White Matter Disease: Causes, Symptoms, Treatment

White matter disease is the wearing away of tissue in the largest and deepest part of your brain that has a number of causes, including aging. This tissue contains millions of nerve fibers, or axons, that connect other parts of the brain and spinal cord and signal your nerves to talk to one another. A fatty material called myelin protects the fibers and gives white matter its color.

This type of brain tissue helps you think fast, walk straight, and keeps you from falling. When it becomes diseased, the myelin breaks down. The signals that help you do these things can’t get through. Your body stops working like it should, much like a kink in a garden hose makes the water that comes out go awry.

White matter disease happens in older or elderly people. There are ways to prevent or even reverse this condition, but you need to start now.

What Causes It?

Many different diseases, injuries, and toxins can cause changes in your white matter. Doctors point to the same blood vessel problems that lead to heart trouble or strokes:

It may be worse for women. You may also be more likely to get it if you have:

• Diabetes
• High cholesterol
• Parkinson’s disease
• History of stroke

Genetics may also play a role.

What Are the Symptoms?

White matter helps you problem-solve and focus. It also plays an important role in mood, walking, and balance. So when something’s wrong with it, you might notice:

• Trouble learning or remembering new things
• A hard time with problem solving
• Slowed thinking
• Leaking urine
• Depression
• Problems walking
• Balance issues and more falls

White matter disease is different from Alzheimer’s, which affects the brain’s gray matter. If you’re having memory problems or a loved one is, a doctor will need to run tests to make a diagnosis.

How Is It Diagnosed?

Advances in medical imaging have made white matter disease easier to spot. A magnetic resonance imaging (MRI) test, which takes pictures of the inside of your brain, can show any damage. Changes to white matter will show up super-bright white (your doctor may call this “hyperintense”) on an MRI scan. You may need more tests to rule out other causes.

How Is It Treated?

There isn’t a specific treatment. The goal is to treat the cause of the damage and stop the disease from getting worse. Your doctor may prescribe medicines to lower your blood pressure or cholesterol.

Can It Be Prevented?

Age-related white matter disease is progressive, meaning it can get worse. But you can take steps to stop it from spreading. Scientists think you might even be able to repair the damage, if you catch it early.

Keep your blood pressure and blood sugar in check. That can lead to white matter changes. To keep your heart healthy, follow a low-fat, low-salt diet, and get about 2 and a half hours of moderate-intensity exercise each week. Manage diabetes if you have it and keep your cholesterol in check. If you smoke, stop now.

White Matter Hyperintensities on MRI

Posted on:May 26, 2017

Last Updated: October 2, 2020

Time to read: 5 minutes

White matter hyperintensities (WMHs) are lesions in the brain that show up as areas of increased brightness when visualised by T2-weighted magnetic resonance imaging (MRI).

WMH’s are also referred to as Leukoaraiosis and are often found in CT or MRI’s of older patients. The prevailing view is that these intensities are a marker of small-vessel vascular disease and in clinical practice, are indicative of cognitive and emotional dysfunction, particularly in the ageing population.

The initial discovery of WMH’s was made in the late 1980’s by Hachinski and colleagues. They described WMH’s as patchy low attenuation in the periventricular and deep white matter.

WHAT DO WMH’S LOOK LIKE ON MRI?

As MRI’s have greater sensitivity to subtle changes in brain water content, they are better at visualising WMH’s. These areas are hyperintense on T2-weighted (T2) and fluid-attenuated inversion recovery (FLAIR) MRI sequences, and by consensus are now referred to as “white matter hyperintensities” (WMH), or “subcortical hyperintensities” where deep gray matter is also involved.

Periventricular White Matter Hyperintensities on a T2 MRI image

WHAT IS THE NEUROPATHOLOGY OF WMH’S?

WMH’s are associated with vascular risk factors such as diabetes, smoking and hypertension and hence WMH’s are considered part of small vessel disease.

Some potential neuropathological associations are:

1. Demyelination and axonal loss
2. Reduced glial density and atrophy
3. Cortical thinning and cerebral atrophy
4. Endothelial and immune activation
5. Ischaemic damage
6. Hypoxia and hypoperfusion

WMH’s are known to disappear as they do not always signify permanent glial or axonal loss; instead subtle shifts in water content.

WHAT IS THE CLINICAL SIGNIFICANCE OF WMH’S?

Until relatively recently, WMH were generally dismissed as inevitable consequences of “normal” advancing age. This is clearly not true. Although WMH do become more common with advancing age, their prevalence is highly variable.

There is strong evidence that WMH are clinically important markers of increased risk of stroke, dementia, death, depression, impaired gait, and mobility, in cross-sectional and in longitudinal studies. They associate with brain damage such as global atrophy and other features of small vessel brain damage, with focal progressive visible brain damage, are markers of underlying subvisible diffuse brain damage, and predict infarct growth and worse outcome after large artery stroke. They could be considered as the neuroimaging marker of brain frailty. (Wardlaw et al., 2015)

A review by Debette and Markus sought to review the evidence of the association between WMHs and the risk of cognitive impairment, dementia, death and stroke.

WMH’S AND STROKE

White matter hyperintensities are a predictor for vascular disease for which age and high blood pressure are the main risk factors.

The review showed that WMHs are significantly associated with an increased risk of stroke. Even when adjusting for vascular disease risk factors, such as age and high blood pressure, this association was still significant.

WMH’S AND COGNITIVE IMPAIRMENT

White matter hyperintensities are also associated with both impaired mobility and reduced cognitive functioning.

Specifically, WMHs can impact on memory, vigilance and executive functioning, depending on its localisation and severity.

Periventricular WMHs can affect cognitive functioning while subcortical WMHs disrupt specific motor functions based on location.

WMH’S AND DEMENTIA

Although WMH’s are associated with a faster decline in global cognitive performance as well as in executive function and processing speed, the jury is out in relation to their association with dementia.

WMH’s have a high association with Vascular dementia but their role in Alzheimer’s dementia is unclear.

According to Debette and Markus –

The presence of white matter hyperintensities may increase the risk that an individual will develop mild cognitive impairment or have declining performances on cognitive tests but may not be enough to facilitate progression from mild cognitive impairment to dementia, the latter being overwhelmingly driven by neurodegenerative lesions. An exception could be the rare cases of pure vascular dementia, where diffuse white matter hyperintensities could be important also at later stages of cognitive decline and conversion.

WMH’S AND MORTALITY

There seems to be a significant association between WMHs and mortality in both the general population and in high-risk populations such as those with a history of stroke and depression.

The Rotterdam and the Framingham Offspring Study showed an association between WMH’s and mortality independent of vascular risk events and risk factors. The association is particularly strong with cardiovascular mortality.

WMH’s may, therefore, be a marker for diffuse vascular involvement including peripheral and coronary arteries increasing the risk of cardiovascular mortality.

WMH’S AND SEVERE AND RESISTANT DEPRESSION

Deep white matter hyperintensities (DWMH’s) are associated with a more severe (melancholic) AND resistant form of depression [Khalaf A et al., 2015] and the patient is more likely to present with cognitive dysfunction, psychomotor slowing, and apathy. [Read more on melancholic depression and association of WMHs with structural melancholia)

They are also closely associated with late-onset depression and their progression is associated with worse outcomes in geriatric depression. [Taylor W et al., 2003]

WMH accumulation occurs over significantly shorter intervals (ie 12 weeks) than has been previously shown. Additionally, these changes are differentially distributed among those patients who are eventually classified as non-remitters, which indicates that the relationship between WMH accumulation and Late life depression (LLD) is consequential even during short antidepressant treatment courses. [Khalaf A et al., 2015]

This ‘Vascular depression’ is regarded as a subtype of late-life depression characterised by a distinct clinical presentation and an association with cerebrovascular damage.

49 year old female presenting with resistant depression and mixed features. Frontal lobe testing showed executive dysfunction. Required augmentation strategies to achieve remission

54 year old female presenting with resistant depression, cognitive impairment and somatic symptomatology

The radiology report for the above patient states –

Moderate to severe leukoaraiosis with scattered areas of T2 hyperintensity involving subcortical white matter, right and left corona radiata of the frontoparietal and to a lesser extent temporal lobes. Area of old cortical damage involving the ventral left frontal and very small area involving the ventral left temporal lobe with some surrounding gliosis, very suggestive of previous trauma.

THE BIG PICTURE

The presence of WMHs significantly increases the risk of stroke, dementia, and death. WMH’S  are significantly associated with resistant depression.

Detecting WMHs by diagnostic brain imaging gives clinicians an opportunity to screen for other vascular risk factors and proactively treat them.

They have important clinical and risk factor associations, and that they should not simply be overlooked as inevitable “silent” consequences of the aging brain.

Want to learn more? We covered the neuropsychiatric aspects of Multiple Sclerosis, an autoimmune condition characterised by significant involvement of white matter.

QUIZ

White Matter Matters | Department of Neurology

White matter inflammation causes the brain-blood barrier to become partially ineffective.

When it comes to diseases of the brain and nervous system, two UC Davis neurology pioneers have a simple way to sum up a lifetime of complex and cutting-edge research: White matter matters.

“White matter is that part of the brain made of cells called ‘axons’ that connect one to the other so that nerves can communicate,” says UC Davis Alzheimer’s Disease Center director Charles DeCarli. “White matter enables the brain to operate intact.”

Full of myelin – a fatty insulation that speeds up nerve impulses – white matter is, of course, white in color, says neurology professor David Pleasure, who directs the Institute for Pediatric Regenerative Medicine, a joint research effort between UC Davis and Shriners Hospitals for Children – Northern California.

Studying Alzheimer’s, multiple sclerosis, cerebral palsy and other neurological impairments, DeCarli and Pleasure have made several profound discoveries that seem to hinge on a simple idea.

“Initially, white matter was not too interesting to the scientific community. But they are slowly coming around.”
— Charles DeCarli, UC Davis Alzheimer’s Disease Center director

High blood pressure, atherosclerosis, inflammation and other basic disease processes may travel the brain on a superhighway of white matter, causing some of neurology’s most mysterious and troubling disorders.

If the nervous system were a computer network, gray matter – a non-myelinated portion that contains nerve cells and capillaries – would be the computers and white matter the cables.

Although diseased white matter impairs the nervous system much like broken, frayed or poorly operating cables impair a computer network, research was mostly focused on gray matter until Charles DeCarli came along.

One of the world’s foremost experts in neurological dementia, DeCarli jokingly refers to himself as “the king of white matter.”

“I have a humorous side, but the moniker reflects that I have been doing research in this area since 1990,” DeCarli says. “Initially, white matter was not too interesting to the scientific community. But they are slowly coming around.”

Brain rust

DeCarli has zeroed in on white matter hyperintensity and its role in dementia.

Seen on brain magnetic resonance images as ultra-white patches, “white matter hyperintensity indicates injury to the axons,” DeCarli explains, “possibly representing loss of blood flow. “

Neurologist Charles DeCarli is zeroing in on the role that vascular disease plays in Alzheimer’s disease.

Also called “brain rust,” DeCarli says that when he began his research in 1990, “everyone thought these hyperintensities were just innocent changes associated with aging.”

He has since focused his attention on an emerging connection between white matter and neurological maladies and their less-mysterious counterparts in other parts of the body: stroke, heart attack, diabetes, hypertension and atherosclerosis.

Stroke and white matter hyperintensities, for instance, share the same risk factors, DeCarli says. “Having these hyperintensities on your brain scan indicates that you are at risk for stroke.”

Referring to it as “the million-dollar question of my research,” DeCarli has sought links between Alzheimer’s disease and white matter hyperintensities.

“We found that hyperintensities injure the frontal lobes of the brain and impair the brain’s ability to manipulate and store information,” he explains. DeCarli’s research team also discovered that white matter hyperintensity-causing vascular disorders add insult to Alzheimer’s injury and might accelerate the disease by damaging axons and weakening neurons.

Using a novel mapping technique, DeCarli has observed that Alzheimer’s patients share large amounts of white matter hyperintensity with a common distribution.

“This is important as it helps us understand what brain connections are impaired,” he explains.

“Once we know which connections are impaired, we can do something to improve those connections.” Obesity, diabetes, high blood pressure and coronary artery disease are well-known menaces to 21st century heart health, but what about their effects on the brain?

“Our current research suggests that some of the changes in memory and thinking associated with aging are actually the consequence of under-treated vascular disease,” DeCarli says.

“There is also some evidence that these diseases can create Alzheimer’s pathology. Forming the plaques and tangles of Alzheimer’s disease may be one way nerve cells in the brain react to injuries of any type.”

He also suspects that an MRI study of obese children and young adults would show increased white matter hyperintensity.

The good news: DeCarli says research indicates that “vascular risk factors are treatable and much of vascular disease is preventable through healthy lifestyle choices.”

Inflammation implications

Pediatric neurologist David Pleasure is studying how inflammation of white matter contributes to certain autoimmune disease like multple sclerosis.

Where DeCarli is studying how reduced blood flow harms white matter, David Pleasure wants to know the impact of inflammation.

Inflamed white matter is implicated in multiple sclerosis, cerebral palsy and several inherited childhood diseases such as adrenoleukodystrophy.

Decoding the pathways that inflammation opens is a puzzle Pleasure is solving with genetic, immune and vascular pieces.

For instance, inflammation causes the normally immunoprivileged central nervous system to become immunocompromised.

“The blood-brain barrier becomes partially ineffective, and peripheral immune cells and antibodies can enter the central nervous system,” Pleasure says.

Once that happens, complications such as multiple sclerosis can result. Using what he calls “the most commonly used model for MS” – experimental autoimmune encephalomyelitis – Pleasure says his team can duplicate “many of the pathological features of MS, trying out new treatment regimens before applying them to patients.”

Pleasure also is focusing on periventricular leukomalacia (PVL) – a disorder of developing white matter in premature infants – that frequently results in cerebral palsy.

Pleasure’s studies on immature oligodendroglia – cells that make myelin – contributed significantly to the understanding of both disorders.

“A common complication of pregnancy – intrauterine infection – increases the incidence of PVL and cerebral palsy by raising levels of inflammatory cytokines, such as interferon-gamma, in the brain of the fetus,” Pleasure says.

Cytokines are signaling proteins that help cells communicate with one another.

Historian of medicine

With a history degree from Yale University, David Pleasure explains medicine like a historian.

“Experimental autoimmune encephalomyelitis was first discovered in the late 19th century, when Louis Pasteur developed an anti-rabies vaccine by growing rabies virus in monkeys,” he says.

And although most people think of MS as a disease of the spinal cord, it has a historical connection with white matter “first described by the French neurologist Jean-Martin Charcot, who named multiple sclerosis back in the late 19th century,” Pleasure explains.

History’s important, and having an historical background gives some perspective to medicine, he says. White matter inflammation causes the brain-blood barrier to become partially ineffective.

“For instance, without Charcot’s discovery that MS affected axons – white matter – as well as myelin, for instance – we would not have the important discovery that followed: that the permanent disability that eventually develops in patients with progressive MS is chiefly due to axonal loss, rather than to demyelination. “

White matter matters

In “The Mysterious Affair at Styles,” Agatha Christie’s quirky Belgian detective Hercule Poirot introduced gray matter into the popular lexicon by tapping his forehead.

“This affair must be unraveled from within,” Poirot said. “These little gray cells. It is up to them.”

Eighty-seven years later, David Pleasure and Charles DeCarli have tapped their own gray cells – and those of the UC Davis research community – to find that it may be up to white matter to unravel the brain’s unique mysteries.

Tension-type headache has association with white matter hyperintensities

by Deena Kuruvilla, MD

One of the most common questions posed to me in my headache practice is “why do I have white spots on my brain?” I often obtain magnetic resonance imaging (MRI) of the brain in my patients with a worrisome story to make sure there is not an underlying cause for the headaches. I then end up with an MRI report that shows white matter hyperintensities (WMH). WMH are lesions in the brain that show up as areas of increased brightness on specific MRI sequences. They may be caused by wear and tear of the cerebral vessels which can result in strokes or in inflammatory disorders such as multiple sclerosis. Migraine patients, especially those with migraine with aura have a higher risk of stroke and cardiovascular disease than the general population. While these associations exist, WMH are usually benign depending on the location and how extensive the lesions are. Benign WMH are found in >90% of people over the age of 60. Larger or more extensive WMH can be seen in cerebrovascular disease, infection, neurodegenerative conditions or multiple sclerosis. Previous studies showed that WMH are more common in patients who experience migraine compared to those who are headache free. In the most recent study about WMH and headache disorders, Honningsvag et al, found that having tension-type headache (TTH) or new onset headache in adulthood is associated with significant WMH. The WMH were specifically found in the deep white matter. Interestingly they did not find an association between WMH and migraine. The finding that WMH are more prominent in TTH suggests that there may be a vascular or inflammatory component to the underlying cause.

In January, the British Medical journal published an article by Adelborg and colleagues which showed that patients with migraine are more likely to have cardiovascular disease, venous thromboembolism, atrial fibrillation and atrial flutter. This finding is relevant for providers and patients because previous research has shown that managing cardiovascular risk factors such as blood pressure, can slow the progression of WMH. While we do not routinely obtain imaging in every person with headache, advanced age or other red flags such as a complicated medical history should certainly prompt providers to consider it.

This study certainly has some pitfalls. It is unclear which definitions were used for tension-type headache and migraine in this study. The authors state that subjects were given a questionnaire to fill out with the details of the headache but the defining points of the headache disorder are unclear. In many cases, we find that what is classified as TTH is truly migraine. We most commonly see this in our Chronic migraine patients who suffer from 15 or more headache days monthly for at least 3 months. Some of these 15 headache days may be mild headache days and incorrectly labeled as TTH.

Articles: http://journals.sagepub.com/doi/pdf/10.1177/0333102418764891
http://www.bmj.com/content/360/bmj.k96

Association of White Matter Hyperintensity Markers on MRI and Long-term Risk of Mortality and Ischemic Stroke

Abstract

Objective To determine whether white matter hyperintensity (WMH) markers on MRI are associated with long-term risk of mortality and ischemic stroke.

Methods We included consecutive patients with manifest arterial disease enrolled in the Second Manifestations of Arterial Disease–Magnetic Resonance (SMART-MR) study. We obtained WMH markers (volume, type, and shape) from brain MRI scans performed at baseline using an automated algorithm. During follow-up, occurrence of death and ischemic stroke was recorded. Using Cox regression, we investigated associations of WMH markers with risk of mortality and ischemic stroke, adjusting for demographics, cardiovascular risk factors, and cerebrovascular disease.

Results We included 999 patients (59 ± 10 years; 79% male) with a median follow-up of 12.5 years (range 0.2–16.0 years). A greater periventricular or confluent WMH volume was independently associated with a greater risk of vascular death (hazard ratio [HR] 1.29, 95% confidence interval [CI] 1.13–1.47) for a 1-unit increase in natural log-transformed WMH volume and ischemic stroke (HR 1.53, 95% CI 1.26–1.86). A confluent WMH type was independently associated with a greater risk of vascular (HR 1.89, 95% CI 1.15-3.11) and nonvascular death (HR 1.65, 95% CI 1.01–2.73) and ischemic stroke (HR 2. 83, 95% CI 1.36-5.87). A more irregular shape of periventricular or confluent WMH, as expressed by an increase in concavity index, was independently associated with a greater risk of vascular (HR 1.20, 95% CI 1.05–1.38 per SD increase) and nonvascular death (HR 1.21, 95% CI 1.03–1.42) and ischemic stroke (HR 1.28, 95% CI 1.05–1.55).

Conclusions WMH volume, type, and shape are associated with long-term risk of mortality and ischemic stroke in patients with manifest arterial disease.

