What are the causes of memory loss, behavioral changes, and slurred speech in a 49-year-old man? How can such a case be diagnosed and treated?

Case Presentation

A 49-year-old left-handed man presented with a history of slurred speech, memory loss, and behavioral changes. His symptoms began a year earlier while on vacation in Tuscany, Italy, where his sister noticed he appeared unusually quiet. Over the following months, his co-workers and family members observed continued changes in his speech and behavior, including difficulties arriving to work on time, disorganization, and memory problems.

Medical History and Examination

The patient had a history of poorly controlled hypertension and hyperlipidemia. Neurological examination revealed a flat affect, disorientation to time, deficits in attention and concentration, and difficulties with memory tasks and clock drawing. His past medical history was noteworthy for meningitis at age 19, mononucleosis at age 29, and recently diagnosed arterial hypertension.

Diagnostic Workup

The patient underwent a detailed workup during his hospitalization, the results of which are discussed in the following sections.

Neuroimaging

Neuroimaging studies, including magnetic resonance imaging (MRI), were remarkable for multiple subcortical white matter lesions.

Laboratory Findings

The patient’s laboratory evaluation, including blood tests and other diagnostic tests, did not reveal any specific underlying cause for his rapidly progressing cognitive decline.

Diagnosis and Treatment

Based on the clinical presentation and diagnostic findings, the patient was diagnosed with a rapidly progressing cognitive decline. He underwent rehabilitation therapy, with slow improvements noted in his memory and organizational skills. However, his condition fluctuated, and he experienced episodes of gait difficulties, increased drowsiness, and an overall decline in his ability to perform daily living activities. The patient was started on antiseizure medication (levetiracetam) after a witnessed seizure.

Prognosis and Ongoing Management

The patient’s condition continued to decline, with significant impairment in his cognition and daily functioning. He required ongoing rehabilitation and supportive care to address his memory, speech, and behavioral issues.

Discussion

The case presented here highlights the diagnostic and therapeutic challenges associated with rapidly progressing cognitive decline in a middle-aged individual. The underlying cause of the patient’s symptoms, which included memory loss, slurred speech, and behavioral changes, was not immediately clear and required a comprehensive evaluation.

What are some potential causes of the patient’s symptoms?

The patient’s presentation could be indicative of various neurological conditions, such as vascular dementia, Alzheimer’s disease, Lewy body dementia, or a rapidly progressing neurodegenerative disorder. The presence of multiple subcortical white matter lesions on neuroimaging suggests a vascular etiology, which may be related to the patient’s history of poorly controlled hypertension and hyperlipidemia.

How would you approach the diagnosis and management of this case?

A thorough diagnostic workup, including neuroimaging, laboratory tests, and neuropsychological assessments, is essential to identify the underlying cause of the patient’s cognitive and behavioral changes. Addressing any underlying medical conditions, such as hypertension and hyperlipidemia, is an important aspect of management. Additionally, rehabilitation therapy, cognitive interventions, and supportive care may be necessary to address the patient’s functional impairments and improve his quality of life.

Conclusion

This case highlights the complex and challenging nature of rapidly progressing cognitive decline in a middle-aged individual. A comprehensive evaluation and a multidisciplinary approach to diagnosis and management are crucial in such cases to identify the underlying cause and provide appropriate interventions to optimize the patient’s outcomes.

Memory Loss, Behavioral Changes, and Slurred Speech in a 49-Year-Old Man

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Front Neurol. 2011; 2: 27.

Published online 2011 Apr 28. Prepublished online 2011 Mar 26. doi: 10.3389/fneur.2011.00027

,¹,² and ^1,*

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A 49-year-old man presented with slurred speech, memory loss, and behavioral changes. His clinical course was marked by decline in functional status and cognition. He had poorly controlled hypertension and hyperlipidemia. Neuroimaging was remarkable for multiple subcortical white matter lesions. We discuss the diagnostic and therapeutic approach of rapidly progressing cognitive decline in the given clinical setting.

