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Lesions on your brain: Brain lesions – Mayo Clinic

Brain lesions – Mayo Clinic

A brain lesion is an abnormality seen on a brain-imaging test, such as magnetic resonance imaging (MRI) or computerized tomography (CT). On CT or MRI scans, brain lesions appear as dark or light spots that don’t look like normal brain tissue.

Usually, a brain lesion is an incidental finding unrelated to the condition or symptom that led to the imaging test in the first place.

A brain lesion may involve small to large areas of your brain, and the severity of the underlying condition may range from relatively minor to life-threatening.

 

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Jan. 11, 2018

Show references

  1. Sandeman EM, et al. Incidental findings on brain MR imaging in older community-dwelling subjects are common but serious medical consequences are rare: A cohort study. PLOS One. 2013;8:e71467.
  2. Magnetic resonance imaging (MRI). National Multiple Sclerosis Society. http://www.nationalmssociety.org/Symptoms-Diagnosis/Diagnosing-Tools/MRI. Accessed Aug. 14, 2017.
  3. Maher CO, et al. Incidental findings on brain and spine imaging in children Pediatrics. 2015;135:e1084.
  4. Cole AJ. Magnetic resonance imaging changes related to acute seizure activity. https://www.uptodate.com/contents/search. Accessed Aug. 14, 2017.
  5. Sports-related concussion. Merck Manual Professional Version http://www.merckmanuals.com/professional/injuries-poisoning/traumatic-brain-injury-tbi/sports-related-concussion. Accessed Aug. 14, 2017.


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White Matter Lesions – StatPearls

Continuing Education Activity

White matter lesions (WMLs) are areas of abnormal myelination in the brain. These lesions are best visualized as hyperintensities on T2 weighted and FLAIR (Fluid-attenuated inversion recovery) sequences of magnetic resonance imaging. They are considered a marker of small vessel disease. However, there are numerous non-vascular causes, as well. An increase in WMLs increases the risk of stroke, cognitive decline, depression, disability, and mortality in the general population. This activity reviews the evaluation and treatment of patients with WMLs and highlights the role of the interprofessional team in evaluating and treating patients with this condition.

Objectives:

  • Identify the etiology of white matter lesions.

  • Describe the typical imaging findings associated with various diseases presenting with white matter lesions.

  • Outline the management options available for patients with white matter lesions.

  • Explain the importance of improving care coordination among the interprofessional team to enhance the delivery of care for patients with white matter lesions.

Access free multiple choice questions on this topic.

Introduction

The white matter (WM) constitutes the network of nerve fibers that serves to allow the exchange of information and communication between different areas of the gray matter (GM). It lies beneath the GM in the brain and superficial to GM in the spinal cord. It has evolved more than GM and occupies almost half of the brain.[1] From the comparison of several cross-sections of the spinal cord performed in different regions, it is evident that the size of the area occupied by the WM varies from region to region, depending on the extent of the central GM. In particular, the GM/WM ratio grows from the cervical region to the lumbar region as the WM is decreasing as it proceeds towards the terminal portion of the spinal cord.

The WM contains neural networks formed by bundles of axons to mediate essential connectivity between different key motor and cognitive cortical regions. It comprises of myelinated and unmyelinated axons along with glial cells, including myelin-producing oligodendrocytes, microglia, astrocytes, and oligodendrocyte progenitor cells.

Myelin acts as electrical insulation for axons and is responsible for rapid saltatory impulse propagation and protects the nerve fibers from injury. [2] It has a water content of about 40%. The remaining dry mass (60%) is mainly composed of proteins (15% to 30%) and lipids (70% to 85%), with phospholipids, cholesterol, galactolipids, and plasmalogens in a molar ratio of 2:2:1:1.[3]

The chapter of WM lesions (WMLs) or leukoaraiosis encompasses small vessel vascular brain diseases and non-vascular conditions. Any process leading to change in chemical composition, damage, or ischemia of myelinated fibers can present as WMLs on magnetic resonance imaging (MRI) that represents the gold standard for WMLs investigation. The term WM hyperintensity (WMH) is quite a descriptive expression used on MRI. These lesions are best seen as hyperintensities on T2 weighted and FLAIR (fluid-attenuated inversion recovery) sequences of MRI. FLAIR sequences have a particular role in assessing WMLs close to the ventricular margin by nullifying the cerebrospinal fluid (CSF) signal.

While the WMHs are well-described on MRI, the lesions were firstly illustrated based on brain computed tomography (CT). In 1985, Hachinski in 1985 described “leukoaraiosis” as “diminished density of white matter which is seen on brain computed tomography.”[4]

Concerning small vessel vascular brain processes, WMLs are commonly present in MRI of asymptomatic elderly individuals typically located in periventricular (PV-WMH) and deep subcortical regions (DS-WMH). For instance, WMLs are frequently detected in people with untreated chronic hypertension. The volume of WMLs tends to increase with age from small punctate lesions to large confluent lesions. Nevertheless, although the occurrence of WMLs was initially considered a normal, age-related finding, recent investigations proved that large areas of disease in the WM of the brain must be considered as neuroimaging markers of brain frailty. Of note, various longitudinal studies described WMLs as a predictor for future risk of stroke, cognitive decline, depression, disability, and mortality in the general population.[5][6] The clinical significance of the lesions is confirmed by the results of a meta-analysis that demonstrated three times increased risk of dementia and stroke, and a doubled risk of death in people with WMLs. [7] For instance, the ischemic microvascular disease, vascular cause of WML, may cause about 45% of dementia cases and 20% of strokes. Again, WMLs are associated with poor post-stroke outcomes and increased risk of parenchymal hematoma following mechanical thrombectomy.[8][9]

Apart from WMLs secondary to small vessel disease, however, these lesions are also common features of demyelinating inflammatory disorders, leukodystrophies, and degenerative disorders. Clinical aspects, prognosis, management varies according to the distribution and spread of the WM damage.

This group of lesions and diseases, therefore, includes very different clinical conditions in terms of etiology, pathogenesis, pathological features, clinical presentations, imaging, and therapy. This article is aimed at discussing the clinical features and treatment of patients with several types of WMLs. The role of the interprofessional team in evaluating and treating patients is also highlighted.

Etiology

The etiology of white matter lesions (WMLs) is heterogeneous. Based on etiology, WMLs can be divided into vascular and non-vascular causes.

Vascular causes of WMLs include:

  • Microvascular ischemic disease or small vessel disease (SVD)

  • Atherosclerosis

  • Migraine

  • Amyloid angiopathy

  • Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) 

  • Vasculitis

  • Susac syndrome

Non-vascular causes for WMLs include:

  • Inflammatory: Multiple sclerosis (MS), acute disseminated encephalomyelitis (ADEM), neuromyelitis optica spectrum disorders (NMOSD)

  • Infectious: HIV encephalopathy, progressive multifocal leukoencephalopathy (PMLE), neuroborreliosis, HSV and CMV encephalitis, neurosyphilis, CNS cryptococcal infection, Whipple disease, Lyme encephalopathy, subacute sclerosing panencephalitis (SSPE). 

  • Toxic: Chronic alcohol abuse, carbon monoxide (CO) intoxication, inhalation of toluene, heroin, and cocaine, methotrexate-related leukoencephalopathy.

  • Metabolic: Vitamin B12 deficiency, copper deficiency, acute intermittent porphyria, hepatic encephalopathy, Hashimoto encephalopathy.

  • Neoplastic: Glial tumors, CNS Lymphoma

  • Traumatic: Radiotherapy, post-concussion (traumatic axonal injury, TAI)

  • Genetic: 
    • Lysosomal Storage Diseases: Metachromatic leukodystrophy (MLD), Krabbe disease, Fabry disease, gangliosidosis, mucopolysaccharidosis

    • Peroxisomal Disorders: X linked adrenoleukodystrophy, Zellweger syndrome, Refsum disease

    • Mitochondrial Disorders: MERF (myoclonic epilepsy with ragged red fibers), MELAS (mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes), Leigh disease, Kearns-Sayre disease.

    • Aminoacidopathies and Organic Acidopathies: Canavan disease, glutaric aciduria, urea cycle disorders

    • Unknown Etiology: Alexander disease, Vander Knapp encephalopathy

    • Others: Vanishing white matter disease, myotonic dystrophy

Another nosographic approach distinguishes primary WMLs, derived from an unknown etiology, from secondary ones; these latter due to a great variety of known etiologies.

Epidemiology

In the general population, the prevalence of age-related vascular WMLs is approximately 10% to 20% at 60 years and approaches 100% in those older than 90 years.[10] Studies have reported that WMLs are common in Japanese, Chinese, Caucasian, African-American, and Caribbean Black populations.[11]

MS represents the most common inflammatory neurological condition in young adults. Again, it has been estimated that the disease affects approximately 2,500,000 people worldwide. In the United States (US), the rate is 57 to 78 cases per 100,000 people in the southern states and 100 to 140 cases in the northern states.[12] The prevalence of NMOSD  is approximately 1/100,000 in the White population and up to 10/100,000 in Blacks. In East Asians, the prevalence is about 3.5/100,000 population.[13]

PMLE is present in 1% to 4% of patients with AIDS. Furthermore, gliomas account for up to 35% of the CNS tumors in adolescents and young adults.[14]

The incidence of WMLs secondary to heritable WM disorder is approximately 1 per 8,000 live births. [15] However, for acquired WM disorders in children, it is estimated to be 1.66 per 100,000 children.[16]

Pathophysiology

Cerebrovascular risk factors such as age, hypertension, diabetes mellitus, hyperlipidemia, hyperhomocysteinemia, and hypersensitive C-reactive protein are well-known risk factors for vascular WMLs.[11] Genetic factors also play an essential role in the development of WMLs as many genetic loci have been identified, and twin studies have suggested 55-80% heritability.[17][18] 

Pathophysiology for the development of vascular WMLs in elderly patients is thought to be secondary to chronically reduced blood flow by arteriosclerosis, lipohyalinosis, or fibrinoid necrosis of small vessels. Incomplete infarction secondary to persistent hypoxia leads to altered cerebral autoregulation promoting the transcription of many inflammatory genes, leading to the breakdown of the blood-brain barrier (BBB) and entry of pro-inflammatory proteins into the brain parenchyma and vessel wall. This will lead to demyelination, axonal loss, vacuolation, and reduced glial density. Some studies also suggest the role of venous collagen deposition in the pathogenesis of ischemic WMLs.[19] 

The different distribution of the lesions could be linked to different pathogenetic mechanisms. PV-WMH is featured by gliosis, loosening of the WM, loss around convoluted venules in perivascular spaces. In contrast, the primary characteristics of DS-WMH are demyelination, gliosis, and augmented tissue loss as the lesions become more serious.  By summarizing, the pathological characteristics of WMLs may encompass myelin rarefaction, reactive gliosis, axonal loss, infarction, venular collagenosis, arteriosclerotic small vessel alterations. Moreover, BBB impairment plays a pivotal role in the genesis of WM damage, and a different pattern involves PV-WMH and DS-WMH.[20]

In WMLs secondary to non-vascular diseases like MS, demyelination is caused by autoimmune inflammation-mediated primarily by T cells against myelin proteins. [21] While the cause of MS is still unknown, it probably presupposes a combination of genetic susceptibility and nongenetic factors such as viral infection, low vitamin D levels. This combination results in an autoimmune disorder that leads to myelin loss, destruction of oligodendrocytes, and reactive astrogliosis. However, the axon is usually undamaged; in some patients, it is aggressively destroyed.[22]

NMOSD is a group of inflammatory disorders of the CSN featuring severe immune-mediated demyelination and axonal damage, involving optic nerves and spinal cord mostly. Although these disorders were studied as a variant of MS, they have distinct pathophysiology. The autoimmune pathogenesis for NMOSD, indeed, involves IgG autoantibody against the aquaporin-4 (AQP4) water channel [23] or the myelin oligodendrocyte glycoprotein. In a subset of NMOSD, no antibodies (double-seronegative disease).

