Theme: Cerebral vascular diseases of the Brain and Spinal cord

Theme: Cerebral vascular diseases of the Brain and Spinal cord

Initial signs of cerebral vascular insufficiency. Dynamic disorders of cerebral circulation (Transient Ischemic Attack (TIA), hypertensive crisis, acute hypertonic encephalopathy (AHE)), Ischemic stroke, Chronic cerebral ischemia – dyscirculative encephalopathy (DE)

 

1. Epidemiology of cerebrovascular diseases.

Among all the neurological diseases of adult life the cerebrovascular ones clearly rank first in frequency and importance. At least 50 % of the neurological disorders are of this type. The prevalence of strokes all over the world is about 1.5 – 7.4 per 1000 of the general population. In Ukraine it is 3.27 per 1000 of the general population. Cerebral stroke is the commonest vascular disease of the brain. Every year there are about 6 mln cases of stroke: among them – 1 mln in Western Europe, about 500 000 in the United States, 300 000 – in Russia, 200 000 – in Japan and 130 000 – in Ukraine.

Stroke after heart diseases and cancer is the third commonest cause of death according to the World Health Organization data.

During the last 15 years there has been a marked enlargement in the prevalence of stroke in Ukraine in about 3.4 times and in incidence in 3 times approximately.

 

 

ANATOMY OF THE BLOOD SUPPLY OF THE BRAIN

The brain is supplied by two paired arteries, the inter­nal carotid arteries anteriorly and the vertebral arter­ies posteriorly. The vertebral arteries unite to form the basilar artery. These two arterial systems form the cir­cle of Willis at the base of the brain, a unique anasto­motic system that gives rise to all of the vessels sup­plying the cerebral hemispheres (Fig. 8-1).

 

Internal Carotid Artery

The internal carotid artery rises in the neck as one of two branches of the common carotid artery. It ascends in the neck and enters the carotid canal in the petrous temporal bone where it ascends, loops for­ward and medially, and ascends again to enter the cranial cavity. The artery enters the cavernous sinus and passes forward, closely related to sella and hy­pophysis medially, and the third, fourth, sixth, and ophthalmic and maxillary divisions of the fifth cranial nerves laterally. The terminal portion of the internal carotid artery ascends and pierces the dura medial to the anterior clinoid process, where the artery is closely related to the optic nerve. The cavernous and terminal portions of the internal carotid artery are fre­quently referred to as the carotid siphon.

The branches of the internal carotid artery in­clude:

1.  Petrous portion                              

A. Caroticotympanic artery—supplies the ante­rior and part of the medial wall of the middle ear.

2.  Cavernous portion

A.  Cavernous arteries—small vessels supplying the hypophysis and the wall of the cavernous sinus.

B.  Hypophyseal arteries — supply the hypophysis.

C.  Semilunar   artery—supplies   the   trigeminal (gasserian: semilunar) ganglion.

D.  Anterior meningeal arteries—supply the dura of the anterior cranial fossa.

3.  Supraclinoid portion

A.  Ophthalmic artery

B.  Anterior choroidal artery

C.  Posterior communicating artery

4.  Terminal portion

A.  Anterior cerebral artery

B.  Middle cerebral artery

 

Ophthalmic Artery

The ophthalmic artery rises from the supraclinoid portion of the internal carotid artery, pierces the dura, and accompanies the optic nerve through the optic foramen and into the orbit. The artery passes medi­ally, superior to the optic nerve, to the roof of the or­bit, where it divides into the supratrochlear and dorsal nasal arteries. Branches of the ophthalmic artery anastomose with branches of the external carotid sys­tem. This anastomosis may supply blood to intracra­nial structures by reversal of flow following insuffi­ciency or occlusion of the internal carotid artery.

The branches of the ophthalmic artery include:

1. Central retinal artery—arises from the oph­thalmic artery and enters the optic nerve close to the eye. The artery emerges from the center of the optic disc in the optic cup and divides into several branches supplying the optic disc and retina.

2.  Ciliary arteries—several iumber, which sup­ply the sclera, choroid, lens and conjunctiva of the eye.

3.  Lacrimal  artery—arises  from the  ophthalmic artery near the optic foramen and runs laterally along the upper border of the lateral rectus mus­cle to supply the lacrimal gland.

4.  Supraorbital artery—arises from the ophthalmic artery and passes above the eye to accompany the \ supraorbital nerve. The artery supplies the skin muscle, and other structures over the foreheads and anastomoses with branches of the superficial! Temporal artery.                                               

5.  Ethmoidal arteries—supply  the ethmoidal si­nuses, the nasal cavity, and the dura of the ante­rior fossa.

6.  Dorsal nasal artery—distributed to the outer surface of the nose and anastomoses with the angu­lar artery.

7.  Frontal artery—supplies the medial aspect of the forehead.

8.  Superior and inferior palpebral arteries—encir­cle the eyelids near the facial margins.

9.  Muscular   branches—supply   the   extraocular muscles.

10. Anterior choroidal artery—arises from the ter­minal portion of the internal carotid artery and passes posteriorly along the optic tract to reach the lateral geniculate body. The artery then enters the choroidal fissure and supplies the choroid plexus in the inferior horn of the lateral ventricle. In its course, the artery supplies the optic tract, the cerebral peduncle, the lateral portion of the lateral geniculate body, the posterior two-thirds of the posterior limb of the internal capsule, the retrolenticular and infralentricular portions of the internal capsule, the optic radiation, the hip­pocampus, the choroid plexus, the tail of the cau­date nucleus, and the amygdala.

 

Posterior Communicating Artery

The posterior communicating artery arises from the terminal portion of the internal carotid artery and passes posteriorly, immediately above the oculomotor nerve, to anastomose with the posterior cerebral artery. Branches of the posterior communicating artery supply the thalamus, subthalamus, internal capsule, mamillary bodies, optic chiasm, and optic tract.

 

Anterior Cerebral Artery

The anterior cerebral artery arises from the terminal portion of the internal carotid artery and passes anteromedially above the optic nerve to come into con­tact with the opposite anterior cerebral artery. The two arteries are connected by a short anterior commu­nicating artery, then pass around the genu and body of the corpus callosum to anastomose with branches of the posterior cerebral artery at the level of the pari­etooccipital fissure.

The branches of the anterior cerebral artery in­clude:

1.  Anterior communicating artery—supplies the op­tic chiasm and hypothalamus.

2.  Perforating branches—penetrate the anterior per­forating substance and lamina terminalis to supply the rostrum of the corpus callosum and the septum pellucidum.

3.  Recurrent branch (medial striate artery, recurrent artery of Heubner)—is distributed to the head of the caudate nucleus and the anterior limb of the internal capsule.

4.  Cortical branches

A.  Orbital branches—supply the orbital and me­dial surfaces of the frontal lobe.

B.  Frontopolar   branch—supplies   the   anterior portion of the medial aspect of the superior frontal gyrus and extends about 1 inch onto the superior lateral surface.

C.  Pericallosal  branch—supplies   the  cingulate gyrus and corpus callosum.

D.  Callosal marginal branch—supplies the cingu­late gyrus, the medial aspect of the superior frontal gyrus, and the paracentral lobule.

 

Middle Cerebral Artery

The middle cerebral artery should be regarded as the intracranial extension of the internal carotid artery. Emboli entering the internal carotid artery invariably enter the middle cerebral artery. The middle cerebral artery runs laterally in the lateral fissure between frontal and temporal lobes (Fig. 8-2) to reach the sur­face of the insula, where it divides into several branches.

1.    Lenticulostriate   arteries   —   perforating branches that arise close to the origin of the middle cerebral artery and penetrate the substance of the brain to supply the head of the caudate nucleus, putamen, globus pallidus, and internal capsule.

2.    Cortical branches—radiate outward from the middle cerebral artery as it lies on the insula. Cor­tical branches that can be recognized by arteriography are  the   orbitofrontal,   frontal,   pre-Rolandic,   post-Rolandic, anterior parietal, posterior parietal, an angu­lar branch following the line of the lateral fissure, and the anterior, middle, and posterior temporal branches extending over the surface of the temporal lobe.