Keywords: memory loss, arterial hypertension, magnetic resonance imaging, vascular dementia

History: A 49-year-old left handed man presented to us with concerns of memory loss, slurred speech and behavioral changes. His symptoms started a year earlier while on vacation (biking) in Tuscany, Italy with his sister. His sister recalled he appeared more quiet than usual. During the ensuing days, other family members also noticed he was unusually quiet and his speech was slurred; this was attributed to fatigue from travel and wine. After he returned from vacation to his work in the Midwest, his co-workers noted similar changes. Subsequently, the patient began to suspect problems himself, when he missed a few days of work, 3 months after his symptoms were recognized while in Italy. Over the ensuing 2 months, he had increasing difficulties arriving to work on time, became more disorganized at home and at work, and had more difficulties remembering things. Six months after onset of symptoms, he was asked to see a physician by his supervisor at work. At the physician’s office, the nurse thought his speech was slurred and recorded a blood pressure of 240/160 mm Hg. He was then admitted to a local hospital where he was noted to have short term memory impairment, slurred speech, word finding difficulties and behavioral changes including wandering, impulsivity and inappropriate sexual overtures to hospital staff. He was then transferred to a tertiary care hospital for further management. A detailed workup was done at the hospital, which is discussed further below. Subsequently, he had rehabilitation therapy and slow improvements were noted on his memory and organizational skills. At this time, he was able to prepare simple meals using the microwave but not the stove. He would accompany family members on errands, medical appointments, taking walks and reading. Moreover, he was independent for personal activities of daily living.

He was subsequently transferred to a rehabilitation center where he continued to show improvement in memory. Some improvement was also noticed in performing activities involving organizational and executive skills.

However, this was followed by episodes of gait difficulties and increased drowsiness, followed by an overall decline in his ability to perform tasks of daily living. He continued to have a fluctuating course and his cognition suffered a significant decline. He was witnessed to have a seizure and was subsequently started on levetiracetam.

Medications include aspirin 81 mg daily, lisinopril–HCTZ 10–12.5 mg daily, nifedipine 90 mg twice daily, folic acid, Coenzyme Q10, Fish oil, Vitamin B complex, atorvastatin 20 mg.

Past medical history was noteworthy for meningitis at the age of 19, mononucleosis at the age of 29, and recently diagnosed arterial hypertension. He worked as a manager in an Information and Technology firm. He smoked a pack of cigarettes a day for the past 20 years. He was divorced. He was not sexually active. He had family history of arterial hypertension.

Neurological examination was remarkable for a flat affect. He was disoriented to time and had deficits in attention and concentration. Four word span was 4/4 at 1 min without distraction, 3/4 at 1 min with distraction, and 2/4 at 6 and 45 min respectively. He could recite the months of the year forward in 9 s (paused between September and October) but took >40 s backward and got stuck at June. Digit span test was 7 forward, and 3 backward. He could draw the face of a clock with correctly placed numbers but could not place the hands of a clock at the right place. He was able to read and write numbers correctly. He could add single and multi-digits correctly but made mistakes in single and multi-digit multiplication. Benton face recognition screening was normal. He had no neglect on letter cancelation test.

His speech was dysarthric with mild word finding pauses. Naming, repetition, comprehension and reading were intact. Writing was “messy” but he was able to spell correctly and the syntax was intact. Cranial nerve examination was normal except for funduscopic examination that showed focal areas of infarct lateral to the left disc and medial to the right disc. He had mildly spasticity in both upper extremities, and moderate spasticity in the lower extremities. He had 5/5 strength in both upper extremities. Hip flexion, knee extension, knee flexion, foot plantar flexion, foot dorsiflexion were 4/5 bilaterally. He had no tremors. He had a right “cortical fist” attitude, and bilateral palmar grasp responses. A snout reflex was present. Vibration and temperature sensation was intact except for slight reduction on the left foot. Position sense was intact. Sensation to light-touch was intact. There was no extinction to double simultaneous stimulation. Graphesthesia and stereognosis were unremarkable. He had slow and clumsy bilateral rapid alternating movements. Mild dysmetria was observed on finger to nose test bilaterally and on heel knee shin test on the left. Muscle stretch reflexes were hyperactive throughout. There was a Hoffman’s sign on the right. The left plantar response was flexor. He had a right Babinski sign. There was mild ideomotor and limb-kinetic apraxia. Oral praxis was intact. He had a mildly unsteady gait. He had normal arm swing and turns, but was mildly unsteady with tandem gait. Romberg was negative.