Glossary

CI=

confidence interval;

CSVD=

cerebral small vessel disease;

FLAIR=

fluid-attenuated inversion recovery;

HR=

hazard ratio;

SMART-MR=

Second Manifestations of Arterial Disease–Magnetic Resonance;

TE=

echo time;

TI=

inversion time;

TR=

repetition time;

WMH=

white matter hyperintensities

White matter hyperintensities (WMH) of presumed vascular origin are frequently observed in older individuals on brain MRI and are an important cause of cognitive decline and dementia. ^1,-,3 They are considered hallmark features of cerebral small vessel disease (CSVD).^4,5

WMH are heterogeneous lesions that correspond to different underlying brain parenchymal changes.^6,-,8 Previous studies on CSVD mainly focused on WMH volume as a marker for CSVD severity.^4,9,-,12 However, there is evidence to suggest that other markers of WMH may also provide clinically relevant information on severity and prognosis of CSVD.^6,7,13,-,16 Specifically, histopathologic studies reported that smooth and periventricular WMH are associated with mild changes of the brain parenchyma, whereas irregular and confluent WMH are associated with more severe parenchymal changes, including loss of myelin and incomplete parenchymal destruction.^6,13 We previously developed an automated MRI method to assess in vivo advanced WMH markers (volume, type, and shape).¹⁴ Using this algorithm, we reported differences in advanced WMH markers such as shape in frail elderly patients, patients with diabetes mellitus, and patients with lacunes on MRI. ^14,-,16 These findings suggest that advanced WMH MRI markers may provide clinically important information on CSVD severity.

The relationship between advanced WMH markers and long-term clinical outcomes, however, is not clear. Examining this relationship is of importance as WMH markers may aid in future patient selection for preventive treatment to ameliorate the risk of CSVD-related death and ischemic stroke. Therefore, in the present study, we aimed to assess whether WMH volume, type, and shape were associated with greater risk of mortality (including vascular death) and ischemic stroke in patients with manifest arterial disease over 12 years of follow-up.

Methods

Standard Protocol Approvals, Registrations, and Patient Consents

The Second Manifestations of Arterial Disease–Magnetic Resonance (SMART-MR) study was approved by the medical ethics committee of the University Medical Center Utrecht according to the guidelines of the Declaration of Helsinki of 1975. Written informed consent was obtained from all patients participating in the SMART-MR study.

Study Population

We used data from the SMART-MR study.¹⁷ The SMART-MR study is a prospective cohort study at the University Medical Center Utrecht with the aim of investigating risk factors and consequences of brain changes on MRI in patients with manifest arterial disease.¹⁷ A total of 1,309 middle-aged and older adult patients referred to our medical center for treatment of manifest arterial disease (cerebrovascular disease, manifest coronary artery disease, abdominal aortic aneurysm, or peripheral arterial disease) were included for baseline measurements between 2001 and 2005.¹⁷ During a 1-day visit to the University Medical Center Utrecht, ultrasonography of the carotid arteries to measure the intima–media thickness (mm), blood and urine samplings, a physical examination, neuropsychological assessment, and a 1.5T brain MRI scan were performed.¹⁷ We used questionnaires for the assessment of demographics, medical history, risk factors, medication use, and cognitive and physical functioning. ¹⁷

Vascular Risk Factors

We assessed age, sex, smoking habits, and alcohol intake at baseline using questionnaires. The body mass index (BMI) was calculated (kg/m²) by measuring weight and height. We measured systolic blood pressure (mm Hg) and diastolic blood pressure (mm Hg) 3 times with a sphygmomanometer and the average of these measurements was calculated. Hypertension was defined as a mean systolic blood pressure of >160 mm Hg, a mean diastolic blood pressure of >95 mm Hg, or the self-reported use of antihypertensive drugs.¹⁷ To determine glucose and lipid levels, an overnight fasting venous blood sample was taken. We defined diabetes mellitus as a fasting serum glucose level of ≥7.0 mmol/L or use of glucose-lowering medication or a known history of diabetes.¹⁷ The degree of carotid artery stenosis at both sides was assessed with color Doppler-assisted duplex scanning using a 10 MHz linear-array transducer (ATL Ultramark 9). ¹⁸ Blood flow velocity patterns were used to evaluate the severity of carotid artery stenosis and the greatest stenosis observed on the left or right side of the common or internal carotid artery was taken to determine the severity of carotid artery disease.¹⁸ We defined a carotid artery stenosis ≥70% as a peak systolic velocity >210 cm/s.¹⁸

Brain MRI

MRI of the brain was performed on a 1.5T whole-body system (Gyroscan ACS-NT; Philips Medical Systems, Best, the Netherlands) using a standardized scan protocol.^17,19 Transversal fluid-attenuated inversion recovery (FLAIR) (repetition time [TR] 6,000 ms; echo time [TE] 100 ms; inversion time [TI] 2,000 ms), T1-weighted (TR 235 ms; TE 2 ms), T1-weighted inversion recovery (TR 2,900 ms; TE 22 ms; TI 410 ms), and T2-weighted images (TR 2,200 ms; TE 11 ms) were acquired with a voxel size of 1.0 × 1.0 × 4.0 mm³ and contiguous slices.^14,19 A neuroradiologist blinded to patient characteristics visually rated brain infarcts on the T1-weighted, T2-weighted, and FLAIR images of the MRI scans. We defined lacunes as focal lesions between 3 and 15 mm according to the STRIVE criteria.⁴ Nonlacunar lesions were categorized into large infarcts (i.e., cortical infarcts and subcortical infarcts not involving the cerebral cortex) and those located in the brainstem or cerebellum.¹⁴

WMH Volumes

WMH and brain volumes (intracranial volume and total brain volume) were obtained using the k-nearest neighbor (kNN) automated segmentation program on the T1-weighted, FLAIR, and T1-weighted inversion recovery sequences of the MRI scans.^19,20 WMH segmentations were visually assessed by an investigator (R.G.) using an image processing framework (MeVisLab 2.7.1.; MeVis Medical Solutions AG, Bremen, Germany) to ensure that cerebral infarcts were correctly removed from the WMH segmentations.¹⁴ Next, we performed ventricle segmentation using the fully automated lateral ventricle delineation (ALVIN) algorithm in Statistical Parametric Mapping 8 (SPM8, Wellcome Trust Centre for Neuroimaging, University College London, UK) for MATLAB (The MathWorks, Inc. , Natick, MA).¹⁴ The procedure is described in detail elsewhere.^14,21 We labeled WMH according to their continuity with the margins of the lateral ventricle and their extension from the lateral ventricle into the white matter.¹⁴ Periventricular WMH were defined as lesions contiguous with the margins of the lateral ventricles and extending up to 10 mm from the lateral ventricle into the white matter.¹⁴ We defined confluent WMH as lesions contiguous with the margins of the lateral ventricles and extending more than 10 mm from the lateral ventricles into the white matter.¹⁴ We defined deep WMH as lesions that were separated from the margins of the lateral ventricles.¹⁴ Examples of periventricular, confluent, and deep WMH visualized in our algorithm are shown in figure 1. Total WMH volume was calculated as the sum of deep WMH and periventricular or confluent WMH.

Figure 1 White Matter Hyperintensities (WMH) on Fluid-Attenuated Inversion Recovery (FLAIR) Images With Corresponding Visualizations in the Automated Algorithm

Examples of confluent (A), periventricular (B), and deep (C) WMH on FLAIR images with the corresponding visualizations in our algorithm shown below. The deep WMH lesion (arrow) is reconstructed in the coronal view, while the periventricular and confluent WMH are viewed from a transverse perspective. Note that the coronal reconstruction of the deep WMH lesion (C) may be influenced by the slice thickness and the lesion may be more punctiform. The confluent WMH lesion in (A) showed a volume of 11.57 mL with an accompanying deep WMH volume of 0.25 mL. The periventricular WMH lesion in (B) showed a volume of 4.98 mL without any accompanying deep WMH lesions. The deep WMH lesion in (C) showed a volume of 0.02 mL with an accompanying periventricular and deep WMH volume of 2.12 and 0.49 mL, respectively.

WMH Types

We categorized patients into the following 3 WMH types: periventricular WMH type without deep WMH, periventricular WMH type with deep WMH, and a confluent WMH type. We did not categorize the latter type according to presence or absence of deep WMH as the number of patients with a confluent WMH without deep WMH (n = 5) was insufficient to perform statistical analyses. ¹⁴

WMH Shape Markers

We hypothesized that a more irregular shape of WMH may indicate more severe cerebral parenchymal damage based on previous histopathologic studies.^{6,-,8,13,22,23} The degree to which deep WMH are punctiform or ellipsoidal may also provide information on CSVD severity.¹⁵

Irregularity of periventricular or confluent WMH was quantified using the concavity index and fractal dimension. In previous work, we established that the concavity index was a robust shape marker that showed a normal distribution in the study sample and provided information on WMH shape irregularity based on volume and surface area.^14,24 The concavity index was calculated by reconstructing convex hulls and calculating volume and surface area ratios of lesions, in which a higher concavity index value corresponds to a more irregular shape of periventricular or confluent WMH.¹⁴ Fractal dimension was calculated using the box counting method and was used to quantify irregularity of periventricular or confluent WMH and of deep WMH. ^14,25,26 A higher fractal dimension value indicated a more irregular WMH shape. As patients frequently show multiple deep WMH, a mean value for the fractal dimension was calculated across all deep WMH per patient.

The degree to which deep WMH are punctiform or ellipsoidal was assessed using the eccentricity, which was calculated by dividing the minor axis of a deep WMH lesion by its major axis.^14,15 A high eccentricity value corresponded to a punctiform deep WMH lesion, whereas a low value corresponded to an ellipsoidal lesion.^27,28 A mean value for the eccentricity was calculated across all deep WMH per patient.

Clinical Outcomes

Patients received a questionnaire every 6 months to provide information on outpatient clinic visits and hospitalization.¹⁸ If a fatal or nonfatal event was reported, original source documents were obtained and reviewed to determine the cause of the event. All possible events were audited independently by 3 physicians of the end point committee. ¹⁸ Follow-up of patients was performed until death, refusal of further participation, or loss to follow-up. Vascular-related death was defined as death caused by myocardial infarction, stroke, sudden death (unexpected cardiac death occurring within 1 hour after onset of symptoms, or within 24 hours given convincing circumstantial evidence), congestive heart failure, or rupture of an abdominal aortic aneurysm.¹⁸ We defined nonvascular-related death as death caused by cancer, infection, unnatural death, or death from another nonvascular cause.¹⁸ Ischemic stroke was defined as the occurrence of relevant clinical features that caused an increase in impairment of at least 1 grade on the modified Rankin Scale, with or without a new relevant ischemic lesion on brain imaging.¹⁸

Study Sample

Of the 1,309 patients included, MRI data were irretrievable for 19 patients and 239 patients had missing data of one or more MRI sequences due to logistic reasons or motion artifacts. Forty-four of the remaining 1,051 patients had unreliable brain volume data due to motion artifacts in all 3 MRI sequences. Four patients were excluded due to undersegmentation of WMH by the automated segmentation algorithm and another 4 patients were excluded because they did not have any WMH greater than 5 voxels. As a result, 999 patients were included in the current study.

Statistical Analysis

Baseline characteristics of the study sample were reported as means or percentages where applicable.

Patients were followed from the date of the MRI until ischemic stroke, death, loss to follow-up, or end of follow-up (March 2017), whichever came first. Cox proportional hazard analysis was used to estimate hazard ratios (HRs) for the occurrence of all-cause, vascular-related, and nonvascular-related death and ischemic stroke associated with WMH volumes, type, and shape markers. The proportional hazards assumption was checked by inspection of Schoenfeld residuals. We concluded that the proportional hazards assumption was met for all covariates.

To reduce the risk of bias due to complete case analysis, we performed chained equations imputation on missing covariates to generate 10 imputed datasets using SPSS 25.0 (Chicago, IL).²⁹ The Cox regression analyses were performed on the imputed datasets and the pooled results were presented. We used SAS 9.4 (SAS Institute, Cary, NC) and SPSS 25.0 (Chicago, IL) to perform the statistical analyses.

WMH Volumes and Clinical Outcomes

To assess whether WMH volumes were associated with clinical outcomes, we separately entered total, periventricular or confluent, and deep WMH volumes in a Cox regression model with age, sex, and intracranial volume as covariates and all-cause death, vascular-related death, nonvascular-related death, and ischemic stroke as outcomes. WMH volumes were natural log-transformed due to a non-normal distribution. In a second model, we in addition adjusted for large infarcts, lacunes, diastolic blood pressure, systolic blood pressure, diabetes mellitus, body mass index, and smoking pack-years at baseline. We also assessed the association between quartiles of WMH volumes (not natural log-transformed) and clinical outcomes, adjusted for all of the aforementioned covariates.

WMH Types and Clinical Outcomes

To assess whether WMH types were associated with clinical outcomes, a categorical variable with the 3 WMH types as outcomes was entered in a Cox regression model with age and sex as covariates and all-cause death, vascular-related death, nonvascular-related death, and ischemic stroke as outcomes. A periventricular WMH type without deep WMH was chosen as the reference category as this type represents the smallest WMH burden. In a second model, we in addition adjusted for the aforementioned covariates.

WMH Shape Markers and Clinical Outcomes

Z scores of WMH shape markers were calculated to facilitate comparison and these were entered in a Cox regression model with age and sex as covariates and all-cause death, vascular-related death, nonvascular-related death, and ischemic stroke as outcomes. In a second model, we in addition adjusted for the aforementioned covariates. If an association between a WMH shape marker and clinical outcome was observed, we in addition adjusted for total WMH volume to assess whether the association was independent of WMH volume.

Data Availability

For use of anonymized data, a reasonable request has to be made in writing to the study group and the third party has to sign a confidentiality agreement.

Results

Baseline characteristics of the study sample (n = 999) are shown in table 1. A total of 784 patients (78%) had periventricular WMH and 215 patients (22%) had confluent WMH. A periventricular with deep WMH type was present in 423 patients (42%) and a periventricular without deep WMH type was present in 361 patients (36%). In total, 274 patients died (149 vascular-related and 125 nonvascular-related) and 75 patients had an ischemic stroke during a median follow-up of 12.5 years (range 0.2–16.0 years; total number of person-years follow-up 11,303).

Table 1

Baseline Characteristics of the Study Sample (n = 999)

Associations Between WMH Volumes and Long-term Clinical Outcomes

Greater total WMH volume was associated with all-cause death (HR 1.32, 95% confidence interval [CI] 1.19–1.46 for a 1-unit increase in natural log-transformed total WMH volume), particularly vascular-related death (HR 1.47, 95% CI 1.29–1.68) and to a lesser extent nonvascular-related death (HR 1.15, 95% CI 0.99–1.34), as well as with ischemic stroke (HR 1.79, 95% CI 1.48–2.16), adjusted for age, sex, and total intracranial volume. These associations persisted after adjusting for cardiovascular risk factors and cerebrovascular disease (table 2).

Table 2

Results of Cox Proportional Hazard Regression Analyses With Total, Periventricular or Confluent, and Deep White Matter Hyperintensity (WMH) Volumes (All Natural Log-Transformed) as Independent Variables and All-Cause, Vascular-Related, and Nonvascular-Related Death and Ischemic Stroke as Dependent Variables

Greater periventricular or confluent WMH volume was associated with all-cause death (HR 1. 29, 95% CI 1.17–1.42), particularly vascular-related death (HR 1.43, 95% CI 1.26–1.63), and to a lesser extent with nonvascular-related death (HR 1.14, 95% CI 0.99–1.32), as well as with ischemic stroke (HR 1.73, 95% CI 1.45–2.08). These associations persisted after adjusting for cardiovascular risk factors and cerebrovascular disease (table 2).

Greater deep WMH volume was associated with all-cause death (HR 1.13, 95% CI 1.04–1.24), vascular-related death (HR 1.15, 95% CI 1.03–1.30), and more strongly with ischemic stroke (HR 1.24, 95% CI 1.05–1.46). Risk estimates slightly attenuated after adjusting for cardiovascular risk factors and cerebrovascular disease (table 2). A nonsignificant association was observed between greater deep WMH volume and nonvascular death (HR 1.10, 95% CI 0.96–1.26), which did not change after adjusting for cardiovascular risk factors and cerebrovascular disease (table 2).

Risk of vascular-related death and ischemic stroke increased per quartile of periventricular or confluent WMH volume (figure 2). Similarly, risk of ischemic stroke increased per quartile of deep WMH volume (figure 3).

Figure 2 Risk of Mortality and Ischemic Stroke in Relation to Quartiles of Periventricular or Confluent White Matter Hyperintensity (WMH) Volume at Baseline

Associations between quartiles of periventricular or confluent WMH volume and risk of all-cause death, vascular death, nonvascular death, and ischemic stroke. Results adjusted for age, sex, intracranial volume, large infarcts on MRI, lacunes on MRI, diastolic blood pressure, systolic blood pressure, diabetes mellitus, body mass index, and smoking pack-years at baseline. The lowest quartile (<0.33 mL) was chosen as the reference category. Range second to fourth quartiles; 0.33–0.74 mL, 0.74–2.04 mL, ≥2.04 mL, respectively. Note that the scale of the y-axis may differ between outcomes. Examples of periventricular or confluent WMH from each quartile are shown in supplemental figure e-1 (available from Dryad: doi.org/10.5061/dryad.qv9s4mwd3). CI = confidence interval.

Figure 3 Risk of Mortality and Ischemic Stroke in Relation to Quartiles of Deep White Matter Hyperintensity (WMH) Volume at Baseline

Associations between quartiles of deep WMH volume and risk of all-cause death, vascular death, nonvascular death, and ischemic stroke. Results adjusted for age, sex, intracranial volume, large infarcts on MRI, lacunes on MRI, diastolic blood pressure, systolic blood pressure, diabetes mellitus, body mass index, and smoking pack-years at baseline. The lowest quartile (<0.03 mL) was chosen as the reference category. Range second to fourth quartiles; 0.03–0.08 mL, 0.08–0.35 mL, ≥0.35 mL, respectively. Note that the scale of the y-axis may differ between outcomes. CI = confidence interval.

Associations Between WMH Types and Long-term Clinical Outcomes

Compared to a periventricular WMH type without deep WMH, a confluent WMH type was associated with a greater risk of all-cause death (HR 2.29, 95% CI 1.64–3.19), particularly vascular-related death (HR 2.81, 95% CI 1.75–4.49) and to a lesser extent nonvascular-related death (HR 1.85, 95% CI 1.15–2.98), as well as with ischemic stroke (HR 4.36, 95% CI 2.20–8.65). These associations persisted after adjusting for cardiovascular risk factors and cerebrovascular disease (table 3). Nonsignificant associations were observed between a periventricular WMH type with deep WMH and vascular-related death (HR 1.53, 95% CI 0.96–2.42) and ischemic stroke (HR 1.75, 95% CI 0.90–3.41), which attenuated after adjusting for cardiovascular risk factors and cerebrovascular disease (table 3).

