NEUROLOGY AND NEUROSURGERY - Y. V. ALEKSEEENKO - 2014

CHRONIC CEREBROVASCULAR DISORDERS. DEMENTIA

Modern classifications of cerebrovascular disorders distinguish variants of chronic progressive cerebrovascular insufficiency, also referred to as dyscirculatory encephalopathy. Dyscirculatory encephalopathy is a syndrome of progressive multifocal or diffuse Brain injury manifested by a range of neurological, neuropsychological, and psychiatric disorders caused by chronic cerebral vascular insufficiency and/or recurrent episodes of acute cerebrovascular accidents. In contemporary English-language literature, this condition is most commonly termed vascular dementia, emphasizing the dominant role of cognitive impairment within the broad spectrum of clinical manifestations associated with this pathology, thereby highlighting the primary cause of patients' functional disability.

The principal causes of dyscirculatory encephalopathy include atherosclerotic lesions of cerebral vessels, arterial Hypertension, Venous Circulation disorders, arterial hypotension, and other universal etiological factors contributing to cerebrovascular pathology. It should be emphasized that, in terms of causality, mechanisms of development, and factors of decompensation, dyscirculatory encephalopathy is an age-dependent yet exceptionally heterogeneous condition. Clinicians most frequently encounter a combination of several mechanisms of chronic vascular brain damage alongside an unfavorable confluence of age-related, endocrine, vascular, metabolic, toxic, and psychological factors. Understanding the complex patterns underlying The Development of this pathology is crucial for adequately assessing the potential for Prevention, slowing its progression, or even reversing the entire spectrum of manifestations associated with dyscirculatory encephalopathy. The complexity of the problem is clearly illustrated by the variety of terms used to describe different variants of chronic cerebrovascular pathology, which help highlight the Specific features of etiopathogenesis, lesion topography, and clinical manifestations in particular conditions: dyscirculatory encephalopathy, progressive vascular leukoencephalopathy, hypertensive encephalopathy, progressive subcortical encephalopathy, vascular dementia, and multi-infarct dementia.

When discussing the dominant Central Nervous system dysfunctions within THE SPECTRUM OF clinical manifestations of chronic cerebrovascular disorders, it must be emphasized that diverse cognitive impairments do not always and immediately reach the threshold of dementia; nevertheless, even in such cases, they profoundly determine the patients' well-being and functional capacity. Dementia is defined as persistent impairment of memory and one or more other cognitive Functions (perception, attention, calculation, language, thinking) associated with organic brain damage, resulting in impaired daily activities and/or occupational performance. A critical criterion is the presence of evident deficits in routine daily activities, occupational performance, and family adaptation.

In addition to vascular brain lesions, well-known neurodegenerative diseases, as well as toxic and dysmetabolic conditions, can lead to the development of cognitive impairment and dementia.

Neurodegenerative Diseases

   • Alzheimer's disease

   • Dementia with Lewy bodies

   • Frontotemporal dementia

   • Primary progressive aphasia

   • Corticobasal degeneration

   • Disorders primarily affecting the Basal Ganglia

   о Parkinson's disease

   о Progressive supranuclear palsy

   о Huntington's disease

   о Other

Dysmetabolic and Toxic Encephalopathies

   • Alcoholism

   • Hypoxic encephalopathy

   • Somatogenic disorders:

   о Hypoxemia (associated with respiratory disorders)

   о Hepatic encephalopathy

   о Renal encephalopathy

   о Hypoglycemic encephalopathy

   • Hypothyroidism

   • Deficiency states (Vitamin B1, B12, and Folic acid)

   • Heavy metal intoxication

   • Adverse drug reactions

Thus, progressive cognitive and behavioral impairments in older adults are most commonly of a mixed nature, involving a specific and variable balance of age-related, circulatory, dysmetabolic, endocrine, and neurodegenerative mechanisms. A critical practical issue in such situations is identifying potentially reversible and treatable disorders.