The exact mechanism of the pathophysiology of ADEM is still unknown. However, it has been related to inflammation initiated by infection or vaccination in genetically susceptible individuals causing demyelination. PMLE is a central demyelinating disease caused by reactivation (usually occurs at CD4 count less than 200/cmm) of latent JC polyomavirus (or John Cunningham virus or Human polyomavirus 2) in oligodendrocytes, in HIV patients. Leukodystrophy causes WMLs secondary to substrate accumulation due to enzymatic defects causing demyelination.

The TAI refers to a severe axonal mechanical damage due to a rotational acceleration of the brain. Although its pathophysiology is complicated, the injury damage is firstly due to a mechanical break involving axonal microtubules. This stretch induces axonal damages through undulations and breaks and direct membrane mechanoporation with calcium influx. This mechanism leads to the activation of several injurious pathways, including the caspase-mediated proteolysis and the cytokine-mediated microglia recruitment with impairment of axonal transport and the agglomeration of transported proteins in varicose swellings.[24]

History and Physical

Clinical presentation can vary from asymptomatic to patients with disabling disease as per the WMLs etiology. Elderly patients with small punctate cerebral vascular white matter lesions (WMLs) are usually asymptomatic, but they progress to large confluent lesions and can present with subtle functional decline, cognitive impairment, dementia, urinary incontinence, or gait and balance impairment and neuropsychiatric disorders. 

Within the group of vascular WM diseases, the distribution of lesions varies greatly, and consequently, the clinical aspects. For instance, in SVD, the WMHs are mainly found in basal ganglia and frontotemporal and periventricular WM. It may induce cognitive impairment, loss of balance or coordination, vision loss, and dizziness. Severe headaches can be present in different types of WMLs.

Patients with non-vascular etiology of WMLs like MS can have heterogeneous presentations, including fatigue, unilateral visual blurring, sensory changes, motor abnormality, urinary incontinence, speech and swallowing difficulties, pain, anxiety, depression, numbness and tingling, cognitive dysfunction. Nevertheless, the clinical scenario varies from patient to patient as well as the evolution of the disease. In some patients, indeed, there is a progressive and rapid deterioration, while in others, an alternation between relapses and remissions can be observed.

Clinical aspects of NMOSD include acute attacks of bilateral optic neuritis with significant visual loss or transverse myelitis, inducing limb weakness, sensory loss, and bladder dysfunction. Other symptoms can include episodes of intractable nausea, vomiting, hiccups, excessive daytime somnolence or narcolepsy, and seizures. There are a commonly relapsing course and variable degrees of recovery within weeks to months.[25]

Children with WMLs presenting with progressive symptoms of declining developmental milestones, cognitive impairment, and motor abnormalities should be suspected for leukodystrophy. However, patients in their first or second decade with WMLs secondary to ADEM present with acute onset and rapidly progressive symptoms of fever, headache, vomiting, confusion, or altered sensorium.  Although migraine was associated with structural changes in the brain WM, these lesions are generally not linked to any neurological issues as well as an increased risk of cognitive decline.[26]

Evaluation

Evaluation of patients presenting with white matter lesions (WMLs) depends on the age of the patient, clinical scenario, and pattern of white matter lesions on MRI. 

WMLs on MRI are common manifestations of cerebral small vessel disease and are associated with vascular risk factors. These patients should be screened for vascular risk factors by routine laboratory tests, including complete metabolic panel, lipid profile, and HbA1c. Also, in these patients, it is worthwhile to quantify WMLs to monitor their progress with time. Various grading scales like the Fazekas scale, age-related white matter changes (ARWMC) rating scale, and Van Swieten scale can be used to assess the extent and progression of WMLs. 

Patients with non-vascular WMLs require further evaluation to identify the etiology of the lesions. CSF analysis is helpful in cases of suspected MS (oligoclonal bands), ADEM (lymphocytic pleocytosis with raised proteins), and infectious demyelination (antiviral antibodies). MR spectroscopy can help in the etiological diagnosis of WMLs to differentiate lesions based on different metabolites peaks.

Additional tests like serology for autoantibodies in case of suspected vasculitis, anti-MOG antibodies in ADEM, and anti AQP4 antibodies in NMOSD. Also, metabolic and toxicology screens can be helpful in suspected cases. Children with WMLs and clinical scenarios for leukodystrophy require genetic testing.

Treatment / Management

White matter lesions (WMLs) detected incidentally or in MRI of elderly patients with a transient ischemic attack (TIA) require management of vascular risk factors by:

Prophylaxis of migraine with aura can also help decrease the risk of WMLs. The use of B vitamins to lower homocysteine levels is useful in managing patients with SVD.

Management of patients with non-vascular WMLs is individualized as per etiology. WMLs secondary to MS flares are treated with steroids. However, patients need long term maintenance therapy with disease-modifying treatment to halt disease progression. Furthermore, in patients with ADEM, immunosuppression with high-dose intravenous glucocorticoids is used. Acyclovir has also been reported to have benefits in some cases. Leukodystrophies do not have a specific treatment, and treatment is supportive and symptomatic only.

Differential Diagnosis

Pattern recognition of white matter lesions (WMLs) in MRI is crucial as it may make the diagnosis in many conditions. 

The differential diagnosis for symmetric WMLs:

  • Bilateral Hemispheres: Toxic encephalopathy, HIV encephalopathy, autoimmune encephalopathies, and Vitamin B12 deficiency

  • Periventricular Lesions: Small vessel disease, HIV encephalopathy, vitamin B12 deficiency, metachromatic leukodystrophy, X-linked adrenoleukodystrophy, and vanishing white matter disease

  • Subcortical Including Arcuate Fibers: Alexander disease, Kearns-Sayre syndrome, and CADASIL

  • Frontal Predominance: Alexander Disease, and metachromatic leukodystrophy

  • Parietal/Temporal/Occipital Lobes: PRES (posterior reversible encephalopathy), heroin abuse, and Krabbe disease.

  • Corpus Callosum: Marchifava-Bignami disease, metachromatic leukodystrophy, and Krabbe disease

  • Cerebellum: Toxic encephalopathy, and mitochondriopathies

  • Central Pons: Central pontine myelinolysis (CPM) 

The differential diagnosis for asymmetric WMLs:

  • Patchy Multifocal Confluent Lesion: MS, autoimmune encephalopathies, and CADASIL

  • Parieto-Occipital Regions: PMLE

Prognosis

The prognosis of patients with white matter lesions (WMLs) depends on the etiology of the lesions. Patients with age-related WMLs are irreversible and progressive. Large and confluent WMLs have a poor prognosis and lead to cognitive impairment and global functional decline. A study by Hassan et al. confirmed the association of severity of white matter lesions with mortality.[27]

WMLs secondary to MS have interpatient variability in prognosis. Severe disabilities are present in 5% of patients within the first five years of onset, and 10–20% of patients of MS remain unimpaired without therapy even after 20 years. [28] NMO and ADEM have a variable prognosis from complete recovery to the development of permanent physical disability, especially in post measles ADEM.[29] Acute demyelinating disease prognosis depends upon the severity of the initial illness. Patients responding to treatment have a favorable prognosis. However, leukodystrophies have poor prognosis. Reversible causes, including metabolic and toxic encephalopathies, have a good prognosis.

Complications

Severe white matter lesions (WMLs) are associated with cognitive impairment, global functional decline, cerebrovascular accident, mood disorders, gait, and balance dysfunction. WMLs are also associated with grey matter atrophy and accelerate neurodegeneration.[30] Furthermore, severe, extensive involvement of white matter by non-vascular causes like MS, ADEM, and NMO causes disability.

Deterrence and Patient Education

Patients with vascular risk factors should be identified early and counseled on lifestyle changes as well as control of comorbid conditions. Self-monitoring of blood pressure and blood sugar, dietary modifications, weight reduction, and improving physical fitness has proven to decrease the progression of white matter lesions.[31] Involvement in cognitively complex leisure activity to improve cognitive reserve has been associated with a protective effect on cognitive functioning and late-life depression in patients with WMLs.[32]

Enhancing Healthcare Team Outcomes

As described, white matter lesions (WMLs) have varied clinical presentations, differential diagnoses, and complications. Managing these patients requires extensive collaboration and coordination among a team of professionals, which consists of neurologists, radiologists, internists, ophthalmologists, psychiatrists, neurosurgeons, rheumatologists, microbiologists, pain specialists, nurse specialists, mental health nurses, pharmacists, physical therapists, and nutritionist. It is compulsory to identify the right set of professionals depending on the etiology of a case. Clear and effective communication between these professionals while monitoring the progression and complications of WMLs can decrease mortality.

Figure

Fazekas grade three white matter lesions in a case of stroke. Contributed by Sunil Munakomi, MD

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What Multiple Sclerosis Looks Like in Your Brain

All people tend to lose brain volume as they age — a process known as atrophy. But in people who have MS, this process typically happens much faster.

It’s normal to lose 0.1 to 0.5 percent of brain volume each year as you age. However, in people with MS, this range is typically 0.5 to 1.35 percent, according to an article published in September 2016 in the journal Multiple Sclerosis and Related Disorders. This greater atrophy may begin even before an MS diagnosis.

When nerve fibers die off in significant numbers due to an MS lesion, myelin is lost from the areas of the brain outside that lesion. That’s because nerve fibers can be very long, extending from one area of the brain to another. A lesion may affect only a small portion of a nerve fiber at first, but when the nerve fiber dies, myelin is lost from the entire length of that fiber beyond the lesion.

There are two main types of tissue in the brain: gray matter and white matter. Gray matter consists of the main bodies of nerve cells, while white matter consists of the nerve fibers that extend from these bodies. White matter gets its color from the myelin that surrounds nerve fibers. So when myelin is lost in areas outside lesions, it tends to cause atrophy of white matter.

But brain atrophy due to MS isn’t limited to white matter. Loss of nerve fibers can lead to the death of entire nerve cells, which means loss of the main nerve cell bodies that make up gray matter. This gray matter atrophy “is more associated with functional consequences than white matter atrophy” is, says Cross.

Scientists are still trying to figure out which symptoms are likely to be caused by atrophy of particular areas of the brain. “The human brain is so interconnected that it’s difficult to say, ‘This dysfunction is due to that region,’” Cross explains. “Memory and cognition are particularly difficult to pin down to any particular region.”

Brain Cysts (Cystic Brain Lesions)

A brain cyst or cystic brain lesion is a fluid-filled sac in the brain. They can be benign (not cancer) or malignant (cancer). Benign means that the growth does not spread to other parts of the body. A cyst may contain blood, pus, or other material. In the brain, cysts sometimes contain cerebrospinal fluid (CSF). CSF is a clear liquid that bathes and cushions the brain and spinal cord. Some brain cysts begin before birth. 

Even if a brain cyst is not cancer, it can still cause problems. The cyst may press against brain tissue and cause symptoms, such as headache, vision problems, or nausea. If this happens, you may need surgery to remove the cyst. In some cases, if the cyst is small and not growing and is not likely to cause symptoms, your healthcare provider may advise watching it instead of surgery.  

There are different types of brain cysts:  

  • An arachnoid cyst is also known as a leptomeningeal cyst. This is a cyst between the brain and the arachnoid membrane. This membrane is one of the protective coverings around the brain. An arachnoid cyst contains CSF. These appear most often in children, but they may also happen in adults. This type of cyst happens more often among males than females.
  • A colloid cyst is a gel-filled cyst. It often forms in one of the 4 ventricles of the brain. The ventricles are the CSF reservoirs in the brain. Colloid cysts usually happen in the third ventricle. This is in a central spot in the brain. The cysts can lead to blockage of CSF flow off and on, and cause positional headaches. These are headaches that happen when a person is in a certain position. These tend to appear during adulthood.
  • A dermoid cyst is a rare type of cyst. It forms when a few skin cells get trapped when the brain and spinal cord form before birth. These cysts may even contain sweat gland cells or hair follicle cells. These often appear in children.
  • An epidermoid cyst is also called an epidermoid tumor. Like a dermoid cyst, it forms from a bit of tissue that gets trapped when the brain and spinal cord form. Epidermoid cysts do not contain sweat glands or hair follicle cells. They grow very slowly. These cysts usually first appear when a person is an adult.
  • A pineal cyst happens on the pineal gland in the middle of the brain. This type of cyst usually only shows up during imaging scans done for another reason. Pineal cysts seldom cause problems. If they do grow large, they can sometimes affect vision. They can appear in people of any age.
  • A brain abscess happens anywhere in the brain as a single t or multiple cysts. Abscesses are usually caused by a bacterial infection . They are sometimes caused by a parasite or a fungus.
  • A neoplastic cyst is due to a benign or malignant tumor. When a brain tumor starts outside the brain, it is called metastatic.

