STROKES

STROKES

 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

·         TIA

·         Hypertonic crisis

·         Acute hypertonic encephalopathy

2.    Strokes

·         Haemorrhage (subdural, epidural, intracerebral, ventricular)

·         Brain infarction (atherothrombotic, cardioembolic, hemodynamic, hemorheologic, lacunar infarction)

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

STROKE – is rapidly developing clinical signs of focal disturbance of cerebral function, lasting more then 24 hours or leading to death

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

Classification of Ischemic stroke

      Brain infarction is divided into:

1.    atherothrombotic

2.    cardioembolic

3.    hemodynamic

4.    hemorheologic

5.    Lacunar infarction

 

Atherothrombotic – occurs in case of plugging of extracranial or intracranial vessel by atherosclerotic plague

Cardioembolic – occurs in case of plugging of extracranial or intracranial vessel by 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.

Lacuna – focus of ischemia without meningeal and cortical symptoms

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

 

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

 

Cardioembolic brain infarction occurs at embolus plugged cerebral vessel.

 

Clinical features of Cardioembolic stroke:

•         Precursors are absent

•         Acute onset at emotional and physical 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 the beginning of stroke

•         More often medial cerebral arteries are involved

 

The reasons of embolism:

•         Aortal or arterial thrombus

•         Thrombus in case of heart abnormalities, such as:

–          Mitral stenosis

–          Aortal abnormality

–          Rheumatic or bacterial endocarditis

–          Myocardial infarctions

–          Cardiosclerosis

–          Cardiomyopathy

–          Different kinds of arrhythmia

–          Embolism can occur at thrombophlebitis, lung abscess, malignant tumors, sepsis

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

–          Gas embolism occurs at surgery on lungs, at pneumothorax

Hemorheologic brain infarction

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

Clinical peculiarities of haemodynamic stroke:

•         The acute onset

•         Haemodynamic factor (acute decreasing of BP, angina pectoris, hypovolume, orthostatic hypotension)

•         Pathology of extra- and intracranial arteries

•         Localization – zones of collateral blood circulation

•         More often present bilateral infarctions

•         Infarction at parietal-occipital areas

 

The lacuna 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.

 

Clinical features:

Periods of brain infarction:

•         Acute

•         Renewal

•         Residual

 

Acute period of brain infarction is divided into three stages:

1.     Precursors

2.     Apoplectic stroke

3.     Focal signs

 

Clinical features of ischemic stroke:

•         Precursors – transient ischemic attacks in the same region where brain infarction is developed

•         Onset is gradually

•         During several hours focal neurologic symptoms are developed

•         The prevalence of focal symptoms over the general cerebral ones

 

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, visual disorders – Hemianopsia, speech disorders (such as motor, sensory, total aphasia) occur when the lesion is in left hemisphere –  apractice – agnostic syndrome occur when the lesion is right hemisphere.

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

·         hemiparesis on the opposite side.

·         There is absence of internal carotid artery pulsation oeck.

On thrombosis side present:

o   miosis, Decreasing of retinal pressure, Painful percussion of skull, Decreasing or lost of Carotid artery pulsation on the neck

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.

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.

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 intracranially.

In case of extracranial lesion: systemic dizziness, hearing disorders , visual disorders, eye movements disorders, vestibular disorders, equilibrium disorders, paresis with sensory disturbances in extremities are observed.

·         Some patients have “drop- attacks “

·         hypersomnia

·         Autonomic disorders

·         Disorders of breathiness, heart function

·         Mental disorders – Korsakov syndrome

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

Alternate intramedular syndromes:

Jackson’ syndrome (medial medullar syndrome)

Awelis’s syndrome (palatine-pharyngeal syndrome)

Schmidt’s syndrome

Valenberg – Zakcharchenko’ syndrome

Babinski-Najott syndrome:

Bilateral thrombosis of Vertebral artery:

–        Bulbar synrome

–        Breathiness disorders and lesion of heart function

–        Paralysis of extremities

–        Loss of consciousness  and deep cerebral coma

  

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, 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.

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.

Diagnostics of Brain Infarction

•         Rheologic disturbances

•         Liquor is pellucid, without significant changes.

•         EEG – There is focus of pathologic activity

•         USD finds out occlusion, stenosis of carotid and vertebral arteries

•         CT reveals hypodensive focus on the second day

•         MRI helps to find out small focuses and those, located in the brain stem

•         Angiography

 

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

 

Hemorrhagic stroke means hemorrhage.