Ancillary studies showed a normal complete blood count, normal basic metabolic profile, a serum cholesterol of 137 mg d/l, Triglycerides 91/mg/dl, HDL of 39 mg/dl, LDL of 80 mg/dl. HbA1c was 5.4. Urine drug screen was negative. Plasma homocysteine was elevated at 24.2 μmol/l. Urine analysis and erythrocyte sedimentation rate were normal. RPR was non-reactive. Serum B12 and Folate levels, and TSH were all normal.

Transesophageal echocardiogram showed normal left and right ventricular size. The left ventricular ejection fraction was 60%. There was no left atrial thrombus. The left atrial appendage was free of thrombus. There was no evidence of interatrial communication or R–L shunt by bubble contrast study. The heart valves were normal.

MRI of the brain showed bilateral periventricular white matter and subcortical white matter ischemic changes (Figures and ). Gradient Echo imaging showed multiple subcortical microbleeds (Figure ). MRA (not shown) of the extracranial and intracranial circulation showed a 1.2 mm × 2 mm right A1–A2 junction aneurysm, and a 1.1 cm × 0.4 cm irregular outpouching from the right vertebral (V2)segment consistent with a pseudoaneurysm likely related to a chronic dissection. There was no evidence of flow-limiting stenosis within intracranial or extracranial vessels. Catheter cerebral angiogram showed a single M3 branch vessel of the right MCA with mild irregularity on magnification lateral views, a 3-mm anterior communicating artery (ACom) aneurysm, and a right V2 segment mild vertebral artery pseudoaneurysm consistent with remote dissection. There was also mild to moderate intracranial dolichoectasia, particularly of the basilar artery.

EEG revealed mild background slowing but no epileptiform activity was noticed. Chest X-ray was normal. CT chest abdomen pelvis were unremarkable. MRI of the cervical and thoracic spine were normal. Cerebrospinal fluid (CSF) testing showed, clear and colorless CSF with glucose of 59 (normal when compared to blood glucose), WBC:1, RBC:0. Cytology was negative for malignancy. Viral (HSV, VZV, CMV, JC virus), bacterial, and fungal cultures were all negative. Hypercoagulable profile, Apo E genotyping, CADASIL gene testing, autoantibody screen (C-ANCA, P-ANCA, SS-A, SS-B, complement levels, Scl-70, Anti Jo, RNP, ANA, Anti Smith Ab, cryoglobulins), and catecholamine levels. All of the above tests were normal.

The patient underwent a brain biopsy (Figures –).

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Hematoxylin and eosin staining.

Figures and shows thickened hyalinized barrel-shaped arterioles. Figure shows a focal area of lack of myelination. The myelin loss was variable with white matter reactive astrocytosis (GFAP stain; Figure ) and microgliosis (CD68 stain; not shown). In general, the blood vessels showed narrowing and hyalinization without occlusion. These features were consistent with subcortical arteriosclerotic leukoencephalopathy (Binswanger’s disease).

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Hematoxylin and eosin staining.

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Luxol fast blue staining.

Binswanger’s disease, also known as Subcortical Arteriosclerotic Encephalopathy was initially recognized by Otto Binswanger in 1894, and Alois Alzheimer first coined the term “Binswanger’s disease” in 1902 (1994; Pantoni et al., 1996). Binswanger recognized a total of eight cases in his original study, but defined the gross pathology in only one of them. Later on Alzheimer described the pathology and clinical characteristics of the disease and proposed it as a separate entity. An earlier review by Babikian and Ropper (1987) reported only 47 cases before 1987. Since then, additional cases of Binswanger’s disease have been reported primarily due to the use of modern neuroimaging.

