ODESSA NATIONAL MEDICAL UNIVERSITY



ODESSA NATIONAL MEDICAL UNIVERSITY

Department of Neurology and Neurosurgery

Methodical guidelines for the students

of the practical classes

Discipline “Neurology”.

Section 2 “Special neurology”.

3. Vascular diseases of the brain and spinal cord, paroxysmal states, cephalgias, sleep disorders, neurointoxications. Traumatic affections of the nervous system.

Theme 17. Vascular diseases of the brain and spinal cord. Chronic disturbances of the cerebral blood circulation.

Course 4 year Faculty medical

Speciality 222 «Medicine»

Approved

at a methodical conference chair

«__» ________

Protocol № __

Head of the department,

Prof. ________ Son A.S.

Odessa – 2020

1. Theme of practical class: Vascular diseases of the brain and spinal cord. Chronic disturbances of the cerebral blood circulation.

2. Actuality of theme:

The vascular diseases of brain take leading seat among the nervous diseases and make the frequent reason of death, temporal or permanent loss or decline of capacity, and also acute states which need urgent help from the doctor of some speciality.

3. Aims of the class:

3.1. Educational aims:

- to acquaint students with modern classification of cerebro-vascular diseases

- a student must know:

1) Classification of acute and chronic disorders of cerebral blood circulation.

2) Etiologic factors and pathogenesis of acute disorders of cerebral blood circulation in patients with haemorhrage strokes.

3) Syndromes of lesion of anterior cerebral artery, middle cerebral artery and posterior cerebral artery.

4) Syndrome of occlusion and stenosis of main vessels of brain.

- to give possibility to capture research skills to the students:

1) Paralyses.

2) Disorders of speech.

3) Disorders of sensation.

4) Disorders of praxis.

5) Disorders of sight.

6) Disorders of reading, writing, calculation.

-to give to the students of ability to explore patients:

1) With acute disorders of cerebral blood circulation and to set the type of stroke.

2) To find the site of lesion.

3) To appoint therapy in the acute period of stroke.

3.2. Educational aims are connected with:

-forming professionally of meaningful substructures of personality;

-the actual aspects of deontological, patriotic, professional, psychological, legal, ecological responsibility and others like that.

3.3. Educating whole are related to:

- by forming at the students of professional approaches to diagnosis of acute disorders of cerebral blood circulation and getting of adequate therapy depending on etiology of disease.

- by the actual aspects of deontologic, sociological, legal, psychological, professional responsibility and others like that.

4. Interdisciplinar integration

5. Table of contents of the class:

The term stroke is applied to a sudden focal neurologic syndrome, specifically the type due to cerebrovascular disease.

The term cerebrovascular disease designates any abnormality of the brain resulting from a pathologic process of the blood

vessels.

Pathologic process is given an inclusive meaning—namely, occlusion of the lumen by embolus or thrombus, rupture of a vessel, an altered permeability of the vessel wall, or increased viscosity or other change in the quality of the blood flowing through the cerebral vessels. The vascular pathologic process may be considered not only in its grosser aspects—embolism, thrombosis, dissection, or rupture of a vessel—but also in terms of the more basic or primary disorder, i.e., atherosclerosis, hypertensive arteriosclerotic change, arteritis, aneurysmal dilation, and developmental malformation. Equal importance attaches to the secondary parenchymal changes in the brain resulting from the vascular lesion.

These are of two main types—ischemia, with or without infarction, and hemorrhage—and unless one or the other occurs, the vascular lesion usually remains silent. The only exceptions to this statement are the local pressure effects of an aneurysm, vascular headache (migraine, hypertension, temporal arteritis), multiple small vessel disease with progressive encephalopathy (as in malignant hypertension or cerebral arteritis), and increased intracranial pressure (as occurs in hypertensive encephalopathy and venous sinus thrombosis).

Also, persistent acute hypotension may cause ischemic necrosis in regions of brain between the vascular territories of cortical vessels, even without vascular occlusion.