New findings could alter how doctors predict whose disease will become more severe — ScienceDaily

For decades, clinicians treating multiple sclerosis (MS) have interpreted the appearance of new or expanding brain lesions on magnetic resonance imaging (MRI) scans as a sign that a patient’s disease is getting worse. Now, University at Buffalo researchers are finding that it may be the atrophy or disappearance of these lesions into cerebrospinal fluid (CSF) that is a better indicator of who will develop disability.

The five-year study, conducted by MS researchers in the Jacobs School of Medicine and Biomedical Sciences at UB, was published in the Journal of Neuroimaging. Similar findings also resulted from their 10-year study of 176 patients that they presented at the annual meeting of the American Academy of Neurology (AAN) in Los Angeles in April.

Robert Zivadinov, MD, PhD, first author on the 10-year study and senior author on the five-year study, said: “Using the appearance of new brain lesions and the enlargement of existing ones as the indicator of disease progression, there was no sign of who would develop disability during five or 10 years of follow-up, but when we used the amount of brain lesion volume that had atrophied, we could predict within the first six months who would develop disability progression over long-term follow-up.

Zivadinov, a professor of neurology in the Jacobs School and director of the Buffalo Neuroimaging Analysis Center (BNAC) in the Jacobs School, also directs the Center for Biomedical Imaging at UB’s Clinical and Translational Science Institute.

Brain lesions and MS

Brain lesions in general are a sign of damage to the brain, such as physical trauma, a stroke, normal aging or chronic disease. Patients with MS receive MRI scans as part of their routine care so that doctors can track the appearance of new lesions and the enlargement of existing ones, typically seen as indicators of disease progression. Approval by the Food and Drug Administration for new MS drugs typically depends on the drug’s ability to reduce the number of brain lesions over 24 months.

Zivadinov noted that according to this premise, the loss of brain lesions could inadvertently be seen as a sign that the patient’s condition is improving. MS is characterized by the loss of myelin sheaths surrounding axons in the brain and disrupting the brain’s ability to send and receive neuronal messages. The growth of new myelin sheaths around axons may demonstrate that some brain tissue has been repaired spontaneously or as the result of medication.

In order to focus specifically on the disappearance of lesions that likely indicate pathological change like atrophy, not beneficial change, like resolution or remyelination, the researchers looked exclusively at lesions seen on previous scans that were later replaced by cerebrospinal fluid.

“How do we know the lesions have disappeared?” asked Zivadinov. “Because where there was brain lesion tissue before, there now is just fluid.”

Lesions disappearing into cerebrospinal fluid

“The big news here is that we did the opposite of what has been done in the last 40 years,” said Michael G. Dwyer, PhD, assistant professor of neurology and bioinformatics in the Jacobs School and first author on the five-year study in the Journal of Neuroimaging. “Instead of looking at new brain lesions, we looked at the phenomenon of brain lesions disappearing into the cerebrospinal fluid.”

The researchers looked specifically at the rate of brain lesion loss due to atrophy compared to accumulation of lesion volume seen both at baseline and follow-up. They found that the amount of lesion volume that atrophied was the only significant lesion parameter that correlated with clinical disability as measured by the Expanded Disability Status Scale (EDSS), the most widely used method of quantifying disability in MS.

“We didn’t find a correlation between people who developed more or larger lesions and developed increased disability,” said Dwyer, “but we did find that atrophy of lesion volume predicted the development of more physical disability.”

While patients with relapsing remitting MS showed the highest amount of new lesions during the study, patients with progressive MS — the most severe subtype — had the most accelerated volume of brain lesion atrophy. The UB researchers said this indicates that this new imaging biomarker could be particularly important in transitional phases between relapsing and progressive MS subtypes.

“Paradoxically, we see that lesion volume goes up in the initial phases of the disease and then plateaus in the later stages,” said Zivadinov. “When the lesions decrease over time, it’s not because the patient lesions are healing but because many of these lesions are disappearing, turning into cerebrospinal fluid.”

More robust than whole brain atrophy

Another important scientific finding of the studies, Zivadinov continued, is that atrophied brain lesions were a more robust predictor of disability progression than the development of whole brain atrophy itself, the most accepted biomarker of neurodegeneration in MS.

“Our data suggest that atrophied lesions are not a small, secondary phenomenon in MS, and instead indicate that they may play an increasingly important role in predicting who will develop a more severe and progressive disease,” he said.

The five-year study involved 192 patients with one of the three subtypes of the disease: clinically isolated syndrome, the earliest stage; relapsing remitting, an intermediate stage; or progressive, the most severe stage. In that study, patients underwent imaging studies in the Center for Biomedical Imaging in the Clinical and Translational Science Institute at UB and BNAC.

The volume of lesions was quantified at the start of the study and patients received yearly scans on the same 3 Tesla MRI machine for more than five years. Lesion volumes were calculated over the five years of the study.

In the 10-year study, the researchers conducted analyses at the Center for Biomedical Imaging in the Clinical and Translational Science Institute and the BNAC at UB. Patients in that study were scanned at the Department of Radiology and followed in the Department of Neurology and the Center of Clinical Neuroscience, all in the Charles University in Prague, Czech Republic.

6 Things to Know About MS Brain Lesions

What causes scarring in multiple sclerosis? Why is treatment so important, and do lesions ever heal?

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When you have the autoimmune disorder multiple sclerosis (MS), lesions on your brain are part of the package—in fact, the word “sclerosis” means scarring, and scarring is just another way of describing lesions.

“You can’t diagnose MS without having brain lesions in at least two areas of the [central] nervous system, one of which has to be in the brain,” confirms Pavan Bhargava, M.D., assistant professor of neurology at the Johns Hopkins University School of Medicine in Baltimore, MD.

But what, exactly, are they? How do they form? And why do they trigger MS symptoms? Here are the answers to your top questions about MS-related brain lesions.

1. How Do Brain Lesions Form?

Brain lesions are caused by a rogue attack from your body’s own immune system, Dr. Bhargava explains. A lesion, or scarring, forms when your immune cells mistakenly target and damage the protective coating, called myelin, that surrounds your nerve fibers, which are also called axons. (This protective coating works much like cables in your home do, sheathing the live wires within them—and you can imagine what happens when that sheathing gets frayed or destroyed.) The medical term for myelin damage and loss is demyelination. And while lesions from MS are often found on different parts of the brain, they can occur anywhere in your central nervous system (CNS), which also includes the two optic nerves and spinal cord.

“Basically, immune cells in the bloodstream get activated for some reason,” Dr. Bhargava says. “They cross into the brain, are activated again, and then produce substances that bring other immune cells into the brain. This causes damage that ends up forming lesions.” In some cases, these immune cells cut through the actual nerve fibers, causing permanent damage, since severed nerves can’t send or receive signals.

When brain lesions first form, Dr. Bhargava says there is active inflammation that can be seen on a magnetic resonance imaging (MRI) scan. If your doctor suspects you have active lesions, you’ll likely have an MRI with gadolinium contrast, he explains. Gadolinium is a rare earth metal that’s used as a contrasting agent to show areas of recent inflammation in your body. Normally, the contrast can’t get into your brain or spinal cord, thanks to what’s known as the blood-brain barrier. But when lesions are active, they upset the blood-brain barrier’s normal defenses. The contrast leaks through to the lesions, and they show up clearly on an MRI.

Over time, the inflammation dies down, the blood-brain barrier goes back to normal, and the contrast no longer shows up on imaging scans. “You’re then left with an area where there’s a loss of myelin, what we call demyelination,” Dr. Bhargava says. You may eventually develop scar tissue in these areas that’s made up of immune cells called microglia.

2. Why Do Lesions Cause MS Symptoms?

The CNS controls everything in your body. So, “wherever the lesions are, they disrupt that signaling pathway,” says Le Hua, M.D., director of the Mellen Program for Multiple Sclerosis at Cleveland Clinic Lou Ruvo Center for Brain Health in Las Vegas, NV.

If a lesion forms on one of your optic nerves, it affects your vision. If it develops on your spinal cord, you might experience numbness or difficulty moving your arms or legs. If it attacks your brainstem, this can impact your eyes and facial movements, speech, and even swallowing. Lesions can also cause fatigue and brain fog, Dr. Hua says.

MS is a relapsing-remitting disease, which means you have periods of disease activity (relapse), followed by periods where inflammation decreases and disease activity stops (remission). “All the symptoms that we typically associate with MS relapses … can be caused by lesions, depending on where they are,” says Dr. Bhargava. “As the inflammation dies down in those lesions, the symptoms can then improve.”

3. Are Lesions on the Brainstem More Serious?

Where, exactly, lesions show up can make a difference, according to Dr. Hua. Lesions in your brainstem or spinal cord are associated with more physical symptoms and a higher risk of disability than lesions that form in other parts of the brain.

She offers an analogy: “If you think about streets, if you block off a road in a neighborhood, there’s not going to be a lot of impact,” Dr. Hua says. “But as those roads and pathways come together in the brainstem and then in the spinal cord, now you’re on a highway. If you block off the highway, you’ve caused significant problems.”

In other words, depending on where it’s located, a lesion in your brain might not affect you that much. You might not even have any symptoms. This is called a silent lesion. Dr. Bhargava says that oftentimes, when people come in with their first relapse from lesions on the optic nerve or spinal cord, “we find that they actually have 10 or 15 lesions in the brain, none of which ever caused any symptoms before,” he says.

Keep in mind, too, that where a lesion appears doesn’t necessarily indicate how much you’ll improve once inflammation decreases after a relapse, notes Dr. Bhargava. How well you bounce back depends more on the lesion’s size and how severe the damage was in the first place.

He also points out that the number of lesions you have doesn’t always correlate with how severe your disease is, or how much MS affects you. “There are some people who have lots of lesions and have very few symptoms, while others can have just a handful of lesions and be really affected by them,” he explains. Again, it depends on where the lesions are located, plus the amount of damage caused.

4. Can Lesions Be Slowed Down or Prevented?

The goal of MS treatment, then, is to stop relapses from occurring: “We prevent new relapses by preventing new lesions from forming,” explains Dr. Bhargava.

Disease-modifying MS therapies, such as beta interferon drugs, infusion treatments, and oral medications, have been shown to be powerfully effective when it comes to preventing new lesions. These treatments can reduce existing inflammation, too.

“We can slow down the inflammation of some lesions when they’re actively inflamed by starting therapy so the lesion itself might not be as drastic,” Dr. Hua says.

5. Can Lesions Heal Once They Appear?

“Absolutely,” says Dr. Hua. “It’s not specific to MS, but in any process where there’s some sort of brain injury, there will always be healing, as well. There will also be the formation of scar tissue,” a process called gliosis, she adds.

In some people, myelin in the lesions is actually repaired to some degree, known as remyelination. However, “it won’t be as robust as the original,” Dr. Hua says, meaning you may gain back some nerve functionality over time, but perhaps not all.

Pathology reports on the brains of deceased people with MS have shown that some lesions appear to show remyelination, agrees Dr. Bhargava. “It does seem that the body can at least partially heal some of these lesions, but this may vary from person to person, and then from lesion to lesion within the same brain,” he says.

Research is in the works to find ways to help the nervous system repair damaged myelin. Scientists are looking into options such as stem cell therapy and certain medications such as clemastine (an oral antihistamine), lipoic acid (an antioxidant), ibudilast (anti-inflammatory), and phenytoin (epilepsy drug) that show promise.