Vascular dementia is the second most common form of dementia in the United States, and causes an estimated 50% of dementia cases in Japan. Binswanger’s disease is a cause of vascular dementia (World Health Organization, 1993), and is most commonly observed in the fifth and sixth decades of life. Slightly more common among men, it is associated with arterial hypertension and diabetes mellitus. The disease starts with mild decrease in cognitive function, referred to as vascular cognitive impairment (Bowler and Hachinski, 1995, 2003). The cognitive decline is gradual in the beginning and worsens with new clinical events. As the disease progresses further decrease in the cognitive function may not be associated with new clinical events (Pohjasvaara et al., 2003). According to criteria defined by Bennett et al. , Binswanger’s disease is diagnosed by the presence of dementia on clinical examination or neuropsychological testing and the presence of either vascular risk factors with cerebrovascular disease or subcortical dysfunction. There should be bilateral subcortical white matter involvement, without cortical involvement on cranial computed tomography or magnetic resonance imaging (Bennett et al., 1990).The dementia is characterized by a predominantly frontal dysexecutive syndrome with mild memory impairment. Dysarthria, gait impairment, and bladder incontinence may occur early in the disease process (Baezner et al., 2008). Some patients may have mania (Caplan and Schoene, 1978), depression (Pohjasvaara et al., 2003) or mood instability with clinical fluctuations (Delong et al., 1974).

Gross pathology is characterized by gyral atrophy and lacunar infarctions involving the basal ganglia, centrum semiovale or internal capsule. The corpus callosum may be atrophic (Babikian and Ropper, 1987). Microscopically, swelling of the myelin sheath and oligodendrocytes is one of the earliest changes seen. There are microcystic areas of infarction, with relative demyelination (Pellissier and Poncet, 1989). The arterioles supplying the deep white matter exhibit lipohyalinosis with perivascular lymphocytes, thickened walls and basal lamina. There is increased deposition of normal collagen, disruption of the media, narrowed lumina and splitting of the internal elastic lamina, with some occluded vessels. The endothelium is often intact. Some vessels show hypertrophy of smooth muscle cells (Akiguchi et al., 1997).

The degree of cognitive decline in Binswanger’s disease correlates with the progression of white matter changes. The Cardiovascular Health Study showed a 28% increase in white matter disease among patients older than 65 years, which correlated with decline in cognitive function (Longstreth et al., 2005). The leukoaraiosis and disability study (LADIS), observed that 10.5% of patients with mild white matter disease progressed to death or disability as compared to 29. 5% with extensive white matter disease every year (Inzitari et al., 2007).The PROGRESS trial showed that patients with mild leukoaraiosis at the time of entry had a slower rate of progression to severe cognitive impairment as compared to patients with severe leukoaraiosis (Dufouil et al., 2009). Other factors correlating with cognitive decline are microvascular retinopathy (Lesage et al., 2009) and hypertension (Gottesman et al., 2010).

Management is primarily aimed at controlling risk factors like arterial hypertension and diabetes mellitus. It is important to always take into account the autoregulatory changes associated with chronic hypertension as these patients may be more likely to have hypotensive events at pressures otherwise considered as normal (Sulkava and Erkinjuntti, 1987). These events may be responsible for white matter changes leading to further memory impairment. Lipid lowering drugs and platelet antiaggregants (mainly aspirin) are used in the prevention of cardiovascular and cerebrovascular disease (Sterzer et al. , 2001). In one study pravastatin improved vasomotor reactivity in small vessel ischemic disease, but had no effect on volume of leukoaraiosis (Zijlmans et al., 2004). L-Dopa has been used to improve gait in patients with features of vascular parkinsonism (Molnar et al., 1998). Memantine, donepezil, and rivastigmine have been used to benefit vascular dementia to a modest degree (Mobius and Stoffler, 2002; Wilkinson et al., 2003).

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Aphasia – Symptoms – NHS

Aphasia affects everyone differently, but most people will have difficulty expressing themselves or understanding things they hear or read.

If aphasia has been caused by a sudden brain injury, such as a stroke or severe head injury, symptoms usually develop straight after the injury.

In cases where there’s gradual damage to the brain as a result of a condition that gets worse over time, such as dementia or a brain tumour, the symptoms may develop gradually.

Expressive aphasia

Someone with expressive aphasia experiences difficulty communicating their thoughts, ideas and messages to others.