Table 3

Results of Cox Proportional Hazard Regression Analyses With White Matter Hyperintensity (WMH) Types as Independent Variables and All-Cause, Vascular-Related, and Nonvascular-Related Death and Ischemic Stroke as Dependent Variables

Associations Between WMH Shape Markers and Long-term Clinical Outcomes

A greater concavity index of periventricular or confluent WMH was associated with a greater risk of all-cause death (HR 1.30, 95% CI 1.18–1.43 per SD increase), particularly vascular-related death (HR 1.34, 95% CI 1.18–1.52) and to a lesser extent nonvascular-related death (HR 1.25, 95% CI 1.07–1.45), as well as with ischemic stroke (HR 1.47, 95% CI 1.23–1.76), adjusted for age and sex. These associations persisted after adjusting for cardiovascular risk factors and cerebrovascular disease (table 4). After in addition adjusting for total WMH volume, the association of concavity index with all-cause and nonvascular-related death persisted (HR 1.21, 95% CI 1.02–1.42; HR 1.23, 95% CI 1.02–1.49, respectively), whereas the association with vascular-related death and ischemic stroke attenuated (HR 1.11, 95% CI 0.89–1.39; HR 1.23, 95% CI 0.95–1.77, respectively).

Table 4

Results of Cox Proportional Hazard Regression Analyses With Standardized White Matter Hyperintensity (WMH) Shape Markers as Independent Variables and All-Cause, Vascular-Related, and Nonvascular-Related Death and Ischemic Stroke as Dependent Variables

A greater fractal dimension of periventricular or confluent WMH was associated with a greater risk of all-cause death (HR 1.33, 95% CI 1.16–1.52 per SD increase), vascular-related death (HR 1.52, 95% CI 1.27–1.82), and ischemic stroke (HR 2.06, 95% CI 1.60–2.65), adjusted for age and sex. These relationships persisted after adjusting for cardiovascular risk factors and cerebrovascular disease (table 4). After in addition adjusting for total WMH volume, the association of fractal dimension with all-cause death, vascular-related death, and ischemic stroke attenuated (HR 1.10, 95% CI 0.93–1.30; HR 1.20, 95% CI 0.95–1.51; HR 1.09, 95% CI 0.52–2.27, respectively). A greater fractal dimension of periventricular or confluent WMH was not associated with a greater risk of nonvascular-related death (HR 1.13, 95% CI 0.92–1.37).

No associations were observed between eccentricity and fractal dimension of deep WMH and long-term clinical outcomes (table 4).

Discussion

In this cohort of patients with manifest arterial disease, we observed that WMH volume, type, and shape were associated with long-term clinical outcomes. Specifically, we found that a greater volume and a more irregular shape of periventricular or confluent WMH were related to a higher risk of death and ischemic stroke. A confluent WMH type was also associated with a greater risk of death and ischemic stroke. These relationships were independent of demographics, cardiovascular risk factors, and cerebrovascular disease at baseline.

Our finding that total WMH volume was related to risk of mortality and stroke is in line with previous studies.^30,-,34 However, the associations of WMH volume subclassifications and WMH types with clinical outcomes presented in this study are novel. We found that the risk of mortality and ischemic stroke was predominantly determined by the volume of periventricular or confluent WMH, rather than the volume of deep WMH. This was supported by the observation that risk estimates for mortality and ischemic stroke were higher for a confluent WMH type than a periventricular WMH type with deep WMH. A possible explanation for this finding may be that confluent WMH represent more severe parenchymal changes due to their relatively central location in the brain. Previous studies showed that pathologic changes in the smaller vessels of the brain can induce secondary ischemia, which may be more profound in the white matter surrounding the lateral ventricles as these regions are furthest removed from collateral circulation.^4,35 This notion may explain the relatively strong association between a confluent WMH type and occurrence of ischemic stroke in the present study.

To our knowledge, no previous studies reported on the longitudinal association of WMH shape with clinical outcomes. In the present study, we observed that a more irregular shape of periventricular or confluent WMH was related to an increased risk of mortality and ischemic stroke, which was only partly explained by WMH volume. An explanation for this finding may be that CSVD consists of a heterogeneous group of small vessel changes and a more irregular shape of WMH may indicate the presence of a more severe CSVD subtype.^35,36 Support for this notion is provided by histopathologic studies that reported ischemic damage, loss of myelin, and incomplete parenchymal destruction in more irregular shaped WMH, whereas smooth WMH correlated with more benign pathologic changes such as venous congestion.^6,8,13 Furthermore, a previous study reported an association between a more irregular shape of WMH and frailty in elderly patients¹⁶ and in previous work we showed that presence of lacunes on MRI was related to a more irregular shape of WMH.¹⁴ These investigations and the results of the present study suggest that in addition to WMH volume, shape of WMH may represent a clinically relevant marker in patients with WMH on MRI.

We observed that a confluent WMH type and a more irregular shape of periventricular or confluent WMH were not only associated with a greater risk of vascular death, but also of nonvascular death. In previous work, we similarly reported that presence of lacunes on MRI was related to a greater risk of nonvascular death.³⁷ An explanation for these findings is that CSVD may be a marker of overall increased vulnerability to adverse outcomes, possibly through the concomitant presence of generalized microvascular disease.^2,4,35 Further studies in different cohorts are needed to confirm this hypothesis, but the reported associations with vascular and nonvascular death suggest that WMH markers may be important in determining overall prognosis of patients with manifest arterial disease.

Key strengths of the present study are the large number of patients included, the longitudinal design, the relatively long follow-up period, and the use of automated image processing techniques that enabled us to examine multiple and also novel features of WMH in relation to clinical outcomes. Furthermore, all MRI scans were visually checked and corrected if needed to ensure that WMH segmentation and subsequent analysis of WMH type and shape were accurate.

Limitations of this study include, first, the use of 1.5T MRI instead of 3.0T MRI, which is likely more sensitive in detecting small WMH lesions. Clinical 3.0T MRI scanners were not readily available during the inclusion period of our study, starting in 2001. Second, we did not categorize deep WMH into lesions located directly under the cerebral cortex (i.e., infracortical) and those located more centrally in the subcortical white matter, which may differ in terms of etiology.³⁸ Third, MRI sequences were used with a relatively large slice thickness of 4 mm, which is likely less accurate in determining WMH shape markers than 3D MRI sequences. The impact of slice thickness, however, may be less profound on measurements of the concavity index as it is calculated by determining volume and surface area ratios of periventricular or confluent WMH, which are expected to remain relatively constant.¹⁴ On the other hand, a more profound impact can be expected on measurements of the fractal dimension, which is directly dependent on voxel size.¹⁴ A larger slice thickness will therefore lead to reduced information in the z-axis. Similarly, shape determination of smaller deep WMH in the size range of several millimeters may also be affected by a relatively large slice thickness. Despite this limitation, however, we were able to detect associations between WMH shape markers and clinical outcomes, suggesting that WMH shape may represent a clinically relevant marker for occurrence of ischemic stroke and death.

Our findings demonstrate that WMH volume, type, and shape are associated with long-term risk of mortality and ischemic stroke in patients with manifest arterial disease. These findings suggest that WMH markers on MRI may be useful in determining patient prognosis and may aid in future patient selection for preventive treatment.

Study Funding

Funding for this article was received as part of a grant from the Netherlands Organization for Scientific Research–Medical Sciences (NWO-MW: project 904-65-095). This funding source had no role in the design, data collection, data analyses, or data interpretation of the study or writing of the report. Funding also was received from the European Research Council under the European Union’s Horizon 2020 Programme (h3020)/ERC grant agreements 637024 and 66681 (SVDs@target).

Acknowledgment

The authors thank the research nurses, R. van Petersen (data manager), and B. van Dinther (study manager).

Appendix 1 Authors

Appendix 2 The Utrecht Cardiovascular Cohort-Second Manifestations of Arterial Disease Study Group

Footnotes

• Go to Neurology.org/N for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article.

• The Article Processing Charge was funded by European Research Council.

• The Utrecht Cardiovascular Cohort-Second Manifestations of Arterial Disease Study Group is listed in Appendix 2.

• Editorial, page 781

• Received July 5, 2020.
• Accepted in final form January 28, 2021.

• Copyright © 2021 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology.

A View Into the MS Brain: What New Imaging Techniques Reveal

Gray Matter Is Made of Nerve Cell Bodies, or Neurons

Gray matter, made up of the cells of the central nervous system called neurons, is thickly located in the outer areas of the brain, called the cortex. If you look at the outside of the brain, it looks gray.

“The white matter carries messages from point A to point B,” Stone says. “The gray matter is point A and point B.”

As MS progresses, changes occur in the gray matter that are different from those occurring in the white matter.

“If you cut off the connections between nerve cells, they eventually die,” Voskuhl explains. “This causes a shrinking of brain tissue, called gray matter atrophy. MS causes inflammation in white matter and atrophy in gray matter. You can measure atrophy by actual loss of brain volume.”

But demyelination and lesions can also happen in gray matter, even if this isn’t visible using conventional magnetic resonance imaging (MRI) scans, according to Léorah Freeman, MD, PhD, a neurologist and assistant professor at Dell Medical School at the University of Texas at Austin.

In fact, Dr. Freeman says, “We know from postmortem studies that in the most severe cases, up to 70 percent of the gray matter can be demyelinated” in people with MS.

Newer Types of MRI and PET Scans Reveal Disease Progression in the MS Brain

Researchers and doctors who treat MS commonly use MRI scans to study the brain. MRI is imaging created with computers and radio wave energy. New types of MRI provide more detail, making it easier to see gray matter.

Magnetic resonance spectroscopy shows areas of the brain where proteins found only inside neurons are located.

Functional MRI (fMRI) makes images of the brain while a person is doing a specific task, like reading. When fewer areas light up during this test, it may be a sign of gray matter atrophy.

Gray matter damage has been shown to play an important role in MS disease progression, according to a study study published in July 2013 in the journal Annals of Neurology that followed more than 400 people with relapsing-remitting MS.

Using a model that included a patient’s age, gray matter lesions, and gray matter atrophy, researchers were able to correctly predict MS progression in about 94 percent of participants who maintained relapsing-remitting MS status, and 88 percent of those who transitioned to the secondary-progressive stage.

Knowledge of how gray matter damage affects MS has lagged behind what’s known about white matter, due to the limitations of conventional imaging techniques.

“It’s easy to see white matter inflammation, because it lights up like a Christmas tree on MRI,” Stone says. “Gray matter atrophy is harder to see. Eventually, it shows up as an increase in the fluid-filled parts of the brain as the brain shrinks. But that can be confusing, because the truth is that everybody’s brain shrinks over time — with or without MS.”

Freeman notes that newer imaging techniques, like positron emission tomography (PET), can help identify gray matter changes that may not be visible on a conventional MRI.

In a small pilot study published in October 2015 in the journal Annals of Neurology, a research team led by Freeman found that PET scans could effectively map and reveal measurements of neuronal damage in the gray matter of people with various stages of MS.

Symptoms of Gray and White Matter Disease

“In general, white matter disease causes acute MS symptoms, like numbness and weakness,” Stone says. “Gray matter disease causes progressive symptoms, like fatigue and memory loss. These higher brain functions are called cognitive functions. Most MS disability actually comes from cognitive dysfunction.”

Voskuhl provides another angle: “I think it makes sense to think of some white matter damage like inflammation as temporary, and some gray matter damage like neuron loss as permanent,” she says. “It’s important to know that cognitive changes in MS are not like in Alzheimer’s disease. They don’t affect a person’s intelligence, long-term memory, or their ability to read or carry on a conversation.”

It’s the cumulative damage to both gray and white matter that adds up to MS symptoms, Stone adds. The problem is that even with increasingly detailed imaging techniques, visible changes in the brain don’t correlate exactly with symptoms like fatigue or cognitive impairment.

“Part of the whole discussion is that we are missing something in MS, and we are constantly trying to figure out what it is we are missing,” says Stone.

Freeman is optimistic that advances in imaging will make it easier to pinpoint how communication between different areas of the brain contributes to a wide range of MS symptoms. “We’re trying to make more correlations between specific symptoms and specific locations of lesions or damage,” she notes.

Better Imaging May Lead to Better Drugs for MS

Gaining a better understanding of how MS operates in the brain is critical to developing the next generation of MS drugs, according to Voskuhl.

“We have drugs that can suppress the immune system, reduce MS attacks, and decrease white matter damage. But what we need now are drugs that prevent or reverse long-term disability of all types, including not only cognition but also walking, balance, and vision,” Voskuhl says. “Research focused on gray matter protection may be the critical next step in this goal.”

Freeman notes that recent advances in imaging, and the better understanding of gray matter damage that they allow, are already affecting how trials of potential new MS drugs are conducted.

“Clinical trials are more consistently looking at the impact of the drug on brain atrophy” in different gray matter structures, Freeman says, “because those are meaningful end points” that the U.S. Food and Drug Administration (FDA) is interested in.

Aside from informing new drug development, advances in imaging may also prove useful to doctors in deciding what course of treatment is best for an individual patient, according to Freeman. Her lab is studying computing techniques to extract more meaningful information from conventional MRIs that are already part of the standard of MS care.

“Right now, the information we’re using from these MRIs to monitor therapy is [whether] patients develop new or active lesions within the white matter,” Freeman explains. “I think we could be using MRI in a different way, to maybe predict treatment response before we even start therapy.”

Artificial Intelligence Could Play a Role in MS Treatment Advances

This vision of MS imaging and treatment could involve using artificial intelligence (AI) technologies to look at the entire brain in MRI scans, and predict individual outcomes and responses to different MS drugs.

In this way, AI could help doctors know “what therapy we should initiate, or when it is time to switch, before patients fail their medication,” says Freeman, as part of a “move from a trial-and-error approach to therapy, and more into a personalized, precision-medicine approach to therapy.”

The best way to get there, the experts agree, is to keep developing and refining imaging techniques that advance our knowledge of the MS brain.

Additional reporting by Quinn Phillips.

Cerebral White Matter Hyperintensities on MRI: Current Concepts and Therapeutic Implications – FullText – Cerebrovascular Diseases 2006, Vol. 22, No. 2-3

Abstract

Background: White matter hyperintensities (WMH) are commonly observed MRI abnormalities in the elderly, which generally reflect covert vascular brain injury. WMH cumulatively produce substantial neurologic, psychiatric, and medical morbidity. This review provides an overview of current knowledge on vascular WMH, and describes some pharmacological agents that may have a role in mitigating this condition. Summary of Review: This review has two main focus areas. The first is a discussion of currently available knowledge regarding the public health burden, pathogenesis, and various risk factors associated with the presence of vascular white matter lesions noted on brain MRI. The second section of the article details the mechanistic and clinical basis for promising pharmacological treatment modalities that could potentially prevent progression of ischemic cerebral white matter brain injury. Many of these therapies are already of proven efficacy in preventing recurrent stroke. Conclusions: Individuals with vascular white matter lesions on MRI may represent a potential target population likely to benefit from secondary stroke prevention therapies.

© 2006 S. Karger AG, Basel

Current Concepts

Public Health Burden of Ischemic White Matter Injuries

About 750,000 Americans experience first-ever or recurrent stroke annually [1, 2]. However, these estimates reflect only clinically manifest, symptomatic strokes and fail to take into account the annual toll of vascular cerebral white matter injury within the American population. In the elderly, symptomatic stroke has a prevalence of 4.7% [3], but MRI white matter hyperintensities (WMH) are found in a significant proportion of the community-dwelling elderly population and the incidence of these lesions approaches 100% by the age of 85 [4, 5]. WMH may initially produce no symptoms or only mild, nonspecific and/or unrecognized symptoms, but eventually can lead to substantial neurological, psychiatric, and medical morbidity. WMH are associated with cognitive dysfunction, frank dementia, depression [6, 7], psychosis, gait impairment and falls [8,9,10], hand incoordination [9, 10], and markedly increased risk of future symptomatic stroke.

MRI White Matter Hyperintensities

WMH are areas of bright, high signal intensities noted on MRI T₂-weighted and proton density sequences, representing regions of scattered brain white matter loss associated with local increases in brain water content. These hyperintensities reflect leukoaraiosis (from the Greek leuko = white, araios = rarefied), a term coined by Hachinski et al. [11 ]to indicate ‘a diminution of the density of representation of the white matter’ on neuroimaging.

WMH of vascular origin can also be divided into punctate, early confluent and confluent hyperintensities [12, 13]. Punctate lesions tend to correspond to a perivascular reduction in myelin content with atrophy of the neuropil and seem to constitute a negligible extent of tissue damage from low permeability through thickened arteriolar walls. Early confluent and confluent (fig. 1) hyperintensities, however, indicate more extensive ischemic damage consistent with advanced microangiopathy. [12, 13].

Fig. 1

MRI T₂-weighted sequences showing confluent WMH.

Progression of WMH and the Distinctly High Risk of Subjects with Confluent Lesions

The presence of confluent WMH at the time of initial observation has been shown to be a potent predictor of subsequent WMH progression [14]. Early confluent and confluent white matter abnormalities are progressive, and likely malignant. Two large population studies have provided detailed information regarding the dramatic differences in the rate of progression of lesion volume in individuals with different degrees of baseline WMH (table 1). The Austrian Stroke Prevention Study investigators performed a population-based study assessing the progression of white matter lesions in community-dwelling volunteers aged 50–75 years without neuropsychiatric disease [15]. MRIs were obtained in 296 volunteers at baseline, 3 years and 6 years, and the total volume of white matter lesions was measured. Those participants with no lesions and with punctate abnormalities at baseline had a low tendency for lesion progression, whereas those participants with early confluent and with confluent lesions showed substantial median increases in lesion volume at 6 years. Lesion grade at baseline was found to be a significant predictor of lesion progression (p < 0.0001) [15].

Table 1

Annual increase in white matter lesion volume (cm³) in subjects with different grades of WMH at study entry

In the PROGRESS MRI substudy, a multicenter study group in France obtained baseline and 3-year MRIs in consecutive stroke subjects enrolled in the international PROGRESS trial of poststroke antihypertensive therapy [16]. In the placebo group, lesion grade at baseline was powerfully related to lesion progression, with no progression seen in mild baseline subjects, and fivefold greater progression seen in confluent subjects compared to early confluent subjects.

Pathogenesis

Pathologic correlation has shown that these patchy white matter lesions correspond primarily to areas of ischemic demyelination and gliosis, and occasionally to clinically silent infarcts [17]. Chronic low-grade vascular insufficiency produces atrophic perivascular demyelination rather than acute tissue necrosis created by more severe ischemia. The WMH are presumably mostly caused by hypoperfusion and arteriolar disease [18]. Lipohyalinosis of the media and thickening of the vessel walls narrow the lumen of the small perforating arteries and arterioles which nourish the deep white matter [19]. The perforating vessels, which originate from cortical and leptomeningeal arteries, have a relatively poor anastomotic system, which makes the white matter vulnerable to cerebral ischemia. Postmortem studies have indicated that WMH seen on MRI scans are associated with degenerative changes in arterioles that are related to atherosclerosis, suggesting that cerebral arteriosclerosis of the penetrating vessels is a major factor in the pathogenesis of ischemic WMH [19].

Risk Factors for Cerebral Ischemic White Matter Injury

Hypertension

Besides age, hypertension is consistently reported to be the most common risk factor for cerebral WMH and spinal cord injury [20,21,22]. The association between hypertension and WMH has been established in cross-sectional [19], and longitudinal studies [20]. Several studies have examined the prevalence of WMH in hypertensive and high normotensive subjects [23,24,25]. For instance, the ARIC study [23] reported a 24.6% prevalence of WMH among individuals aged 55–72 years, 49% of whom were hypertensives. Previously increased blood pressure may increase the risk for dementia by inducing small vessel disease and white matter lesions [26]. There is also a suggestion of greater association of hypertension with confluent white matter lesions; van Swieten et al. [27 ]found diastolic blood pressures were higher in individuals with confluent lesions than in those with no or focal lesions 13 ± 9 years earlier.