Causes of cerebral abnormalities from alterations of arteries

and veins

1. Atherosclerotic thrombosis

2. Transient ischemic attacks

3. Embolism

4. Hypertensive hemorrhage

5. Ruptured or unruptured saccular aneurysm or AVM

6. Arteritis

a. Meningovascular syphilis, arteritis secondary to pyogenic and tuberculous meningitis, rare infective types (typhus, schistosomiasis, malaria, mucormycosis, etc.)

b. Connective tissue diseases (polyarteritis nodosa, lupus erythematosus), necrotizing arteritis. Wegener arteritis, temporal arteritis, Takayasu disease, granulomatous or giantcell arteritis of the aorta, and giant-cell granulomatous angiitis of cerebral arteries

7. Cerebral thrombophlebitis: secondary to infection of ear, paranasal sinus, face, etc.; with meningitis and subdural empyema; debilitating states, postpartum, postoperative, cardiac failure, hematologic disease (polycythemia, sickle cell disease), and of undetermined cause

8. Hematologic disorders: anticoagulants and thrombolytics, clotting factor disorders, polycythemia, sickle cell disease, thrombotic thrombocytopenic purpura, thrombocytosis, intravascular lymphoma, etc.

9. Trauma and dissection of carotid and basilar arteries

10. Amyloid angiopathy

11. Dissecting aortic aneurysm

12. Complications of arteriography

13. Neurologic migraine with persistent deficit

14. With tentorial, foramen magnum, and subfalcial herniations

15. Miscellaneous types: fibromuscular dysplasia, with local dissection of carotid, middle cerebral, or vertebrobasilar artery, x-irradiation, unexplained middle cerebral infarction in closed head injury, pressure of unruptured saccular aneurysm, complication of oral contraceptives

16. Undetermined cause in children and young adults: moyamoya disease and others

Cerebrovascular diseases characteristic of each age period

1. Prenatal circulatory diseases leading to

a. Porencephaly

b. Hydranencephaly

c. Hypoxic-ischemic damage

d. Unilateral cerebral infarction

2. Perinatal and postnatal circulatory disorders resulting in

a. Cardiorespiratory failure and generalized ischemia—e’tat

marbre

b. Periventricular infarcts

c. Matrix hemorrhages and ischemic foci in premature infants

d. Hemorrhagic disease of the newborn

3. Infancy and childhood: vascular diseases associated with

a. Ischemic infarction

b. Congenital heart disease and paradoxical embolism

c. Moyamoya

d. Bacterial endocarditis, rheumatic fever, lupus erythematosus

e. Sickle cell anemia

f. Mitochondrial disorders (MELASa)

g. Homocystinuria and Fabry’s angiokeratosis

4. Adolescence and early adult life: vascular occlusion or hemorrhage with

a. Pregnancy and puerperium

b. Estrogen-related stroke

c. Migraine

d. Vascular malformations

e. Premature atherosclerosis

f. Arteritis

g. Valvular heart disease

h. Sickle cell anemia

i. Antiphospholipid arteriopathy, plasma C-protein deficiency

and other coagulopathies

j. Moyamoya, Takayasu disease

k. Arterial dissections

l. Amyloid angiopathy

5. Middle age

a. Atherosclerotic thrombosis and embolism

b. Cardiogenic embolism

c. Primary (hypertensive) cerebral hemorrhage

d. Ruptured saccular aneurysm

e. Dissecting aneurysm

f. Fibromuscular dysplasia

6. Late adult life

a. Atherosclerotic thrombotic occlusive disease

b. Embolic occlusive disease

c. Lacunar state

d. Brain hemorrhage (multiple causes)

e. Multi-infarct dementia

f. Binswanger disease

The association between cerebrovascular disease and dementia has been recognized for many years. Some authors propose using the term vascular cognitive impairment (VCI) to describe the contribution of cerebrovascular disease to various dementia syndromes. This applies whether the dementia is primarily related to cerebrovascular disease or mixed with another dementing disorder. Indeed in the early and mid-20th century, cerebrovascular disease was postulated to be the specific etiology for senile dementia. It was not until the 1960s, that AD was recognized to be the most common pathophysiologic mechanism for the majority of individuals who have dementia. In subsequent decades, the concept of VCI underwent several revisions. Given the wide array of clinical syndromes possible with stroke, VCI presentation varies considerably. The heterogeneity of stroke complicates one’s ability to specifically define VCI as a single clinical entity with specific diagnostic criteria. Autopsy series show cerebrovascular disease coexisting with AD, and influencing clinical dementia, in approximately 20% of dementia cases.