6. Why Is It Important to Monitor MS Lesions?

Dr. Hua says that lesions show up much more frequently on MRI than they do clinically (the aforementioned “silent” lesions.). This is why doctors monitor MS with frequent MRI scans instead of waiting for patients to present with symptoms. “We want to see the silent disease activity. We want to make sure that no new lesions are formed, because if we can stop lesion formation, we will significantly reduce disability,” says Dr. Hua.

MRIs are typically done every year, she explains. If you’ve started a new medication, Dr. Hua says you might have one in six months’s time to make sure the medication is doing its job. Once you’re older, inflammation tends to slow down. You won’t need MRIs as often as long as your MS is stable.

Though MRI scans are an important tool doctors use to monitor MS, they don’t provide the whole picture. “We still rely on clinical tools, other tests, and other measures to really help us understand the best way to care for patients,” Dr. Hua says.

Meet Our Writer

Sarah Ludwig Rausch

Sarah Ludwig Rausch is a health writer and editor whose specialties include mental health, diseases, research, medications, and chronic conditions. She’s written for The Christian Science Monitor, American Cancer Society, Cleveland Clinic, PsychologyToday.com, MedShadow Foundation, the ACT Test, and more.

White Spots on a Brain MRI: What It Means

Your brain MRI results have come back and they show bright, white spots amid the gray brain tissue. Should you be alarmed?

Experts say such spots, called white matter hyperintensities (WMHs) or leukoaraiosis, can be a sign that you are at risk for certain illnesses, depending on how many spots you have, their size and location in your brain, and your age. WMHs increase with aging and have been linked to cognitive impairment, stroke (potentially triple the risk compared to someone without WMH) and dementia (double the risk), as well as other problems.

The good news is that knowing you have WMHs can help your doctor determine steps you can take to prevent conditions from occurring or slow their progression, if caught in time.

What Causes White Matter Hyperintensities?

White spots on your MRI can show up even if you have no symptoms of illness. MRI, or magnetic resonance imaging, reveals these spots with greater intensity because they have increased water content compared to normal, higher fat content, myelinated tissue in the brain. The “watery” lesions, or WMHs become more common in your later decades, though they can be seen at any age. At age 60, about 10 to 20% of asymptomatic patients have WMHs. This value increases to almost 100% for those over 90.

Doctors used to consider white spots on a brain MRI a normal and benign sign of aging, like wrinkles or gray hair. More recent MRI technology has enabled doctors to study them more carefully and to recognize them as indicators of illness. They now are considered a sign of small blood vessel disease in the brain and may occur when blood flow is reduced due to various medical conditions.

Causes for WMH include:

  • Small “silent” strokes
  • Metabolic leukodystrophies (rare genetic diseases that affect white matter in the brain)

Sometimes, WMHs go away—for example, if an infection is cured or a tumor removed. Sometimes, the white lesions improve, but then worsen. This can occur with an episodic, inflammatory condition like lupus, which can cycle between periods of inflammation and remission.

If you have WMH, you may be at increased risk for:

  • Decline in gait (how you walk and move) and disturbances in balance

Your doctor is your best resource to explain what your MRI white spots mean and what steps you may need to take.

What to Do About White Matter Hyperintensities

Some people are more likely to have WMHs than others. Research has shown that people of Hispanic or African American heritage are at higher risk. WMHs also have a genetic component, meaning they can run in families.

Medical conditions that put you at risk of developing WMHs include:

  • Vitamin deficiency (B12, B6 and folic acid)
  • Tension or migraine headaches (especially with aura)

You may be able to control some of these risk factors through lifestyle changes. For example, smoking is associated with greater WMHs, so quitting smoking can help reduce or avoid this problem. Studies show exercise may help reduce WMHs. Improving your diet can help too. One clinical trial currently in progress is examining whether consuming more omega-3 fatty acids (found in such fish as salmon and tuna) can help.

Researchers also have found older adults (60 and older) who have greater exposure to stress tend to have higher rates of WMH. Learning how to reduce stress may help reduce WMH.

In addition to lifestyle changes, make sure you control high blood pressure and other health conditions associated with WMH. This may mean taking medicine as well as following other guidance from your physician.

Scientists are continuing to study WMHs and how these white spots on the brain may be prevented, reversed or slowed. In the meantime, if your MRI shows white spots, the healthcare provider will work with you on any necessary follow-up tests and steps you can take to improve your long-term outcomes.

90,000 Insidious brain. Why “black” neurons die and how to stop it

https://ria.ru/20200611/1572643126.html

Insidious brain. Why “black” neurons die and how to stop it

Insidious brain. Why “black” neurons die and how to stop it – RIA Novosti, 06/11/2020

Insidious brain. Why “black” neurons die and how to stop it

In the world, according to various sources, from ten to sixteen million people suffer from Parkinson’s disease, and the WHO predicts that by the middle of the century this figure will be like… RIA Novosti, 11.06.2020

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MOSCOW, June 11 – RIA Novosti, Tatyana Pichugina. In the world, according to various sources, from ten to sixteen million people suffer from Parkinson’s disease, and the WHO predicts that this figure will at least double by the middle of the century. Pathology develops imperceptibly for many years, then progresses rapidly, reducing life expectancy. Neurons and Dopamine The midbrain contains a group of neurons rich in the dark pigment neuromelanin, the substantia nigra.Their processes reach other parts of the brain, primarily the striatum (striatum). Here they release dopamine, a signaling molecule that regulates muscle function. If its synthesis and metabolism are normal, the muscles contract and relax in a timely manner, if not, their tone is increased. The death of neurons in the substantia nigra leads to a constant lack of dopamine and, as a consequence, severe impairment of motor function – Parkinson’s disease. Its symptoms are coordination problems, stiffness of movements, slowness, stoop, limb tremors.The disease progresses rapidly, cannot be treated, substitution therapy only temporarily improves the condition. A person gradually turns into a disabled person, and an untimely death awaits him. Many famous people suffered from Parkinson’s disease – including the American boxer Muhammad Ali, the Soviet actor Mikhail Ulyanov, Pope John Paul II. The diagnosis was recently reported by the British rock singer Ozzy Osbourne. Difficulties in early diagnosis Some signs of Parkinson’s disease appear several years before the apparent impairment of movement.The sense of smell disappears, in the phase of REM sleep, a person drops objects from the bedside table, touches the sleeping person next to him, can fall off the top shelf in the train. Each of these symptoms is characteristic of many pathologies, but together they indicate the latent course of Parkinson’s disease (pre-motor phase). It takes several months or even years to clarify the diagnosis. In controversial cases, they resort to positron emission (PET) or single-photon emission computed tomography (SPECT). “We introduce radioisotope drugs into the body, they are included in the metabolism of neurons that synthesize dopamine.We scan the brain and see how the synthesis is going. These methods make it possible to diagnose several years before movement disorders, “says Professor, Corresponding Member of the Russian Academy of Sciences Sergei Illarioshkin, Head of the Brain Research Department of the Scientific Center of Neurology. True, PET and SPECT are very rare: these procedures are mainly intended for oncology. Transcranial sonography (ultrasound of the brain) and MRI on devices with a high magnetic field intensity are more accessible, which also record signs of degradation of the substantia nigra.However, all current diagnostics of Parkinson’s disease have a common problem – it is effective only in combination with clinical symptoms. Like any neurodegenerative pathology associated with the death of a specific group of neurons, Parkinson’s disease is very insidious. It all starts at a relatively young age and develops slowly for many years without making itself felt. This is due to the exceptional plasticity of the brain. To compensate for the loss of nerve cells, the remaining ones work more actively – they generate more dopamine, target neurons become more sensitive to it, and only when all possibilities are exhausted does the nervous system fail with obvious symptoms.”The clinic occurs after the death of 50-55% of the cells in the substantia nigra. It is too late to treat. Therefore, preventive therapy, such as antioxidants and others, is ineffective. It should be applied until no more than 15-20% of neurons have died. But how to recognize pathology on this stage? Hence the idea of ​​biomarkers – substances in the body that indicate a pathogenic process or a predisposition to it long before clinical symptoms “, – explains the professor. RNA as biomarkers” One of the serious problems of any neurodegenerative pathology is that it is available for research , only the blood of patients.Of course, there is a lot of work with the brain of the deceased, but it is not very correct to look for markers of the early stage of the disease there after many years of the disease, its active treatment, against the background of other frequent diseases characteristic of old age – cardiovascular, cancer, “says the doctor of biological sciences Peter Slominsky, Head of the Laboratory of Molecular Genetics of Hereditary Diseases at the Institute of Molecular Genetics, Russian Academy of Sciences, His group is looking for molecules in the blood of patients – the harbingers of Parkinson’s disease: micro-RNA, mRNA.”The death of neurons in the substantia nigra is accompanied by pronounced changes in gene expression, and we assume that the same happens in blood cells. The hypothesis is based on the fact that a number of genes associated with dopamine metabolism are expressed in peripheral blood lymphocytes,” the scientist clarifies. The expectation that the blood-brain barrier – a conditional border that prohibits the exchange of substances between the brain and the rest of the body – is not so impenetrable and the degradation of the substantia nigra will somehow echo in the peripheral blood.The task is to determine a group of genes that act differently in sick and healthy people by comparing their transcriptome – the entire set of RNA cells. “For such a study, blood samples from people at the very initial stage of the disease – before treatment, possibly affecting gene expression, are especially suitable. Therefore, samples are taken from patients diagnosed with suspected Parkinson’s disease and, after a few months, from those who have been diagnosed, “he continues. To create a complete panel of biomarkers, many samples are needed.It would be ideal to observe a large group of people, regularly test, identify risk groups and then compare with those who are diagnosed with the disease, which is one percent among people over 60 years old, regardless of place of residence, ethnicity. Therefore, the study must be long – it is necessary to monitor the person’s condition for at least several years. The problem is also that microRNA and mRNA analyzes are still inconvenient for prophylactic screening in clinical laboratories. PCR is required, and this time, rather expensive equipment, laborious procedures.The hope is that when molecules specific for Parkinson’s disease are found, there will be available methods for their study – given the powerful leap forward now in rapid tests of RNA-containing viruses. in the exchange of signals between nerve cells, but all of its functions are not fully understood. In healthy neurons, this protein, having worked out, is destroyed, and in pathology it accumulates, its long filaments – fibrils stick together into conglomerates (Lewy bodies) and become toxic.A mutation in the alpha-synuclein gene leads to one of the hereditary forms of Parkinson’s disease. In about one in ten cases, this pathology has genetic causes. Most often, these are mutations in the LRRK2 or PARK8 genes, which encode the proteins dardarin and parkin, respectively. They are involved in many biochemical processes in different types of cells, but for some reason a failure in them turns into the formation of Lewy bodies and the death of primarily dopaminergic neurons in the substantia nigra. “Obviously, the alpha-synuclein protein is important for pathology, but is it the root cause? There are diseases when it is also postponed, for example, dementia with Lewy bodies, ”says Doctor of Biological Sciences Maria Shadrina, a colleague and co-author of Slominsky.- There are many parallels with Alzheimer’s disease, which is somewhat more common than Parkinson’s. There, neurons of a certain type, cholinergic in the hippocampus, also die, and the protein beta-amyloid accumulates in the brain. And this disease develops covertly for many years before a person’s memory and other cognitive functions weaken. “There is no shortage of hypotheses explaining the occurrence of both diseases. This is neuroinflammation, triggered by a viral infection in youth, and neurotoxins in the environment, such as herbicides , and the now fashionable gut microbiome, which is suspected of spoiling alpha-synuclein.It is not so easy to test all this in an experiment. Rodents – the favorite laboratory models of biologists – do not get sick with Parkinson’s. “To mimic the disease, mice inject a toxin and after six hours they observe the death of neurons in the substantia nigra, a sharp decrease in dopamine. In humans, this stage lasts for decades. On the other hand, in rodents it is possible to simulate hereditary forms of the disease by introducing mutations into the genome “, – explains Slominsky. Experiment with twins Now scientists have a unique chance – among patients in the Far East, three were found with monozygous twins who do not have Parkinson’s disease.”They grew up together, live in the same region, work is not associated with toxins. The DNA is identical, so if there is a genetic predisposition, other factors were superimposed on it,” says Maria Shadrina. The task is to analyze the transcript of twins, find genes that are expressed in them in different ways, to establish micro-RNA regulating them and to associate with Parkinson’s disease. However, the question of the root causes of the pathology remains open. “One of the explanations is the mitochondrial genome, which is transmitted from the mother.It is different for twins. Mitochondria multiply in the cell by simple division and mutate rapidly. Just a change in the energy of the cell, for which mitochondria are responsible, is one of the signs of Parkinson’s disease, – Sergei Illarioshkin gives an example. He does not exclude the possibility that the second twin will develop the disease later. – We can check it on PET, do an EEG video polysomnography to see the reactions in the REM sleep phase, evaluate the structure of the nigrosome (clusters of dopamine neurons) using 3-Tesla MRI data in a new mode.It is possible that the disease is already developing. There are such examples. “How neurons are grown. Pluripotent stem cells also allow the study of Parkinson’s disease. In fact, these are embryos that can turn into any kind of mature cells, including neurons. Previously, stem cells were taken from an abortive material, the placenta. Now, thanks to the discovery of the Japanese scientist Shinyi Yamanaki, they can be obtained from the tissue of an adult. You need to chew a little in the laboratory to artificially age, and please – mature neurons in a Petri dish.There are no other options to take them from a living patient. “We have created the first in Russia collection of cell lines from fifty patients with Parkinson’s disease. Three of them already have induced pluripotent stem cells. There are also transgenic neurons, into whose DNA biosensors have been inserted using the CRISPR-Cas9 system They highlight various processes at the cellular level, for example, the accumulation of reactive oxygen species, “says Sergei Medvedev from the Development Epigenetics Laboratory of the Institute of Cytology and Genetics of the Siberian Branch of the Russian Academy of Sciences.Together with colleagues from the Novosibirsk Institute of Organic Chemistry. NN Vorozhtsov and the International Tomographic Center of the SB RAS, on such artificial neurons of the substantia nigra, they will test potential drugs that slow down their death, look for genetic factors of the disease and biomarkers. death of neurons, because we do not know the cause, and there can be a huge number of them. The strategy of struggle is aimed at early diagnosis and preventive neuroprotective therapy in order to slow down the process as much as possible.Ideally, the threshold for neuronal death at which clinical symptoms appear is a loss of 70-80 percent of dopamine, occurring at the age of 120-150 years. The person will get sick, but the quality of life will remain acceptable, “says academician Mikhail Ugryumov, head of the laboratory of nervous and neuroendocrine regulation of the Koltsov Institute of Developmental Biology, Russian Academy of Sciences. In his laboratory, mice with the earliest stage of Parkinson’s disease are obtained. Then, in their blood look for matches with potential biomarkers found in the blood of patients with a confirmed diagnosis.”There are dozens of biomarkers and not a single specific one, since we find them in other diseases. In any case, you need to use a set of markers, but even for them, the diagnosis will still not be definitive,” the researcher notes. He suggests creating a stress test to detect the disease. In psychiatry and neurology, this approach is not used, but in other fields of medicine it is completely. For example, there is a glucose tolerance test for diagnosing diabetes mellitus. Scientists have already found a substance that blocks the synthesis of dopamine in the brain and a dose that temporarily increases symptoms in pathology, without side effects.Experiments on mice were successful, and now, together with colleagues from Taiwan, researchers are preparing trials on primates. “There is reason to believe that this diagnosis will be specific.” They form in an embryo between eight and 15 weeks of age. As the body ages, they die: on average, every ten years, the brain loses four percent of nerve cells. In a neurodegenerative disease, for unknown reasons, the rate of neuronal death increases significantly.And although there are progenitor stem cells in the hippocampus and striatum, it was not possible to prove that they replace dead ones. In the early 1990s, with the development of cellular technologies, the idea arose to transplant healthy donor neurons into patients. “Swedish professor Andres Bjorklund conducted experiments on mice, which caused Parkinson’s disease by neurotoxins, but the neurons transplanted from the healthy animal died, so he transplanted the neurons from the embryo to the diseased rodents, and their behavior was restored.It was a triumph, “recalls Mikhail Ugryumov. On this wave, Bjorklund launched a program of clinical trials of cell technologies for the treatment of Parkinson’s disease in the EU. Ugryumov led a research group from Russia. In total, we performed 13 neuron transplants. “They took abortive material, cut out the area of ​​the brain where dopaminergic neurons were supposed to form, made a suspension and injected the patient where there was a dopamine deficiency. The operation is non-traumatic, under local anesthesia.For ten years in all European countries – members of the consortium have collected a lot of material. The patients’ condition improved, but after six months the disease returned, “- says the scientist. In the United States, the same results were obtained. Improvement of cell technologies did not change the situation.” Everywhere they use the same methodology: they test therapy in rodents, then in humans. The general picture: one hundred percent success on animals, no lasting effect on humans, “- sums up the academician. The human brain is too complex, he believes.Neurons cannot be transplanted into the substantia nigra, where the environment is suitable for them, because in the adult brain they cannot grow into another section. Therefore, they are implanted immediately where dopamine is required – in the striatum. The mouse brain is flooded with various signaling substances, all neurons work in this cocktail. In humans, neurons are specialized, they have their own signaling substances, and their delivery should be directed. The neuron is controlled not over the entire surface, but at points – synaptic contacts.And each is connected with ten to fifteen thousand other strictly defined neurons. All of this must re-form the cell that has been transplanted. In the next fifty years, according to Mikhail Ugryumov, this task is most likely unsolvable.