Large-Vessel Atherosclerosis

Breteler et al. [25 ]reported that WMH were related to atherosclerosis, indicated by increased common carotid intima-media thickness and carotid plaques. Similarly, Manolio et al. [28 ]found that MRI infarcts, ventricular and sulcal widening, and white matter score were strongly associated with carotid intimal-medial thickness and stenosis degree after adjustment for age and sex (all p < 0.01). Furthermore, de Leeuw et al. [29] showed that the presence of aortic atherosclerosis during midlife, assessed on abdominal radiographs, was significantly associated with the presence of periventricular WMH 20 years later.

Endothelial Dysfunction

Several studies suggest that cerebral leukoaraoisis is associated with impaired endothelial relaxation and reactivity of both cerebral and system vessels. Transcranial Doppler ultrasound studies have shown significantly impaired vasomotor reactivity in subjects with periventricular white matter lesions [30] and lacunar strokes [31]. A prolonged arteriovenous cerebral transit indicating disordered cerebral microcirculation has been demonstrated in subjects with microangiopathy and vascular dementia [32].

Several authors have drawn upon epidemiologic, pathologic, and experimental studies to suggest that cerebral small vessel endothelial dysfunction, with leakage of plasma components into the vessel wall and surrounding brain tissue leading to neuronal damage, may contribute to the development of lacunar stroke, leukoaraiosis, and dementia [33, 34].

A study by Hassan et al. [35 ]measuring circulating levels of markers of endothelial activation and damage, intercellular adhesion molecule 1, thrombomodulin, tissue factor (TF) and tissue factor pathway inhibitor (TFPI) in a prospective series of subjects with lacunar stroke found that the ischemic leukoaraiosis group had a different endothelial marker profile, with lower levels of TFPI (p = 0.01) and a higher TF/TFPI ratio (p = 0.01) compared with the isolated lacunar infarction group. Thrombomodulin levels were associated with the number of lacunes (p = 0.008) and the leukoaraiosis score (p = 0.03), but TF levels and the TF/TFPI ratio were associated only with the extent of leukoaraiosis (p ≤ 0.02). These results suggested that there is evidence of chronic endothelial dysfunction in cerebral small vessel disease and that endothelial prothrombotic changes may be important in mediating the ischemic leukoaraiosis phenotype.

Diabetes

Some studies have suggested that WMH are associated with diabetes [12, 13]. However, other studies have not confirmed this association [27, 36]. It has been suggested that the reasons for these conflicting results may be differences in sample sizes, grades of WMH, diabetes severity, and diabetes duration across the various study populations [37]. Most recently, a study of nondemented elderly persons has found a significant Pearson correlation with WMH for elevated hemoglobin level, an index of recent (preceding 3 months) glycemic control [38]. Further investigation of any potential relationship between diabetes and WMH is most certainly needed.

Therapeutic Implications

Promising Treatment Modalities for Preventing Progression of Ischemic Cerebral White Matter Brain Injury

Antiplatelet Agents

Antiplatelet agents have an established role in reducing secondary stroke and primary cardiac risk [39]. However, up until recently, antiplatelet agents could not be recommended for routine use in the primary preventionof clinically manifest cerebrovascular disease. This was largely due to a lack of high-quality evidence supporting efficacy and the potentially increased risk of hemorrhagic stroke, as noted with prophylactic aspirin use for primary stroke prevention [40]. The results from the Women’s Health Study have now suggested that there may be a role for a primary stroke prevention strategy using antiplatelet therapy in selected populations [41]. This study showed a 24% reduction in ischemic stroke risk (relative risk 0.76; 95% CI 0.63–0.93; p = 0.009) and a nonsignificant slight increase in the risk of hemorrhagic stroke in favor of aspirin (vs. placebo) among women 45 years of age or older, with no prior history of stroke [41]. The results of the Women’s Health Study and the proven efficacy of various antiplatelet agents acting via distinct mechanisms in secondary stroke prevention (please see below) may support the need for developing studies to assess the potential for antiplatelet therapies to mitigate the adverse consequences of WMH in individuals without clinically manifest cerebrovascular disease.

Aspirin. Aspirin (acetylsalicylic acid) prevents platelet activation by inhibiting the enzyme cyclooxygenase resulting in the blockage of thromboxane generation, and has been shown to be protective in most types of subjects at increased risk of occlusive vascular events [39]. Cyclooxygenase also produces superoxide radicals within vascular endothelial cells. Decreasing superoxide radicals abolishes amyloid-mediated vasoactivity and damage. Thus, aspirin may also reduce endothelial damage through its inhibition of cyclooxygenase [42]. Another mechanism for aspirin’s cerebroprotective effects may lie in its known inhibition of matrix metalloproteinase activity [43]. It has been suggested that ongoing cerebral white matter injury is related to matrix metalloproteinase production by microglia/macrophages [44].

Dipyridamole. Dipyridamole is well known to exert antiplatelet activity [45]. Dipyridamole is not only an antiplatelet agent exerting its effects directly on platelets by inhibition of adenosine uptake but it is also an antithrombotic agent utilizing other mechanisms [46]. One of the pharmacological effects of dipyridamole is vasodilatation, which in turn may result in lowering blood pressure [47]. Dipyridamole also directly stimulates the release of endothelial PGI₂, as well as reduces the thrombogenicity of subendothelial structures by increasing the productive mediator 13-hydroxyoctadecadienic acid. One study suggested that dipyridamole may act primarily on mediators of inflammation (as determined by C-reactive protein) and endothelial dysfunction (assessed by von Willebrand factor) [48].

Aspirin and Dipyridamole. Preclinical studies have shown a synergistic effect of dipyridamole and acetylsalicylic acid in reducing thrombus formation [49]. The combination of aspirin and dipyridamole is superior to either agent alone in preventing overt recurrent ischemic stroke. The large European Stroke Prevention Study 2 trial found that low-dose aspirin plus dipyridamole more than doubled the reduction in stroke risk achieved with aspirin alone, i.e. a 37% risk reduction for the combination versus 18.1% for aspirin alone. The results also suggested that the effects of aspirin and dipyridamole are additive [50].

Clopidogrel. Clopidogrel is an adenosine diphosphate receptor antagonist, which inhibits adenosine diphosphate-induced fibrinogen binding to platelets, a necessary step in the platelet aggregation process. The CAPRIE study revealed a slight advantage for clopidogrel over aspirin in the composite endpoint of ischemic stroke, myocardial infarction or vascular death among a cohort of 19,185 patients with recent ischemic stroke, myocardial infarction or peripheral arterial disease [51, 52].

Antihypertensive Agents

Subjects taking antihypertensive drugs and who have controlled blood pressure have a reduced risk of severe WMH [20]. Although mean blood pressure is an important predictor of stroke events, the results of recent clinical trials showing benefit of blood pressure reduction even in normotensive individuals [53] indicate that blood pressure likely represents a continuum of risk for stroke, and that the categorical distinction of hypertension from normotension is somewhat artificial [54], thereby implying that the scope of subjects who can be treated with effective stroke-preventive therapies could be widened, and reinforcing the view that the use of antihypertensives should be determined by a person’s overall level of risk rather than level of blood pressure alone.

Most salient to this reasoning is the recent report of the French MRI substudy of the PROGRESS clinical trial, which represents the first clinical trial to examine progression of white matter abnormalities in subjects treated with add-on antihypertensive therapy. In the PROGRESS trial, hypertensive and high normotensive subjects with a history of stroke received add-on thiazide diuretic and angiotensin-converting enzyme inhibitor (ACEI) therapy (added to their existing blood pressure regimen). A French multicenter group performed an MRI substudy of the PROGRESS trial to determine if active diuretic plus ACEI therapy resulted in a decrease of incidence of new WMH during MRI follow-up, compared to the placebo-treated group of individuals. Dufouil et al. [16] obtained baseline and 3-year follow-up MRI to measure the presence and volume of incidental white matter lesions on 225 persons with prior cerebrovascular disease (stroke or transient ischemic attack). The results demonstrated a statistically significant effect of diuretics plus ACEIs in reducing the occurrence of new white matter lesions, with the treatment effect most pronounced in the subgroup of subjects with advanced leukoaraiosis at the time of study entry.

Of those subjects in the active treatment group who had severe white matter lesions upon entry, none experienced an increase in lesions. The results clearly suggest that an add-on blood-pressure-lowering regimen in subjects with prior stroke stops or delays further covert ischemic brain damage. However, these promising results in subjects who have already suffered an overt clinical stroke need to be extended to subjects with no past history of overt stroke, who may have different rates of progression of covert vascular injury. It is noteworthy that the PROGRESS MRI substudy findings suggest that only subjects with more advanced leukoaraoisis at entry will experience substantial enough progression to benefit from therapy to avert progressive covert vascular brain injury within a few years of intervention.

The general consensus is that blood pressure lowering is the most important factor in the stroke prevention benefit conferred by antihypertensive treatment regardless of the antihypertensive agent class, and that this should be the focus of any management geared at reducing stroke risk. However, there is mounting evidence that certain antihypertensive classes may confer clinical benefit in stroke prevention through additional mechanisms [55].

The Renin-Angiotensin-Aldosterone-Kinin System

Angiotensin II receptor blockers (ARBs) and ACEIs are two classes of antihypertensive drugs that reduce the activity of the renin-angiotensin II system (RAS). Pharmacological modulation of the renin-angiotensin-aldosterone-kinin system is an attractive therapeutic target for the treatment of covert vascular brain injury because abnormalities in the renin-angiotensin-aldosterone-kinin cascade have been implicated in the pathogenesis and clinical expression of brain small vessel disease [56, 57]. ACEIs and ARBs have both been shown beneficial in preventing first and recurrent symptomatic strokes [53, 58, 59]. These agents also appear to lower blood pressure without reducing measures of cerebral perfusion [60].

Genetic association studies in the setting of the Austrian Stroke Prevention Study indicated that polymorphisms in the RAS increase the susceptibility for progression of cerebral small vessel disease. Homozygosity for the T allele of the M235T polymorphism of the angiotensinogen gene was associated with a 3.19-fold increased risk for lesion progression independently of arterial hypertension. These data suggest that drugs influencing the RAS may allow interference of the unfavorable course of cerebral small vessel disease [61].

Angiotensin II (ANG II), the main effector peptide of the RAS, is implicated in the development of vascular pathologies. Considered to be central to the whole vascular continuum, recent investigations have also established a role for ANG II in the recovery of the brain after cerebral insult. ANG II exerts its actions through two receptors: ANG II type 1 (AT1) and type 2 (AT2). Drugs that activate the AT2 receptors, such as ARBs, have consistently been more beneficial for stroke reduction than drugs devoid of such activation, despite an equal fall in arterial pressure [62, 63]. These clinical and epidemiologic observations are supported by experimental data documenting greater cerebroprotection with ARBs (which increase ANG II levels and stimulate the AT2 receptors) than with ACEIs [62]. Among the many potential effects mediated by stimulation of the AT2 is the neuronal regeneration after injury and inhibition of pathological growth. Indeed, experimental data indicate that ARBs offer double protection in that they inhibit the AT1 receptor-mediated proatherothrombotic effects and enhance the AT2 receptor-mediated protection against ischemia by increasing the generation of ANG II, particularly in small arteries [62]. This latter effect may give ARBs an advantage over ACEIs, because although ACEIs inhibit the AT1-mediated proatherothrombotic effects as well, they also reduce circulating ANG II levels and thereby AT2 receptor-dependent cerebroprotection [62]. However, this potential advantage has not been proven in the clinical arena. The Ongoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial (ONTARGET) is an ongoing double-blind randomized study comparing the efficacy and safety of add-on therapy of an ARB vs. ACEI in the prevention of cardiovascular events, and will confirm or disconfirm any additional benefits of ARBs over ACEIs [64].

Statins

The use of statins (HMG-CoA reductase inhibitors) intuitively has potential appeal for preventing WMH injury. Numerous trials have shown that treatment with statins is associated with a significant decrease in the risk of stroke and transient ischemic attack in patients with symptomatic coronary artery disease or multiple risk factors for atherosclerosis [65], and some studies indicate that pretreatment with statins may result in lesser stroke severity [66]. The mechanism by which statins confer vascular protection is likely multifactorial and includes lipoprotein alterations (upregulation of low-density lipoprotein receptor activity and reducing the entry of low- density lipoprotein into the circulation), improved endothelial function (upgrade endothelial nitric oxide synthase, inhibit inducible nitric oxide synthase), plaque stabilization, antithrombosis, attenuation of inflammatory cytokine responses, and antioxidant effects [67].

All of this notwithstanding, no study has yet shown that statins are effective in preventing secondary stroke. The SPARCL trial is currently investigating this issue [68]. Pertinent to patients with WMH, the Cardiovascular Health Study examined the association of statin drug use with changes in white matter measures on serial MRI scans separated by 5 years, and found no notable differences in evolution of white matter measures between treatment (statin vs. no statin) groups [69]. However, only limited inferences can be made from these MRI data of the Cardiovascular Health Study subset since the study was observational, the sample size was relatively modest (n = 1,730), and the grading system used to measure white matter disease in the study may not have had sufficient sensitivity or interreader reliability to detect significant changes within the study interval. Future larger randomized studies will be needed to explore the role of statins, if any, in reducing ischemic white matter brain injury.

Conclusions

Although associated with cognitive impairment and dementia, and likely predictors of future vascular events, the varied and covert nature of WMH presents an important obstacle in evaluating the efficacy of therapies. Large sample sizes are likely to be required for treatment trials using clinical endpoints alone, and by the time clinical endpoints become manifest, the burden of brain injury caused by these lesions would be substantial. Clinical endpoints set the ultimate standard for definitive clinical trials, but more sensitive surrogate markers could be useful in evaluating the efficacy of new treatments and selecting the most promising treatments for large trials. An analogy is provided by multiple sclerosis, for which detection of new lesions by contrast-enhanced MRI has been implemented as a surrogate marker of disease activity [70, 71], and new lesion detection has been incorporated into guidelines for disease monitoring in therapeutic trials in multiple sclerosis [71]. The European Task Force on Age-Related White Matter Changes has recently concluded that MRI white matter lesions are an appropriate biometric marker for use in phase 2 clinical trials [72]. With the emergence of promising new (and not so new) therapies that may limit cognitive decline in persons with MRI WMH, opportunities may abound for exploring avenues to reduce the immense public burden of cerebral vascular white matter ischemic injury.

References

1. 
   Broderick J, Miller R, Khoury JC, Alwell K, Kissela MB, Woo D, Shukla R, Moomaw C, Gebel J, Pancioli AM, Brott TG, Kothari RU: Incidence rates of stroke for blacks and whites: preliminary results from the greater Cincinnati/northern Kentucky stroke study. Stroke 2001;32:320.
   




2. 
   Williams G: Incidence and characteristics of total stroke in the united states. BMC Neurol 2001;1:2.
   




3. 
   Mittelmark M, Psaty BM, Rautaharju PM, Fried LP, Borhani NO, Tracy RP, Gardin JM, O’Leary DH: Prevalence of cardiovascular diseases among older adults. The cardiovascular health study. Am J Epidemiol 1993;137:311–317.
   




4. 
   Awad I, Johnson PC, Spetzler RF, Hodak JA: Incidental subcortical lesions identified on magnetic resonance imaging in the elderly. Postmortem pathological findings. Stroke 1986;17:1090–1097.
   




5. 
   Kertesz A, Black SE, Tokar G, Benke T, Carr T, Nicholson L: Periventricular and subcortical hyperintensities on magnetic resonance imaging. ‘Rims, caps, and unidentified bright objects’. Arch Neurol 1988;45:404–408.
   




6. 
   Kidwell C, Saver JL: Causes and consequences of leukoaraiosis: a review. Facts Res Gerontol 1996(suppl stroke):115–135.
   




7. 
   de Groot J, de Leeuw FE, Oudkerk M, Hofman A, Jolles J, Breteler MM: Cerebral white matter lesions and depressive symptoms in elderly adults. Arch Gen Psychiatry 2000;57:1071–1076.
   




8. 
   Baloh R, Yue Q, Socotch TM, Jacobson KM: White matter lesions and disequilibrium in older people. 1. Case-control comparison. Arch Neurol 1995;52:970–974.
   




9. 
   Price T, Manolio TA, Kronmal RA, Kittner SJ, Yue NC, Robbins J, Anton-Culver H, O’Leary D: Silent brain infarction on magnetic resonance imaging and neurological abnormalities in community-dwelling older adults. The Cardiovascular Health Study. CHS Collaborative Research Group. Stroke 1997;28:1158–1164.
   




10. 
    Longstreth W: Brain abnormalities in the elderly: frequency and predictors in the United States (the Cardiovascular Health Study). Cardiovascular Health Study Collaborative Research Group. J Neural Transm Suppl 1998;53:9–16.
    




11. 
    Hachinski V, Potter P, Merskey H: Leukoaraiosis: an ancient term for a new problem. Can J Neurol Sci 1986;13:533–534.
    




12. 
    Schmidt R, Fazekas F, Kleinert G, Offenbacher H, Gindl K, Payer F, Freidl W, Niederkorn K, Lechner H: Magnetic resonance imaging signal hyperintensities in the deep and subcortical white matter. A comparative study between stroke patients and normal volunteers. Arch Neurol 1992;49:825–827.
    




13. 
    Fazekas F, Niederkorn K, Schmidt R, Offenbacher H, Horner S, Bertha G, Lechner H: White matter signal abnormalities in normal individuals: correlation with carotid ultrasonography, cerebral blood flow measurements, and cerebrovascular risk factors. Stroke 1988;19:1285–1288.
    




14. 
    Schmidt R, Schmidt H, Kapeller P, Enzinger C, Ropele S, Saurugg R, Fazekas F: The natural course of MRI white matter hyperintensities. J Neurol Sci 2002;203–204:253–257.
    




15. 
    Schmidt R, Enzinger C, Ropele S, Schmidt H, Fazekas F: Progression of cerebral white matter lesions: 6-year results of the Austrian stroke prevention study. Lancet 2003;361:2046–2048.
    




16. 
    Dufouil C, Chalmers J, Coskun O, Besancon V, Bousser MG, Guillon P, MacMahon S, Mazoyer B, Neal B, Woodward M, Tzourio-Mazoyer N, Tzourio C: Effects of blood pressure lowering on cerebral white matter hyperintensities in patients with stroke: the PROGRESS (Perindopril Protection Against Recurrent Stroke Study) Magnetic Resonance Imaging Substudy. Circulation 2005;112:1644–1650.
    




17. 
    Fazekas F, Kleinert R, Offenbacher H, Schmidt R, Kleinert G, Payer F, Radner H, Lechner H: Pathologic correlates of incidental MRI white matter signal hyperintensities. Neurology 1993;43:1683–1689.
    




18. 
    Liao D, Cooper L, Cai J, Toole J, Bryan N, Burke G, Shahar E, Nieto J, Mosley T, Heiss G: The prevalence and severity of white matter lesions, their relationship with age, ethnicity, gender, and cardiovascular disease risk factors: the ARIC study. Neuroepidemiology 1997;16:149–162.
    




19. 
    Pantoni L, Garcia JH: The significance of cerebral white matter abnormalities 100 years after Binswanger’s report. A review. Stroke 1995;26:1293–1301.
    




20. 
    Dufouil C, de Kersaint-Gilly A, Besancon V, Levy C, Auffray E, Brunnereau L, Alperovitch A, Tzourio C: Longitudinal study of blood pressure and white matter hyperintensities: the EVA-MRI cohort. Neurology 2001;56:921–926.
    




21. 
    Lee S, Park SJ, Ki HK, Gwon HC, Chung CS, Byun HS, Shin KJ, Shin MH, Lee WR: Prevalence and risk factors of silent cerebral infarction in apparently normal adults. Hypertension 2000;36:73–77.
    