Vertebral Artery   –

The vertebral artery arises from the first portion of the subclavian artery in the neck. The anatomical course can be considered in four parts.

First part—ascends posteromedial^ and enters the foramen of the transverse process of the sixth cer­vical vertebra.

Second part—ascends through the foramina of the transverse processes of the upper sixth cervical vertebra.

Third part—curls backward in a groove behind the superior articular process of the atlas and passes through the foramen magnum.

Fourth part—pierces the dura to lie on the ven­tral surface of the medulla, where it ascends to the lower border of the pons to unite with the vertebral artery from the opposite side, forming the basilar artery.

The branches of the vertebral artery include:

1.    Spinal branches accompany the nerve roots into the spinal canal. Only one or two of these branches anastomoses with the anterior spinal artery.

2.    Muscular branches — supply the deep mus­cles of the neck.

3.    Meningeal branches—arise from the verte­bral arteries at the level of foramen magnum and sup­ply the dura of the posterior fossa and the falx cere­bri.

4.    Anterior spinal artery—arises from the vertebral artery near its termination and descends over the surface of the medulla to unite with the artery from the opposite site and form one anterior spinal artery. This artery lies on the ventral surface of the spinal cord and terminates as a fine vessel in the cauda equina. The anterior spinal artery supplies the medial and inferior portions of the medulla, including the medullary pyramids, and all of the spinal cord, except the posterior columns and posterior horns of the gray matter.

5. Posterior inferior cerebellar artery—arises from the fourth portion of the vertebral artery and passes around the medulla, onto the inferior surface of the cerebellum, where it divides into two branches. The posterior inferior cerebellar artery supplies the lateral portion of the medulla and the inferior cerebel­lar peduncle. The medial branch supplies the inferior vermis, the medial aspect of the cerebellar hemi­sphere, and the choroid plexus of the fourth ventricle. The lateral branch supplies the inferior surface of the cerebellar hemisphere. There is a well-developed anastomosis with the anterior inferior cerebellar and superior cerebellar arteries.

 

Basilar Artery

The basilar artery (Fig. 8-3) takes origin at the in­ferior border of the pons from the junction of the two vertebral arteries and ascends in the median groove of the pons to terminate at the upper border of the pons by dividing into the two posterior cerebral arteries.

The branches of the basilar artery include:

1.  Pontine branches—supply the pons.

2.  Internal auditory artery—accompanies the sev­enth and eighth cranial nerves into the internal au­ditory meatus and supplies the inner ear.

3.  Anterior inferior cerebellar artery—arises just above the lower border of the pons and passes around the pons onto the inferior surfaces of the cerebellar hemisphere and anastomosis with the posterior inferior cerebellar artery.

4.  Superior cerebellar artery—arises just below the termination of the basilar artery and passes around the pons, separated from the posterior cerebral artery by the oculomotor nerve. The superior cere­bellar artery supplies the superior and middle cerebellar peduncles, the pineal gland, the choroid plexus of the third ventricle, and the superior sur­face of the cerebellum.

 

Posterior Cerebral Artery

The posterior cerebral artery arises at the termination of the basilar artery, where it is separated from the superior cerebellar artery by the oculomotor nerve. The posterior communicating artery, a branch of the internal carotid artery, joins the posterior cerebral artery, which winds around the cerebral peduncle onto the tentorial surface of the occipital lobe.

The branches of the posterior cerebral artery in­clude:

1.  Posteromedial arteries—enter the posterior perfo­rated substances to supply the medial surface of the thalamus and the wall of the third ventricle.

2.  Posterior choroidal artery—runs beneath the splenium of the corpus callosum to supply the choroid plexus of the third ventricle.

3.  Posterolateral arteries—supply the lateral thala­mus and the midbrain.

4.  Anterior temporal branches—supply the uncus and the fusiform gyrus of the temporal lobe.

5.  Posterior temporal branches—supply the inferior temporal gyrus.

6.  Calcarine branches—supply the medial surface of the occipital lobe with a short extension onto the superior lateral surface of the hemisphere and the occipital pole. The posterior cerebral artery anas­tomoses with the anterior cerebral artery at the level of the parietooccipital fissure on the medial surface of the hemisphere.

 

 

 

Arterial Circle of Willis

This unique anastomosis, which lies at the base of the brain, is derived from the internal carotid and verte­bral arterial systems (see Fig. 8-1). The anterior por­tion of the circle is formed by the two anterior cere­bral arteries derived from the internal carotid arteries and connected by the anterior communicating artery. The posterior portion of the circle consists of the two posterior cerebral arteries, which are the terminal branches of the basilar artery. The posterior cerebral

arteries are connected to the internal carotid artery on each side by the posterior communicating arteries. The circle of Willis encloses the optic chiasm, the infundibulum, the tuber cinereum, and the mamillary bodies.

 

ANATOMY OF THE VENOUS DRAINAGE OF THE BRAIN

The cerebrovenous system can be divided into two subdivisions, the superficial external venous drainage and the deep internal venous drainage. Both systems eventually drain into the venous sinuses.

The upper lateral surface of the cerebral hemi­sphere is drained by the superficial cerebral veins, which enter the superior longitudinal sinus. The su­perficial middle cerebral vein also drains the lateral surface of the cerebral hemispheres and passes for­ward in the lateral fissure to enter the cavernous si­nus. The superficial middle cerebral vein communi­cates with the superior longitudinal sinus through the superior anastomotic vein of Trolard and with the transverse sinus through the inferior anastomotic vein of Labbe. The inferior cerebral veins drain the orbital surface of the frontal lobe, the lateral aspect of the temporal lobe, and the lateral aspect of the occipital lobe to empty into the cavernous sinus and transverse sinuses. The veins over the insula unite to form the deep middle cerebral vein, which passes anteriorly deep to the lateral fissure and joins the basal vein of Rosenthal. This latter structure arises in the anterior perforating substance by the union of the anterior cerebral vein and the veins of the corpus callosum. The basal vein is joined by the deep middle cerebral vein as it passes posteriorly in close relationship to ^l the uncus and hippocampus. The basal vein then 1 winds around the midbrain to unite with the basal vein from the opposite side, at the origin of the great cerebral vein.

The deep internal group of cerebral veins drain the central structures of the cerebral hemisphere and are closely related to the ventricular system.

The terminal (thalamostriate) vein arises from the inferior horn of the lateral ventricle and follows the tail of the caudate nucleus into the body of the lat­eral ventricle, lying between the caudate nucleus and the thalamus. The terminal vein runs forward to the intraventricular foramen and is joined by the anterior caudate vein, the septal vein, which drains the septum pellucidum, and the choroidal vein, which drains the choroid plexus of the lateral ventricle to form the in­ternal cerebral vein. This structure turns at its origin, forming the venous angle, and then passes along the roof of the third ventricle and through the velum interpositum to join with the opposite internal cerebral vein. The great vein of Galen is formed by the union of the internal cerebral veins and the junction of the basal veins of Rosenthal. After a short course, the great cerebral vein is joined by the inferior sagittal si­nus to form the straight sinus.

The intracranial venous sinuses are thin-walled endothelial-lined structures lying within the dura. The superior longitudinal sinus takes origin at the fora­men cecum anteriorly and passes in the superior sur­face of the falx cerebri to the internal occipital protu­berance, then turns to the right to form the right transverse sinus. The superior longitudinal sinus re­ceives the superior cerebral veins. The walls of the si­nus contain granulations that are responsible for the absorption of cerebrospinal fluid (CSF) into the ve­nous system. The inferior longitudinal sinus arises in the free margin of the falx cerebri by the union of a number of small veins and runs posteriorly to termi­nate in the straight sinus at the junction of the falx cerebri and the tentorium cerebelli. The straight sinus is formed by the union of the great vein of Galen and the inferior longitudinal sinus and passes posteriorly in the junction of the falx cerebri and tentorium cere­belli. The straight sinus terminates at the internal oc­cipital protuberance by becoming the left transverse sinus. The transverse sinuses arise at the internal oc­cipital protuberance and run along the edge of the tentorium cerebelli to end at the base of the petrous temporal bone, where they become the sigmoid si­nuses. The transverse sinuses receives most of the ve­nous drainage from the cerebellum. The sigmoid si­nuses are a direct continuation of the transverse sinuses, beginning at the base of the petrous temporal bone and terminating at the jugular foramen as the in­ternal jugular vein.