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MOSCOW, June 11 – RIA Novosti, Tatyana Pichugina. In the world, according to various sources, from ten to sixteen million people suffer from Parkinson’s disease, and the WHO predicts that by the middle of the century this figure will at least double. Pathology develops imperceptibly for many years, then progresses rapidly, reducing life expectancy. This ailment is incurable, so it is imperative to diagnose it as early as possible.

Neurons and dopamine

The midbrain contains a group of neurons rich in the dark pigment neuromelanin – the substantia nigra.Their processes reach other parts of the brain, primarily the striatum (striatum). Here they release dopamine, a signaling molecule that regulates muscle function. If its synthesis and metabolism are normal, the muscles contract and relax in a timely manner, no – their tone is increased.

The death of neurons in the substantia nigra leads to a constant lack of dopamine and, as a result, severe impairment of motor function – Parkinson’s disease. Its symptoms are coordination problems, stiffness of movements, slowness, stoop, limb tremors.

The disease progresses rapidly, cannot be treated, substitution therapy only temporarily improves the condition. A person gradually turns into a disabled person, and an untimely death awaits him. Many famous people suffered from Parkinson’s disease – including the American boxer Muhammad Ali, the Soviet actor Mikhail Ulyanov, Pope John Paul II. British rock singer Ozzy Osbourne recently reported this diagnosis.

Difficulties in early diagnosis

Some signs of Parkinson’s disease appear several years before a clear movement disorder.The sense of smell disappears, in the phase of REM sleep, a person drops objects from the bedside table, touches the sleeping person next to him, can fall off the top shelf in the train. Each of these symptoms is characteristic of many pathologies, but together they indicate the latent course of Parkinson’s disease (pre-motor phase).

Clarification of the diagnosis takes several months or even years. In controversial cases, they resort to positron emission (PET) or single-photon emission computed tomography (SPECT).

“We introduce radioisotope drugs into the body, they are included in the metabolism of neurons that synthesize dopamine.We scan the brain and see how the synthesis is going. These methods make it possible to diagnose several years before movement disorders, “says Professor, Corresponding Member of the Russian Academy of Sciences Sergei Illarioshkin, Head of the Brain Research Department of the Scientific Center of Neurology.

January 21, 2020, 18:15 Culture Ozzy Osbourne was diagnosed with Parkinson’s disease

True, PET and SPECT is very rare: these procedures are mainly intended for oncology.Transcranial sonography (ultrasound of the brain) and MRI on devices with a high magnetic field intensity are more available, which also record signs of degradation of the substantia nigra.However, all current diagnostics of Parkinson’s disease have a common problem – it is effective only when combined with clinical symptoms.

Like any neurodegenerative pathology associated with the death of a specific group of neurons, Parkinson’s disease is very insidious. It all starts at a relatively young age and develops slowly for many years without making itself felt. This is due to the exceptional plasticity of the brain. To compensate for the loss of nerve cells, the remaining ones work more actively – they generate more dopamine, target neurons become more sensitive to it, and only when all possibilities are exhausted does the nervous system fail with obvious symptoms.

“The clinic occurs after the death of 50-55% of the cells in the substantia nigra. It is too late to treat. Therefore, preventive therapy, such as antioxidants, etc., is ineffective. It should be used until no more than 15-20% of neurons have died. But how to recognize pathology at this stage? Hence the idea of ​​biomarkers – substances in the body that indicate a pathogenic process or a predisposition to it long before clinical symptoms “, – explains the professor.

RNA as biomarkers

“One of the serious problems of any neurodegenerative pathology is that, in fact, only the blood of patients is available for research.Of course, there is a lot of work with the brain of the deceased, but it is not very correct to look for markers of the early stage of the disease there after many years of the disease, its active treatment, against the background of other frequent diseases characteristic of old age – cardiovascular, cancer, “says the doctor of biological sciences Petr Slominsky, Head of the Laboratory of Molecular Genetics of Hereditary Diseases at the Institute of Molecular Genetics of the Russian Academy of Sciences

His group is looking for molecules in the blood of patients – the harbingers of Parkinson’s disease: micro-RNA, mRNA.

“The death of neurons in the substantia nigra is accompanied by pronounced changes in gene expression, and we assume that the same happens in blood cells. The hypothesis is based on the fact that a number of genes associated with dopamine metabolism are expressed in peripheral blood lymphocytes”, – specifies scientist.

April 11, 2018, 08:00 Science Deprived of the “happiness hormone”: what is known about Parkinson’s disease

The calculation that the blood-brain barrier is a conditional border that prohibits the exchange of substances between the brain and the rest of the body is not so impenetrable and the degradation of the substantia nigra as- it will echo in the peripheral blood.The task is to determine a group of genes that act differently in sick and healthy, comparing their transcript – the entire set of RNA cells.

“Blood samples from people at the very initial stage of the disease are especially suitable for such a study – before treatment, possibly affecting gene expression. Therefore, samples are taken from patients with a diagnosis of” suspected Parkinson’s disease “and, after a few months, from those who the diagnosis was confirmed, “he continues.

It takes a lot of samples to create a complete biomarker panel.It would be ideal to observe a large group of people, regularly test, identify risk groups and then compare with those who are diagnosed with the disease, which is one percent among people over 60 years old, regardless of place of residence, ethnicity. Therefore, the study should be long-term – it is necessary to monitor the person’s condition for at least several years.

Another problem is that micro-RNA and mRNA analyzes are still inconvenient for prophylactic screening in clinical laboratories.PCR is required, and this time, rather expensive equipment, laborious procedures. The hope is that when molecules specific for Parkinson’s disease are found, available methods for their study will appear, taking into account what a powerful breakthrough is now taking place in express tests of RNA-containing viruses.

June 5, 2020, 18:00 Science Scientists have substantiated the need for another test for COVID-19

Chorus of genetic mutations

There is a lot of alpha-synuclein protein in the brain, which is involved in the exchange of signals between nerve cells, but all of its functions are not fully understood …In healthy neurons, this protein, having worked out, is destroyed, and in pathology it accumulates, its long filaments – fibrils stick together into conglomerates (Lewy bodies) and become toxic. A mutation in the alpha-synuclein gene leads to one of the inherited forms of Parkinson’s disease.