This may affect speech, writing, gestures or drawing, and causes problems with everyday tasks like using the telephone, writing an email, or speaking to family and friends.

People with expressive aphasia may have some of the following signs and symptoms:

• slow and halting speech – with difficulty constructing a sentence
• struggling to get certain words out – such as the names of objects, places or people
• only using basic nouns and verbs – for example, “want drink” or “go town today”
• spelling or grammatical errors
• using a wrong but related word – such as saying “chair” instead of “table”
• including nonsense words or their speech not making sense (speech-sound errors)

Receptive aphasia

A person with receptive aphasia experiences difficulty understanding things they hear or read. They may also have difficulty interpreting gestures, drawings, numbers and pictures.

This can affect everyday activities such as reading an email, managing finances, having conversations, listening to the radio, or following TV programmes.

People with receptive aphasia may have some of the following signs and symptoms:

• difficulty understanding what people say
• difficulty understanding written words
• misinterpreting the meaning of words, gestures, pictures or drawings
• giving responses that may not make sense if they’ve misunderstood questions or comments
• not being aware of their difficulties with understanding, or their own speech errors

Aphasia symptoms associated with dementia

People with the most common types of dementia, such as Alzheimer’s disease and vascular dementia, usually have a mild form of aphasia.

This often involves problems finding words and can affect names, even of people they know well.

It doesn’t mean they don’t recognise the person or don’t know who they are, they just can’t access the name or get mixed up.

Primary progressive aphasia

This is a rare type of dementia, where language is heavily affected. As it’s a primary progressive condition, the symptoms get worse over time.

Usually, the first problem people with primary progressive aphasia (PPA) notice is difficulty finding the right word or remembering somebody’s name.

The problems gradually get worse, and can include:

• speech becoming hesitant and difficult, and making mistakes with the sounds of words or grammar
• speech becoming slow with short, simple sentences
• forgetting the meaning of complicated words, and later also simple ones, making it more difficult for them to understand other people
• speech becoming more vague and the person having difficulty being specific or clarifying what they’re saying
• becoming less likely to join in with or start conversations

A person with PPA may also experience other symptoms later in their illness, including:

• changes in their personality and behaviour
• difficulties with memory and thinking – similar to Alzheimer’s disease
• difficulties with movement – similar to Parkinson’s disease

Page last reviewed: 23 March 2021
Next review due: 23 March 2024

90,000 causes of poor memory, absent-mindedness, forgetfulness. Treatment of memory problems

Memory fails everyone from time to time. For example, how many times have you forgotten the right thing at home or could not remember the name of a person you recently met?

A decrease in memory and other cognitive indicators can occur for natural reasons and be temporary, for example, due to overwork. Few people complain about forgetfulness from childhood, but the brain, like other body structures, inevitably changes with age. Unfortunately, it is not always possible to see in time the line between when absent-mindedness or age-related memory impairment remain within the normal range, and when they flow into a pathological state. You should not experience tangible difficulties in everyday affairs, the quality of work and life should not suffer. When this happens, you should contact a specialist to clarify the diagnosis. Even if memory problems are caused by a disease, with the right treatment, they can be reversible.

Memory is one of the most complex structures of the psyche. Its violation entails a disorder in the ability to know, the ability to reason, remember, make decisions and communicate. Memory problems are out of the norm if you notice the following signs:

• not only trifles are forgotten, but also important events;
• it is impossible to concentrate, the thread of conversations is lost, the head does not think well, it is difficult to grasp the plots of books or films, the same questions are asked many times;
• inability to make decisions, plan things or learn instructions;
• it became harder to navigate in familiar conditions and perform familiar tasks;
• the functions of speech and writing are disturbed: words are confused, syllables change places, the ability to express thoughts deteriorates;
• weak memory and behavioral changes become noticeable to your surroundings;
• the chronology of events is confused or false memories appear;
• Memory deterioration becomes more and more noticeable over time.

Diseases that include memory pathology usually begin insidiously, but progress over time and deprive a person of the ability to work, communicate, and even serve himself. Therefore, if your memory has noticeably worsened, do not delay visiting a doctor, because this may be the first sign of a serious neurological or mental illness. The sooner treatment is prescribed, the more successfully it will be possible to restore lost functions.