According to the localization of hemorrhage it is divided into such groups:

1.    Intracerebral (when the hemorrhage is into the substance or parenchyma of the brain)

2.    Membrane

a)    subarachnoid (when the bleeding originates in the subarachnoid spaces surrounding the brain)

b)    epidural and subdural (traumatic)

3.    Combined

a)    subarachnoid – parenchymatous

b)    parenchymatous– subarachnoid

c)    parenchymatous–ventricular

d)    ventricular

     

Etiology

The most common causes of hemorrhage are:

1.    Hypertension

2.    Symptomatic arterial hypertension (at kidney diseases, systemic  vessel processes)

3.    Inborn arterial and arterial – venous malformations

4.    Blood diseases (leucosis, polycythemia)

5.    Cerebral atherosclerosis

6.    Intoxications, such as uremia, sepsis

 

Pathogenesis

       Hemorrhage results from rupture of the vessel anywhere within the cranial cavity or diapedesis in case of increased penetrance of vessel’s wall. Rupture of the vessel is much more common and takes about 80 % of all stroke cases while diapedesis occurs only in 20 % of cases.

       Hypertension has been implicated as the main cause of hemorrhage. Hypertension is the cause of a weakening in the walls of arterioles and the formation of micro aneurysms. Among elderly nonhypertensive patients with recurrent hemorrhages, amyloidal angiopathy has been implicated as an important cause. Others causes include arterial-venous malformations, aneurysms, bleeding disorders or anticoagulation, trauma, tumors, cavernous angiomas and drug abuse.

Pathomorphology 

    In case of hemorrhagic stroke we distinguish hematoma – like hemorrhage and transudation – like hemorrhage.

     According to the localization there are:

1.    Lateral hemorrhage (they are located laterally compared with the internal capsule. They take about 40 % of all hemorrhages).

 

2.    Medial hemorrhage (they are located medially compared with the internal scapule and take about 10 % of all hemorrhages).

 

3.    Combined hemorrhages (they take the whole region of basal nuclei: subcortical nuclei, thalamus, and internal capsule. They take about 16 % of all hemorrhages).

 

4.    Cerebellar hemorrhages (6 – 10 %)

 

5.    Brain stem hemorrhages (5 %).

 

       Primary ventricular hemorrhages are very rare. In case of large hemorrhage brain edema is developed. The last is associated with dislocation of brain stem which is the main cause of patients’ death.

 

     The main cause of death is rupture into the ventricular system and brain stem hemorrhage with lesion of main vital centres.

 

Clinical picture There are three main periods of stroke:

1.    Acute (up to 3 – 4 months)

2.    Renewal (up to 1 year)

3.    Residual

Acute period is divided into such stages:

1.    Precursors

2.    Apoplectic stroke

3.    Focal signs

      Usually hemorrhage has rapid development in day time during physical or emotional stress. The patients are usually young. And they have risk – factors in anamnesis. Precursors are very rare.

      Two main groups of symptoms are typical for hemorrhage – general cerebral and focal. Typically general cerebral symptoms prevail over focal ones in case of hemorrhage.

      General cerebral symptoms mean severe headache, vomiting, consciousness disorders.

       While examining patients with consciousness disorders we should pay attention to the possibility of contact with patient, his ability to follow commands, to say what has happened with him, to orient in the space and time and so on.

Clinical features

•         Acute onset:

–        in day time during physical or emotional stress

–        the patients are usually young

–        they have risk – factors in anamnesis

–        precursors are very rare

•         Acute severe headache

•         nausea, vomiting with blood

•         Consciences disorders – from stupor to the deep coma

•         Hyperemia of the face

•         neck vessels are pulsing

•         pulse is strained and slow

•         blood pressure is increased

•         meningeal symptoms

•         seizures

•         automatic gesticulation

•         autonomic disorders

•         psychomotor agitation

         Sometimes sopor occurs at the beginning of hemorrhage, which can develop in coma in a few hours.  

Coma is characterized by deep consciousness disorder, disturbance of breathing and heart activity. The patient doesn’t respond to stimuli.

        At atonic coma all reflexes are lost, blood pressure is decreased and there is breathing disturbance.

       In case of coma development:  response to stimuli is absent,  eyes are closed, mouth is opened, face is red, lips are cyanotic, neck vessels are pulsing, there is breathing disturbance, skin is cold, pulse is strained and slow, blood pressure is increased, temperature increases in 24 hours.  Patient is lying on his back. All muscles are relaxed.  Pupils are changed (there can be anizokoria, cross – eyes, sometimes gaze paresis can be observed).     Mouth angle is a little bit lower.  On the opposite side hemiplegia is often observed: the arm is falling down like bine, there is hypotonia of muscles, reflexes are low, and Babinski sign is often observed too. Sometimes meningeal signs, vomiting and dysphagia are observed too. Retention of urine or involuntary urination can also occur. In case of cortex irritation epileptic attacks can be developed.

Brain stem hemorrhage is associated with:  tetraparesis,  alternating syndromes,  eye movement disorders, nystagmus,  gorge disorders,  cerebellar syndromes.