In many dementia patients, short-term and long-term memory impairments come to the fore. In addition, at least one of the following abnormalities must be present:

   • impaired Abstract thinking (inability to find Similarities and differences between related words, difficulty defining words and concepts, failure to grasp the meaning of proverbs and sayings, and inability to solve basic semantic and arithmetic problems, etc.);

   • impairment of several higher cortical functions (aphasia, apraxia, agnosia, constructional and spatial apractagnosia);

   • impaired judgment (inability to formulate a goal-directed plan or maintain relationships with other people and family);

   • personality changes (alteration or accentuation of premorbid traits, neglect of personal appearance, apathy, and narrowing of interests).

Social and domestic maladaptation of the patient remains the key criterion for dementia.

The pathomorphological picture in dyscirculatory encephalopathy includes both focal and diffuse Changes in the brain tissue. There is Atrophy of the cerebral grey and White matter, ventricular enlargement, evidence of prior lacunar strokes, cysts and consequences of extensive ischemic or hemorrhagic brain lesions, and signs of leukoaraiosis.

The clinical manifestations of dyscirculatory encephalopathy at all stages of this chronic, gradually progressive condition are complex and mosaic in nature, with a predominance of subjective symptoms. Mild cognitive, emotional, and behavioral abnormalities, as well as Sleep disturbances, often dominate from the very beginning. Patients typically complain of headaches, dizziness, tinnitus, unexplained mood swings, tearfulness, irritability, difficulty controlling emotional responses, and the like. Various autonomic regulation and sensory disorders are also detected. All these Complaints are systematic and persistent, tending to decompensate under adverse conditions such as informational, emotional, and physical overload, sleep deprivation, intoxication, weather changes, and so on. In advanced Stages of the disease, psychopathological symptoms may develop, requiring the involvement of psychiatric specialists. Many patients exhibit The formation of mild signs of extrapyramidal insufficiency (hypokinesia),

movement coordination disorders (ataxia), and the appearance of pseudobulbar symptoms involving changes in vocal volume, articulation, and swallowing disorders.

Taking into account the aforementioned neuropsychological disorders, internal organ dysfunction, and the condition of the musculoskeletal and Sensory systems, it is possible to outline a set of core problems that significantly limit the functional independence of patients with dyscirculatory encephalopathy, serve as a reason for seeking medical care, and form the focus of preventive, therapeutic, and rehabilitative interventions.

   • Subjective disorders (cephalic syndrome, dizziness, tinnitus, etc.)

   • Gait disturbances and frequent falls

   • Paroxysmal states (autonomic and hypertensive crises, transient ischemic attacks, syncopal episodes, epileptic syndrome, etc.)

   • Impairments of cognitive functions, emotional sphere, and sleep

   • Psychopathological disorders

It should be noted that the onset of such disorders as gait disturbances and frequent falls can result from a range of pathological abnormalities—movement coordination disorders and mild extrapyramidal insufficiency, dizziness, visual impairment, leg weakness due to polyneuropathy, leg pain and general weakness, syncopal episodes, and others.

The stages or degrees of dyscirculatory encephalopathy are distinguished as follows. The First stage—initial (compensated)—is characterized by a predominance of subjective disorders and autonomic regulation disturbances; the second—moderate (subcompensated)—differs in its multisystem manifestations; and the third—severe (decompensated)—implies the presence of persistent neurological function deficits and prior acute cerebrovascular accidents.

The Diagnosis of dyscirculatory encephalopathy involves clarifying the underlying cause and pathogenetic variant of the chronic progressive cerebrovascular disorder, as well as identifying factors and mechanisms leading to the patient's decompensation.

The instrumental examination plan includes funduscopy, rheoencephalography, ultrasound of the neck and HEAD vessels, and occasionally cerebral MR angiography, CT, and MRI of the brain. However, a thorough analysis of complaints and medical history can in many cases prove far more fruitful than instrumental examination. The reason is that current understanding of cerebral Blood flow autoregulation and the mechanisms of systemic and local compensation in cerebrovascular pathology remains clearly insufficient. At the same time, the sensitivity and informative value of many non-invasive Methods for Assessing cerebral blood flow and METABOLISM are limited. The development and widespread adoption of functional neuroimaging methods will help improve the diagnosis of these conditions.