Vascular cognitive impairment occurs when multiple cerebral infarcts or hemorrhages cause enough neuronal or axonal loss to impair cognitive function. The core pathologic VCI syndromes include (1) lacunar disease (penetrator-vessel disease), (2) multi-infarct dementia (MID; medium- and large-vessel disease), (3) strategic single-infarct dementia (thalamus, angular gyrus, e.g.), and (4) Binswanger dementia. These conditions are not mutually exclusive; there are many instances wherein the patient has a mixture of small-vessel and medium-vessel infarcts. Furthermore, age-related microvascular disease, frequently defined by brain MRI scans of elderly patients, may also contribute to the onset, progression, and symptoms of old-age dementia.

Epidemiology The risk of VCI increases with age just as the risk of stroke increases with age. Most epidemiologic studies of dementia do not differentiate among AD, cerebrovascular, and mixed dementia. The prevalence of a pure vascular cause of dementia in autopsy studies is probably less than 10% of old-age dementia cases. However, the prevalence of VCI may be much greater. There is often a prevalence of patients with mixed dementia, including the effects of both vascular and neurodegenerative disorders; this in fact may be much higher than current esti mates. In general, diagnostic criteria for VCI lack sufficient sensitivity and specificity to recognize cases of VCI reliably. Many patients may also have other dementia types, like AD, DLB, or normal pressure hydrocephalus. Interestingly, cerebrovascular disease is extremely common and shares several risk factors for AD. These include hypertension, diabetes, and hyperlipidemia. Recent investigations also suggest a link between AD and metabolic syndrome. Stroke is identified more commonly in AD patients than in age-matched controls. It is, there- fore, reasonable to suspect that cerebrovascular disease contributes significantly to old-age dementia.

Clinical Presentation and Differential Diagnosis. The potential for prevention of VCI highlights the importance of recognizing and treating the various vascular causes that may predispose to or contribute to dementia. Standard criteria for diagnosing vascular dementia are difficult to define given the variable nature of cognitive deficits following stroke, mainly depending upon the anatomical location of the stroke. The most common dementia is AD, typically characterized by short-term memory loss in the early stages. While vascular dementia may present in this way, it is not necessarily the “cardinal” feature of VCI. The cognitive consequence of stroke may include execu- tive dysfunction, neglect, or aphasia. Additionally, the degree of cerebrovascular disease progression varies greatly. Residual symptoms following acute stroke may seem to initially but incompletely improve and then later on contribute to eventual cognitive dysfunction in the setting of mixed demention. More- over, there is now considerable evidence that stroke increases the risk of AD. “Silent” lacunar infarcts are particularly associated with increased risk of AD. Almost all standard diagnostic criteria for VCI require imaging studies demonstrating evidence of stroke.