      Pons hemorrhage manifests as: ptosis, gaze paresis, increased muscular tone (hormetonia).

 Cerebellar hemorrhage usually starts with:    dizziness,  severe headache in occipital lobe,  vomiting,  eye movement disorders,  ptosis, Gervig – Mazhandi syndrome, Parino syndrome are observed.  Cerebellar symptoms, such as nystagmus, dysartria, hypotonia, and ataxia. Paresis of extremities is not common.   

The most common complication of intracerebral hemorrhage is rupture into the ventricle system. This is usually associated with:  worsening of patient’s state, hyperthermia, breathing disorders, hormetonia.

Hormetonia manifests as changes of muscle tone in extremities, when hypotonia is changed into hypertonia in a few seconds or minutes.

     On the side of lesion there is: anizokoria, Bechterev phenomena, painful trigeminal and occipital points, automatic movements, gaze paralysis, Kerning sign.

    On the opposite side:  positive Bare’s sign,  mouth angle is located lower thaormally, foot is turned outside,    pathological signs, hypotonia,  hyporeflexia

The run of the disease

      The patients with brain hemorrhage are in very severe state. 70 % to 95 % of them died. About 40 % – 45 % of them die during the first day, the rest of them – live 3 or 5 days.

      The main cause of death is compression of brain stem as a result of brain edema and rupture into ventricular system associated with disorders of vital centers.

       In case of good prognosis the patients usually recover from coma, then reflexes appear, general cerebral symptoms regress, the patients start to gorge, then they start to move, sensation and speech renew also.

Diagnostics

     In case of rapid development of all symptoms with loss of consciousness, high blood pressure and presence of focal symptoms there is no problem with putting diagnosis. But when the hemorrhage starts gradually without loss of consciousness, then it is much more difficult to put a diagnosis. In this case instrumental and laboratory examination has a great meaning.

    In blood usually leucocytosis, related lymphopenia, hyperglycemia (up to 8 – 10 mmole/l) is observed.

     In liquor which is flowing out under high pressure during lumbar puncture a great number of erythrocytes are found.

    On eye fundus – retinal hemorrhages, hypertonic angioretinopathy and Salus symptoms are observed.

     At echoencephaloscopy there is dislocation of middle structures on 6 –7 sm to the healthy side.

    By means of angiography we can find out aneurysm, dislocation of blood vessels, to find out zone “without vessels “.

    EEG – present pathological activity focus

     CT and MRI find out hyperdensive focuses.

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

Brain edema treatment

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

Improving of brain metabolism

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

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/

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.

Differential treatment of haemorrhage:

The main directions of treatment are:

1.    To lower increased blood pressure

2.    To liquidate brain edema and lower intracranial pressure

3.    To increase coagulative properties of blood and decrease penetrance of vessels’ wall

4.    To prevent and treat cerebral vessels spasm

5.    To normalize vital and autonomic functions and prevent complications

6.    To treat hypoxia and brain metabolism disorders

 

1.     To lower increased blood pressure

Clofelini, b-aqdrenoblockers (anaprilini, obzidani, inderali), Calcium antagonists (nifidipini, adalat) IACE (capoten, enalapril, renarapril) are used.

At too high blood pressure ganglioblockers are used:

–       Pentamini 5% 1.0

–       Benzohexonium 2.5 % 1 ml

–       Arfonad 5 ml 5 % i/v in physiologic solution

 

2.     To liquidate brain edema and lower intracranial pressure

The same measures as in nondifferential treatment are used.

3.     To increase coagulative properties of blood and decrease penetrance of vessels’ wall

a)    CaCl2 10 – 20 ml 10 % i/v

      Vicasoli 1 – 2 ml 1 % i/v

         ascorbinic acid 2 – 5 ml 5 – 10 % solution I/m

b)    Antifibrinolytics:

   EAKA 100 ml 5 % solution 1–2 times per day I/v by drops during 5 – 7 days. Then we use it orally – 3 g every 3 –4 hours up to 3 weeks.

c)    At decompensated fibrinolysis we use

Trasiloli 20 – 30 000 U i/v by drops in 250 ml of physiologic solution

Hordox 5 000 U i/v by drops every other day

d)    to normalize microcirculation we use:

dicinoni 2 ml 12.5 % solution 2 – 3 times per day during 10 days, then 2 tablets (0.5 g) every day.

Ascorutini, rutamini (1 ml i/m 1 – 2 times per day)

4.     To prevent and treat cerebral vessels spasm:

Antagonists of Calcium are used:

Nimotop is introduced I / v 15 mg per kg per day during 5 – 6 hours. On the 5^th – 7 th day it is used orally 60 mg every 4 hours during 7 – 10 days.

5. To normalize vital and autonomic functions and prevent complications

6. To treat hypoxia and brain metabolism disorders.

The same measures as in nondifferential treatment are used.