22. 
    Longstreth WT Jr, Bernick C, Manolio TA, Bryan N, Jungreis CA, Price TR: Lacunar infarcts defined by magnetic resonance imaging of 3,660 elderly people: the cardiovascular health study. Arch Neurol 1998;55:1217–1225.
    




23. 
    Liao D, Cooper L, Cai J, Toole JF, Bryan NR, Hutchinson RG, Tyroler HA: Presence and severity of cerebral white matter lesions and hypertension, its treatment, and its control. The ARIC study. Atherosclerosis Risk in Communities Study. Stroke 1996;27:2262–2270.
    




24. 
    Longstreth W, Manolio TA, Arnold A, Burke GL, Bryan N, Jungreis CA, Enright PL, O’Leary D, Fried L: Clinical correlates of white matter findings on cranial magnetic resonance imaging of 3,301 elderly people. The Cardiovascular Health Study. Stroke 1996;27:1274–1282.
    




25. 
    Breteler MM, van Swieten JC, Bots ML, Grobbee DE, Claus JJ, van den Hout JH, van Harskamp F, Tanghe HL, de Jong PT, van Gijn J, et al: Cerebral white matter lesions, vascular risk factors, and cognitive function in a population-based study: the Rotterdam study. Neurology 1994;44:1246–1252.
    




26. 
    Skoog I, Lernfelt B, Landahl S, Palmertz B, Andreasson LA, Nilsson L, Persson G, Oden A, Svanborg A: 15-year longitudinal study of blood pressure and dementia. Lancet 1996;347:1141–1145.
    




27. 
    van Swieten J, Geyskes GG, Derix MM, Peeck BM, Ramos LM, van Latum JC, van Gijn J: Hypertension in the elderly is associated with white matter lesions and cognitive decline. Ann Neurol 1991;30:825–830.
    




28. 
    Manolio T, Burke GL, O’Leary DH, Evans G, Beauchamp N, Knepper L, Ward B: Relationships of cerebral MRI findings to ultrasonographic carotid atherosclerosis in older adults: the Cardiovascular Health Study. CHS Collaborative Research Group. Arterioscler Thromb Vasc Biol 1999;19:356–365.
    




29. 
    de Leeuw FE, De Groot JC, Oudkerk M, Witteman JC, Hofman A, van Gijn J, Breteler MM: Aortic atherosclerosis at middle age predicts cerebral white matter lesions in the elderly. Stroke 2000;31:425–429.
    




30. 
    Bakker S, de Leeuw FE, de Groot JC, Hofman A, Koudstaal PJ, Breteler MM: Cerebral vasomotor reactivity and cerebral white matter lesions in the elderly. Neurology 1999;52:578–583.
    




31. 
    Molina C, Sabin JA, Montaner J, Rovira A, Abilleira S, Codina A: Impaired cerebrovascular reactivity as a risk marker for first-ever lacunar infarction: a case-control study. Stroke 1999;30:2296–2301.
    




32. 
    Puls I, Hauck K, Demuth K, Horowski A, Schliesser M, Dorfler P, Scheel P, Toyka KV, Reiners K, Schoning M, Becker G: Diagnostic impact of cerebral transit time in the identification of microangiopathy in dementia: a transcranial ultrasound study. Stroke 1999;30:2291–2295.
    




33. 
    Wardlaw J, Sandercock PA, Dennis MS, Starr J: Is breakdown of the blood-brain barrier responsible for lacunar stroke, leukoaraiosis, and dementia? Stroke 2003;34:806–812.
    




34. 
    Baloh R, Vinters HV: White matter lesions and disequilibrium in older people. 2. Clinicopathologic correlation. Arch Neurol 1995;52:975–981.
    




35. 
    Hassan A, Hunt BJ, O’Sullivan M, Parmar K, Bamford JM, Briley D, Brown MM, Thomas DJ, Markus HS: Markers of endothelial dysfunction in lacunar infarction and ischaemic leukoaraiosis. Brain 2003;126:424–432.
    




36. 
    Bogousslavsky J, Regli F, Uske A: Leukoencephalopathy in patients with ischemic stroke. Stroke 1987;18:896–899.
    




37. 
    Fukuda H, Kitani M: Differences between treated and untreated hypertensive subjects in the extent of periventricular hyperintensities observed on brain MRI. Stroke 1995;26:1593–1597.
    




38. 
    Murray A, Staff RT, Shenkin SD, Deary IJ, Starr JM, Whalley LJ: Brain white matter hyperintensities: relative importance of vascular risk factors in nondemented elderly people. Radiology 2005;237:251–257.
    




39. 
    Collaborative meta-analysis of randomised trials of antiplatelet therapy for prevention of death, myocardial infarction, and stroke in high risk patients. BMJ 2002;324:71–86.
    




40. 
    Rodondi N, Bauer DC: Assessing the risk/benefit profile before recommending aspirin for the primary prevention of cardiovascular events. Am J Med 2004;117:528–530.
    




41. 
    Ridker P, Cook NR, Lee IM, Gordon D, Gaziano JM, Manson JE, Hennekens CH, Buring JE: A randomized trial of low-dose aspirin in the primary prevention of cardiovascular disease in women. N Engl J Med 2005;352:1293–1304.
    




42. 
    Broe GA, Grayson DA, Creasey HM, Waite LM, Casey BJ, Bennett HP, Brooks WS, Halliday GM: Anti-inflammatory drugs protect against Alzheimer disease at low doses. Arch Neurol 2000;57:1586–1591.
    




43. 
    Jiang MC, Liao CF, Lee PH: Aspirin inhibits matrix metalloproteinase-2 activity, increases E-cadherin production, and inhibits in vitro invasion of tumor cells. Biochem Biophys Res Commun 2001;282:671–677.
    




44. 
    Rosenberg GA, Sullivan N, Esiri MM: White matter damage is associated with matrix metalloproteinases in vascular dementia. Stroke 2001;32:1162–1168.
    




45. 
    Emmons PR, Harrison MJ, Honour AJ, Mitchell JR: Effect of dipyridamole on human platelet behaviour. Lancet 1965;ii:603–606.
    




46. 
    Eisert WG: Near-field amplification of antithrombotic effects of dipyridamole through vessel wall cells. Neurology 2001;57:S20–S23.
    




47. 
    Aktas B, Utz A, Hoenig-Liedl P, Walter U, Geiger J: Dipyridamole enhances NO/cGMP-mediated vasodilator-stimulated phosphoprotein phosphorylation and signaling in human platelets: in vitro and in vivo/ex vivo studies. Stroke 2003;34:764–769.
    




48. 
    Zhao L, Leonardi-Bee J, Weaver C, Heptinstall S, Bath P: Effect of aspirin, clopidogrel and dipyridamole on soluble markers of vascular stress in patients with prior stroke. 13th Eur Stroke Conf, Mannheim-Heidelberg, May 2004.
    




49. 
    Honour AJ, Hockaday TD, Mann JI: The synergistic effect of aspirin and dipyridamole upon platelet thrombi in living blood vessels. Br J Exp Pathol 1977;58:268–272.
    




50. 
    Diener HC, Cunha L, Forbes C, Sivenius J, Smets P, Lowenthal A: European stroke prevention study. 2. Dipyridamole and acetylsalicylic acid in the secondary prevention of stroke. J Neurol Sci 1996;143:1–13.
    




51. 
    Ringleb PA, Bhatt DL, Hirsch AT, Topol EJ, Hacke W: Benefit of clopidogrel over aspirin is amplified in patients with a history of ischemic events. Stroke 2004;35:528–532.
    




52. 
    Hirsh J, Bhatt DL: Comparative benefits of clopidogrel and aspirin in high-risk patient populations: lessons from the CAPRIE and CURE studies. Arch Intern Med 2004;164:2106–2110.
    




53. 
    Randomised trial of a perindopril-based blood-pressure-lowering regimen among 6,105 individuals with previous stroke or transient ischaemic attack. Lancet 2001;358:1033–1041.
    




54. 
    Gorelick PB: New horizons for stroke prevention: PROGRESS and HOPE. Lancet Neurol 2002;1:149–156.
    




55. 
    Ruland S, Gorelick PB: Are cholesterol-lowering medications and antihypertensive agents preventing stroke in ways other than by controlling the risk factor? Curr Neurol Neurosci Rep 2003;3:21–26.
    




56. 
    Takami S, Imai Y, Katsuya T, Ohkubo T, Tsuji I, Nagai K, Satoh H, Hisamichi S, Higaki J, Ogihara T: Gene polymorphism of the renin-angiotensin system associates with risk for lacunar infarction. The Ohasama study. Am J Hypertens 2000;13:121–127.
    




57. 
    Hassan A, Lansbury A, Catto AJ, Guthrie A, Spencer J, Craven C, Grant PJ, Bamford JM: Angiotensin converting enzyme insertion/deletion genotype is associated with leukoaraiosis in lacunar syndromes. J Neurol Neurosurg Psychiatry 2002;72:343–346.
    




58. 
    Dahlof B, Devereux RB, Kjeldsen SE, Julius S, Beevers G, Faire U, Fyhrquist F, Ibsen H, Kristiansson K, Lederballe-Pedersen O, Lindholm LH, Nieminen MS, Omvik P, Oparil S, Wedel H: Cardiovascular morbidity and mortality in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol. Lancet 2002;359:995–1003.
    




59. 
    Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G: Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med 2000;342:145–153; errata in N Engl J Med 2000;342:748 and N Engl J Med 2000;342:1376.
    




60. 
    Bath P: High blood pressure as risk factor and prognostic predictor in acute ischaemic stroke: when and how to treat it? Cerebrovasc Dis 2004;17(suppl 1):51–57.
    




61. 
    Schmidt R, Fazekas F, Enzinger C, Ropele S, Kapeller P, Schmidt H: Risk factors and progression of small vessel disease-related cerebral abnormalities. J Neural Transm Suppl 2002:47–52.
    




62. 
    Fournier A, Messerli FH, Achard JM, Fernandez L: Cerebroprotection mediated by angiotensin II: a hypothesis supported by recent randomized clinical trials. J Am Coll Cardiol 2004;43:1343–1347.
    




63. 
    Schrader J, Luders S, Kulschewski A, Hammersen F, Plate K, Berger J, Zidek W, Dominiak P, Diener HC: Morbidity and mortality after stroke, eprosartan compared with nitrendipine for secondary prevention: principal results of a prospective randomized controlled study (MOSES). Stroke 2005;36:1218–1226.
    




64. 
    http://www.ontarget-micardis.com/studyprog/ontar/ontarget.htm). Last accessed November 16, 2005.
    




65. 
    Ovbiagele B, Kidwell, CS, Saver JL: Expanding indications for statins in cerebral ischemia: a quantitative study. Arch Neurol 2005;62:67–72.
    




66. 
    Greisenegger S, Mullner M, Tentschert S, Lang W, Lalouschek W: Effect of pretreatment with statins on the severity of acute ischemic cerebrovascular events. J Neurol Sci 2004;221:5–10.
    




67. 
    Davignon J, Laaksonen R: Low-density lipoprotein-independent effects of statins. Curr Opin Lipidol 1999;10:543–559.
    




68. 
    Amarenco P, Bogousslavsky J, Callahan AS, Goldstein L, Hennerici M, Sillsen H, Welch MA, Zivin J: Design and baseline characteristics of the stroke prevention by aggressive reduction in cholesterol levels (SPARCL) study. Cerebrovasc Dis 2003;16:389–395.
    




69. 
    Bernick C, Katz R, Smith NL, Rapp S, Bhadelia R, Carlson M, Kuller L: Statins and cognitive function in the elderly: the cardiovascular health study. Neurology 2005;65:1388–1394.
    




70. 
    Miller D, Barkhof F, Nauta JJ: Gadolinium enhancement increases the sensitivity of MRI in detecting disease activity in multiple sclerosis. Brain 1993;116:1077–1094.
    




71. 
    Miller D, Albert PS, Barkhof F, Francis G, Frank JA, Hodgkinson S, Lublin FD, Paty DW, Reingold SC, Simon J: Guidelines for the use of magnetic resonance techniques in monitoring the treatment of multiple sclerosis. US National MS Society Task Force. Ann Neurol 1996;39:6–16.
    




72. 
    Schmidt R, Scheltens P, Erkinjuntti T, Pantoni L, Markus HS, Wallin A, Barkhof F, Fazekas F: White matter lesion progression: a surrogate endpoint for trials in cerebral small-vessel disease. Neurology 2004;63:139–144.
    

Author Contacts

Bruce Ovbiagele, MD

Stroke Center and Department of Neurology, University of California at Los Angeles

710 Westwood Plaza

Los Angeles, CA 90095 (USA)

Tel. +1 310 794 6379, Fax +1 310 267 2063, E-Mail [email protected]

Article / Publication Details

First-Page Preview

Received: September 28, 2005
Accepted: December 08, 2005
Published online: July 14, 2006

Issue release date: July 2006

Number of Print Pages: 8

Number of Figures: 1

Number of Tables: 1

ISSN: 1015-9770 (Print)
eISSN: 1421-9786 (Online)

For additional information: https://www.karger.com/CED

Copyright / Drug Dosage / Disclaimer

Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.

Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.

Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

90,000 Cases from blogs related to the head

This section describes the detection of diseases related to the head. Practice shows that mri diagnostics of the head in the early stages of the disease helps to significantly reduce the risk of developing diseases

July 25
Detection of ACVA in the basin of the left PCA and SMA of the brain using MRI

Patient N. 85 years old after a hypertensive crisis (pressure rise up to 280 mm Hg) notes partial speech impairment, headache, memory impairment, dizziness, visual impairment in the right eye.With a diagnosis of stroke (acute cerebrovascular accident), she was hospitalized in a hospital where an MRI scan of the brain was performed.

More details

13 MAY
Detection of a huge arachnoid cyst with signs of lateral and axial dislocation using MRI

Patient H., 73 years old, higher education, worked as a doctor all his life. Now retired. For 2-3 years, relatives began to notice in him a decrease in memory and intelligence, lethargy, a shuffling gait, which they regarded as age-related changes.The last two months have been joined by a state of stunnedness. The patient was referred by a neurologist for an MRI of the brain.

On MRI scans in the anterior and middle cranial fossa on the left, a large arachnoid cerebrospinal fluid cyst is determined, which compresses the left hemisphere, the left lateral ventricle, displaces the midline structures up to 15 mm to the right. The left frontal, temporal, and insular lobes are reduced in volume, with signs of hypogenesis. The right lateral ventricle is moderately dilated, the enclosing cistern and convexital subarachnoid spaces are compressed.

More details

18 JAN
MRI diagnostics of acute cerebrovascular accident

Patient J., 70 years old, was taken to the department of magnetic resonance imaging of the Federal State Budgetary Institution “FTSSKE named after V.A. Almazov Ministry of Health and Social Development “with suspected acute cerebrovascular accident.

According to the MRI of the brain in the left fronto-parietal region, in the basin of the left middle cerebral artery, the zone of hyperintense MR signal on T2 VI, FLAIR PI, DWI corresponding to the zone of acute cerebrovascular accident by ischemic type is determined.

More details

06 DEC
MRI diagnostics of S-shaped tortuosity of the LVA

A 56-year-old man turned to a neurologist with complaints of recurrent headaches, in connection with which he was referred for MR-angiography of the cerebral vessels.

On the obtained images of cerebral vessels in 3D-TOF mode, S-shaped tortuosity of the left internal carotid artery in the extracranial sections is determined, which is most likely responsible for the patient’s clinical symptoms.

More details

27 NOV
MRI diagnostics of a vascular genesis gliosis focus in a 53-year-old patient

Patient H.53 years old consulted a general practitioner complaining of headaches. After a neurological examination, the patient was referred for an MRI of the brain in order to exclude organic pathology.

According to MRI data of the brain in the white matter of the left frontal lobe, at the supraventricular level, a single focus is determined (most likely a focus of gliosis of vascular origin, less likely a demyelinating process), 12 mm in size.

More details

16 NOV
MRI diagnostics of the brain without pathology

Patient L.27 years old consulted a general practitioner with complaints of a single episode of loss of consciousness. After a neurological examination, the patient was referred for an MRI of the brain in order to exclude organic pathology.

According to MRI data, no areas of pathological intensity of the MR signal in the substance of the brain were detected.

More details

15 NOV
MRI diagnosis of asymmetry of the calibers of the vertebral arteries in a 53 year old man

A 53-year-old man consulted a neurologist with complaints of recurrent headaches, in connection with which he was referred for MR-angiography of the cerebral vessels.

On the obtained images of cerebral vessels in 3D-TOF mode, the asymmetry of the calibers of the vertebral arteries in the V4 segment is determined (the caliber of the PAD is less than the LA), which is most likely responsible for the clinical symptoms of the patient.

More details

02 NOV
MRI diagnostics of asymmetry of the calibers of the vertebral arteries in a 57-year-old man

A 57-year-old man consulted a neurologist with complaints of recurrent headaches, in connection with which he was referred for an MRI angiography of the cerebral vessels.

On the obtained images of the cerebral vessels in 3D-TOF mode, the asymmetry of the calibers of the vertebral arteries in the V4 segment (the caliber of the LA is less than the PPA) is determined, which is most likely responsible for the clinical symptoms of the patient.

More details

29 OCT
MRI diagnostics of arachnoid cyst of the left temporal region

Patient K., 15 years old, is being examined by a neurologist for epilepsy. This year he decided to have an MRI of the brain.

On a series of MRI of the brain, it is determined: in the pole of the left temporal lobe, cystic expansion of the external cerebrospinal fluid space is determined, measuring 3.8 x 4.8 x 5.2 cm, with clear even contours, with a pronounced mass effect, without signs of perifocal edema ( most likely an arachnoid cyst).The median structures are minimally displaced to the right by 0.3 cm.

More details

24 OCT
MRI diagnosis of S-shaped tortuosity of the left internal carotid artery

A 60-year-old man consulted a neurologist with complaints of recurrent headaches, and therefore was referred for an MRI angiography of the cerebral vessels.

On the obtained images of cerebral vessels in 3D-TOF mode, S-shaped tortuosity of the left internal carotid artery in the extracranial sections is determined, which is most likely responsible for the patient’s clinical symptoms.

More details

22 OCT
MRI diagnostics of arachnoid cyst

The mother of a 12-year-old child turned to a neurologist with complaints of convulsions for the first time in the child, accompanied by loss of consciousness.

After MRI it was revealed that in the left frontal region there is an arachnoid cyst, which compresses the adjacent parts of the brain and causes atrophy from compression of the frontal bone.

More details

19 OCT
MRI diagnostics of asymmetry of the calibers of the vertebral arteries in a 55-year-old man

A 55-year-old man consulted a neurologist with complaints of recurrent headaches, and therefore was referred for an MRI angiography of the cerebral vessels.

On the obtained images of cerebral vessels in 3D-TOF mode, the asymmetry of the calibers of the vertebral arteries in the V4 segment is determined (the caliber of the PAD is less than the LA), which is most likely responsible for the clinical symptoms of the patient.

More details

18 OCT
MRI diagnostics of cerebrovascular atherosclerosis

A 45-year-old man consulted a neurologist with complaints of recurrent headaches, and therefore was referred for an MRI angiography of the cerebral vessels.

On the obtained images of cerebral vessels in 3D-TOF mode, it is determined: the right vertebral artery is not visualized.The contours of the rest of the cerebral vessels are uneven, which is most likely associated with atherosclerotic lesions.

More details

17 OCT
MRI diagnostics of migraine

Patient G., 30 years old, consulted a general practitioner with complaints of a single episode of loss of consciousness. After a neurological examination, the patient was referred for an MRI of the brain in order to exclude organic pathology.