However, there is no specific characteristic appearance on imaging studies that provide a diagnosis of VCI per se. The absence of specific cerebrovascular lesions of course mitigates this diagnosis. MRI is more sensitive than CT in showing sub- cortical and periventricular white matter changes consistent with small-vessel disease, and smaller infarcts. Therefore, a VCI diagnosis requires recognition of various syndromic features to correlate with findings on imaging studies. Clinical presentation is arbitrarily divided into large-vessel and small-vessel disease, which are not mutually exclusive clinically. Large-vessel disease tends to affect large vascular territories, producing well-known clinical syndromes. For example, frontal lobe involvement may produce aphasia, apraxia, disinhibition, or apathy. Mesial temporal involvement produces amnesia, angular gyrus lesions lead to constructional apraxia, and parietal lesions produce alexia or apraxia. The clinical syndrome of MID typically proceeds in a step- wise fashion with clear-cut stroke events leading to successive, cumulative impairment of various cognitive domains. Small- vessel disease typically eventuates in subcortical infarcts. These are sometimes localized within strategic locations, such as the thalamus or basal ganglia, and involve white matter tracts such as frontosubcortical and thalamocortical tracts. Moreover, small-vessel pathology is often seen in the context of “normal” aging, where the smallest branches become increasingly tortuous, producing twists and loops along paths deep in the brain. Morphologic changes are amplified by hypertension and diabetes. This results in diffuse myelin loss within deep vascular territories such as periventricular and subcortical white matter regions. The clinical correlates of small-vessel disease may include executive dysfunction, apathy, inattentiveness, and personality changes typical of frontal lobe syndromes as occur with hydrocephalus and frontotemporal dementia. Involvement of specific circuits correlates with recognized clinical manifestations

Dorsolateral prefrontal circuit dysfunction correlates with executive dysfunction, decreased verbal fluency, poor performance on sequencing tasks, impersistence, set shifting, and perseveration. Subcortical orbitofrontal circuits are associated with disinhibition, manic behavior, and compulsive behavior. Medial frontal circuits produce apathy, psychomotor retardation, and mood lability.

Binswanger Disease. This is the clinical representation of VCI dementia resulting from small-vessel disease. Characteristically, patients are aged between 50 and 70 years; more than 80% have a history of hypertension, diabetes, or both. Initial symptoms vary but often include behavioral changes such as depression, emotional lability, or abulia. Gait disturbances are characterized by lower extremity parkinsonism, ataxia, or spasticity. Dysarthria and other focal motor signs may be present. Urinary incontinence is common. Patients often have histories of dizziness or syncope. Progressive executive dysfunction, slow mental processing, and memory impairment affecting information retrieval rather than encoding characterize cognitive impairment. Binswanger disease follows a clinical course having intermit- tent progression, often without clear stroke-like events. Typically, this follows a 3- to 10-year course. Pathologically, one finds numerous subcortical and periventricular infarcts that spare cortical u-fibers. When patients present with the clinical picture typical for Binswanger disease but do not have hyper- tension or diabetes, a diagnosis of cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoariosis (CADASIL) should be considered. It is one of the few hereditary causes of VCI. In the elderly, the possibility of mixed dementia exists when patients exhibit clinical features of AD and VCI. Imaging studies reveal evidence of infarct, widespread microvascular disease, or both. Silent brain infarction, especially in the basal ganglia and thalamic regions, and significant ischemic white matter changes enhance the clinical presentation and progression of AD. In addition, various vascular risk factors, such as hypertension, hypercholesterolemia, and hyperhomocysteinemia (levels 14 mmol/L), also increase the risk of AD. Brains with mixed pathologies, matched for dementia severity, reveal fewer AD lesions compared with pure AD cases. Clearly the specific clinical presentation is influenced by cerebrovascular disease in these cases. Finally, the risk of developing poststroke dementia increases with advancing age, recurrent stroke, and larger periventricular white matter lesions on MRI. Hypoxic and ischemic stroke complications, such as pneumonia or seizure, also increase the risk of poststroke dementia.