The cavernous sinus arises anteriorly from the superior ophthalmic vein at the superior orbital fis­sure and passes posteriorly, close to the sella turcica and terminates by dividing into the superior and infe­rior petrosal sinuses. The cavernous sinuses commu­nicate with each other through the intercavernous si­nuses, which lie anteriorly and posteriorly to the sella turcica. The lateral walls of the cavernous sinuses contain the third, fourth, and sixth nerves and the ophthalmic and maxillary divisions of the trigeminal nerve. The intracavernous portion of the internal carotid artery is contained within the cavernous sinus. The superior petrosal sinus arises from the cavernous sinus at the apex of the petrous temporal bone and passes along the edge of the tentorium cerebelli to terminate in the transverse sinus. The inferior petrosal sinus also rises at the apex of the petrous temporal bone and enters a groove lying in the junction of the petrous temporal and occipital bones to terminate in the jugular bulb of the internal jugular vein.

 

2. The main reasons and risk – factors of cerebral blood – circulation disturbances.

    There are a lot of reasons and risk – factors of cerebral blood – circulation disturbances. But the commonest are 3 of them:

1.    Atherosclerosis of cerebral vessels and general atherosclerosis. In 75 % of all cases it is the main reason of all acute cerebral blood – circulation disturbances.

2.    Hypertension – the frequency of hypertension in case of stroke is about 72 %.

3.    Combination of atherosclerosis and hypertension.

      Besides these main reasons there are some others which can cause cerebral blood – circulation disturbances.

4.    Symptomatic arterial hypertension (for example caused by kidney diseases)

5.    Heart diseases such as inborn and acquired cardiac abnormalities, arrhythmias, IHD, atherosclerosis, cardiosclerosis, angina pectoris, myocardial infarction.

6.    Infectious and infectious – allergic vasculitis (at rheumatism, connective tissue diseases, lues)

7.    Arterial hypotension.

8.    Vasomotor dystonia.

9.    Blood diseases (polycythemia, leucosis, haemophilia)

10. Kidney diseases.

11. Endocrine diseases (diseases of thyroid gland, pancreas, suprarenal glands)

12. Diabetes mellitus.

13. Toxic lesion of vessels at endogenous and exogenous intoxication ( at acute and chronic kidney or liver failure, alcoholic intoxication )

14. Traumatic lesion of vessels (at haemorrhage – subdural, epidural, ventricular, parenchymatous).

15. Artery and vein compression (especially in cervical part of spinal cord – for example at osteochondrosis)

16. Inborn and acquired Willis circle abnormalities – occlusion, stenosis of MAH and neck, aneurism, constriction of vessels.

17. Brain tumours.

 

For these reasons’ realization they should be combined with risk – factors, such as

·         Age (the elder person is, the highest risk of cerebrovascular disease is)

·         Sex (at the age of up to 55 – 60 years fatality from cerebrovascular disease is higher in men, after 55 – 60 years – it is higher in women)

·         Heredity (in particular to heart and cerebrovascular diseases)

·         Alcohol abuse

·         Cigarette smoking

·         Hyperlipidemia and hyperglycaemia

·         Arterial hypertension

·         Hypodynamia

·         Meteorological dependence ( especially people with labile autonomic nervous system )

·         Personal type (picnotic type), stress, high carbohydrate diet.

Combination of three and more factors increases risk of development of acute neurological deficit.

 

Classification of cerebrovascular diseases

According to World Health Organization classification all cerebrovascular diseases are divided into 3 groups:

A.   Premonitary and initial symptoms of brain blood supply insufficiency

B.   Acute cerebral blood circulation disturbances

1.    Dynamic cerebral blood circulation disturbances

2.    Acute hypertonic encephalopathy

3.    Haemorrhage – subdural, epidural

4.    Intracerebral hemorrhage

5.    Brain infarction

a) cardioembolic,

b) atherothrombotic,

c) hemodynamic,

d) hemorheologic,

e) lacuna

C.   Dyscirculative encephalopathy or chronic cerebral blood circulation insufficiency or slowly progressive insufficiency of cerebral blood circulation.

 

Dynamic cerebral blood circulation disturbances (DCBCD)

DCBCD – are acute brain dyscirculation events which usually are developed against the main diseases. They are associated with temporary general and focal brain symptoms. They have tendency to involution during 24 hours.

    To DCBCD belong

1.    Transient ischemic attacks ( TIA ) – they take about 1/3 of all DCBCD

2.    Hypertonic crisis  – it takes about 2/3 of all DCBCD

     This disease is very common and takes about 1/3 of all cases of cerebrovascular diseases.

 

Etiology

TIA is usually associated with:

·         Atherosclerosis

·         Stenosis of MAH

·         Heart diseases (abnormalities, myocardial infarction)

·         Sometimes vasculitis, systemic vascular diseases

In 30 – 40 % of patients with TIA stroke is developed in 5 years. In 20 % of them stroke is developed in 1 month, in 50 % – it is developed in a year. The possibility of stroke development is higher at repeated TIA and depends on age of the patient (it is getting higher in 1.5 times with every 10 years).

 

Pathogenesis

 

 

The main pathogenic mechanisms are:

A.   Thromboembolic

B.   Hemodynamic

 

They are very closely associated with each other.

A.   The commonest of them are thromboembolic. That means microembolism of cerebral vessels.

Microembols are divided into arteriogenic and cardiogenic.

   

Arteriogenic microembols are small units that originate from clots and are the result of destroyed atherosclerotic plaques.

Thrombocytic embols are crumbling. That is the main reason of rapid involution of neurological deficit.

Cardiogenic microembols can cause TIA in patients with arrhythmias, heart abnormalities, after myocardial infarction, in patients with rheumatic endocarditis.

 

B.   Haemodynamic  mechanisms

1.     Atherosclerotic stenosis of cerebral vessels or MAH, especially in association with hypotension, arrhythmias and myocardial infarction.

2.     Thrombosis of neck magistral artery.

 

Thrombosis of Medial cerebral artery

 

     

 

3.     In the subclavian steal syndrome the patient has a narrowed subclavian artery and the arm “steals” blood from the basilar artery via the vertebral artery. There may be a cervical bruit and a difference in blood pressure between the arms. At times of arm exercise the patient may experience vertebrobasilar insufficiency.

4.     Spasm of cerebral vessels and as a result perivascular oedema and hypoxia of brain tissue.

5.     Inborn stenosis , abnormalities of MAH

6.     Compression of vertebral artery by osteophytes at cervical osteochondrosis.

7.      Vessels insufficiency (contradiction between real and demandable blood supply). This can occur at heart failure, hypotension, internal bleeding.

 

Clinical picture of TIA

      TIA is usually characterized by focal neurological symptoms. The last usually dominate over general brain symptoms. Thus TIA is regional DCBCD. They are usually acute and develop suddenly.

There are 2 main groups of TIA’s symptoms:

a.    focal

b.    general brain symptoms

General, if they present, usually manifest as headache, dizziness, short loss of consciousness. Focal symptoms depend on the vessel territory.

 

TIAs in carotid distribution (They take 30 % of all TIAs)

 

 

 

 

Carotid distribution – is a territory of internal carotid arteries and their branches – ophthalmic artery, anterior cerebral artery, and middle cerebral artery. Via anterior cerebral artery carotid distribution supplies anterior part of frontal lobe, internal surface of hemisphere to sulcus parietooccipitalis , via middle cerebral artery – the cortex of frontal, parietal, temporal lobe, internal capsula and nucleus.