Brain CT or MRI allows for the exclusion of dangerous structural lesions, such as a brain tumor or abscess, cerebral infarction, intracranial Hemorrhage, chronic traumatic intracranial hematoma, and Hydrocephalus. Neuroimaging methods help differentiate between degenerative, metabolic, and vascular lesions of the central nervous system.

Batteries of special neuropsychological tests are used to identify and quantify cognitive impairment; however, performing a full neuropsychological assessment requires trained specialists and significant time expenditure.

Various Forms of dyscirculatory encephalopathy must be differentiated from vegetative dysfunction, asthenoneurotic and depressive disorders, vertebrogenic reflex-vascular and radiculovascular disorders, Primary and secondary cephalgias, dysmetabolic encephalopathies, Brain Tumors, neuroinfections, neurointoxications, and several other conditions.

The therapeutic management plan for dyscirculatory encephalopathy involves the simultaneous Structure/175.html">Implementation of 1) therapy for the underlying disease; 2) optimization of cerebral blood flow, neurometabolic, and neurophysiological processes; and 3) secondary stroke prevention. This ensures the normalization of blood pressure, correction of Cardiac Arrhythmias, management of Lipid Metabolism disorders, and Treatment of Diabetes Mellitus. It is not uncommon for systemic Hemodynamic changes in the Pathogenesis of chronic cerebrovascular disorders to be underestimated. It should be noted that adequate control of elevated blood pressure not only reduces the risk of stroke but also slows the progression of cognitive impairment in dyscirculatory encephalopathy. Promising data in this regard have been obtained from The Study of angiotensin receptor blockers (sartans).

There is a wide range of vasoactive and neurometabolic agents available for the treatment of dyscirculatory encephalopathy, but optimal Selection requires compliance with the following criteria:

  • good tolerability during long-term use;

  • ease of dosing, simple administration regimen, and convenient dosing frequency;

◊ absence of pronounced systemic effects;

◊ compatibility with other therapeutic prescriptions.

In many cases of chronic forms of cerebrovascular insufficiency, vasoactive and neurometabolic agents with multiaction (polymodal) properties are most effective and convenient. They are administered in repeated courses as a preemptive neuroprotective therapy in the event of potential decompensation.

The following vasoactive agents are widely used:

◊ Vinpocetine (Cavinton) 5–10 mg 3 times a day

◊ Nicergoline (Sermion) 10 mg 3 times a day

◊ Pentoxifylline (Trental) 200 mg 3 times a day

◊ Theophylline (Euphyllin) 15 mg 3 times a day

◊ Phezam (piracetam + cinnarizine) 1–2 capsules 3 times a day

◊ Vasobral 1–2 tablets 2 times a day (2–4 ml 2 times a day)

◊ Instenon 1 dragee 3 times a day

The term "nootropics" (from the Greek "noos" meaning mind and "tropos" meaning turning/towards) was first coined in 1972 by Corneliu Giurgea to describe the effects of piracetam produced by the Belgian pharmaceutical company UCB. This marked the very beginning of modern neuroprotection. According to WHO experts, nootropic drugs are medications that have a direct activating effect on learning, improve memory and mental performance, and increase the brain's resistance to various adverse influences. A broader field—neurometabolic pharmacotherapy—involves The Use of nootropics, neuroprotectants, and agents with predominantly neurotrophic effects, which typically feature multiple Mechanisms of action and sites of application. The best-known agents include piracetam, emoxypine, actovegin, phenibut, mildronate, Glycine, gliatilin, cytoflavin, citicoline, cerebrolysin, cerebromedin, thiocetam, and others. Many vasoactive and neuroprotective agents can be administered either as intravenous infusions or in tablet form. The use of injectable forms at the very beginning of a treatment course may be fully justified; however, it should be kept in mind that sustained clinical improvement and stabilization of vascular and metabolic processes in dyscirculatory encephalopathy are more successfully achieved through the prolonged, multi-week oral administration of moderate doses of the same medications. Aggressive pharmacotherapy regimens should be avoided, especially in elderly and senile patients.