Prevention and Treatment. Primary prevention must be pursued aggressively. When at-risk patients are identified, treatment of arterial hypertension, cardiac disease, lipid abnormality, and diabetes are important in reducing dementia risk. Secondary prevention, that is, treatment when cerebrovascular disease is initially recognized, begins with appropriate acute management of stroke and its complications. Prevention of stroke recurrence by appropriate antiplatelet or anticoagulant therapy and addressing primary risk factors are also very important. Use of calcium channel blockers in the treatment of hypertension may be more effective in dementia prevention than other antihypertensive medications. Dietary supplementation with folic acid and vitamins B6 and B12 may help to reduce the levels of homocysteine, a possible contributory precursor to VCI. The role of “neuroprotective agents” in prevention of poststroke dementia is unknown. To date, evidence-based controlled trials have not yet identified any pharmacologic agents for treatment of ischemic vascular (multiinfarct) dementia. However, when dementia develops, cholinesterase inhibitors may be helpful. As in AD, titration of these medications to maximum doses is recommended; their long-term efficacy in VCI is unknown. The efficacy of cholinesterase inhibitor treatment may be greater in cases of mixed dementia. However, acetylcholine deficits may be significant in VCI as well as in AD. Subcortical vascular disease often interrupts major cholinergic pathways from the basal forebrain to widespread regions of the cerebral cortex. Deficits of CSF acetylcholine levels are found in VCI cases when compared with healthy controls. As in all dementia cases, caregiver education and support are essential to long-term success and quality of patient life.

6. Materials in relation to the methodical providing of the class:

6.1. Control materials to the preparatory stage of the class:

Questions (right answer in bold):

A 62-year-old man with a history of myocardial infarction awakens with a dense right-sided hemiplegia. His eyes are tonically deviated to the left, and he does not respond to threat on the right side of his visual field. He appears to be alert and responds to pain on the left side of his body. His speech is unintelligible and nonfluent, and he follows no instructions. Efforts to get him to repeat simple phrases consistently fail.

Pick the language disturbance that best explains the clinical picture.

a. Broca’s aphasia

b. Wernicke’s aphasia

c. Transcortical sensory aphasia

d. Transcortical motor aphasia

e. Anomic aphasia

f. Global aphasia

g. Conduction aphasia

h. Mixed transcortical aphasia

A 45-year-old woman with chronic atrial fibrillation discontinues warfarin treatment and abruptly develops problems with language comprehension. She is able to produce some intelligible phrases and produces sound quite fluently; however, she is unable to follow simple instructions or to repeat simple phrases. On attempting to write, she becomes very frustrated and agitated. Emergency MRI reveals a lesion of the left temporal lobe that extends into the superior temporal gyrus. Pick the language disturbance that best explains the clinical picture.

a. Broca’s aphasia

b. Wernicke’s aphasia

c. Transcortical sensory aphasia

d. Transcortical motor aphasia

e. Anomic aphasia

f. Global aphasia

g. Conduction aphasia

h. Mixed transcortical aphasia

A 71-year-old man develops headache and slight difficulty speaking while having sexual intercourse. He has a long-standing history of hypertension, but has been on medication for more than 7 years. He makes frequent errors in finding words and follows complex commands somewhat inconsistently. The most obvious defect in his language function is his inability to repeat the simplest of phrases without making repeated errors. An emergency CT scan reveals an intracerebral hemorrhage in the left parietal lobe that appears to communicate with the lateral ventricle. Pick the language disturbance that best explains the clinical picture.

a. Broca’s aphasia

b. Wernicke’s aphasia

c. Transcortical sensory aphasia

d. Transcortical motor aphasia

e. Anomic aphasia

f. Global aphasia

g. Conduction aphasia

h. Mixed transcortical aphasia

A 24-year-old woman abruptly loses all speech during the third trimester of an otherwise uncomplicated pregnancy. She has a history of severe migraines during which she occasionally develops a transient right hemiplegia. Her comprehension is good, and she is frustrated by her inability to speak or write. She is unable to repeat simple phrases, but she does begin to produce simple words within 5 days of the acute disturbance of language. Pick the language disturbance that best explains the clinical picture.

a. Broca’s aphasia

b. Wernicke’s aphasia

c. Transcortical sensory aphasia

d. Transcortical motor aphasia

e. Anomic aphasia

f. Global aphasia

g. Conduction aphasia

h. Mixed transcortical aphasia

A 78-year-old man has a cardiac arrest while being treated in an emergency room for chest pain. Resuscitation is initiated immediately, but profound hypotension is observed for at least 20 min. A cardiac rhythm is restored, but the patient remains unconscious for the next 3 days. When he is awake, alert, and extubated, his speech is limited to repetition of words and sounds produced by those around him. He has no apparent comprehension of language and produces few sounds spontaneously. Whenever the patient is spoken to, he fairly accurately repeats what was said to him. Pick the language disturbance that best explains the clinical picture.