Causes of memory impairment

Risk factors are advanced age, genetic predisposition, arterial hypertension, high cholesterol, overweight, low level of education, lack of physical and social activity. Age is the most common reason for memory impairment. Most people start complaining at age 65-70. The reason is the age-related change in the functional activity of the brain. The presence of these factors should be alarming, but they are not enough for the development of the pathological process.

More than a hundred diseases can be the reasons why memory is lost. Among them are both reversible and irreversible. Often this symptom becomes the first signal of the onset of the disorder, and then other cognitive and somatic disorders are added. With memory impairment, the reasons may be as follows:

1. head injuries: falls, fights and accidents can lead to cognitive impairment even if the person has not lost consciousness;
2. dementia: the most common cause of poor memory in adults over 65 years of age. There are several varieties of dementia, and each has its own characteristics of the clinical picture. Among them, dementia in Alzheimer’s disease, vascular dementia, frontotemporal dementia, dementia with Lewy bodies;
3. diseases of the brain: tumor or infectious processes in the brain can be the reason why memory deteriorates;
4. Creutzfeldt-Jakob disease: a rapidly progressive neurodegenerative disease. If memory impairment is caused by this rare but dangerous pathology, then immediate help is needed, since CJD has a high mortality rate;
5. Mental and emotional problems: Stress, depression and anxiety can lead to forgetfulness, poor concentration and other reasons for disrupting daily activities;
6. drugs: side effects may include cognitive impairment;
7. alcoholism: dependence on alcohol significantly impairs the functioning of the brain, which affects the deterioration of memory and the ability to mental activity;
8. hypothyroidism: among its symptoms are weakness, fatigue, sleep disturbances, intellect and memory;
9. Vitamin deficiencies: Vitamins, particularly B-12, help keep nerve cells healthy. If a person has a bad memory and attentiveness, the reasons may be in their deficiency and poor diet;
10. insomnia: sleep disorders lead to fatigue and lethargy, which negatively affects thinking and memory.

Impairments can range from mild to severe, but they are all the result of damage to brain structures that impair memory by preventing the storage, retention, and recall of memories.
For example, the medial temporal lobe is involved in the formation of episodic memory, and the limbic system processes information and organizes long-term memory.

With memory problems, the causes can lead to progressive forms, as in Alzheimer’s or Huntington’s disease, or to acute ones, for example, as a result of a head injury. Memory may be lost for current events or for events that occurred during or after the traumatic situation. In any case, with a weak memory, the reasons must be clarified, which is not always possible to do on your own. Try to honestly answer the question: “Do I have signs of memory impairment?”. If you or a loved one is concerned about your condition, see your doctor. Usually, with poor memory, the causes can only be identified and corrected with the help of a specialized examination.

What to do if memory deteriorates

It is difficult to come to terms with memory loss and the development of the disease. Some try to hide the symptoms, which may cause loved ones not to realize the problem for a long time.

If you notice that memory has worsened with age, you will understand what to do with it better if you find out the reasons. What causes age-related memory decline? First, the hippocampus, the area of ​​the brain that is involved in the formation and retrieval of memories, is declining in function. Secondly, the activity of hormones and proteins that perform a protective and stimulating function for neurons is lost. And thirdly, there is a decrease in blood flow to the brain, which leads to a deterioration in memory and cognitive skills.

To be in good shape, our brain, like the whole body, requires care and regular training. If you already notice memory problems, your doctor will tell you what to do, but you yourself can improve the situation with tips that will help you adapt and keep your brain active. Please note that with cognitive impairment, all problems should be discussed with the family, as the patient will need the help and participation of loved ones.