According to MRI data, no areas of pathological intensity of the MR signal in the substance of the brain were detected.

More details

01 OCT
MRI diagnostics of cystic formation of the pineal gland

Patient M., 34 years old, consulted a neurologist at a medical center with complaints of headaches, insomnia. In order to exclude focal brain damage, the patient was referred for MRI.

MRI of the brain revealed: no focal changes in the substance of the brain were found. However, in the projection of the pineal gland, a cystic formation with clear even contours measuring 1.2×0.9 cm was found without signs of volumetric effect on the surrounding structures.

More details

26 SEP
MRI diagnosis of multiple sclerosis in a 29-year-old patient

Patient N., 29 years old, consulted a neurologist with complaints of visual impairment, dizziness, unsteadiness of gait, numbness of the hands. After a neurological examination, the patient was referred for an MRI of the brain to rule out demyelinating disease.

According to MRI data of the brain in the white matter of both hemispheres periventricularly, as well as in the corpus callosum, multiple foci of “confluent” character of various shapes and sizes are determined (most likely foci of demyelination).

More details

25 SEP
MRI diagnostics of cerebrovascular accident

Patient D., 73 years old, was taken to the department of magnetic resonance imaging of the Federal State Budgetary Institution “FTSSKE named after V.A. Almazov Ministry of Health and Social Development “with suspected acute cerebrovascular accident.

According to MRI data of the brain in the right frontal lobe at the level of the basal nuclei, the zone of hyperintense MR signal on T2 VI, FLAIR PI, DWI corresponding to the zone of acute ischemic cerebrovascular accident is determined.

More details

SEP 24
MRI diagnostics of a single focus of gliosis, 3 mm in size

Patient R. 34 years old consulted a general practitioner with complaints of sleep disorder. After a neurological examination, the patient was referred for an MRI of the brain in order to exclude organic pathology.

According to MRI data of the brain in the white matter of the right frontal lobe, at the level of the anterior horn of the right lateral ventricle, a single focus of gliosis of vascular origin, 3 mm in size, is determined.

More details

SEP 17
MRI diagnostics of cerebral vessels

A 54-year-old man consulted a neurologist complaining of daily headaches in the afternoon, and therefore was referred for an MRI angiography of the cerebral vessels.

On the obtained images of cerebral vessels in the 3D-TOF mode, no narrowing and pathological tortuosity of the vessels were detected. The MR signal from the cerebral vessels is not changed.

More details

SEP 13
MRI diagnostics of brain lesions and cerebrovascular accident

Patient Z.76 years old, consulted a neurologist at a medical center with complaints of headaches, periodic dizziness. In order to exclude focal brain damage, the patient was referred for MRI.

MRI of the brain revealed that in the white matter of both hemispheres, subcoritical and periventricular, multiple foci of a vascular nature are determined. Mixed hydrocephalus of replacement genesis is also noted. Diagnosis: chronic cerebral circulation insufficiency.

More details

28 AUG
Mri head diagnostics

Patient G., 27 years old, consulted a general practitioner with complaints of headaches and periodic dizziness. After a neurological examination, the patient was referred for an MRI of the brain in order to exclude organic pathology.

According to MRI data, no areas of pathological intensity of the MR signal in the substance of the brain were detected.

More details

21 AUG
MRI diagnostics of discirculatory encephalopathy

Patient K.64 years old, consulted a neurologist at a medical center with complaints of headaches, periodic dizziness. In order to exclude focal brain damage, the patient was referred for MRI.

MRI of the brain revealed that in the white matter of both hemispheres, the foci of vascular gliosis were determined subcoritically and periventricularly. Diagnosis: discirculatory encephalopathy.

More details

15 AUG
MRI diagnosis of pineal cyst

Patient D.36 years old, consulted a neurologist at a medical center with complaints of headaches. In order to exclude focal brain damage, the patient was referred for MRI.

MRI of the brain revealed: no focal changes in the substance of the brain were found. However, in the projection of the pineal gland, a cystic formation with clear even contours measuring 1.2×0.7 cm was found without signs of volumetric effect on the surrounding structures.

More details

13 AUG
MRI diagnosis of a single focus of gliosis in the right frontal lobe

Patient J.34 years old consulted a general practitioner complaining of headaches. After a neurological examination, the patient was referred for an MRI of the brain in order to exclude organic pathology.

According to MRI of the brain in the white matter of the right frontal lobe, subcortically, a single focus of vascular genesis of gliosis, 3 mm in size, is determined.

More details

July 30
MRI diagnostics of hydrocephalus of replacement genesis

Patient S., 68 years old, consulted a neurologist at a medical center with complaints of headaches, recurrent dizziness, and a sharp decrease in memory.In order to exclude focal brain damage, the patient was referred for MRI.

MRI of the brain revealed that in the white matter of both hemispheres, subcoritical and periventricular, multiple foci of a vascular nature are determined.

More details

July 25
MRI diagnostics of LVSA tortuosity

Patient By the age of 24 she consulted a neurologist with complaints of frequent headaches. The neurologist recommended that the patient undergo an MRI of the vessels of the brain.

According to the MRI of the cerebral vessels, it is determined: S-shaped tortuosity in the extracranial section of the left internal carotid artery.Also hypoplasia of the left vertebral artery.

More details

JUL 24
MRI diagnostics of a single focus of gliosis

Patient L., 34 years old, consulted a general practitioner complaining of headaches. After a neurological examination, the patient was referred for an MRI of the brain in order to exclude organic pathology.

According to the MRI of the brain in the white matter of the left frontal lobe, at the paraventricular level, a single focus of vascular genesis of gliosis, 3 mm in size, is determined.

More details

July 20
MRI diagnostics of multifocal brain lesions (CMC)

Patient Z. 76 years old, consulted a neurologist at a medical center with complaints of headaches, periodic dizziness, and a sharp decrease in memory. In order to exclude focal brain damage, the patient was referred for MRI.

MRI of the brain revealed that in the white matter of both hemispheres, subcoritical and periventricular, multiple foci of a vascular nature are determined.Mixed hydrocephalus of replacement genesis is also noted. Diagnosis: chronic cerebral circulation insufficiency.

More details

23 MAY
MRI diagnostics of liquor kittens

Patient K., 50 years old, turned to a neurologist with complaints of headaches, memory impairment. From the anamnesis it is known that the patient suffers from atherosclerosis of the brachiocephalic arteries. After the consultation, the patient was referred for an MRI of the brain.

At MRI of the brain in the projection of the basal nuclei of both hemispheres, multiple liquor cysts are determined, due to previously transferred lacunar strokes.

In addition, when examining the vessels, a sharp depletion of blood flow in the vertebral arteries was revealed, as well as occlusion of the middle third of the basilar artery. With MRI data, the patient was referred to a neurologist in order to select the necessary therapy.

More details

21 MAY
MRI diagnosis of cerebellar meningioma

A 70-year-old female patient consulted a neurologist complaining of a headache. After a neurological examination, the patient was referred for an MRI of the brain. MRI of the brain in the left half of the posterior cranial fossa revealed a pathological extracerebral mass, heterogeneous structure due to calcifications, compressing the left cerebellar hemisphere.

More details

21 JUN
MRI diagnostics of subdural hematoma

Patient K., 28 years old in a state of alcoholic intoxication, was hit by a motorcycle, did not lose consciousness, and refused medical assistance. After the injury, he began to notice a headache, the intensity, frequency and duration of which gradually increased. Sometimes it was accompanied by vomiting. Two weeks after the injury, the patient consulted a neurologist, who referred him for an MRI of the brain.

More details

11 JUN
MRI detection of left cerebellopontine cholesteatoma

Patient B.For 38 years, recurrent pains in the left side of the face were worried. Three months later, the pain became constant, there was numbness in the left half of the face, more in the area of ​​the nose and lower jaw, which intensified when brushing teeth and shaving. He did not seek medical help. Numbness of the dorsum and base of the thumb gradually joined. A neurologist directed for an MRI of the brain.

More details

23 MAY
Identification of triventricular hydrocephalus of the brain

Patient H.At 36 years after severe TBI, gross ataxic disorders and mild tetraparesis remained.

After courses of rehabilitation therapy, the patient still had unsteadiness of gait. Gradually, the patient’s condition progressively worsened: instability, unsteadiness of gait increased, headaches became more frequent, their intensity increased, efficiency decreased, fatigue increased, memory decreased, and urinary dysfunction appeared. He was hospitalized in a planned manner, an MRI of the brain was performed.

More details

14 JAN
MRI diagnosis of PCF cholesteatoma

We bring to your attention a clinical case of a 53-year-old patient P., who, after a traumatic brain injury, began to notice hearing loss in his left ear. On this occasion, he was not examined, did not seek medical help, considering it a consequence of the injury. Headache, pain in the left side of the face gradually joined. The neurologist sent for an MRI of the brain.

More details

10 JAN
MRI diagnosis of a tumor of the posterior cranial fossa

We bring to your attention a clinical case of patient R.51 years old, who developed unsteadiness of gait, gradually (within 3-4 months) weakness in the legs joined. I performed an MRI of the brain on my own.

More details

09 JAN
MRI diagnostics of demyelination of the white matter of the brain

We bring to your attention a clinical case of a 52-year-old female patient, who began to notice a decrease in vision in the left eye. I performed MRI on my own, revealed an extracerebral convexital mass in the right frontal region. For diagnostic purposes, selective cerebral angiography was performed, after which speech impairment appeared in the form of simplification, impoverishment, difficulty in formulating a statement, impaired motility, up to the difficulty and impossibility of performing purposeful activity, significant dispersal of attention.Disinhibition and euphoria were noted. Repeated MRI of the brain was urgently performed.

More details

13 DEC
MRI diagnostics of a tumor of the temporal lobe

Patient F., 54, developed generalized convulsions against the background of complete well-being. He turned to a neurologist, was sent for an MRI of the brain.

MRI examination in the medio-basal parts of the right temporal lobe reveals a formation with blurred contours, a hyperintensive MR signal on T2 VI and Tirm,

More details

11 DEC
MRI diagnostics of craniopharyngioma

Patient V.At the age of 23, against the background of prolonged and severe headaches, she began to notice narrowing of the visual fields, deterioration of visual acuity. She turned to a neurologist, who sent her for an MRI of the brain.

On MRI scans in the chiasmatic-sellar region, a large formation of a cystic-solid structure is determined, spreading suprasellar, compressing the corresponding cistern, third ventricle, knee, anterior and middle parts of the corpus callosum.

More details

03 DEC
MRI diagnostics of pituitary adenoma

A clinical case of patient G.62 years old, who has been worried for six months with headaches and progressive weakness, narrowing of the visual fields on both sides. Examined by a neurologist and endocrinologist. An MRI scan of the brain was prescribed.

More details

30 NOV
MRI diagnostics of discirculatory hydrocephalus

We bring to your attention a clinical case of patient S., 68 years old, who developed unsteadiness of gait, increasing in the dark. Relatives began to note emotional lability, memory impairment, sleep disturbance. In addition, the patient was worried about headaches in the temporo-occipital region, dizziness, pain in the cervical and lumbar regions.The patient was admitted to a neurological hospital with a diagnosis of Dyscirculatory encephalopathy of mixed genesis. MRI of the brain was performed.

More details

29 NOV
MRI diagnosis of convexital meningioma

We bring to your attention a clinical case of a patient M., 48 years old, who has been suffering from intense headaches for three years. In addition, he began to notice the appearance of a dense outgrowth in the left frontal region. I performed an MRI of the brain on my own.

More details

09 NOV
MRI diagnostics of microadenoma of the central pituitary gland

We bring to your attention a clinical case of patient A, 31 years old, who has been troubled by headaches and increased blood pressure for several years (up to high numbers: 190/100 mm.Hg), in addition, notes the appearance of excess weight. He is receiving treatment from a therapist for arterial hypertension. The patient independently performed an MRI of the brain.

More details

08 NOV
MRI diagnostics of glioma

We bring to your attention a clinical case of patient L., 41 years old, who, during the last month, had a feeling of a foreign smell and was noted to have lost consciousness for 2-3 minutes, periodically dizziness. The appearance of complaints does not connect with anything, the attacks were repeated daily.The patient was referred by a neurologist for an MRI of the brain.

More details

06 NOV
MRI diagnosis of central pontine myelinolysis

We bring to your attention a clinical case of patient D., 40 years old, suffering from chronic alcoholism, who had two convulsive seizures with loss of consciousness, weakness in the left leg appeared. To exclude organic changes in the brain, the neuropathologist referred the patient to an MRI.

More details

05 NOV
MRI diagnostics of a tumor of the frontal region

We bring to your attention a clinical case of patient K., 31 years old, who has been experiencing persistent nasal congestion for several years. On this occasion, he was not examined and was not treated. Headaches gradually joined in, mainly in the frontal region, which had been intense for the last two weeks. The patient was referred by a neurologist for an MRI of the brain.

More details

23 OCT
MRI diagnosis of cervical cancer

We bring to your attention a clinical case of patient V., 43 years old, who for several years has been troubled by periodic pulling pains in the lower abdomen.I have not been to a gynecologist for several years. Abundant bloody discharge, not associated with the menstrual cycle, has joined. Directed for MRI of the pelvis.

More details

15 OCT
MRI diagnosis of meningioma

A clinical case of a 57-year-old patient B. is presented to your attention. According to the patient, she considers herself a patient over the past few years, when pressing pains gradually appeared in the left fronto-parietal region, which arose periodically, and were poorly controlled with medication.Over the past year, he has noted deterioration in vision. A neurologist recommended an MRI of the brain.

More details

10 OCT
MRI diagnostics of tumor lesions of the lymph nodes

We bring to your attention a clinical case of patient D., 67 years old, who began to notice episodes of shortness of breath, weakness, and excessive sweating. The patient was worried about attacks of a significant drop in blood pressure (up to 80 and 40 mm Hg), about one of them was admitted to the hospital.In addition, the patient noted an increase in the size of the neck on the left (within three months), with which she consulted a surgeon. To clarify the nature of the changes, an MRI scan of the soft tissues of the neck was performed.

More details

04 OCT
MRI diagnostics of cerebellar tumor

We present to your attention a clinical case of a 65-year-old female patient K., who suddenly felt a tinnitus, the next morning, unsteadiness of gait, dizziness joined in. With a diagnosis of acute cerebrovascular accident for 10 days, she was treated by a neurologist at the place of residence, with a weak clinical effect.To clarify the nature of changes in the brain, the patient was referred for MRI.

More details

02 OCT
MRI diagnostics of a brain tumor

We bring to your attention a clinical case of a 56-year-old female patient K., who gradually developed severe apathy, had convulsions once. On this occasion, she did not seek medical help, was not examined. After a few weeks (outdoors), generalized seizures developed. I went to a neurologist and was sent for an MRI of the brain.

More details

04 SEP
MRI diagnosis of multiple sclerosis

Patient N., 29 years old, consulted a neurologist with complaints of visual impairment, dizziness, unsteadiness of gait, numbness of the hands. After a neurological examination, the patient was referred for an MRI of the brain to rule out demyelinating disease.

According to MRI data of the brain in the white matter of both hemispheres periventricularly, as well as in the corpus callosum, multiple foci of “confluent” character of various shapes and sizes are determined (most likely foci of demyelination).

More details

03 SEP
MRI diagnosis of pelvic organ prolapse

We bring to your attention a clinical case of patient K, 67 years old, who was observed by a gynecologist for pelvic organ prolapse. She repeatedly refused the proposed surgical treatment. The patient is worried about the practically constant prolapse of the genitals with their maceration, impaired urination and defecation, pulling pain in the lower abdomen. The attending doctor is directed to an MRI of the pelvis.

More details

14 AUG
Mri examination of headaches

Patient E.32 years old consulted a general practitioner complaining of headaches. After a neurological examination, the patient was referred for an MRI of the brain in order to exclude organic pathology.

According to MRI data, no areas of pathological intensity of the MR signal in the substance of the brain were detected.

More details

01 Aug
MRI diagnostics of cavernous angioma

Patient S., 58 years old, consulted a local neurologist with complaints of frequent headaches and dizziness. After the consultation, the patient was referred for an MRI of the brain at the CMR in order to exclude various pathologies.

MRI of the brain in the right frontal lobe at the level of the basal nuclei revealed a rounded formation with clear even contours, a somewhat non-uniform structure, surrounded by a hypointense rim – a cavernous angioma.

More details

July 27
MRI diagnosis of posterior trifurcation

Patient C, 57 years old, was hospitalized at FBSI “FTSSKE named after V.A. Almazov of the Ministry of Health and Social Development of the Russian Federation “for planned heart surgery. Before surgery, anesthesiologists recommended performing an MRI scan of the cerebral vessels in order to assess their condition before applying general anesthesia in order to avoid complications of ischemic origin.

More details

16 JUL
MRI diagnostics of multifocal brain lesions

Patient R, 70 years old, consulted a neurologist at a medical center with complaints of headaches, periodic dizziness. In order to exclude focal brain damage, the patient was referred for MRI.

MRI of the brain revealed that in the white matter of both hemispheres, subcoritcal and periventricular, multiple “confluent” vascular foci are determined.Diagnosis: chronic cerebral circulation insufficiency. Also, the patient has a mixed hydrocephalus of substitutional genesis.

More details

13 JUL
MRI diagnostics of a vascular genesis gliosis focus in a 34-year-old patient

Patient Z. 34 years old consulted a neurologist with complaints of headaches. After a neurological examination, the patient was referred for an MRI of the brain in order to exclude organic pathology.

According to MRI data of the brain in the white matter of the left frontal lobe at the level of the anterior horn of the left lateral ventricle, a single focus of vascular genesis of gliosis, 3 mm in size, is determined.

Based on the obtained MRI data, the patient was referred for a consultation with a neurologist.

More details

06 JUL
MRI diagnostics of hydrocephalus

Patient N., 56 years old, consulted a general practitioner with complaints of memory impairment. It is known from the anamnesis that the patient worked at a chemical plant for a long time. After a neurological examination, the patient was referred for an MRI of the brain in order to exclude organic pathology.

More details

05 JUL
MRI diagnostics of a retrocerebellar cyst

Patient R.At the age of 28, a planned MRI examination of the brain for recurrent dizziness revealed a local expansion of the retrocerebellar space – a retrocerebellar cyst.

Based on the MRI examination data, the patient was referred to a neurologist at the medical center to determine further treatment tactics.

More details

26 JUN
MRI diagnosis of vascular plexus cysts

In a 34-year-old patient N., CT of the brain revealed enlargement of the posterior horns of the lateral ventricles of the brain.In order to clarify the nature of the changes, the patient was prescribed an MRI of the brain. At MRI of the brain in the projection of the posterior horns of the lateral ventricles of the brain, in the projection of the choroid plexus, cystic formations corresponding to the cysts of the vascular plexuses are determined.

More details

20 JUN
MRI diagnostics of multiple brain formations

We bring to your attention a clinical case of a 56-year-old female patient K., who gradually developed severe apathy, had convulsions once.On this occasion, she did not seek medical help, was not examined. After a few weeks (outdoors), generalized seizures developed. I went to a neurologist and was sent for an MRI of the brain.

More details

14 JUN
MRI diagnosis of vascular malformation in a newborn baby

A clinical case of a 5-day-old patient D. is presented to your attention. During the feeding, the mother noticed a twitching of the pen in the newborn daughter, which she reported to the pediatrician. There were no other changes in the child’s condition.To exclude pathology of the brain, MRI was performed.

According to MRI in the left parietal lobe and in the region of the posterior horn of the left lateral ventricle, a vascular ball associated with the choroid plexus of the ventricle is determined.