a. Broca’s aphasia

b. Wernicke’s aphasia

c. Transcortical sensory aphasia

d. Transcortical motor aphasia

e. Anomic aphasia

f. Global aphasia

g. Conduction aphasia

h. Mixed transcortical aphasia

6.2. Information necessary for forming of knowledge-abilities it is possible to find in textbooks:

basic:

1. Duus’ Topical Diagnosis in Neurology / Mathias Baehr, Michael Frotscher. Fifth Edition, 2012. – 344 pp.;

2. Roger Simon, David Greenberg, Michael Aminoff - Clinical Neurology (7th Edition) Published: 2009. - 408 pp.;

3. H. Royden Jones et al. (eds.) - Netter’s Neurology (2nd ed.) – 2012. – 749 pp.

4. Merritt's Neurology / Lewis P. Rowland, Timothy A. Pedley - Merritt's Neurology (12th edition) – 2009. - 1216 pp.

additional:

5. Laboratory Diagnosis in Neurology Wildemann / Oschmann / Reiber. – 2010 (1st Edition). - 296 pp;

6. Anatomic Basis of Neurologic Diagnosis Alberstone / Steinmetz / Najm / Benzel. – 2009.- 600 pp.

6.3. Orienting card from organization of independent work of students with educational literature

|№ п.п. |Basic tasks |Pointing |Answers |

|1. |To repeat the blood supply of brain and |Duus’ Topical Diagnosis in Neurology / Mathias Baehr, Michael | |

| |spinal cord |Frotscher. Fifth Edition, 2012. – P. 270-288. | |

|2. |To learn the symptoms of disorders of |Duus’ Topical Diagnosis in Neurology / Mathias Baehr, Michael | |

| |blood supply of the brain |Frotscher. Fifth Edition, 2012. – P. 288-302. | |

| | |H. Royden Jones et al. (eds.) - Netter’s Neurology (2nd ed.) – 2012. | |

| | |– P. 493-514. | |

|3. |To learn the syndromes of disorders of |Duus’ Topical Diagnosis in Neurology / Mathias Baehr, Michael | |

| |blood supply of the brain |Frotscher. Fifth Edition, 2012. – P. 288-302. | |

| | |H. Royden Jones et al. (eds.) - Netter’s Neurology (2nd ed.) – 2012. | |

| | |– P. 493-514. | |

|4. |To be able to find affected vascular zone |Duus’ Topical Diagnosis in Neurology / Mathias Baehr, Michael | |

| | |Frotscher. Fifth Edition, 2012. – P. 270-302. | |

| | |H. Royden Jones et al. (eds.) - Netter’s Neurology (2nd ed.) – 2012. | |

| | |– P. 493-515. | |

7. Materials for self-control of quality of preparation:

A 50-year-old man had a brainstem stroke following a vertebral artery dissection secondary to an acute sports-related injury. This patient might be expected to develop dysphagia secondary to involvement of which of the following structures?

a. Nucleus solitarius

b. Nucleus and descending tract of CN V

c. Nucleus ambiguus

d. Lateral spinothalamic tract

e. Inferior cerebellar peduncle

Occlusion of which of the following arteries typically produces Wallenberg (lateral medullary) syndrome?

a. Basilar artery

b. Vertebral artery

c. Superior cerebellar artery

d. Anterior inferior cerebellar artery (AICA)

e. Anterior spinal artery

A 75-year-old man with a history of recent memory impairment is admitted with headache, confusion, and a left homonymous hemianopsia.

He has recently had two episodes of brief unresponsiveness. There is no history of hypertension. Computed tomography (CT) scan shows a right occipital lobe hemorrhage with some subarachnoid extension of the blood.