 

 

1.    The most common symptoms are subjective sensory disorders, such as numbness, tingling in face and extremities; and objective sensory disorders such as hyperesthesia of superficial sensation in face and extremities, sometimes deep sensation in fingers and toes.

2.    Very often motor disorders together with sensory ones are observed. They are central paresis of extremity or fingers with hyperreflexia, pathologic signs of Babinski, Rossolimo. Hemiparesis or hemiplegia is observed only in severe cases.

3.    Sometimes distorting language (transient aphasia) is observed.

4.    When TIA occurs in the internal carotid artery territory ophthalmic – piramidal syndrome is developed. It usually manifests as blindness or reduction of vision on the same side and hemiparesis on the opposite side. It is known as Lasko – Radowich syndrome.

5.    Focal Jackson motor or sensory epileptic attacks are observed in patients with MAH pathology.

 

TIAs in vertebrobasilar distribution (They take about 70 % of all TIAs)

      

             

 

 

This territory provides blood supply of brainstem, cerebellum, occipital lobe cortex, mediobasal structures of temporal lobes.

1.    Vestibular syndrome. It manifests as systemic dizziness, occipital headache, nystagmus, equilibrium disorders.

2.    Brainstem – cerebellum syndrome. It manifests as equilibrium, coordination and synergy of action disorders.

3.    Paresis of oculomotor muscles with convergence disorders, diplopia, cross – eye.

4.    Bulbar syndrome with swallowing, voice and speech disorders.

5.    Alternation syndromes are quite rare.

6.    Vision disorders of cortex character such as photopsias, hemianopsia, quadric hemianopsia and optic phenomena.

7.    Atonic – adynamic syndrome. It is observed at acute ischemia of reticular formation and lower olives in medulla oblongata in case of “drop – attacks “ – the attacks of sudden loss of muscle tone that cause patient’s falling down without loss of consciousness .These attacks manifest at cervical spinal cord disorders in case of sudden turning out or head retroversion.  Sometimes symptom of Sistine chapel can occur when loss of muscle tone is associated with loss of consciousness.

8.    At ischemia of mediobasal structures of temporal lobe one can Korsakov syndrome observe – the attacks of temporary memory disorders on current events associated with confabulator component and disorientation.

9.    Paroxysmal hypersomnic and katalepsic syndromes with autonomic – vascular crisis are observed at ischemia of hypothalamic structures.

10. Syndrome of temporal epilepsy.

11. In the subclavian steal syndrome the patient has a narrowed subclavian artery and the arm “steals” blood from the basilar artery via the vertebral artery. There may be a cervical bruit and a difference in blood pressure between the arms. At times of arm exercise the patient may experience vertebrobasilar insufficiency.

 

      Except carotid and vertebrobasilar cerebral ischemic crisis there are associated dynamic cerebral blood circulation disturbances such as:

·         Coronary – cerebral crisis

·         Aorto – cerebral crisis

·         Liver- cerebral crisis

·         Cholecysto – cerebral crisis

 

TIA with neurological symptoms that clinically disappear within 24 hours but leave changes  at CT such as low density zones  are regarded as “ minor ischemic strokes “.

      It is important to mention that the duration of TIAs is from several minutes up to 24 hours. But usually it is 10 – 15 minutes.

     One of TIA‘s characteristic features is relapse, when attacks are observed 3 – 5 times per year. There is one more peculiarity, which is necessary to remember – the attacks in vertebrobasilar territory are more common and are frequently repeated in spite of TIA in carotid territory.

But TIA in carotid territory prognosis is much more serious. Usually in one or two years after first attack stroke is developed.

     Another peculiarity is that if TIA is observed several times per 24 hours it means there is pathology of MA. Transient in word TIA concerns only neurological clinical picture, but has nothing to do with hemodynamic cerebral disturbances, as they are observed during the next 3 weeks.

 

Hypertensive cerebral crisis

It takes about 13 – 15 % of all acute disturbances of cerebral blood circulation.

Pathogenesis In course of a set of experiments it was found out that the spasm of veins during increasing of blood pressure displays a reaction of cerebral blood circulation regulation. The spasm of veins protects our brain from excessive perfusion. In case of rapid and severe increasing of blood pressure the system of self-regulation cannot compensate it. That is the main reason of disturbance of self-regulation system of blood circulation and brain hyperemia. It also promotes brain oedema, blood circulation deficiency and ischemia of brain tissues.

 

Clinical features of hypertensive crisis:

• General

• Regional

• Mixed

Hypertensive crisis is a manifestation of hypertension or symptomatic arterial hypertension exacerbation. It manifests as general cerebral and focal symptoms.

Except high blood pressure severe headache, heavy head, psychomotor agitation, obscured consciousness , heart beating, shortness of breath, heart pain, nausea, vomiting, sometimes epileptic attacks are observed in case of hypertensive cerebral crisis . It is also usually accompanied by autonomic disturbances, such as sweating, feeling of cold in extremities, change of face colour, heart and breathe rate.

According to the system of hemodynamics  there are three types of crisises

·         Hyperkinetic

·         Hypokinetic

·         Eukinetic

 

1.    Hyperkinetic type usually is accompanied by increasing of heart outflow with increased heart index more than 4.5 l per min in m² and normal general peripheral resistance.

2.    Hypokinetic type is accompanied by decreasing of heart outflow with decreased heart index to 2.8 l per min in m² and high general peripheral resistance.

3.    Eukinetic type is accompanied by normal heart outflow and slightly increased general peripheral resistance.

 

The main clinical features of hyperkinetic crisis are:

1.    There is a rapid development of crisis without portents.

2.    Mainly systolic blood pressure is increased (More than 180-200 mm)

3.    General cerebral symptoms are well – expressed. That means psychomotor agitation, severe headache with nausea and vomiting.

4.    There are well – expressed autonomic disorders, such as shortness of breath, red or pale skin, and polyuria.

5.    The duration of crisis is up to several hours.

 

The main clinical features of hypokinetic crisis are:

1.    There is gradual development against long lasting hypertension background.

2.    Mainly diastolic blood pressure is increased.

3.    There is well – expressed EKG – changes: slow intra – ventricular conductivity, decreasing of ST – segment.

 In this case the risk of ischemic stroke is too high.

The main clinical features of eukinetic crisis are:

1.    A rapid development.

2.    Both systolic and diastolic blood pressures are increased.

3.    The symptoms of acute left – ventricular insufficiency and lung oedema can be observed.

 

According to the duration hypertensive crisises are divided into:

1.    Mild, which last up to 1 hour

2.    Mediate (they last several hours)

3.    Severe (they last from 5 –6 hours up to 24 hours)

 

The frequency:

·      Mild hypertensive crisis are:

Frequent – means they are observed more than 4 times per month;

Moderate frequent – means they are observed 3 – 4 times per month;

Rare – means they are observed 1 – 2 times per month;

 

·      Mediate and severe hypertensive crisis are:

Frequent – means they are observed more than 5 times per year;

Moderate frequent – means they are observed 3 – 5 times per year;

Rare – means they are observed 1 – 2 times per year.

 

Diagnostics of dynamic blood circulation disturbances

      When the symptoms of blood circulation disturbances last from several minutes up to hour there are no problems with diagnosis of dynamic blood circulation disturbances, such as transient ischemic attack or hypertensive crisis. In case of rapid development of general cerebral and focal symptomatic and duration up to several hours usually the diagnosis of dynamic blood circulation disturbances is put afterwards, as nobody knows the results (sometimes stroke is developed in such a way).

      Very often transient ischemic attack or hypertensive crisis is the first sign of heart – vascular system disorders. That’s why it is very important to reveal the main disease. That’s why we need additional methods of patient’s examination.

 

Additional methods of patients’ with DCBCD medical examination

1.    Ultrasonic doplerography – finds out the absence or presence of stenosis and occlusions of magistral arteries of head and neck.

 

 

 

 

2.    Rheoencephalography – finds out asymmetry of blood circulation, the state of vessel tonus and elasticity of vessels.