More details

11 JUN
MRI diagnostics of a single focus of gliosis

Patient I., 28 years old, consulted a neurologist with complaints of headaches. After a neurological examination, the patient was referred for an MRI of the brain in order to exclude organic pathology.

According to the MRI of the brain in the white matter of the left frontal lobe, a single focus of vascular genesis of gliosis, 3 mm in size, is determined. There is also an uneven thickening of the mucous membrane in the right and left maxillary sinus with the presence of fluid.

More details

08 JUN
MRI diagnostics of internal hydrocephalus

Patient W., 83 years old, turned to a district neurologist with complaints of memory loss, increased fatigue. The patient was referred for an MRI of the brain in order to exclude various pathologies.

MRI of the brain revealed: MRI signs of chronic cerebral circulation insufficiency; pronounced open internal hydrocephalus, indicating signs of atrophic changes in the brain.

More details

06 JUN
MRI diagnostics of cerebral astrocytoma

Patient F., 54 years old, applied to the CMRT in order to control the continued tumor growth, because noted a deterioration in his health over the past month.

On a series of MRI tomograms of the brain after intravenous contrasting, against the background of postoperative gliocystic changes, there is a selective increase in the intensity of the MR signal, which indicates a continued growth of the pathological formation.

More details

05 JUN
MRI diagnostics of chiasmatic-sellar tumor

We bring to your attention a clinical case of patient E., 53 years old, who is worried about headaches and decreased vision, more in the left eye. I turned to a neurologist with these complaints. The ophthalmologist revealed signs of congestion in the fundus. The patient is referred for an MRI of the brain.

On MRI tomograms in the chiasmatic-sellar region, a volumetric pathological formation is visualized, with ante-, infra-, supra- and laterosellar (left) growth, a homogeneous structure, with a total size of 5.7×3.6×4.0 cm.

More details

17 MAY
MRI diagnostics of vascular diseases

The patient developed a severe headache with a single loss of consciousness, then gradually developed nausea, vomiting, and dizziness. The next day, MRI was performed. MRI in the vascular mode (a, b, c) revealed spontaneous intracranial hemorrhage (1) and its cause – an aneurysm (2) measuring 3x4x6 mm. Hospitalized in the hospital. X-ray angiography (d) performed at the hospital confirmed the cause of the hemorrhage – aneurysm.

More details

17 MAY
MRI diagnostics of anterior trifurcation

A 50-year-old man consulted a neurologist complaining of daily headaches in the afternoon, and therefore was referred for an MRI angiography of the cerebral vessels. On the obtained images of cerebral vessels in 3D-TOF mode, the variant of the divergence of both anterior cerebral arteries from the right internal carotid artery (anterior trifurcation) and the absence of visualization of the right vertebral artery are determined, which causes the patient’s clinical symptoms.The patient was referred for a consultation with a neurologist, where he was prescribed specialized therapy.

More details

09 MAY
MRI diagnostics of pituitary microadenoma

We present to your attention a clinical case of a patient with a pituitary microadenoma revealed by MRI.

Patient R., 24 years old with complaints of menstrual irregularities, consulted a regional endocrinologist. The doctor ordered the patient to have a blood test for pituitary hormones. Blood tests showed an increase in prolactin levels (1000 μIU / ml).Further, to clarify the nature of the changes in the pituitary gland, the patient was referred for MRI of the pituitary gland with intravenous contrast enhancement.

More details

03 MAY
MRI diagnosis of multiple sclerosis in a 22-year-old patient

A clinical case of a 22-year-old patient L. with complaints of hand numbness, unsteadiness of gait, visual disturbances is presented to your attention. The patient decided to perform an MRI of the brain on his own. No changes were found on a series of MRI tomograms of the brain. The patient himself calmed down and decided not to go to the doctors again.However, the patient’s mother noticed some symptoms in her son and took him to the district neurologist. The neurologist, relying on the absence of changes in the brain, interpreted the symptoms as signs of overwork. The patient’s mother decided to consult her son additionally in the hospital with another neurologist, who suspected a demyelinating disease and prescribed an MRI of the cervical spine.

More details

The role of magnetic resonance imaging in detecting early signs of brain damage in arterial hypertension

The article presents data on the prevalence of increased intensity foci in the white matter, lacunar infarctions and cerebral microbleeds in patients with essential arterial hypertension.The possibilities of magnetic resonance imaging in identifying the initial signs of brain damage as a target organ for arterial hypertension are considered. In the given clinical case, magnetic resonance imaging revealed the initial signs of brain damage in a middle-aged patient with untreated uncomplicated first-degree arterial hypertension.

Rice. 1. Single focal changes in the white matter of the brain, leukoaraiosis in the anterior horns of the lateral ventricles as “caps” (MRI image in T1 mode)

Rice.2. Single microhemorrhage (MRI image in SWI mode)

In middle-aged patients with arterial hypertension (AH) without a history of cardiovascular and / or cerebrovascular diseases, cerebrovascular lesions are found in 44% of cases [1]. Neuroimaging using various pulse sequences of magnetic resonance imaging (MRI) can be used to detect early signs of brain damage in small vessel disease [2].Currently, three standard MRI sequences are used: T1, T2 and FLAIR modes [3].

In most cases, foci of hyperintensity in the white matter of the brain on T2-weighted MRI images are located bilaterally and symmetrically [4], more often in the periventricular areas and deep white matter, less often in the infratentorial regions of the brain [5]. For their assessment, visual analog scales are used – the Fazekas scale and the Sheltens scale [6].

In elderly and senile people suffering from hypertension, during MRI, in addition to foci of increased intensity in the white matter of the brain, asymptomatic heart attacks are often detected, mainly small in size with localization in the deep parts of the brain (the so-called lacunar heart attacks). The incidence of such heart attacks varies from 10 to 30% [7]. Focuses of hyperintensity in the white matter and silent cerebral infarctions, in turn, are associated with an increased risk of stroke, cognitive impairment, and dementia [7–10].

According to the results of MRI of patients with hypertension without cardiovascular diseases, latent cerebrovascular foci are more common than subclinical heart and kidney damage (44, 21 and 26%, respectively), while signs of damage to other target organs may be absent [11].

Investigation of the relationship between arterial hypertension and brain lesions using MRI

The effect of hypertension on the risk of developing pathologies of the brain as a target organ has been evaluated in several large studies [12–20].

In a multicenter neuroimaging MRI study (3C) -Dijon, 1319 people (61.6% of women) took part, of which 75% suffered from hypertension. The average age of patients is 72.4 ± 4.1 years [12]. The observation period is four years. At the time of inclusion in the study, patients underwent three measurements of blood pressure (BP) in a sitting position and MRI of the brain on a tomograph with a magnetic field power of 1.5 T in standard sequences.

In the group of patients with hypertension, there was a greater volume of lesions in the white matter of the brain compared with the group of patients without hypertension (p = 0.002).At the same time, the maximum values ​​of the volume of lesions of the white matter were recorded among those who received antihypertensive therapy, but did not reach the target BP values ​​compared to those who received it, reached the target BP values ​​and did not previously take antihypertensive drugs (p = 0.0009). In addition, a linear relationship was found between the increase in diastolic blood pressure (DBP) for every 5 mm Hg. Art. and the volume of lesions of the white matter of the brain (p = 0.01). After four years of follow-up, patients who received antihypertensive therapy but did not reach the target BP values ​​still had the largest volume of brain lesions (p

The ARIC multicenter epidemiological cohort study investigated the causes and clinical outcomes of atherosclerosis, as well as cardiovascular risk factors in middle-aged people [13].From 1987 to 1989, the study included 15 792 people (8710 women and 7082 men) aged 45 to 64 years. The study was designed for four visits every three years. During the third visit (1993–1995), 1920 patients (539 women, mean age 62 ± 4.4 years) underwent MRI of the brain on a tomograph with a magnetic field power of 1.5 T in modes T1, T2, FLAIR. Focal brain damage was assessed on a ten-point scale, where zero is the absence of focal changes, nine are pronounced focal changes.AH was found in 49% of patients, of whom 11% did not receive antihypertensive therapy, 22% achieved the target BP level while taking antihypertensive drugs, 16% received antihypertensive therapy, but did not reach target BP values. At an additional fifth visit (2004–2006), 983 patients (605 women, mean age 72 ± 4.0 years) underwent a repeat MRI of the brain. It was found that the total mean systolic blood pressure (SBP) is a predictor of the progression of lesions of the white matter of the brain (2.6 cm ³ , p

The cross-sectional neuroimaging study CARDIA analyzed the relationship between vascular risk factors and early signs of brain damage [14].In 1985-1986. the study included 5115 patients from 18 to 30 years old. In 2010–2011. 75% of the cohort were re-examined. The examination involved a three-fold measurement of blood pressure and an MRI of the brain on a tomograph with a magnetic field power of 3 T in modes T1, T2, MPRAGE, FLAIR, DTI, pCASL. In the group of patients with hypertension (n = 280, mean age – 50.3 ± 3.5 years), an increase in SBP significantly correlated with a more pronounced atrophy of the white matter of the brain (p = 0.002) and a decrease in the total volume of the brain compared with the control group …

In a prospective study by W.B. White et al., Evaluated the progression of focal brain lesions in 72 elderly patients (mean age 82 years) [15]. AH was diagnosed in 70% of patients, 64% of them were taking antihypertensive therapy. The observation period was two years. All patients underwent daily monitoring of blood pressure, measurement of office blood pressure, as well as MRI of the brain on a tomograph with a magnetic field power of 3 T in standard pulse sequences.

The authors of the study found that office BP levels did not correlate with the degree of progression of hyperintense lesions. However, the relationship between individual indicators of daily blood pressure monitoring and the volume of foci in the brain was statistically significant. Thus, at baseline and at the end of observation in the group of patients with an average daily SBP ≤ 135 mm Hg. Art. the total volume of lesions in the white matter of the brain was significantly less than in the group of patients with an average daily SBP ≥ 135 mm Hg.Art. (1.26 ± 0.15%, p = 0.03 versus 1.96 ± 0.26%, p = 0.03).

In a longitudinal population-based study involving 665 patients from the Rotterdam study, it was demonstrated that only the SBP level affects the progression of focal brain damage [16]. In the group of untreated patients with hypertension, there was also a more rapid progression of the volume of foci in the white matter of the brain compared with the group of patients who did not reach the target blood pressure against the background of regular antihypertensive therapy (p

The AGES-Reykjavik study included 4057 patients who participated in the population-based study Reykjavik [17].The latter was carried out from 1967 to 1996. Persons born in 1907–1935 were selected for it. and living in Reykjavik. The patients were divided into two groups. Patients of the first group (n = 1365, 49% of women, mean age – 51 ± 7.0 years) suffered from hypertension in middle age, 251 (6%) of them were taking antihypertensive therapy. Patients of the second group (n = 2692, 64% of women, mean age – 50 ± 6.0 years) did not suffer from hypertension in middle age. In the first group, the mean SBP was 148 ± 15 mm Hg. Art., DBP – 92 ± 9 mm Hg.Art., in the second – 123 ± 9 and 78 ± 6 mm Hg. Art. respectively.

From 2002 to 2006, new data were obtained and used in the AGES-Reykjavik study. In patients, blood pressure was measured three times, cognitive functions and the brain were examined (MRI on a tomograph with a magnetic field power of 1.5 T in the T1, T2, FLAIR sequences).

The average age of patients in the first group was 77 ± 5.0 years, the average SBP was 149 ± 21 mm Hg. Art., DBP – 76 ± 10 mm Hg.Art. 82% of patients received antihypertensive therapy. The average age of patients in the second group was 75 ± 5.0 years, the average SBP was 139 ± 19 mm Hg. Art., DBP – 73 ± 9 mm Hg. Art. Antihypertensive drugs were taken by 53% of patients.

In patients with hypertension, significantly more pronounced focal lesions of the white matter of the brain were observed (relative risk (RR) 1.3, 95% confidence interval (CI) 1.1–1.6) and lacunar infarctions (RR 1.2, 95% CI 1.1-1.4).

High SBP values ​​in the older age group were associated with an increased risk of lacunar infarctions (p = 0.01) and focal brain lesions (p = 0.002), but only for middle-aged patients without hypertension.

High DBP in the older age group correlated with a high risk of focal brain damage both in patients with hypertension (p = 0.007) and in patients without hypertension in middle age (p

In a study by Z. Gao et al. 148 patients were included (143 men and five women, mean age 82.2 years). AH was recorded in 113 (76.4%) patients, type II diabetes mellitus – in 57 (38.5%), hyperlipidemia – in 31 (20.9%) patients [18].

A history of eight patients (mean age 81.3 ± 13.0 years) had hemorrhagic stroke, 63 (mean age 84.4 ± 6.9 years) had ischemic stroke, 20 (mean age 83.1 ± 6.8 years) – transient ischemic attack, 57 (average age – 79.6 ± 8.7 years) – lacunar stroke.

The patients underwent three measurements of office blood pressure and MRI of the brain using a tomograph with a magnetic field power of 1.5 T in standard pulse sequences and SWAN mode. The frequency of damage to the deep parts of the white matter of the brain in patients with hypertension was significantly higher than in the control group – 64.6 and 42.9%, respectively, p = 0.002.

In a cross-sectional study, J.C. Foster-Dingley et al. included 220 elderly patients (mean age 80.7 ± 4.1 years, 125 (56.8%) women) [19].Inclusion criteria: age 75 and older, taking antihypertensive therapy, presence of mild cognitive impairment according to the Short Mental Status Assessment Scale, SBP ≤ 160 mm Hg. Art. Exclusion criteria: dementia, history of ischemic stroke or transient ischemic attack, myocardial infarction, coronary heart disease, heart failure, low life expectancy.

Before the start of the study, the patients underwent a two-fold measurement of blood pressure, the mean (1/3 SBP + 2/3 DBP) and pulse (SBP – DBP) values ​​were calculated.MRI of the brain was performed on a tomograph with a magnetic field power of 3 T in standard sequences, as well as in DTI and SWI modes. Periventricular foci were found in 132 (60%) patients, subcortical – in 113 (51.4%), lacunar infarctions – in 59 (26.8%) patients. There was no significant correlation between SBP and / or DBP levels and the volume of lesions in the white matter of the brain, the presence of periventricular or subcortical foci, and lacunar infarctions.

WITH.Rosano et al. evaluated the effect of SBP on the structure of white matter tracts in the brain in a cohort of elderly patients who took part in the HEALTH ABC study [20]. The longitudinal cohort study HEALTH ABC (1997–1998) recruited 3,075 patients aged 70 to 79 years. The main criteria for inclusion in the study were the difficulty in walking independently, the ability to walk a quarter mile or climb ten steps, and the absence of cancer. Patients had to see a doctor every year.

In 2006-2008. only 819 patients in the HEALTH ABC study were able to follow up. They were asked to participate in the Healthy Brain Project Ancillary. The study included 311 patients (130 (41.8%) men, mean age 82.9 ± 2.0 years). AH was detected in 217 (69.3%) of them, only 193 (62.1%) received antihypertensive therapy. The observation lasted ten years. During the study period, the patients were measured twice annually.In addition, all patients underwent MRI of the brain on a 3 T tomograph in the sequences FLAIR, MPRAGE, DTI.

The results of the study demonstrated that increased mean SBP values ​​correlated with a higher prevalence of focal white matter lesions (p = 0.002). Baseline high pulse BP (PAP) was also associated with a high prevalence of lesions in the white matter of the brain (p = 0.03). At the same time, the relationship between the intake of antihypertensive drugs and the severity of focal lesions of the white matter has not been established.Increase in SBP for every 10 mm Hg. Art. increased the risk of focal brain damage approximately tenfold (RR 10.4, 95% CI 10.2-10.6, p = 0.0001). Relatively recently, foci of another type, microbleeds, were identified in 5% of hypertensive patients [21].

MRI in SWI / SWAN mode allows visualizing traces of small hemorrhages after a long period, deposits of iron-containing substances in certain structures of the brain, as well as contrasting venous blood.Cerebral microbleeds are visualized as hypointense foci 3–10 mm in size due to the paramagnetic properties of local macrophage depots containing hemosiderin [22].

In a study by L. Henskens et al. included 218 patients with hypertension (50.5% men, mean age 52.5 ± 12.6 years). The mean SBP was 174 ± 24 mm Hg. Art., DBP – 104 ± 13 mm Hg. Art. [23]. The patients underwent three measurements of office blood pressure in a sitting position, daily monitoring of blood pressure and MRI of the brain on a 1.5 T tomograph in T1, T2, FLAIR and SWI modes.Microbleeds were found in 35 (16.1%) patients (95% CI 11.1–21.0). Patients with microbleeds were older and had higher office BP levels compared to patients without microbleeds (p

Z. Gao et al. found that cerebral microbleeds in patients with hypertension were recorded more often than in patients of the control group (51.3 and 20.0%, respectively, p = 0.001) [18]. Cerebral microbleeds correlated with focal lesions of the white matter of the brain only in the AH group (p

According to a study by J.C. Foster-Dingley et al., 25% of elderly patients with hypertension had cerebral microbleeds [19].

Z. Jia et al. assessed the relationship of cardiovascular risk factors with the localization and frequency of occurrence of cerebral microbleeds [24]. The study included 393 patients with cerebral microbleeds (137 women, mean age 70.7 ± 10.8 years).

Arterial hypertension of the first degree was detected in 141 (35.9%) patients, second degree – in 89 (22.6%), third degree – in 81 (20.6%) patients.Diabetes mellitus of the second type – in 101 (25.7%) patients. 94 (23.9%) patients received antiplatelet therapy. 122 patients had focal brain damage, 72 patients suffered from transient ischemic attack.

The participants of the study underwent MRI of the brain on a tomograph with a magnetic field power of 3 T in the T1, T2, FLAIR, SWI sequences. An increase in SBP by one standard deviation correlated with the presence of cerebral microbleeds in the medial lenticulostriatal artery (RR 1.02, 95% CI 1.00–1.03, p

It should be noted that in almost all studies devoted to this problem, there were significant limitations: different age of patients, the presence of concomitant diseases, for example, diabetes mellitus, a history of transient ischemic attacks that influenced the results obtained, the use of antithrombotic drugs that could cause or a provoking factor in the development of cerebral microbleeds.

Clinical case

Patient K., 44 years old, complained of an episodic increase in blood pressure, decreased memory for current events, difficulties in performing complex work.

From anamnesis: increase in blood pressure to 150/95 mm Hg. Art. was recorded during the last three years when undergoing medical examination. He did not receive examination and treatment for hypertension, and did not measure blood pressure. I did not see a doctor because I believed that blood pressure increased due to stress at work.In the last month and a half, he has been measuring blood pressure quite often, its values ​​vary within 150–160 / 90–100 mm Hg. Art. At high, according to the patient, blood pressure took captopril or nifedipine. He did not receive permanent antihypertensive therapy.

During the last six months, the patient began to find it difficult to concentrate when performing complex professional tasks, forgetfulness appeared (he remembers that he promised to do something, but does not remember what exactly), difficulties in perceiving information and planning his working day.

The patient has never smoked, drinks alcohol once a week (300-500 ml of low-alcohol drinks (beer)).

Family history is burdened. The patient’s mother suffered from hypertension (maximum BP values ​​- 180/100 mm Hg). At the age of 70, she suffered a hemorrhagic stroke. She died at the age of 75 as a result of a malignant stomach formation. The father died of cirrhosis of the liver.