If memory deteriorates, the following list will tell you what to do:

• Continue to participate in daily activities.
• Study regularly, learn new things, and do mental exercises such as strategy games, crosswords, and puzzles.
• Use helpful tools such as reminder notes, to-do lists, and calendars.
• Make time for friends: many people refuse social life when their memory weakens, which is absolutely impossible to do. A study by the Harvard School of Public Health found that people with active social lives have the slowest memory decline.
• Always put the things you need, such as keys or glasses, in the same place.
• Get plenty of rest: sleep deprivation reduces the growth of new neurons in the hippocampus.
• Eat a nutritious diet: Omega-3 rich foods such as salmon, tuna, walnuts, and broccoli are especially good for your brain. But saturated fats and calories should be limited.
• Treat Chronic Illnesses: Studies show that diabetes, cardiovascular problems, and other somatic conditions greatly exacerbate the decline in attention and memory, making combating them a must in the fight for brain activity.
• Get rid of bad habits such as alcohol and smoking: they increase the risk of vascular disorders.
• Introduce moderate exercise into your life – it reduces the risk of developing dementia by up to 50%. Good as simple walking and light aerobics, as well as coordination exercises.
• Share your concerns with your family. In moments when your memory fails critically, it is they who will tell you what to do.

The brain is able to produce new cells at any age, so significant memory loss not is an inevitable result of aging. Your lifestyle, habits, and daily activities have a huge impact on your brain health. Unfortunately, it is possible to cope with this problem on your own only up to a certain point. When memory is lost, the doctor should tell you what to do, because only a full-fledged treatment can improve the long-term prognosis.

Which doctor to contact for memory problems

If a person develops a memory impairment, which doctor to contact should be decided as soon as possible. A full range of diagnostic measures is needed, with the help of which it will be clarified which pathology the symptoms are associated with. Not everyone knows which doctor deals with memory. Please note that multiple consultations may be required.

Which doctor should I contact for memory loss? A psychiatrist, a neurologist and a neuropsychologist will help you. In some cases, you may need to consult a general practitioner and geriatrician. This is a complex problem that manifests itself both at the organic and psychological levels, so their joint work is necessary.

For memory problems, the doctor uses the following diagnostic methods:

• study of anamnesis;
• physical health assessment;
• conversation with relatives: when one of the family members, especially the elderly, begins to lose memory, relatives often decide which doctor to see. Their participation in diagnostic and treatment activities can provide significant assistance;
• neurological, psychiatric and psychological evaluation;
• psychometric testing: measures the accuracy, speed and quality of such mental processes as decision making, attention, planning;
• laboratory and instrumental examination: blood tests, MRI scanning, positron emission tomography, electroencephalography, etc.

Specialists carefully analyze the patient’s condition, taking into account his behavior and the results of the diagnostic measures taken. If you are thinking about which doctor to contact about memory, it is better to look for a place where several related specialists can work together. It is also necessary to have modern diagnostic equipment – this will allow the results to be more accurate and save time.

Subsequently, the results of diagnostic measures are used to develop a treatment plan. If a person is in old age, but does not yet experience serious problems with memory, you need to know which doctor to contact in advance – if you are concerned about the possibility of cognitive decline in the future, it is better to conduct a preventive examination. It will help delay or even avoid the development of a serious pathology. The presence of mild cognitive impairment increases the risk of developing Alzheimer’s disease and other forms of dementia.

With a bad memory, which doctor to contact and which institution to go to, everyone decides for himself: it can be a state psycho-neurological dispensary and a polyclinic at the place of residence, or a private specialized center. Unfortunately, in state institutions one will have to spend too much time, the loss of which is dangerous with the active involutionary process of the brain. Also, doctors are too busy to pay enough attention to patients. In case of memory problems, which doctor will help better can be understood from his work experience, skill level and status of the clinic.

Memory treatment

For impaired memory and attention, treatment depends on the cause. Symptoms associated with mental illness, vascular disorders, Alzheimer’s disease or other organic pathologies require different approaches.

For memory problems, treatment may include:

• Drugs for the correction of concomitant diseases: drugs for controlling blood pressure, angioprotectors, hormone replacement therapy and others.
• If TBI caused memory impairment, treatment may include the appointment of analgesics to eliminate pain.
• Sedatives and antidepressants are used for mental disorders with signs of anxiety and depression.
• Cholinergic drugs, nootropics, drugs that interact with NMDA receptors are prescribed for dementia.
• Vitamin therapy and bioadditives are used as part of complex therapy.
• Psychotherapy: allows the patient to adapt and improves prognosis.
• Recommendations for lifestyle changes and, if necessary, instructions for caring for the patient for relatives.