3.    EEG – finds out diffuse and local changes of brain bioelectric potentials.

4.    X –ray examination of cervical part of spinal cord – finds out osteochondrosis, spinal abnormalities.

 

 

5.    EKG – finds out the state of coronal vessels, rhythm disorders, and coronary insufficiency.

6.    Otoneurological examination is recommended in case of expressed vestibular syndrome in order to exclude labyrinth pathology.

7.    Ophthalmic examination – finds out sclerotic or hypertensive changes on eye fundus.

 

 

8.    Blood analysis.

9.    Coagulation test – finds out increased aggregation of thrombocytes, erythrocytes, and hematocrit.

10. Biochemical blood analysis – finds out proteinemia, increased cholesterin, b– lipoprotein, pre-b– lipoprotein.

 

Differential diagnosis

Dynamic blood circulation disturbances are usually differentiated with:

1.    Migraine crisis

2.    Partial epileptic attacks

3.    Vestibular crisis

4.    Multiple sclerosis

5.    Brain tumor

6.    Hypoglycemia

7.    Faint

 

Treatment of dynamic blood circulation disturbances

      Hospitalization is necessary for the patients with:

a.    Severe cerebral – vascular crisis that can result in stroke

b.    Repeated attacks with well – expressed focal symptoms

c.    Severe hypertensive crisis with high blood pressure

d.    Coronary – cerebral attack, suspected myocardial infarction or angina pectoris.

 

The main principals of DBCD treatment

1.    To normalize blood pressure

2.    To improve brain hemodynamic

3.    To improve microcirculation and rheologic properties of blood, to prevent aggregation of blood cells

4.    To decrease vessels’ penetrance

5.    To prevent brain oedema, to decrease intracranial hypertension

6.    To improve heart activity

7.    To improve brain metabolism

8.    To overcome autonomic syndrome

 

Treatment of hypertensive crisis

1.    At all kinds of crisis  hypotensive medications are used:

·         Clofelin 1ml 0.01 % i/v in 20 ml of physiologic solution

·         Dibasol 0.5% 2 – 4 ml i/m or i/v

·         Euphyllini 2.4% 10.0  i/v in physiologic solution

·         Antagonists of Calcium  (finoptini 0.5% 2 ml i/v in 10 ml of physiologic solution)

·         Cardioselective b-adrenoblockers (athenolol  25 – 50 mg per day)

·         Nifidipine 10- 20 mg

·         Inhibitors of ACE – Enalapril 5 – 10 mg

·         In case of too high blood pressure with left ventricule insufficiency and lung edema ganglioblockers are used – benzohexonium 2.5 % 0.5 – 1 ml i/m or s/c in glucose solution by drops.

 

2.    In case of hypertensive hypokinetic crisis we usually begin with:

• Dibasol 0.5% 4 – 6 ml

• b-adrenoblockers – Anaprilini 0.1% 5 ml i/v 

But the last are contraindicated at bradycardia, disoders of atrioventricular conduction.

 

3.    In case of hypokinetic crisis we start with peripheral vasodilatators:

• Apresin – 2% 1 ml i/v by drops;

• Diazoxid 1.5% 20 ml 3 – 4 times per day.

 

4. At eukinetic crisis we usually use clofelini, antagonists of calcium, spasmolytics.

 

5. At all kinds of hypertensive crisis with psychoemotional and autonomic reaction we prescribe I/v by drops:

• Aminazini 2.5% 1 ml in 200 ml of physiologic solution

• Sibazoni 0.5% 2 ml

• Pipolfeni 2.5% 2 ml

 

1.    In order to prevent brain edema we use euphillini 2.4 % solution 10 ml with 2 ml lazix 

2.    To decrease brain hypoxia we use Na oxybutiras 20% 10 ml i/v in glucose solution.

 

Treatment of TIA

1.     Blood pressure normalization

a.     At heart failure and systolic blood pressure less than 120 mm glycosides are used:

·         Corglyconi 0.06 % 1.0 + strophantini 0.05 % 1.0 in 20 ml of 40 % glucose  i/v

·         Cordiamini 1 ml s/c

·         Sulfocamfocaini 10 % 2ml i/m

·         Cofeini 10 % 1ml s/c

·         Mesatoni 1- 0.05 % 1 ml s/c or i/m at low BP

·         Prednisoloni 60 – 120 mg i/v by drops with 200 ml 5 % glucose

b.     At hypertension hypotensive therapy and spasmolytics are used in usual doses.

 

4.    To improve brain hemodynamic vasoactive medications are used:

·         Euphilini 2.4 % 10 ml

·         Cavintoni 10 – 20 mg i/v with 20 ml 0.9 % NaCl

·         Sermioni 4 –8 mg i/v by drops

·         Ksantinoli nicotinas 15 % 2 ml i/m

 

3. To improve microcirculation and rheologic properties of blood, to prevent    aggregation of blood cells. (It is especially important in case of well expressed focal neurological symptoms in order to prevent stroke).

·         Direct anticoagulants:

– Heparini 5 –10 000 U. s/c 3 –4 times per day during 3 –5 days, than 2 500 U. 4 times per day during 3 – 4 days;

– Fraxiparini 0.3 x 2

·         Indirect anticoagulants:

–     Pelentani 0.1 – 0.3

–     Fenilini 0.015 – 0.03

–     Syncumar 0.004 2-3 times per day during 2-3 weeks

 

4. Antiagregants:

·         Aspirini 70 –80 mg once a day

·         Ticlidi 0.25 2 times per day during 2- 3 months

·         Trentali 2% 5 ml i/v by drops (it is contraindicated at myocardial infarction, do not use it with heparin or on an empty stomach)

·         Agapurini 1 pill 3 times per day

·         Reopoliglucini 200 –400 ml i/v by drops

·         Solcoserili 10 –20 ml i/v by drops during 5 –7 days

·         Ksantinoli nicotinas 15 % 1 –2 ml i/m

·         Curantili 0.025 3 times per day (it is contraindicated at low BP, heart failure)

·         Plavix 75 mg per day

·         Parmidini 0.5 3 times per day

 

1.    To prevent brain edema, to decrease intracranial hypertension:

·         Furasemidi 40 –80 mg per day

·         Lasix 1% 2ml i/v or i/m

·         Manitoli 10 –20 % 200 ml i/v

·         Dexoni 4-6 mg i/v or i/m

·         Albumini 5 % 100 ml

·         Vit E 5% 2 ml i/m, Aevit 1 ml i/m, Unitioli 5 ml

 

6. To improve brain metabolism:

·         Nootropil 20 % 5- 10 ml

·         Instenoni 2 ml i/m or i/v by drops

·         Solcoserili 10 –20 ml i/v by drops

·         Actovegini 2 ml i/m or i/v (it is contraindicated at cardiovascular failure, oliguria, lung edema)

·         Cerebrolisini 15 % 1.0 ml i/m

 

7. Antioxydants:

·         Vit E 1 ml i /m

·         Tiatriasolini 1 ml i /m

·         Emoxipini 2.0 i/m

 

8. Symptomatic treatment:

·         At vomiting and hiccup – cerukal, aminasini, galoperidol, validol

·         At headache – tramadol, analgini

·         At agitation – sedatives and anxyolytics

 

Surgical treatment – is used at stenosis of general or internal carotid artery (when stenosis is more than 70 % according to ultrasonographic data). Thrombinectomy is used.

Prevention means in term diagnosis and treatment of main disease (first of all atherosclerosis, hypertension, and heart diseases).

 

Working efficiency The persons with DCBCD are regarded temporary disabled. In case of frequent and repeated DCBCD it is necessary to employ patient in order to exclude mental and physical strain or direct him to MSEC to fix up the group of disability.

 

Students’ practical Study Program.