Approximately one in ten cases of this pathology have genetic causes. Most often, these are mutations in the LRRK2 or PARK8 genes, which encode the proteins dardarin and parkin, respectively. They are involved in many biochemical processes in different types of cells, but for some reason a failure in them turns into the formation of Lewy bodies and the death, first of all, of dopaminergic neurons in the substantia nigra.

“Obviously, the alpha-synuclein protein is important for pathology, but is it the root cause? There are diseases when it is also postponed, for example, dementia with Lewy bodies,” says Doctor of Biological Sciences Maria Shadrina, colleague and co-author of Slominsky. There are many parallels with Alzheimer’s disease, which is somewhat more common than Parkinson’s. There are also neurons of a certain type, cholinergic in the hippocampus, and the protein beta-amyloid accumulates in the brain. And this disease develops secretly for many years before a person’s memory and others weaken cognitive functions “.

There is no shortage of hypotheses explaining the occurrence of both diseases. These include neuroinflammation, triggered by a viral infection in youth, and neurotoxins in the environment, such as herbicides, and the now fashionable gut microbiome, which is suspected of spoiling alpha-synuclein.

Testing all this in an experiment is not so easy. Rodents, biologists’ favorite laboratory models, do not get Parkinson’s.

“To mimic the disease, mice inject a toxin and after six hours they observe the death of neurons in the substantia nigra, a sharp decrease in dopamine.In humans, this stage lasts for tens of years. On the other hand, hereditary forms of the disease can be simulated in rodents by introducing mutations into the genome, “Slominsky explains. Parkinson’s disease.

“They grew up together, live in the same region, work is not related to toxins. The DNA is identical, so if there is a genetic predisposition, then other factors were superimposed on it, “says Maria Shadrina.

The task is to analyze the transcriptome of twins, find genes that are expressed differently in them, establish micro-RNAs that regulate them, and link them with Parkinson’s disease. However, the question of the root causes of the pathology remains open.

“One of the explanations is the mitochondrial genome, which is passed on from the mother. It is different in twins. Mitochondria multiply in the cell by simple division and quickly mutate. Just a change in the energy of the cell, for which mitochondria are responsible, is one of the hallmarks of Parkinson’s disease, – gives the example of Sergei Illarioshkin.He does not exclude the possibility that the second twin will develop the disease later. – We can check it on PET, do an EEG video polysomnography to see the reactions in the REM sleep phase, evaluate the structure of the nigrosome (clusters of dopamine neurons) using 3-Tesla MRI data in a new mode. It is possible that the disease is already developing. There are such examples. “

May 14, 2020, 08:00 ScienceIn fact, these are embryos that can turn into any kind of mature cells, including neurons.

Earlier stem cells were taken from abortive material, placenta. Now, thanks to the discovery of the Japanese scientist Shinyi Yamanaki, they can be obtained from the tissue of an adult. We need to do a little chemistry in the laboratory in order to artificially age, and please – mature neurons in a Petri dish. There are no other options to take them from a living patient.

“We have created the first collection of cell lines in Russia from fifty patients with Parkinson’s disease.Three of them already have induced pluripotent stem cells. There are also transgenic neurons in whose DNA biosensors have been inserted using the CRISPR-Cas9 system. They highlight various processes at the cellular level, for example, the accumulation of reactive oxygen species, “says Sergei Medvedev from the Development Epigenetics Laboratory of the Institute of Cytology and Genetics of the Siberian Branch of the Russian Academy of Sciences.

Together with colleagues from the N.N. center of the SB RAS, they will test potential drugs that slow down their death on such artificial neurons of the substantia nigra, look for genetic factors of the disease and biomarkers.

Exercise test

“Not a single person has yet been cured of Parkinson’s disease. We cannot stop neuronal death, because we do not know the cause. And there can be a huge number of them. The strategy of struggle is aimed at early diagnosis and preventive neuroprotective therapy, Ideally, if the threshold of neuronal death at which clinical symptoms appear is a loss of 70-80 percent of dopamine, occurs at the age of 120-150 years.A person will get sick, but the quality of life will remain acceptable, “says academician Mikhail Ugryumov, head of the laboratory of nervous and neuroendocrine regulation at the Koltsov Institute of Developmental Biology, Russian Academy of Sciences.

Mice with the earliest stage of Parkinson’s disease are obtained in his laboratory. their blood is looking for matches with potential biomarkers found in the blood of patients with a confirmed diagnosis.

“Dozens of biomarkers are known and not a single specific one, since we find them in other diseases as well.In any case, you need to use a set of markers, but even based on them, the diagnosis will still not be final, “the researcher notes.

He proposes to create a stress test to detect the disease. In psychiatry and neurology, this approach is not used, and in other areas of medicine – For example, there is a glucose tolerance test in the diagnosis of diabetes mellitus

Scientists have already selected a substance that blocks the synthesis of dopamine in the brain and a dose that temporarily increases symptoms in pathology, without side effects.Experiments on mice were successful, now, together with colleagues from Taiwan, researchers are preparing trials on primates.

“There is reason to believe that this diagnosis will be specific,” the academician emphasizes.

22 November 2019, 23:51 They form in an embryo between eight and 15 weeks of age.As the body ages, they die: on average, every ten years, the brain loses four percent of its nerve cells.

In neurodegenerative disease, for unknown reasons, the rate of neuronal death increases significantly. And although there are progenitor stem cells in the hippocampus and striatum, it was not possible to prove that they replace the dead.

In the early 1990s, with the development of cellular technologies, the idea arose to transplant healthy donor neurons into patients.

“The Swedish professor Andres Bjorklund conducted experiments on mice in which Parkinson’s disease was caused by neurotoxins.However, neurons transplanted from a healthy animal died. Then he transplanted neurons from the embryo to sick rodents, and their behavior was restored. It was a triumph, “recalls Mikhail Ugryumov.

On this wave, Bjorklund launched a program of clinical trials of cell technologies for the treatment of Parkinson’s disease in the EU. Six countries took part in it. Ugryumov led a scientific group from Russia. In total, we performed 13 transplant operations.

26 May 2020, 14:36The operation is non-traumatic, under local anesthesia. For ten years in all European countries – members of the consortium have collected a lot of material. The patients’ condition improved, but after six months the disease returned, “- says the scientist.

In the USA, the same results were obtained. Improvement of cell technologies did not change the situation.

” Everywhere they use the same methodology: they test therapy on rodents, then on humans. The general picture: one hundred percent success on animals, no lasting effect on humans, “- sums up the academician.

The human brain is too complex, he believes. Neurons cannot be transplanted into the substantia nigra, where the environment is suitable for them, because in the adult brain they cannot grow into another section. Therefore, they are implanted immediately where dopamine is required – in the striatum.

The mouse brain is flooded with various signaling substances, all neurons work in this cocktail. In humans, neurons are specialized, they have their own signaling substances, and their delivery should be directed.

The neuron is controlled not over the entire surface, but at points – synaptic contacts. And each is connected with ten to fifteen thousand other strictly defined neurons. All of this must re-form the cell that has been transplanted. In the next fifty years, according to Mikhail Ugryumov, this task is most likely unsolvable.

12 January 2020, 08:00 What food does the brain like and what it suffers from? 90,000 Mikhail Ugryumov. Brain Diseases: How to Save Neurons

Phenomena

Anna Natitnik

image

Diseases of the brain are the scourge of the XXI century.In the world, huge sums are spent on people suffering from them – but there is still no hope for a cure for many of these diseases. What is the cause of brain diseases and what are the prospects for combating them, says the vice-president of the Russian Physiological Society. I.P. Pavlova, Head of Laboratories, Institute of Developmental Biology named after N.K. Koltsov Russian Academy of Sciences and Research Institute of Normal Physiology. PC. Anokhina, Academician of the Russian Academy of Sciences, Adviser to the President of the Russian Academy of Sciences for International Scientific Cooperation, Professor, Doctor of Biological Sciences Mikhail Veniaminovich Ugryumov.

What are brain diseases?

These are diseases based on neuronal death. Depending on in which area of ​​the brain they die, one or another function of the brain or the body as a whole is turned off – say, reproductive.

Why do neurons die?

The reasons may vary. For example, acute injuries: trauma, strokes – as a result of which blood is poured out of the vessels and the process of neuronal death begins almost instantly.If you intervene quickly and start therapy, the healing effect can be very good. In the case of strokes, we are talking about 3-5 hours. But if you delay and provide help later, then the process, which goes on as a chain reaction, will become irreversible and will take over many areas of the brain. Worst of all, if this process develops in the medulla oblongata, where the respiratory, vasomotor center is located, then the person stops breathing, the heart stops working and he immediately dies. If the process takes place in the cortex, people lose their memory and the ability to be aware and perceive what is happening.

Another large group of brain diseases are chronic, so-called neurodegenerative diseases. They develop over many years – say, 20-30 – without any external manifestations. A person feels absolutely healthy, but at the same time he has a pathological process – neurons die. In general, neurons die in everyone. Even conventionally, the rate of this death is calculated – four percent in 10 years. But with neurodegenerative diseases, it increases significantly.

Which diseases are neurodegenerative?

Their range is wide, but Alzheimer’s disease and Parkinson’s disease certainly dominate. With Parkinson’s disease, mainly dopaminergic neurons, located in a special part of the brain called the nigrostriatal system, die, and a person’s motor function is impaired: trembling or stiffness of movements occurs. Most often, these symptoms mix over time.In Alzheimer’s disease, cholinergic neurons in the hippocampus and cortex die, that is, the neurons that are responsible for memory and learning – these functions in humans are affected. Another disease associated with the death of dopaminergic neurons is Huntington’s chorea. It manifests itself in impaired cognitive and physical abilities. There is also a disease that affects people of young reproductive age – hyperprolactinemia. In this case, the death of neurons leads to inhibition of reproductive function and infertility.If this disease is started, it goes into an irreversible stage – a pituitary tumor develops. Depression is also associated with neuronal death. It all starts with a reversible functional stage (mood deterioration, anxiety, high fatigue), but then moves on to the level of organic changes.

Why is neuronal death not felt for so long in neurodegenerative diseases?

Because the brain is extremely plastic, it has tremendous compensatory capabilities.Generally speaking, all organs have these possibilities, but in the world they are manifested to the greatest extent, since from the point of view of evolution, this is one of the most important structures. Therefore, when the symptoms of the disease finally appear, this, on the one hand, suggests that the compensatory mechanisms have exhausted themselves, and on the other, that the number of dead neurons has reached a threshold level. This threshold is calculated only for Parkinson’s disease: if dopamine is lost by 70-80 percent, a person’s motor function is immediately impaired.

Please provide examples of compensating mechanisms.

In Parkinson’s disease, as I said, neurons that synthesize dopamine, a substance that determines the interaction (chemical signals) between neurons, die. Not all neurons die, and those that are saved are activated, trying to produce more signals. But sooner or later, the number of these chemical signals decreases: the death of neurons is an irreversible process.And then another group of compensatory mechanisms comes to the fore – neurons receiving signals become more sensitive and “hear” even those neurons that generate a signal at a very low level, that is, “speak quietly.”

What are the causes of neurodegenerative diseases?

In the vast majority of cases, they are not known. Even ten years ago, scientists hoped that neurodegenerative diseases are monogenic, that is, one gene is responsible for their development.In this case, it would be easy to establish diagnostics and treatment – it would only be necessary to find this gene. But it turned out that the overwhelming majority of patients have impaired functions of many genes, so these diseases have passed from monogenic to polygenic.

Another feature: if earlier it was believed that the disease develops as a result of the death of only one group of neurons – in a strictly defined area of ​​the brain, it turned out that this is a systemic disease that spreads to many parts of the brain, to the peripheral nervous system, to internal organs …But the key symptomatology, from which the patient really suffers, really depends on a particular group of cells.

Is there a hereditary predisposition to these diseases?

There is, but we are talking about a very small percentage of patients – no more than three. There are family forms – they appear in people already at a young age, at 25-30 years. But in general, these are not fatal diseases: if parents get sick, children do not necessarily get sick.