An MRI scan with gradient echo (susceptibility) sequences reveals foci of hemosiderin in the right temporal and left frontal cortex. Which of the following is the most likely cause of this patient’s symptoms and signs?

a. Gliomatosis cerebri

b. Multi-infarct dementia

c. Mycotic aneurysm

d. Amyloid angiopathy

e. Undiagnosed hypertension

A 22-year-old male abuser of intravenous heroin has been having severe headaches during sexual intercourse. Within a few minutes of one headache, he develops right-sided weakness and becomes stuporous. His neurologic examination reveals neck stiffness as well as right arm and face weakness. An unenhanced emergency CT scan reveals a lesion of 3 to 4 cm in the cortex of the left parietal lobe. The addition of contrast enhancement reveals two other smaller lesions in the right frontal lobe but does not alter the appearance of the lesion in the left parietal lobe. Which of the following diagnostic studies is most likely to establish the basis for this patient’s neurologic deficits?

a. HIV antibody testing

b. Cerebrospinal fluid (CSF) examination

c. Electroencephalography

d. Nerve conduction studies

e. Cardiac catheterization

A 52-year-old right-handed woman who has abused intravenous drugs for many years has an HIV antigen test that is positive. CD4+ (helper) T lymphocyte count is normal. A brain CT scan reveals several hemorrhagic lesions. Nerve conduction studies reveal generalized slowing in the legs, and EEG exhibits focal slowing over the left parietal lobe. Cardiac catheterization suggests aortic valve disease, and the patient’s CSF is xanthochromic (yellow). Which of the following is the probable site of injury in the CNS?

a. An arterial wall

b. The ventricular endothelium

c. The pia arachnoid

d. The dura mater

e. The perivenular space

8. Materials for audience independent preparation:

8.1. List of educational practical tasks which are necessary to make during practical employment:

1. To explore derivative patient.

2. To explore the clinical findings.

3. To explore ishemic signs.

9. Instructional materials for capturing professional abilities, skills foreseen by this work.

9.1. Method of conducting of researches, stages of execution (see part 5).

10. Materials for self-control of capturing the knowledge, abilities, skills foreseen by this work:

10.1 a) Tests of rector control

b) Test of the task "КРОК-2".

11. Theme of the following class: Ischemic stroke. Transitory ischemic attacks.

-----------------------

|№ |Discipline |To know |To be able |

|1. |a)Human anatomy |Blood supply of brain and spinal cord. |On macropreparations to distinguish extra- and intracranial vessels. |

tion of the circle of Willis. Blood supply of different parts of the brain. |To explore EEG and REG in patients with vascular pathology. | |

| |c) Pathological physiology |Symptoms of damage of different parts of the brain. |To explore disorders of movements, coordination, statics, function of |

| | | |sight. |

|2. |Following disciplines: |Symptoms of violation of cerebral circulation of blood at metabolic |To suspect the lesion of the nervous system at diabetes mellitus, |

| |a) Therapy |diseases, at vasculitis. |rheumatism. |

| |b) Physiotherapy, medical rehabilitations and resort |Indications to sanatorium treatment of patients with vascular pathology |To appoint physical therapy treatment in the acute and chronic period of |

| | |of cerebrum. |disease. |

| |c) Neurosurgery |Blood supply of the brain and symptoms of damage of different vascular |To appoint surgical treatment in patients with stroke. |

| | |zones. | |

|3. |Inwardly subject integration: |Symptoms of damage of different vascular zones. |To diagnose cerebral rheumovasculitis. To appoint treatment. |

| |a) Rheumatic damages of the nervous system. | | |

| |b) Traumatic damages of spinal cord and head. |Symptoms of damage of different vascular zones. |To diagnose the damage of the spinal cord, bain, and appoint adequate |

| | | |therapy. |

| |c) Disease of the vegetative system. |Symptoms of damage of different vascular zones and vegeto-vascular |To diagnose the syndrome of vegetative dystonia. To appoint the adequate |

| | |dystonia. |inspection and treatment. |

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