 

Step I.  Aim: To make the clinical diagnosis. For this purpose it is necessary:

1.    To determine types of acute disorders of the cerebral circulation.

2.    To determine Carotid or Vertebrobasilar vessels distribution.

3.    To find the reasons to cause disorders of cerebral circulation.

4.    To formulate the diagnosis, for example:

a)    TIA in Left Carotid Distribution from cerebral atherosclerosis and hypertensive disease, stenosis of the left vertebral vessel

b)    DE III st (intracerebral subarachnoid hemorrhage – aneurysm of cerebral vessel’s, 1995 y)

TIA may occur in carotid or vertebrobasilar territory. The differential points between these two types of TIAs are:

1.     TIAs in carotid distribution

–          transient blindness in the eye on the same side as a narrowed internal carotid artery (amaurosis fugax). Patient may report a “shade coming down” over his eye.

–          Transient aphasia.

–          Motor and sensory symptoms in a single extremity (upper or lower), or a clumsy “bear’s paw” hand.

2.     TIAs in vertebrobasilar distribution

–          slurred speech, dizziness, ataxia, syncope, numbness around lips or face, double vision,

–          hemiparesis and hemisensory loss do not parallel each other in the individual limb as in carotid disease.

Differential diagnosis. Migraine may be accompanied by transient neurologic deficits (visual disturbances, motor or sensory symptoms) and can usually be identified by the headache that follows the neurologic deficit, the gastrointestinal symptoms, and by the fact that it appears in patients younger than those with cerebrovascular disease. Nevertheless, older people do experience migraines phenomena, and there may not always be prominent headache symptoms.

Keep in mind that focal seizures may produce transient neurologic symptoms (numbness, leg or arm weakness) which may persist for hours. Obtain an EEG if seizures are suspected.

Some systemic factors are known to be associated with TIAs. Well-recognized ones are anemia, polycythemia, thrombocytosis, and hypoglycemia.

Step II. Aim: Administer emergency treatment. For this purpose it is necessary to choose:

1. emergency therapy of TIAs.

2. differentiated emergency therapy of hypertensive crisis.

3. rehabilitation and prophylactic programs for cerebrovascular patients.

 

Strokes

 

Definition

     In broadest sense, the World Health Organization has defined stroke as “rapidly developing clinical signs of focal (at times global) disturbance of cerebral function, lasting more than 24 hours or leading to death with no apparent cause other then that of vascular origin”.

 

Epidemiology

     According to World Health Organization data about 150 to 740 people per 100 000 population suffer from stroke all over the world. In the United States of America there are about 400 000 patients with stroke every year. In Europe there are about 1 mln people with stroke every year. In Ukraine according to 1997 data 130 890 patients had stroke and 54 000 of them died. During the last 30 years the frequency of stroke has increased significantly all over the world.

 

Classification of stroke     Stroke is classified by the pathology of the underlying focal

brain injury into either infarction or hemorrhage. Infarction is much more common than hemorrhage. The proportion between them is 4:1 (80 % to 20%).

 

Brain infarction

 

Classification

      Brain infarction is divided into:

1.    atherothrombotic,

2.    cardioembolic,

3.    hemodynamic,

4.    hemorheologic

5.    Lacunar infarction.

 

Atherothrombotic and cardioembolic occurs in case of plugging of extracranial or intracranial vessel by atherosclerotic plague, thrombus or embolus from the heart.

Hemodynamic – one occurs at angiospasm in case of atherosclerosis, vascular insufficiency, central hemodynamics disorders. Rheologic – occurs in case of disturbance of rheologic blood properties.

 

Etiology

The most common causes of brain infarction are:

·         Atherosclerotic lesion of MAH

·         Combination of atherosclerosis with hypertension

·         Chronic ischemic heart disease with rhythm disorders

·         Combination of atherosclerosis with diabetes

·         Rheumatism, heart abnormalities (inborn and acquired)

·         Vasculitis

 

Pathogenesis

Atherothrombotic brain infarction occurs at thrombosis in case of atherosclerotic lesions, disturbance of rheologic blood properties, central hemodynamic disorders.

 

Cardioembolic brain infarction occurs at embolus plugged cerebral vessel.

The sources of embolus are:

a)    parts of aortal or arterial thrombus

b)    Parts of thrombus in case of heart abnormalities, such as mitral stenosis, aortal abnormality, rheumatic or bacterial endocarditis, myocardial infarctions, cardiosclerosis, cardiomyopathy.

3.   Embolism can occur at thrombophlebitis, lung abscess, malignant tumors, and sepsis.

4. Fat embolism occurs at bone fractures, after surgery associated with trauma of subcutaneous tissue.

5. Gas embolism occurs at surgery on lungs, at pneumothorax. 

      Usually it is difficult to distinguish thrombosis and embolism. That’s why we use the term “thromboembolism“.

 

Hemorheologic brain infarction

      Usually occurs at disturbance of self – regulation of brain blood circulation, in case of MAH abnormalities and long lasting angiospasm.

 

The lacunar syndrome

This condition is associated with small areas of in­farction deep in the cerebral white matter of the cere­bral hemispheres or in the pons, resulting from:

1.  Small vessel disease with lipohyalinosis and fibri­noid degeneration

2.  Decreased perfusion of penetrating arteries from proximal narrowing of larger vessels

3.  Branch artery atheromatous occlusion

4.  Embolism

However, the widespread use of MRI and CT scan­ning has shown that the lacunar state is not uncom­mon in asymptomatic individuals. Consequently, the diagnosis of lacunar syndrome should be approached with caution.

The lacunar stroke may be defined as a unilat­eral motor or sensory deficit without visual field deficit or disturbance of consciousness or language. The CT scan may show a small, sharply marginated hypodense lesion in the subcortical area, with the di­ameter smaller than 20 mm. Multiple lacunes are strongly related to hypertension and diabetes mellitus. Lacunar infarction is an acute onset of focal neurological deficits lasting more than 24 h. There are six recognized lacunar syndromes:

1.  Pure motor, hemiplegia or hemiparesis

2.  Dysarthria, clumsy hand syndrome

3.  Ataxic hemiparesis

4.  Sensorimotor stroke

5.  Pure sensory stroke

6.  Unilateral dystonia and involuntary movements such as choreoathetosis following lacunar infarc­tion of the putamen or globus pallidus  or hemiballismus owing to subthalamic infarction

Risk factors include hypertension, diabetes mellitus, heart disease, heavy alcohol consumption, cigarette smoking, and lack of physical exercise. La­cunar infarcts are the most common finding in cere­bral infarction in young adults.

 

Diagnostic Procedures All patients should re­ceive full evaluation for diseases of the blood vessels, atheroselerosis, arteriosclerosis heart disease abnormal­ities of blood constituents, and reduced cerebral perfu­sion. These investigations have been outlined under di­agnostic procedures for TIAs. Future developments of MRI with diffusion and perfusion studies, PET, and SPECT will define the location and extent of damage to cerebral tissue, and may permit earlier identification of blood vessel involvement in the lacunar state.

 

Treatment Control of risk factors (smoking, hy­pertension, diabetes mellitus) and treatment with an­tiplatelet agents or anticoagulants are of limited value, suggesting that the process of lacunar infarc­tion has advanced to a point where treatment of risk factors is ineffective.

 

Pathophysiology

     As a result of brain infarction in case of blood circulation less than 10 ml per 100 g of brain tissue in 1 min zone of focal necrosis is formed.

 

     During the first 6 hours this zone is surrounded by region with borderline blood circulation (18 – 20 ml per 100 g in 1 min). This region is called penumbra.

The neurons within this region are preserved structurally but their function suffers. During first 3 – 6 hours we can renew their function, that’s why this period is known as “therapeutic window “.

      After 6 hours zone of brain infarction is formed completely. Pathobiochemical and pathophysiological changes are observed in penumbra region. One of the main reasons of neurons death is accumulation of glutamat, which causes brain edema and disturbance of synaptic transference. The number of intracellular enzymes is increased. That causes activation of thrombocytes, microcirculation disorders, and ischemia. As a result ruination of neurons occurs.