In some cases of memory loss, treatment can completely eliminate the problem, but some diseases, such as Alzheimer’s disease, cannot be cured. However, symptoms can be relieved and their progression slowed down. With disorders of the emotional-volitional sphere, poor memory, absent-mindedness, forgetfulness, treatment helps the patient to smooth out the symptoms and better adapt to what is happening, and also facilitates the care of relatives.

Memory disorders are a very complex multifactorial problem, which should be dealt with by highly qualified specialists.

Studies show that proper memory treatment allows patients to control the progression of symptoms for a long time and remain socially active even with the most severe diseases.

Violations of memory, attention, thinking – Help for adults – Speech Development Center in Moscow

A person has unique abilities to catch and pronounce speech; store information and process it. Disorders of these functions may be associated with mental disorders. It may be temporary or permanent. Most often, a malfunction in the brain causes a stroke, which is a consequence of a violation of the supply of blood to a part of the brain. Stroke is a medical emergency and urgent treatment is necessary because the sooner treatment is started, the less damage will be done to the brain .

According to the WHO (World Health Organization), about 15 million people annually face this disease, of these 15 million, 5 million die, and another 5 million are completely immobilized. About 12 million strokes are caused by high blood pressure. According to statistics, stroke ranks fourth among diseases in the world in terms of the number of deaths. Stroke is the main cause of disability in people, and 75% of patients are people over the age of 65.

Only timely diagnosis and proper treatment will allow restoring brain functions. The first step to solving this problem is choosing the right clinic.

Main symptoms and hazards

Memory impairment

Memory impairment refers to the inability to store and process information correctly. A person can stop remembering important dates, events, faces of loved ones and stop navigating in a familiar space. This phenomenon can be both short-term and permanent. At the first symptoms, you need to contact an experienced neurologist, because otherwise, a neurological disorder can develop into a chronic form and adversely affect the quality of life.

Attention disorder

Attention refers to the ability of a person to focus on certain factors. A violation of this function is signaled by several symptoms:

· The person becomes distracted. He quickly gets tired and a long opinion cannot penetrate into the essence of the task.

· Attention quickly switches from one object to another or, on the contrary, a person is unable to switch his attention for a long time.

The most dangerous consequence of this condition is the complete lack of concentration, in which a person loses the ability to adequately perceive and capture information.

Impaired thinking

Thinking refers to the ability of the brain to process information. The most obvious signs of a disorder are:

· incoherent and spasmodic speech;

· loss of orientation in space;

· reduced level of thinking.

The negative consequence is that a person cannot exist independently in society without the support of other people.

If primary symptoms of impaired memory, thinking and attention appear, you should consult a neurologist. It will help to identify the cause of the deviation and select a set of rehabilitation measures aimed at restoring important functions.

There are cases of simultaneous impairment of memory, thinking and attention. This is a very dangerous symptom, which can become a harbinger of cerebrovascular accident, and therefore it is recommended to carefully consider your health. When the primary symptoms of a neurological disorder appear, you need to contact an experienced specialist.

Diagnostic measures

No process in the human body occurs suddenly. Any illness is given a “push” by a certain factor. That is why the first step in working with a client is to identify the cause of the disorder.

If the appearance of an illness is a secondary form of the development of another disease, then in this case, a study of general analyzes and instrumental examination is used.

Possible causes of disturbances

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In all cases, a neurological deviation can be either temporary or permanent.

How specialists of the ACME Center work

Our clinic employs experienced specialists who know how to effectively address these problems. The patient is given trainings, after which memory, attention are strengthened and thinking improves. Modern tests are aimed at repeating words; drawing up a single drawing from several abstract concepts; text analysis; problem solving in a smart way.

If necessary, specialists will select a complex of vitamins and medications necessary to eliminate the problem, which are selected individually, depending on the cause and stage of manifestation of the violations.

The goal of our specialists is to develop a set of measures to restore vital functions. We strive to completely change the patient’s lifestyle, making it the most favorable for recovery.

Why AKME Center

Neurological deviation is a thin border of the mind, in case of violation of which it is necessary to take immediate measures to restore it.