What percentage of the population in Russia and in the world suffers from neurodegenerative diseases?

The number of cases is increasing among people over 60 years old. If we talk about Parkinson’s disease, then among 60-year-olds it is one percent, then, by the age of 70, it reaches five percent. Alzheimer’s disease spreads even faster with age. At 60 years old – this is three percent, at 70-75 years – 15-20 percent. These are world statistics. Our morbidity figures must be taken with great care.It is believed that in Russia one and a half million patients with Alzheimer’s disease, 300 thousand with Parkinson’s disease. But diagnostics is poorly delivered in Russia: in rural areas, people do not undergo outpatient examinations at all. Therefore, in order to understand the general trends, it is necessary to refer to the American and European experience.

Where do these diseases rank in terms of prevalence?

Neurological and mental diseases now rank third after cardiovascular and oncological diseases.However, according to forecasts of the World Health Organization, literally in ten years they will come out on top.

Why?

The number of patients with neurodegenerative diseases increases significantly every ten years. This is a catastrophe. There are three reasons for this – two of them can be understood, the third is not. The first is diseases of old age: the older a person is, the more likely it is that neuronal death will reach a threshold level.And as life expectancy in the world has increased dramatically, so does the number of older people. Although this does not apply to us: our life expectancy is 15 years less than in Europe, and much less than in Japan. The second reason is environmental pollution. Because of this, for example, parkinsonism occurs – about the same as Parkinson’s disease. For example, in hazardous production, heavy metals enter the brain through the nasal passages and cause the death of neurons. In addition, statistics from the World Health Organization and the Society for the Fight against Alzheimer’s Disease show that the number of patients is growing fastest in developing countries.Why – it is not clear: life expectancy there is low, which means there should be fewer patients. Perhaps the reason is environmental pollution – in these countries, little attention is paid to the environment. The third factor cannot be explained – the disease is rejuvenated: people begin to get sick at a younger age.

The number of depressions, often ending in suicide, is growing at the fastest rate today. One of the reasons is the constant stress that wears out a person. Besides, I think this can be partly explained by the economic crisis.In this sense, we are in a privileged position. If in the West life is so regulated that any deviation from the rules completely destabilizes a person, then our people are difficult to knock out of a rut.

How effectively are chronic brain diseases treated?

Parkinson’s disease was identified about 200 years ago, Alzheimer’s disease – 100 years ago. During this time not a single patient has been cured in any country in the world.Drug therapy should be aimed at preserving regulatory neurons and maintaining the functional activity of neurons involved in compensatory processes. However, as I already said, when a person develops symptoms of the disease and goes to a doctor, he has almost no neurons left – there is simply nothing to treat.

Quite recently, 10-15 years ago, scientists thought that they should try to make a diagnosis at the very initial stage of the pathological process, when neurons are just beginning to die.This happens at a fairly young age – 35-40 years old. If at this stage we begin to treat the patient – to reduce the rate of death of neurons, then the number of these neurons will not fall to the threshold level even at 90-100 years. This means that a person will not feel the symptoms of the disease until the end of his life. I think this is the most promising path.

How can a diagnosis be made at an early stage? Should a person, by some indication, understand that something is wrong with him and consult a doctor?

I think that the person himself will not go to the doctor before the onset of symptoms.Therefore, it seems to me, the issue should be resolved by medical examination of the population, during which clinical precursors of the disease can be identified. The process of death of neurons covers many parts of the brain, and before they begin to die in areas specific to a particular disease, they die, for example, in the olfactory bulb – in the region of the brain that is responsible for smell. In addition, patients in the early stages have constipation, heart failure. These harbingers can indicate different diseases, and none of them indicate a specific disease – therefore, you need to collect a whole bunch of harbingers.Changes in the functions of the nervous system and – as a result – of internal organs should be reflected in the composition of blood plasma and the functional activity of its cells. These changes can also serve as markers of neurodegenerative diseases. When all the precursors are found in a person, he is included in the risk group – out of a thousand people, three to five fall into it. And already these people need to carry out differential diagnostics to make sure that we are really talking about Parkinson’s or Alzheimer’s disease. For this there is an expensive and rare method – positron emission tomography.This is a non-invasive (no one gets into a person’s brain) neuroimaging (you can see all the cellular and molecular processes that take place in the brain) method. If it turns out that a person’s neurons do not work well, little chemical signal is synthesized, and at the same time all the precursors have been identified in him, then he definitely needs to be treated.

Isn’t it easier to immediately send everyone to such a tomography during a medical examination?

This method will never be used for general medical examination, even in the richest countries.It requires large financial costs and special technical conditions: the isotopes used in tomography do not live long, from half an hour to two or three hours, so a special neurochemical laboratory with a cyclotron is needed, which will synthesize them and immediately inject them to the patient. The devices themselves are hardware, their work depends on a set of tests, connections that are in the hands of specialists. Unfortunately, in Russia it is very difficult to obtain a license to use the required tests. Therefore, we do not carry out such diagnostics at all.

How can neuronal death be inhibited?

There are several groups of substances for this. As a rule, the death of any cell is associated with oxidative stress: free radicals accumulate in the cell, which ultimately kill it. This is counteracted by drugs – antioxidants. But it seems to me that preventive treatment can be based on the use of growth factors, or neurotrophic factors. These are neuropeptides – molecules that are made up of amino acids.They have three essential properties. First, their action is aimed at stopping or slowing down the death of neurons. Second, they stimulate neuronal differentiation during brain development. Third, they control compensatory processes. This is a unique combination. Different peptides are dominated by different properties, and, accordingly, they have a different effect on certain neurons. Therefore, before using them for treatment, it is necessary to study them carefully.

What can be the source of growth factors?

They can be obtained by chemical, genetic engineering or combinatorial methods.But the main thing is that they themselves are synthesized in the body, in almost any cells, and especially actively in the brain. So you can either use artificial growth factors, or learn how to control their natural synthesis in the brain. The second option is preferable because it significantly reduces the risk of side effects. There are already special substances that stimulate the production of growth factors. Back in Soviet times, apparently by order of the Ministry of Defense, the Institute of Molecular Genetics developed a drug for astronauts and high-altitude pilots that improves brain activity, especially in extreme situations, called Semax.

However, as I said, it is necessary not only to increase the synthesis of growth factors, but also to control this process. It is necessary to understand in which situations and areas of the brain this is necessary and possible to do, and in which not, because growth factors under certain conditions can cause the formation of a tumor. If their concentration is very low (10-11), they have all the positive properties. But it is worth increasing this concentration by three orders of magnitude, and growth factors will begin to destroy cells, in particular neurons.

If we talk about artificially synthesized growth factors, then another question arises: how to deliver them to the brain? Peptides pass very poorly or do not pass at all through the blood-brain barrier, which protects the brain from external harmful influences (bacteria, toxic substances from the external environment can enter the bloodstream, but not into the brain; and vice versa, most substances from the brain do not enter general circulation system). To drag peptides across this barrier, they can be packed in lipid capsules (anything that dissolves in lipids penetrates well into the brain) or planted on nanoparticles.Another way is to take these substances internally: they enter the brain along the cranial nerves.

While we are solving the issue of peptide delivery today, a number of other problems require long and serious work. First of all, these are the problems of dosage and maintenance of the required concentration of the substance and its targeted delivery to those neurons that are affected.

There is a lot of talk about stem cells now. Can they be used to treat neurodegenerative diseases?

As part of a European program, I spent almost 15 years using cell technology to treat Parkinson’s disease – and I became disillusioned with this approach.The creator of this program, the famous Swedish scientist Andres Bjorkland, was guided by the following considerations: if something dies, for example, the heart, kidneys, liver, they are changed; This means that if the neurons synthesizing a chemical signal stop working, you need to put a pump that would pump this signal. He decided that the ideal pump was the neurons themselves. If you transfer neurons from an adult to an adult, they do not take root and die. Therefore, it is necessary to use embryonic neurons – in the brain of an adult organism, they will develop and work well.An experiment on rats gave an ideal therapeutic effect. However, in the course of human trials, the condition of patients improved within six months, a maximum of a year, and then everything was again reduced to zero. No one had any worsening, thank God, but the therapeutic effect was temporary. Therefore, this technology was not recommended to be used in the clinic.

The problem turned out to be much more complicated than we thought. It turned out that rodents have a much more plastic brain than humans. In humans, each neuron is connected with a dozen or even two tens of thousands of other neurons using specialized synaptic contacts.Therefore, in order to cure a person, it is necessary not only to download the necessary substance, but also to reproduce all this microarchitectonics – and this is still impossible to do.

Are there other, non-drug treatments for brain diseases?

As you know, if you disconnect from the brain all external information received through sight, hearing, motor activity, etc., then it degrades very quickly. Information trains the brain and makes it work.This feature can be used for neurodegenerative diseases as well. At last year’s Science and Technology in Society Forum in Kyoto, a Columbia University professor gave a terrific talk. She talked about psychological training – for memorization, for thinking efforts – that was conducted for people with the onset of Alzheimer’s disease. It turned out that such training slows down and even stops the development of the disease for some time. Similar trainings are held in our Center for Speech Pathology and Neurorehabilitation at the Research Institute of Psychiatry of the Ministry of Health.Psychologists of this center work with people who have suffered traumas, strokes, and as a result, many patients even return to their professional activities.

If we talk about the method of early diagnosis and treatment, in how many years, according to your forecasts, will it be applied in practice?

I think success on this path will be achieved in five years, maximum ten. This time could be significantly reduced if specialists from different countries combined their efforts.Several years ago, we agreed to work with the US National Institutes of Health, which is conducting similar research. However, then they unexpectedly refused – probably for them competition in this field has become a defining political issue.

We are constantly talking about the globalization of the world, about the fact that mankind is faced with new problems that cannot be solved by one country, even the richest, that this requires unification. So far, unfortunately, these are mostly words.Nobody understands how to unite: how to combine national economic, political and scientific ambitions, on the one hand, and the interests of patients, on the other.

90,000 Scientists have linked COVID-19 smell loss to brain damage

COVID-19 leads to loss of brain gray matter, British experts warn. This can be the cause of loss of smell and taste and other neurological symptoms. The body is able to adapt to the changes, and the symptoms will go away, but the brain tissue itself will no longer heal.

The cause of neurological symptoms in COVID-19 may be the destruction of gray matter, according to researchers from the University of Oxford. They talked about this in more detail in an unreferenced article posted on the preprint service medRxiv .

The researchers used data from the UK Biobank repository of medical and genetic information. They selected the results of examinations of 394 people who had had coronavirus and who had an MRI of the brain both before and after the illness, and compared them with the results of a control group of 388 people who had not been ill.

The ability to look at a patient’s brain before and after an illness has made it possible to distinguish changes caused by COVID-19 from other possible brain lesions, the researchers note.

They found significant loss of gray matter density and volume in several areas of the brain – the parahippocampal gyrus associated with memory coding, the lateral orbitofrontal cortex, which is involved in decision-making, and the insular lobe, which plays a role in the formation of emotions.

“Our results show gray matter loss in the limbic areas of the cerebral cortex, which are directly related to the primary olfactory and gustatory systems,” the authors write.

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@ ScottGottliebMD / twitter.com

More pronounced changes were observed in the left hemisphere.

Also, the researchers compared the results of hospitalized patients with those who had been ill at home, but found no significant difference. However, hospitalized patients showed a more pronounced loss of gray matter in the cingulate cortex, the central nucleus of the amygdala, and some regions of the hippocampus.All of these areas are also associated with memory and the formation of emotions.

COVID-19, even in a mild form, can lead to brain damage, the researchers conclude.

They recommend that those who have recovered do not neglect timely examinations in order to find out what consequences they could face.

The study design does not allow to confirm the existence of a causal relationship – theoretically, some other factors could have influenced the state of the brain. Nevertheless, the authors of the work are sure that this connection exists.They note other limitations of work: almost all of the patients were white, which does not allow to extend the data to representatives of other ethnic groups, in addition, the researchers did not have data on the saturation of the participants’ brains with oxygen and other factors that could play a role.