 

Clinical features:

Acute period of brain infarction is divided into three stages:

1.     Precursors

2.     Apoplectic stroke

3.     Focal signs

 

To precursors belong transient ischemic attacks in the same region where brain infarction is developed. Brain infarction usually is developed in elderly people at any time. Gradually during several hours focal neurologic symptoms are developed. Sometimes the beginning of brain infarction (BI) is rapid, especially in case of embolic stroke. But one of the most important differential features of BI is the prevalence of focal symptoms over the general cerebral ones.

General cerebral symptoms manifest as headache, vomiting, consciousness disorders. These symptoms are usually observed at thrombembolic stroke and are increased according to the brain edema.

   Focal symptoms depend on localization of the infarction, damaged vessel and state of collateral blood circulation. The most common brain infarctions are in the region of middle cerebral artery.

       Middle cerebral  artery  blood – supplies basal nuclei, internal capsule, a part of temporal lobe, middle and lower parts or pre – and post central gyruses, opercular region, a part of parietal lobe, gyrus angularis, posterior parts of upper and middle frontal gyruses.

 

 

If the artery’s main trunk is occluded hemiplegia, hemianesthesia, gaze paresis, speech disorders (such as motor, sensory, total aphasia) occur when the lesion is in left hemisphere and apractice – agnostic syndrome occur when the lesion is right hemisphere.

If the artery’s cortical branches are occluded motor and sensory disorders in upper extremity, hemianopsia, sensomotor aphasia, apraxia, alexia, acalculia occur when the lesion is in left hemisphere and anozognosia, and autotopognosia occur when the lesion is right hemisphere.

If the artery’s posterior branches are occluded hemianesthesia, bathianesthesia, astereognosis, afferent paresis of extremities, hemianopsia, sensory aphasia, agraphia, alexia, acalculia and apraxia occur.

Anterior cerebral artery blood – supplies the cortex of frontal lobe (superior frontal    gyrus), superior part of anterior central gyrus, superior part of posterior central gyrus, corpus callosum, a part of superior parietal lobulus, orbital part of frontal lobe, lobulus paracentralis.

Infarction in the area of the anterior cerebral artery causes spastic hemiparesis with the prevalence in proximal part of upper extremity and distal part of lower extremity. This kind of BI is associated with the symptoms of oral automatism, psychiatric disorders, dysphagia, dysphonia, astasia, abasia, motor aphasia, retention of urine.

If the internal carotid artery is occluded before ophthalmic artery alternating optic – hemiplegic syndrome takes place. That means blindness or visual disorders on the side of lesion and hemiparesis on the opposite side. There is absence of internal carotid artery pulsation oeck.

If the internal carotid artery is occluded intracranial hemiplegia, hemianesthesia, well expressed general cerebral symptoms as a result of brain edema, compression or dislocation of brain stem are observed.

      When the infarction is in the region of vertebral – basilar vessels occipital lobes and brain stem suffers.

       Infarction in cortical branches region manifest as visual disturbances: homonymic hemianopsia with preserved macular vision or upper qudrantive hemianopsia, sometimes visual agnosia and metamorphopsia can occur. If the lesion is in the left hemisphere alexia, sensory and semantic aphasia can be observed.

If the process is distributed on mediobasal part of temporal lobe, memory disorders, such as Korsak syndrome usually take place.

Posterior cerebral artery blood supplies occipital lobe, posterior part of lower and middle temporal gyruses, basal and mediobasal part of temporal lobe, deep thalamocollicular branches blood supply thalamus, hypothalamus, posterior – lower parts of cortex of parietal lobe.

 

Infarction in the region of the posterior cerebral artery causes hemianopsia, visual agnosia, hemianesthesia, hyperpathia, desorientation in space and time, disorders of space –optical gnosis.

Infarction in the region of deep branches of posterior cerebral artery that blood supplies thalamus, posterior part of occipital lobe, corpus callosum, radiate crown, causes thalamic syndrome of Dejerin – Russi. Than last manifests as hemianesthesia, hyperpathia, dysesthesia, thalamic pains, hemianopsia, pseudoathetosis, hemiataxia, and dynamic hemiparesis on the opposite side.

Infarctions in the region of vertebral artery Vertebral artery blood supplies brain stem; oblongata brain, cerebellum, cortex of occipital lobe, part of cervical part of the spinal cord. It can be damaged extra – or intra cranially.

In case of extracranial lesion systemic dizziness, hearing, visual, eye movements, vestibular, equilibrium disorders and paresis with sensory disturbances in extremities are observed. Some patients have “drop- attacks “.

In case of intracranial lesion alternating syndromes of oblongata brain occur.

      Infarctions in the region of basilar artery cause the lesion of pons, cerebellum, hypothalamus, cortex of occipital lobe. In case of acute occlusion loss of consciousness, eye movements disorders, pseudobulbar syndrome, tetraplegia, muscle tone disturbance, sometimes even cerebellar symptoms and cortical blindness occur. Most of these patients die because of the vital functions disorders.

When the lesion is in pons syndromes of Miyar – Hyubler, Fowil, Brisso – Siquar and alternating hemianesthesia occur.

Infarction in the region of mesencephalon causes Parino syndrome, which manifests as gaze paresis upwards.

Infarction in the region of brain peduncles causes Weber or Benedict alternating syndrome. Sometimes Clode and Fua – Nikolesku syndrome can be observed.

Clinical features Atherothrombotic stroke

      Occur at older age

      Developed during some ours and days

      TIA present in anamnesis

      Developed at night or in the morning time

      Stenosis and occlusion of MAH at ultrasound examination

      Decreased of Internal Carotid artery pulsation on the neck

 

Clinical features Cardioembolic stroke

      Precursors absent

      Acute onset at emotional and physician activity

      General cerebral signs are very intensive:

Loss of consciousness,

Seizures and psychomotor agitation

Severe headache

      Embolism of vessels of retina, extremities, other inner organs

      Embolism of different arteries of the brain

      Embolism of cortical branches of the brain arteries

      Maximal neurological deficit at debut of stroke

      More often Median cerebral artery are lesion

 

 

Lacune

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Diagnostics of Brain Infarction The main peculiarities are:

·         Before stroke period in the previous history (TIA in anamnesis)

·         The beginning of the stroke is gradual

·         Data of somatic and neurological status

·         Additional methods of diagnostics

       Usually the patients with BI have rheologic disturbances.

Liquor is pellucid, without significant changes. There is focus of pathologic activity on EEG. USG finds out occlusion, stenosis of carotic and vertebral arteries.

Angiography

CT reveals hypodensive focus on the second day. MRI helps to find out small focuses and those, located in the brain stem.

 

 

          

 

              

 

Differential diagnosis

1.    Traumatic hemorrhage, trauma of brain

2.    Myocardial infarction

3.    Epilepsy

4.    Uremic coma

5.    Hyperglycemic coma

6.    Hypoglycemic coma

7.    Brain tumor with inside hemorrhage

 

While differentiation we should pay attention on anamnesis, run of the disease, symptoms, blood pressure, MAH state, eye fundus state, EKG, laboratory data, LP data.

Alcoholic coma is characterized by alcohol odour, psychomotor agitation, red eyes and face, seizures, normal blood pressure, low reflexes, enlargement of liver.

Uremic coma is characterized by ammonium odour, oliguria, edema, and ascites.

Diabetic coma is characterized by acetone odour, Kusmaul breathing, dry skin, hypotonia, hyporeflexia, hyperglycemia, glucosuria, acetone and sugar in urine.

      Hypoglycemic coma is characterized by wet skin, normal breathing, seizures, and low sugar level in blood.

Epileptic coma is characterized by seizures, there is episyndrome in anamnesis. EEG helps to put a diagnosis.

Running of the disease There are three main kinds of stroke running:

1.    Favourable, when all damaged functions are renewed.

2.    Remittent when the patient state is worsening because of associated pneumonia or other complications.

3.    Progressive, which usually causes death of the patient.

       The most severe are hemorrhages. Mortality in this case is from 60 to 90 %. Especially increases mortality in case of hemorrhage in ventricles, brain stem and cerebellum.