Survey. Somatic status: the skin is clean, normal moisture and elasticity.Swollen legs and feet. Body mass index – 27.2 kg / m ² , waist circumference – 93 cm. The sound of the lungs is clear, pulmonary. At auscultation of the lungs – over the entire surface, breathing is weakened vesicular, no wheezing. The respiratory rate is 18 per minute. Percussion revealed a displacement of the left border of the relative dullness of the heart to the left (1.5 cm outside of the left midclavicular line). Heart sounds are clear, rhythmic. Heart rate (HR) – 77 per minute. BP – 150-152 / 95-98 mm Hg.Art. On palpation, the abdomen is soft, painless. The size of the liver according to Kurlov is 9.5 × 8.0 × 7.0 cm. The symptom of tapping is negative on both sides.

Neurological status: in clear consciousness, contact, adequate, critical, correctly oriented in place, time and self. The cranial innervation is intact, the proboscis reflex is revealed. There are no paresis. Muscle tone is normal. Tendon reflexes are vivid, D = S, zones of evocation are normal, pathological reflexes are absent.Sensitivity is not changed. Performs coordination tests satisfactorily. Stable in the Romberg position, the Romberg test is negative. Gait – no peculiarities. Controls the pelvic organs.

The results of neuropsychological testing: 29 points on the Montreal scale for assessing cognitive functions, twice mistaken in the serial counting, made a mistake in the generalization test (when asked what is common between a watch and a ruler, he answered that the clock measures time, but there are divisions on the ruler) …

Verbal Association Test. In a test for categorical associations, he named nine animals – fluency is reduced. I performed the test for categorical associations satisfactorily – I named 13 words.

Test of communication of numbers and letters. Completed Part B in 254 seconds (the norm for the corresponding age group and educational level is no more than 106 seconds). The execution time for part A is not violated – 30 seconds.

Stroop test. The first part (reading the names of colors printed in black, T1) – 52 seconds, the second part (naming the colors, T2) – 64 seconds, the third part (naming the color of a word, where the font color differs from the meaning of the word, T3) – 188 seconds.The interference coefficient (T3-T2) is 124 (the greater this difference, the more pronounced the effect of interference and, consequently, the rigidity (narrowness, rigidity) of cognitive control).

General analysis of blood and urine – no pathological changes.

Biochemical blood test: creatinine – 90.9 μmol / l, glomerular filtration rate – 88 ml / min / 1.73 m ² , potassium – 4.7 mmol / l, fasting glucose – 5.3 mmol / l, total cholesterol – 4 mmol / l, low density lipoproteins – 1.3 mmol / l, triglycerides – 0.9 mmol / l, high density lipoproteins – 1.2 mmol / l.

Electrocardiogram: sinus rhythm, correct. Heart rate – 74 per minute. The horizontal position of the electrical axis of the heart.

Echocardiogram: the cavities of the heart are not dilated. The walls of the left ventricular myocardium are not thickened. The global systolic function of the left ventricle is preserved (ejection fraction – 71%). Zones of violation of the local contractility of the myocardium were not revealed. Zero-first degree mitral regurgitation. First degree tricuspid regurgitation.The diastolic function of the left ventricle is not impaired. There were no signs of pulmonary hypertension (mean pressure in the pulmonary artery was 20 mm Hg).

24-hour blood pressure monitoring:

• average daily SBP – 138 mm Hg. Art. (norm – less than 130 mm Hg. Art.), DBP – 82 mm Hg. Art. (normal – less than 80 mm Hg. Art.), PAD – 56 mm Hg. Art., heart rate – 83 per minute;
• average daily SBP – 144 mm Hg. Art. (normal – less than 135 mm Hg. Art.), DBP – 88 mm Hg. Art.(normal – less than 85 mm Hg. Art.), PAD – 57 mm Hg. Art., heart rate – 83 per minute;
• mid-night SBP – 117 mm Hg. Art. (normal – less than 120 mm Hg. Art.), DBP – 63 mm Hg. Art. (the norm is less than 70 mm Hg), PAD – 54 mm Hg. Art., heart rate – 84 per minute;
• daytime SBP variability – 13 mm Hg. Art., DBP during the day – 11 mm Hg. Art., GARDEN at night – 20 mm Hg. Art., DBP at night – 12 mm Hg. Art., the type of diurnal profile – dipper, the magnitude of the morning rise in SBP – 95 mm Hg. Art., DBP – 88 mm Hg. Art., the rate of the morning rise of the SBP is 20 mm Hg.Art. per hour, DBP – 20 mm Hg. Art. at one o’clock.

Triplex scanning of the carotid arteries: the left common carotid artery – the diameter of the middle part – 6.5 mm. The walls are of increased echogenicity, the average thickness of the “intima – media” complex along the posterior wall is 0.78 mm. A heterogeneous, predominantly hypoechoic atherosclerotic plaque with a thickness of up to 3.4 mm and a length of up to 1.8 cm with a transition to the bulb of the internal carotid artery, stenosis up to 36% is located along the anterior wall in the area of ​​bifurcation.With color Doppler mapping, the blood flow is laminar. The peak systolic linear blood flow velocity is 62 cm / s. Right common carotid artery – middle part diameter – 6.6 mm. The walls are of increased echogenicity, the average thickness of the “intima – media” complex in the bulbous part along the posterior wall is 0.63 mm. A heterogeneous atherosclerotic plaque with areas of calcification up to 2.3 mm thick and up to 1.2 cm long, passing into the internal carotid artery, stenosis up to 24% is located along the posterior wall in the area of ​​bifurcation.With color Doppler mapping, the blood flow is laminar. Peak systolic linear blood flow velocity – 61 cm / s.

Conclusion: non-occlusive atherosclerotic plaques in the system of both carotid arteries at the extracranial level. The blood flow through the carotid arteries at the extracranial level is preserved. No hemodynamically significant obstacles to blood flow through the carotid arteries were found.

MRI of the brain on a Siemens Magnetom 3 T tomograph in the sequences T1, T2, FLAIR, SWI (Fig.1 and 2): the midline structures are not displaced. The ventricular system is symmetrical. The Mamillo-Pontine distance has not been reduced. The arachnoid spaces of the convexial surface of the brain are not expanded. Corpus callosum without deformation, thickness not changed. CSF dynamics is compensated. The pituitary gland in the Turkish saddle. The structure of the gland without focal changes. The craniovertebral junction is formed normally. The hippocampus is of normal volume. Coarse leukoaraiosis in the anterior horns of the lateral ventricles of the “cap” type. In moderate amounts, focal changes in the white matter.SWI is a single extravasate. No pathological vascular structures were identified.

Conclusion: disease of small vessels of the brain, the first degree on the Fazekas scale.

Thus, a middle-aged patient with short-term (three years) AH of the first degree has brain lesions: focal changes in the white matter of the brain and a single extravasate. At the same time, other target organs are not damaged – there is no left ventricular myocardial hypertrophy, the glomerular filtration rate is normal.

Conclusion

For patients with hypertension, neuroimaging using various pulse sequences of MRI can be recommended already in the early stages of the disease to detect early signs of brain damage and prescribe appropriate therapy, which will improve the overall prognosis.

90,000 Benefits of MRI | MRI diagnostics

You can make an appointment by calling 8 (3532) 433-505,
or using the appointment form

Magnetic resonance imaging (MRI) allows you to get an image of almost all body tissues, since it is possible to change the time of action of the radio wave flux.

Due to the fact that magnetic resonance imaging gives a very detailed image, it is considered the best technique for detecting various tumors, investigating disorders of the central nervous system and diseases of the musculoskeletal system. As a result of magnetic resonance imaging (MRI), a full, three-dimensional picture of the investigated area of ​​the body is obtained. Thanks to magnetic resonance imaging (MRI), it becomes possible, without using contrast agents, to thoroughly examine many organs and systems.

Modern tomographs allow the scanning method to obtain tomograms in an arbitrarily oriented plane without changing the position of the patient. At the same time, the MRI study uses similar CT principles of spatial information coding and data processing. In a single scan of, for example, the head, data are usually collected from about 20 levels of the skull and brain, with a slice thickness of 4-5 mm. The higher the magnetic field strength of the tomograph, this value is expressed in Tesla, the thinner these sections can be made, the more accurate the study will be, the more accurate the result will be.Most clinical magnetic resonance imaging (MRI) scanners contain 0.5-1.5 Tesla magnets and only a few contain 3T magnets. A stronger magnetic field can provide a more detailed examination. The scanning time depends on the tasks and parameters of the magnetic resonance imager and is on average from 2-7 minutes (for magnetic resonance imaging MRI of the head) to 60 minutes. Ultimately, images of slices of tissue being examined, such as brain tissue, appear on the display screen.

The method of magnetic resonance imaging (MRI) makes it possible to visualize sections of the skull and brain, spinal column and spinal cord on the display screen, and then on X-ray film.The information makes it possible to differentiate the gray and white matter of the brain, to judge the state of its ventricular system, subarachnoid space, to identify many forms of pathology, in particular volumetric processes in the brain, zones of demyelination, foci of inflammation and edema, hydrocephalus, traumatic lesions, hematomas, abscesses, foci of manifestation cerebral circulation disorders of ischemic and hemorrhagic type, by the way, ischemic foci in the brain can be detected in a hypodense form as early as 2-4 hours after a stroke.

An important advantage of magnetic resonance imaging (MRI) over CT is the ability to obtain an image in any projection: axial, frontal, sagittal. This makes it possible to visualize the subtentorial space, the spinal canal, to reveal an auditory nerve neuroma in the cavity of the internal auditory canal, a pituitary tumor, a subdural hematoma in the subacute period, even in cases when it is not visualized on CT.

Magnetic resonance imaging (MRI) has become the main method for detecting some forms of anomalies: anomalies of the corpus callosum, Arnold-Chiari anomalies, foci of demyelination in the paraventricular and other parts of the white matter of the brain in multiple sclerosis.

Magnetic resonance imaging (MRI) reveals foci of cerebral ischemia earlier than computed tomography (CT), and they can be detected in the brain stem, in the cerebellum, in the temporal lobe. On magnetic resonance imaging (MRI), contusion foci, brain abscesses and areas of cerebral edema are clearly visible.

Magnetic resonance imaging (MRI) plays an important role in determining the causes of dementia. At the same time, changes in brain tissue are often nonspecific and sometimes difficult to differentiate, for example, foci of ischemia and demyelination.

Valuable information is revealed on spine MP-tomograms, especially on sagittal sections. At the same time, the structural manifestations of osteochondrosis are visualized, in particular the state of the vertebrae and ligamentous apparatus, intervertebral discs, their prolapse and impact on the dura mater, spinal cord, cauda equina, intravertebral neoplasms, manifestations of hydromyelia, hematomyelia and many other pathological processes are also visualized.

The diagnostic potential of magnetic resonance imaging (MRI) can be increased by prior administration of certain contrast agents.As a contrast agent injected into the bloodstream, an element from the group of rare earth metals is usually used – gadolinium, which has the properties of a paramagnetic, is injected intravenously.

The advantage of magnetic resonance imaging (MRI) over computed tomography (CT) is most obvious when examining those parts of the nervous system that cannot be imaged with CT due to the overlap of the examined brain tissue by adjacent bone structures. In addition, with magnetic resonance imaging (MRI), one can distinguish inaccessible CT changes in the density of brain tissue, white and gray matter, detect brain tissue damage in multiple sclerosis, etc.

With magnetic resonance imaging (MRI), the patient is not exposed to ionizing radiation. However, there are some limitations to the use of magnetic resonance imaging (MRI). Thus, magnetic resonance imaging (MRI) is contraindicated in the presence of metallic foreign bodies in the cranial cavity, since there is a danger of their displacement under the influence of a magnetic field and, consequently, additional damage to nearby brain structures. Magnetic resonance imaging (MRI) is contraindicated if patients have an external pacemaker, pregnancy, severe claustrophobia (fear of being in a cramped room).Complicates the use of MRI examination of its duration (30-60 minutes), during which the patient must be immobile.

Magnetic resonance imaging of the brain with contrast (children)

ANMO “Stavropol Regional Clinical Consultative and Diagnostic Center”:

355017, Stavropol, st. Lenin 304

(8652) 951-951, (8652) 35-61-49 (fax)

(8652) 951-951, (8652) 31-51-51 (information service)

View details

Separate subdivision “Diagnostic center on the Western bypass”:

355029 m.Stavropol, st. Western Bypass, 64

(8652) 951-951, (8652) 31-51-51 (contact phone)

(8652) 31-68-89 (fax)

View details

Family doctor’s clinic:

355017 Stavropol, K. Marx Ave., 110 (behind the Central Department Store)

(8652) 951-951, (8652) 31-51-51 (contact phone)

(8652) 31-50-60 (registry)

View details

Nevinnomyssk branch:

357107, m.Nevinnomyssk, st. Nizyaeva 1

(86554) 95-777, 8-962-400-57-10 (registry)

View details

Separate structural unit in Cherkessk:

369000, Cherkessk, st. Umar Aliyeva 31

8 (8782) 26-48-02, + 7-988-700-81-06 (contact phones)

View details

Separate structural unit in g.Eliste:

358000, Elista, st. Republican, 47

8 (989) 735-42-07 (contact phones)

View details

ZAO Regional Clinical Diagnostic Center:

355017 Stavropol, st. Lenin 304

(8652) 951-951, (8652) 35-61-49 (fax)

(8652) 951-951, (8652) 31-51-51 (information service)

View details

Separate structural unit on the street.Savchenko, 38 bldg. 9:

355021, Stavropol, st. Savchenko, 38, bldg. nine

8 (8652) 316-847 (contact phone)

View details

Separate structural unit on the street. Chekhov, 77:

355000, Stavropol, st. Chekhov, 77

8 (8652) 951-943 (contact phone)

View details

Separate structural unit in g.Mikhailovsk:

358000, Mikhailovsk, st. Lenin, 201 (in the new residential area “Aquarelle”).

8 (988) 099-15-55 (contact phone)

View details

Principles and advantages of the tractography method when MR tractography is shown

The task of tractography, one of the additional functions of magnetic resonance imaging, includes the image of the pathways of the white matter of the brain with high visualization accuracy.

White matter is a whole set of different nerve structures through which impulses are transmitted. If the gray matter is responsible for creating these impulses, then the white only ensures their transmission. The quality of the functioning of the brain depends on the speed of this process.

The examination is based on the diffusion tensor neuroimaging method, which allows examining the pathways (tracts of the white matter), detecting disturbances in the course and structural features of these pathways, which is impossible with standard MRI.

Method principle

White matter is characterized by diffusion of water molecules along nerve fibers. If the integrity of the fibers is violated, the trajectory of the diffusion process changes. MRI scanner with tractography function capable of:

• to identify changes in the direction of water diffusion with the determination of numerical coefficients;
• visualize the area of ​​interest in a graphic image on the monitor screen at the required scale;
• create volumetric tractograms.

The resulting tractogram can be studied in real time, displayed on electronic or paper media.

Make an appointment now!

Advantages of the

method

This research method allows visualization of such microstructural changes that are not recorded by a conventional MR image:

• White matter tract disorders – damage or displacement;
• pathology of myelination (formation of an insulating sheath) of nerve fibers at different ages;
• neurodegenerative destruction of nerve fiber cells;
• the degree of involvement of the pathways in oncogenic processes.

When MR tractography is shown

Brain tractography is used in various branches of medicine – neurology, psychiatry, cardiology, pediatrics for the diagnosis of neurodegenerative, tumor, vascular, ischemic, traumatic, inflammatory pathologies accompanied or caused by damage to the white matter tracts:

• infantile cerebral palsy,
• Alzheimer’s disease;
• Parkinson’s disease;
• brain injuries;
• malignant and benign neoplasms;
• ischemic brain damage in newborns;
• schizophrenia;
• depressive disorders caused by organic disorders;
• multiple sclerosis;
• epilepsy;
• genetically determined hereditary tremor;
• congenital disorders of myelination of tracts.

Tractography is of exceptional importance when planning an operation. For example, when a neoplasm is detected, the surgeon can accurately determine the boundaries of the tumor and the degree of its penetration into healthy tissues. This will ensure the most complete removal of the neoplasm with a good prognosis for a stable therapeutic result without relapse.

Tractography of the brain of men and women

Despite the existing myths, the brains of men and the brains of women do not differ in the structure of neural connections; therefore, MRI tractography for men and women follows the same protocol.

90,000 MRI of the brain with contrast in the network of clinics “Polyclinic.ru”

How is MRI of the brain with contrast

Consider a detailed algorithm for examining the brain with contrast by means of MRI:

• Before the examination, the patient must turn off the phone, if necessary, change into clothes without metal elements.
• An MRI diagnostician gives a short briefing.
• As soon as the patient is fully informed about the upcoming manipulation, a contrast agent is injected. This is done very slowly, while the doctor monitors the patient’s condition. The amount of contrast agent is determined on an individual basis, depending on the injected drug and the body weight of a person.
• After the injection of the contrast agent, the patient is placed on the table, if necessary, it is fixed with belts, the table is brought inside the tomograph.
• As soon as the images are ready, the patient is released from the straps and helped to stand up.

Usually the research lasts no more than half an hour. After the diagnosis, you need to wait until the doctor deciphers the results.

After the procedure, in most cases, unpleasant sensations. Only in some cases, after the administration of a contrast agent, a slight tingling sensation in the mouth or slight dizziness may be felt.Do not worry, this is a variant of the norm – the discomfort goes away on its own over time.

Diagnostic results

When conducting magnetic resonance imaging of the brain with contrast, it is possible to diagnose many pathological processes even at an early stage of development. The specialist can see narrowing of the lumen, varicose veins of the brain, venous malformations, neoplasms in the cranial cavity, etc.

In the event that the brain does not have pathologies and abnormalities, the conclusion should indicate the following:

“Visualized sub- and supratentorial structures in axial, sagittal and frontal projections.

Median structures without features, localization is normal. The bark and white matter are well developed, with normal MR signal intensity.

Convexital grooves of the cerebellum and cerebrum are within normal limits.

Ventricles of the brain of the same shape, correct localization, normal size. Basal cisterns and subarachnoid spaces are normal.

Signs of impaired outflow of cerebrospinal fluid and increased intracranial pressure are absent.No tumors were found. ”

Magnetic resonance imaging with contrast agent is an informative diagnostic procedure. If the doctor insists on it, then it is important for your health. Follow the doctor’s recommendations and seek help at the first unpleasant symptoms.

Center news – MEDEXPERT

06/25/2015

MRI for infantile cerebral palsy

Cerebral palsy, or cerebral palsy, means disorders of body position and movement, which lead to a limitation of physical activity.The cause of these disorders is damage to the child’s brain during intrauterine development or after birth. Motor impairments in cerebral palsy are often accompanied by cognitive and behavioral impairments, defects in sensitivity and perception. More than half of children with cerebral palsy are prone to epileptic seizures (15-90% in different groups). Diagnosis of disorders in the brain is of great importance in cerebral palsy. An invaluable help in this can be provided by MRI for children. With the help of magnetic resonance imaging, it is possible to identify areas of cortical-subcortical atrophy, pseudoporencephaly, a diffuse decrease in the density of the white matter of the brain.So, according to Russian scientists, in almost all children with cerebral palsy, MRI shows atrophic changes in the cerebral cortex, mainly in the anterior sections of the frontal and temporal lobes of the brain.

It is also important that MRI allows you to confidently distinguish cerebral palsy from the consequences of craniocerebral trauma, neuroinfections and strokes, hereditary spastic paraplegia, Giacomini syndrome, hereditary ataxia, early autism, schizophrenia, spinal cord lesions, diseases of Strumpel, Fahr, Hallerwordenz-Spatzes -Merzbach, Sjogren-Larsson syndrome, Verding-Hoffmann amyotrophy and other pathologies.It is no coincidence that the use of MRI in cerebral palsy is one of the most urgent areas of modern diagnostic medicine.