“We were able to identify a consistent pattern of gray matter loss in the limbic regions of the brain that form the olfactory and gustatory network,” the researchers conclude. “Whether these abnormal changes indicate a spread of disease in the brain, which may portend future vulnerability of the limbic system, including memory, in these patients remains to be seen.”

“Research suggests COVID-19 may lead to loss of brain tissue with long-term consequences,” said Dr. Scott Gottlieb, former head of the US Food and Drug Administration. –

The body will be able to compensate for this over time, and the symptoms will disappear, but it will never be possible to restore the destroyed areas. ”

A decrease in brain volume was observed in areas close to those associated with the sense of smell, Gottlieb stresses.

“This shows that the loss of smell is a consequence of a more important process, the reduction in the volume of the cerebral cortex,” he says.

COVID-19 can also lead to the defeat of white matter, found out earlier specialists from the University of Pennsylvania. Of the 2,820 patients with COVID-19 the authors dealt with between March 1 and June 18, 2020, 59 underwent an MRI scan of the brain. Many showed signs of brain damage caused by multiple sclerosis, strokes, lack of oxygen in the blood, insufficient blood supply to the brain, and other factors.But the researchers also noticed that six patients (10.2%) had signs of leukoencephalopathy.

Leukoencephalopathy is a persistent destruction of the white matter of the brain.

With its progression, it can lead to speech and vision impairments, less often – to dizziness, headaches, epileptic seizures. Mental disorders are also possible.

90,000 Ministry of Health reported on the risk of brain damage from coronavirus :: Society :: RBC

As follows from the recommendations of the department, the coronavirus, when it spreads in the body, can infect the brain, and a change in the sense of smell in the early stages of the disease can indicate damage to the central nervous system.

Photo: Artem Geodakyan / TASS

The SARS-CoV-2 virus, which causes the coronavirus infection COVID-19, spreading in the human body, can lead to brain damage.This is reported (* .pdf) in the new version of the temporary guidelines of the Ministry of Health.

“Dissemination of SARS-CoV-2 from the systemic circulation or through the plate of the ethmoid bone (Lamina cribrosa) can lead to brain damage,” – stated in the document.

In Russia, a record number of patients died from coronavirus per day

It is noted that a change in the sense of smell (hyposmia) in a patient at an early stage of the disease may indicate damage to the central nervous system, as well as edema of the nasopharyngeal mucosa.

According to the ministry, the virus enters the body through the epithelium of the upper respiratory tract, stomach and intestines. In the first stage of infection, SARS-CoV-2 enters target cells, the receptors of which are present in the respiratory tract, kidneys, esophagus, bladder, ileum, heart and central nervous system. However, the main target, according to the Ministry of Health, is the alveolar cells of type II (AT2) of the lungs, which leads to the development of pneumonia.

Spinal Cord Injury | Institut Guttmann

The spinal cord is a “nerve cord” covered with membranes, which is freely located in the cavity of the spinal canal.Above, it passes into the medulla oblongata of the brain, below it reaches the lumbosacral region. The spinal cord is part of the Central Nervous System and has a direct connection with the internal organs, skin and muscles of a person. The spinal cord is the main channel that provides the brain with information from the rest of the body and allows the brain to control the executive organs, including the transmission of “orders” that regulate movement.

Its interruption or damage causes paralysis of conscious motor functions and leads to the loss of all kinds of sensitivity below the zone of damage; which also leads to a lack or disorders of sphincter control (urination and bowel movement), disorders in the sexual and reproductive sphere, disorders of the Autonomic Nervous System and the risk of developing other complications (pressure sores, spasticity, pathological processes in the kidneys, etc.)etc.)

Injury to the spinal cord can be the result of an injury (accident, injury at work, sports injury, traffic accident, etc.), disease (tumor, consequences of infectious or vascular diseases, etc.) or congenital disease (splitting spine). Depending on whether the damage is complete or partial, as well as the level of damage, its consequences will be more or less severe.

Damage to the nerve communication at the cervical level leads to TETRAPLEGY, that is, loss or decrease in sensitivity and / or conscious movements of the upper and lower extremities and the entire trunk.The defeat of the spinal cord at the thoracic and lumbar levels leads to PARAPLEGY – lack of sensitivity and / or complete or partial paralysis of the lower extremities and that part of the trunk, which is located below the lesion. Damage at the level of the Conus medullaris or the cauda equina does not cause such serious movement disorders and gross loss of sensitivity, and therefore, in most cases, the ability to walk is preserved; however, the most serious consequences are: anesthesia in the perineum and lower posterior parts of the buttocks, disorders of the pelvic organs of the peripheral type, loss of the anal reflex, trophic disorders in the sacrum.

REHABILITATION AFTER SPINE INJURY

Until now, the consequences of spinal cord injury are irreversible, since the spinal cord lacks the ability to regenerate, and its complexity and structure make reconstructive surgery impossible with modern methods. However, there is active research going on around the world for a cure in the future. Comprehensive rehabilitation of a patient in a specialized center is currently the only alternative for the most effective recovery and care of these people.

90,000 Brain recovery after injuries and injuries

Traumatic brain injury (TBI) – organic damage to the brain and cerebral structures (membranes, vessels, nerves) resulting from mechanical damage to the brain.

As a result of mechanical action, a break or damage to nerve fibers occurs, which leads to a violation of the transmission of a nerve impulse. Such damage can occur in various areas of the brain responsible for speech, hearing, perception, attention, memory.

Therefore, different people as a result of TBI may have different problems – with memory, attention, perception and recognition. Traumatic brain injuries often result in disorders of thinking, emotional sphere (depression, irritability), impairment of hearing, writing, counting, reading and speech.

Most of these violations can be compensated. After TBI treatment received in a hospital, the patient needs rehabilitation (elimination of the consequences of traumatic brain injury), aimed at restoring the lost functions.

At the Center for Speech Neuroscience “DoctorNeuro” the condition of each patient is assessed by an interdisciplinary team of specialists. Doctors assess the problem comprehensively, each from the point of view of his specialization. In the diagnosis of the consequences of TBI, various methods of functional diagnostics are used. The entire process of your rehabilitation will take place under the supervision of an experienced neurologist. He will study the anamnesis, prescribe an examination and a consultation of doctors, select medication and concomitant therapy, and monitor the course of rehabilitation.

“Recovery training can be started at any time, but the first year after injury and recovery from an acute condition is the most important for achieving maximum results.”

Krivtsova Yulianna Pavlovna,
Neurologist
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Survey

Neurologist

Rehabilitation after TBI begins with an appointment with a neurologist. The doctor conducts an examination, examines the already available medical documentation (discharge, CT, MRI) and, if necessary, prescribes an additional examination.This can be functional diagnostics, computer diagnostics, laboratory tests and examination of the patient by other specialists. The scope of the required examination is determined by the neurologist individually in each case.

The purpose of the surveys is to assess the volume, degree and type of disorders that have arisen as a result of traumatic exposure. Based on the results of such a comprehensive examination (diagnosis), the doctor will be able to prescribe therapy and develop a rehabilitation route.

EEG

Electroencephalogram allows you to assess the functional state of the bioelectrical activity of the brain in order to identify or exclude functional pathologies in its individual areas.

UZDG

Doppler ultrasound (USDG) of the vessels of the head and neck is prescribed to assess the degree of arterial and venous blood flow, exclude indirect signs of venous and intracranial hypertension, and diagnose vascular angiospasm.

Oculist

A neurologist may prescribe an additional consultation with an ophthalmologist in order to exclude pathology from the fundus. Stagnation in the fundus can serve as evidence of cerebral hypoxia, which is very important for the selection of drug therapy.

Neuropsychologist

With the help of special methods of neuropsychological diagnostics, the neuropsychologist identifies disorders in the work of higher mental functions that have arisen as a result of traumatic brain injury. The specialist evaluates the state of memory, attention, thinking of the patient, as well as the state of his emotional sphere (the presence of aggression, irritability, depression) – it is with the problems identified during the examination that the neuropsychologist will work in the process of neurorehabilitation of the patient.

Speech therapist

Speech therapist assesses the state of the patient’s speech if it is damaged.

Treatment

On the basis of a comprehensive examination and determination of the degree of damage to higher mental functions, a neurologist prescribes an individual neurorehabilitation program: both the necessary drug therapy and restorative sessions with a neuropsychologist and speech therapist.

As an effective innovative method of treatment, a neurologist can prescribe the method of transcranial magnetic stimulation (TMS).This is a modern non-invasive technique for the treatment of neurological disorders. The effectiveness of TMS has been proven by both foreign and Russian experience.

The principle of TMS operation is the painless and safe effect of short-term magnetic impulses on the affected nerve cells of the cerebral cortex, which significantly accelerates the restoration of the function of brain areas lost as a result of traumatic effects.

TMS can be prescribed both as monotherapy and work in conjunction with drug therapy.

TBI symptoms with recent head impact

  • Headaches,
  • Vertigo,
  • Loss of consciousness even for a few seconds,
  • Falling asleep within the first two hours,
  • Nausea, vomiting,
  • Visual impairment: pain in the eyes, displacement (bifurcation) of the image,
  • Tinnitus,
  • Retrograde amnesia (after a blow, events lasting from a few seconds to 2 hours may fall out of the victim’s memory).

Symptoms of a head injury in the past (sometimes after 3-5 years)

  • Frequent headaches,
  • Sleep and / or sleep / wake cycle disorders,
  • Visual impairment,
  • Impaired cognitive functions (impaired memory, concentration, fatigue, difficulty following the sequence of actions, etc.).

90,000 Brazilian scientists suspect coronavirus in the destruction of brain neurons in patients

Coronavirus infection leads to the death of neurons in the cerebral cortex and can cause diseases such as Alzheimer’s and Parkinson’s and schizophrenia.This was reported by the G-1 portal with reference to the research data of Brazilian scientists, published in the electronic scientific library medRxiv. Scientists have come to the conclusion that lesions of brain neurons occur not only in seriously ill patients with coronavirus, but also in those who have had a mild to moderate disease.

A study by a group of more than 70 Brazilian researchers showed that the new coronavirus affects the human brain, causing neuronal death, even in COVID-19 patients who did not need hospitalization, the Brazilian newspaper writes.Researchers from the State University of Campinas (Unicamp), the University of São Paulo (USP), the Federal University of Rio de Janeiro (UFRJ), the National Laboratory for Biological Sciences (LNBio) and the private research institute D’Or took part in the scientific work.

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“In the case of severe patients, neuronal death is expected because they have a low level of oxygen saturation in the blood, which is very damaging to the brain. But when such serious changes are detected in someone who has had a mild or moderate illness, this is already a cause for concern, “- quotes the publication of one of the curators of the study, Daniel Martins-de-Sousa from Unicamp.According to the researchers, the virus infects astrocytes – cells that are responsible for communication between neurons and for their nutrition. This, in turn, leads to significant changes in the cerebral cortex, up to atrophy of certain areas, with the work of which mood changes are associated. As the newspaper notes, it was this symptom that was most often observed in the studied group of patients.

“We have encountered many patients who, even after recovering from COVID-19 about two months ago, still have symptoms of neurological disorders: headache, excessive sleepiness, memory impairment, loss of taste and smell.In some rare cases, convulsions are observed, although these people did not have this before, ”said neurologist Clarissa Lin Yasuda of Unicamp. “What we don’t know yet is how serious such damage is, whether it is temporary or irreversible. Therefore, we will monitor our patients for at least the next three years to understand whether the virus leads to the development of degenerative diseases in those who have a genetic predisposition to them, ”she explained. Science has reason to believe that the coronavirus can activate genetic diseases such as schizophrenia, Parkinson’s and Alzheimer’s, Yasuda said.“By understanding how the virus changes cells, we can start thinking about how to use the right drugs,” added Martins de Sousa.

Photo MARTIN DIVISEK / EPA / TASS

Countries that were wrong: who is returning quarantine measures due to a new surge in COVID-19 infections

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