Favourable prognosis is in case of limited hemorrhages, small in size, without brain edema and secondary brain stem syndrome development.

Mortality at brain infarction is in 20 – 27 % of all cases.

 

Strokes treatment

There are nondifferential and differential kinds of stroke treatment.

Nondifferential treatment includes:

1.    Prevention and treatment of pulmonary insufficiency

2.    Liquidation of heart – vascular disorders

3.    Brain edema treatment

4.    Normalization of water – electrolytes balance and acid – alkali balance

5.    Osmose correction

6.    Improving of brain metabolism

7.    Liquidation of hyperthermia and other autonomic disorders

 

1.    Prevention and treatment of pulmonary insufficiency

a)    the patient is lying on the bed with his head elevated

b)    cleaning of patient’s oral cavity

c)    tracheostomia (at inspiratory muscles paralysis)

d)    at lung edema patient is given oxygen; narcosis, Bobrov’s apparatus, 2 ml 1 % lazix, 2 ml 1% dimedroli, 2 ml 0.1 % atropini I / m  are used.

e)    Antibiotics are used in order to prevent pneumonia

2.    Liquidation of heart – vascular disorders

a)    At increased blood pressure we use:

·         Clofelini 1 – 3 ml 0.01 % solution i/m, i/v.

·         Dibasoli 3 – 4 ml 1 % solution i/v

·         Droperidoli 1 ml 0.25 % solution i/v

·         Rasedili 1 – 2 ml 0.1 % i/v, I / m,

·         In case of hyperkynetic type of blood circulation we use b– adrenoblockers (anaprilini, obzidani, inderal )

·          In case of hypokynetic type of blood circulation we use peripheral vasodilatators (Natrii nytroprussidi , appresini) in combination with euphyllini

b)    At low blood pressure we prescribe

·         Dexamethazoni 4 – 8 mg i/v by drops in physiological solution

·         Prednizoloni 60 – 120 mg i/v by drops in physiological solution

·         In order to improve heart activity we use strofantini, corgliconi, cordiamini

3. Brain edema treatment

Diuretics, corticosteroids, albumini, ganglioblockers, 20 % mannit, manitoli, glycerini, lazix, diakarbi are used.

4. Normalization of water – electrolytes balance and acid – alkali balance

      We should estimate patient’s necessity in water according to his secretion, the level of Na in blood, hematocritis. An average water necessity is 35 ml per kg, in patients with loss of consciousness it is 50 ml per kg. We should correct patient’s hyper- or hyponatriemia,   hyper- or hypokaliemia.  4 % solution of natrium bicarbonates i/v, trisaminum is used at metabolic acidosis. KCl i/v is used at metabolic alkalosis.

5.  Osmose correction

    Normally blood osmose is within 280 – 295, urine osmose is 600 – 900 mosm per liter.

   At stroke usually we have hyperosmose, which manifests as increased hematocritis, hyperagrigation.

 

6. Improving of brain metabolism

 Vit E, piracetami, aminaloni, cerebrolysini natrii oxybutiras are used.

7. Liquidation of hyperthermia and other autonomic disorders.

At hyperthermia we use

·         reopirini 5ml

·         analgini 50 % 2.0

·         aspizoli 0.5 g

 At autonomic disorders we introduce

·         sibazoni 0.5 % 1 ml

·         haloperidoli 0.5 % 1 ml

·         dimedroli 1 % 2 ml

·         natrii oxybutiras  20 % 10 ml

 

Differential treatment of brain infarction

The main directions are:

1.    To renew blood circulation in zone of ischemia.

2.    To correct rheologic and coagulative properties of blood, to improve microcirculation.

3.    To prevent disorders of cerebral metabolism.

4.    To decrease brain edema.

5.    To treat brain hypoxia.

 

1.  To renew blood circulation in zone of ischemia

a)    . Actilaza 100 mg I/v by drops every 2 – 3 hours.

b)    Inhibitors of glutamat excretion (difenin, nimotop, MgSO4) are used. Nimotop is used 15 mg in 1500 ml of physiologic solution i/v by drops, or in tablets 30 – 60 mg 4 times per day.

In order to improve perfusion we use cavinton 20 mg I/v by drops.

At hyperperfussion we use:

·         euphyllini 10 ml 2.4 % solution,

·         penthoxiphyllini,

·         diuretics (manitol 15 % 100 – 200 ml) 

·         albumini 100 ml I/v

 

2.  To correct rheologic and coagulative properties of blood, to improve microcirculation

a) anticoagulative therapy is used only at progressive stroke:

·         heparini 5 000 U 4 times per day during 5 – 7 days, the 2 500 U during next 3 –4 days.

·         Fraxiparini is considered to be even more effective.

b)  Antiagregants are used also:

·         penthoxiphyllini 5 – 10 ml 2 % solution I /v by drops during 10 days, then 200 mg 3 –4 times per day up to 1 month.

·         Sermioni 4 mg I / v by drops during 10 days, then 1 tablet 3 times per day up to 1 month.

·         Ticlid 250 mg twice a day.

·         Aspirini 250 mg once a day.

·         Dipiridamoli 1 – 2 ml i/v by drops during 10 days, then 25 mg 2 –3 times per day.

c)    Hemodilution is reached by introduction of reopoliglucini 400 ml I / v by drops during 5 – 7 days.

3.    To decrease brain edema.

·         Glycerini 1 g per 1 kg is used I/v

·         Dexamethazoni 16 – 32 mg per day

4.    To treat brain hypoxia.

·         Vit E 1 ml i/m.

·         Piracetam 10 – 20 ml i/v by drops.

In case of stenosis, occlusion of MAH surgical treatment can be used.

Prognosis During the first two days the state of patients with brain infarction is very severe. In a few days it is going better. Recurrent stroke can occur during the first year, sometimes during the first 2 or 3 years.

Prevention means in time treatment of heart – vascular diseases, hypertension and rhythm disorders.

 

HYPERTENSIVE ENCEPHALOPATHY

Hypertensive encephalopathy is a syndrome charac­terized by marked elevation of blood pressure and ev­idence of increased intracranial pressure.

 

Etiology and Pathology Most patients with hy­pertensive encephalopathy have a long history of es­sential hypertension. In other cases, the elevation of blood pressure is secondary to another disease process such as acute glomerulonephritis, chronic nephritis, pheochromocytoma, Cushing disease, or acute toxemia of pregnancy.

There is diffuse cerebral edema and cerebral vasospasm. Microscopic examination reveals pe­techial hemorrhages and fibrinoid necrosis of the ar­teries.

The patient complains of severe headache with nausea and vomiting. Visual disturbances, including blurring of vision and scotomata, are frequent. Con­fusion, with progression to stupor, convulsions, and coma are seen in untreated cases. Examination of the fundi reveals papilledema and hypertensive retinal changes. Focal neurological signs are not characteris­tic but may be seen as a postictal phenomenon or when intracranial hemorrhage occurs.

 

Diagnostic Procedures The MRI and CT scans reveal diffuse cerebral edema.

 

Treatment Hypertensive encephalopathy is a med­ical emergency and the blood pressure should be re­duced as rapidly and safely as possible.

 

Prognosis Untreated hypertensive encephalopa­thy is fatal. Follow-up care and appropriate long-term medication allow patients to survive for many years.

 

Students’ practical Study Program.

Step I.  Aim: To make the topical diagnosis. For this purpose it is necessary:

1. To determine types of stroke.

2. To determine Carotid or Vertebrobasilar vessels distribution.

3. To find the reasons to cause disorders of cerebral circulation.

4. To find the periods of stroke.

5. To formulate the diagnosis, for example:

a)      Ischemic atherothrombotic stroke in Left Carotid Distribution from cerebral atherosclerosis and

   Hypertensive disease, acute period.

Step II. Aim: Administer emergency treatment. For this purpose it is necessary to choose:

1. Undifferentiated emergency therapy of strokes.

2. Differentiated emergency therapy.

3. Rehabilitation and prophylactic programs for stroke patients.