  In case of impaired venous outflow, the use of theophylline, vinpocetine, caffeine, instenon, and vasobral is recommended. For complaints of systemic (vestibular-type) dizziness, betahistine dihydrochloride is prescribed. The correction of emotional and anxiety disorders often requires the intervention of a psychotherapist or psychiatrist; antidepressants, sedatives, and hypnotics are utilized. Tranquilizers or antipsychotics should be used with extreme caution in elderly and senile patients.

Great attention must be paid to the identification and management of concomitant endocrine and Metabolic Disorders. Constant monitoring of blood glucose levels, timely detection and correction of thyroid dysfunction, and the prevention and correction of deficiency states (Vitamins B₁, B₆, B₁₂) are essential.

Clinical Case Studies

Option 1

A 68-year-old female complains of systematic headaches in the temporal and occipital regions, tinnitus, periodic paroxysmal dizziness, recent memory impairment, mood instability, difficulty falling asleep, and rapid fatigue. She lives alone. For the past 14 years, she has noted elevated blood pressure and takes antihypertensive medications irregularly. Hypertensive crises have been documented on several occasions. Three days ago, while working at her dacha in hot weather, she suddenly felt unwell, experiencing dizziness, tinnitus, visual impairment, nausea, sudden generalized weakness, and palpitations. She lost her balance and fell; there was likely a brief loss of consciousness. Her blood pressure was recorded at 150/95 mm Hg. Following injections of antispasmodics, her condition improved, but generalized weakness, a feeling of fullness and ringing in the head, and gait instability still persist.

  Physical examination reveals signs of oral automatism, mild Asymmetry of Reflexes (brisk on the left), intact coordination tests, and no meningeal signs. Brain CT scan reveals mild atrophy of both cerebral hemispheres.

  • List the main neurological disorders.

   • Explain The Nature and possible mechanisms of the sudden deterioration in the patient's condition.

   • Formulate a preliminary clinical diagnosis.

   • Outline the directions for the Differential diagnosis.

   • What additional examination Procedures are necessary?

   • Outline the patient management plan.

   • Describe the pharmacotherapy regimen.

   • Determine the prognosis of the disease.

Option 2

A 78-year-old female patient with a history of Essential Hypertension, coronary artery disease, and cardiac arrhythmias has experienced a gradual memory decline over the past 6-7 years. Her instrumental activities of daily living have become impaired, and she now requires ongoing assistance from relatives when shopping and paying utility bills due to difficulties with counting money and filling out paperwork. Relocating to live with her daughter's family was accompanied by a decompensation of her mental status; she became irritable, expressed persecutory delusions directed at her relatives, and claimed they wanted to misappropriate her property. She was unable to adapt to the kitchen and use unfamiliar household appliances. Episodes of acute confusional state with disorientation in place and time were observed; she failed to recognize relatives, was restless, attempted to leave the apartment, and experienced a disturbed sleep-wake cycle. Upon examination, she is disoriented in time, active, somewhat anxious, and exhibits a marked impairment of memory for both past and current events. She cannot perform calculations, has writing difficulties, and shows impaired spatial orientation; her speech is free of gross impairments. Delusional ideas of persecution are present. Her intellect is significantly reduced. Neurological examination reveals oral primitive reflexes, with no other focal neurological deficits.

   • How would you classify the patient's condition?

   • Name the primary neuropsychiatric disorders.

   • Which impairments limit her legal capacity?

   • Explain the Water/144.html">Origin of the neuropsychiatric symptoms.

   • Formulate a probable topical diagnosis.

   • Formulate a preliminary clinical diagnosis.

   • Describe the protocol for instrumental neurological examination.

   • Determine The Scope of the somatic examination.

   • Outline the main directions for the differential diagnosis.

   • Propose a management plan and a comprehensive therapy regimen.

   • Provide recommendations for the patient's relatives.

   • Determine the prognosis of the disease.