Crib Neuroscience.

Acute disorders of cerebral circulation.

To acute disorders of cerebral circulation (cerebral vascular accident) are occurring acute cerebral lesion of vascular origin, characterized by meningeal, cerebral and focal symptoms or their combination. Depending on the duration of persistent neurological deficits distinguish transient disorders of cerebral circulation and strokes. Risk factors of stroke are genetically predisposed to diseases of the cardiovascular system, dislipoproteinemia, hypertension, diabetes, overweight, frequent emotional stresses. Stroke flowing on the type of acute cerebral ischemia are a result of the mismatch between the needs of the brain of oxygen and energy substrates delivered by the blood, and a sharp decrease in cerebral perfusion. The basis of stroke hemorrhagic is a breach of the integrity of the vascular wall and penetration of blood in the brain tissue, the ventricles or under the membranes.

Classification. Acute disorders.

Pnmk (transient violation of cerebral blood flow.

Stroke (acute cerebrovascular blood flow.

CEREBRAL syndrome, including depression of consciousness, headache, nausea and vomiting, sense of faintness is not vestibular vertigo and less generalized convulsions, reflects the degree of violation functionsthe of the brain. The reasons for its cause are cerebral hypoxia, ischemia, edema, increased intracranial pressure, intoxication and the combination of these factors. The severity of cerebral syndrome and its dynamics are the main criteria in the assessment of the severity of the patient’s condition. The examination begins with an assessment of level of consciousness, the most complex indicator of the activities of the brain. It is necessary to allocate the following levels of oppression of consciousness torpor, stupor, coma.

MENINGEAL syndrome is a sign of irritation of the meninges seen in meningitis, encephalitis, and severe stroke. The most elementary study include: – determination of rigidity of the muscles of the neck, by passive flexion of the head and estimation in cm of the distance between the chin and sternum – the study of symptom Kernig, by bending the legs at a right angle at the hip and knee joints with subsequent extension and evaluation, in degrees, of the angle between the Shin and the thigh, check zygomatic phenomenon spondylitis, by percussion of the zygomatic arch with the assessment of facial grimaces.

FOCAL symptoms: movement disorders (from mild paresis to plegia), the vast majority of movement disorders are distributed on gametype; numbness (hypoesthesia); aphasia; dysarthria; hemianopsia; oculomotor disorders (horizontal gaze palsy); decreased visual acuity; anosognosia; disorders of memory.

1. Embolic type.

·- Thromboembol (cardiogenic – rheumatic fever, endocarditis.

·- Atheromatous embolus (destruction of the atheromatous plaque.

· Fat embolus (fractures of large tubular bones.

Embolus to any type of obstructs the lumen of intracerebral arteries, as a consequence, there are certain higher focal symptoms.

Clinical picture. For the disease characterized by acute beginning sociophysiological symptoms. In most cases, onset of the disease occurs on the background of active hemodynamics: physical activity, psycho-emotional stress.

The cause of embolic stroke, the localization and amount of focal symptoms are evident. Cerebral symptoms appear due to a sharp violation of cerebral autoregulation of cerebral blood flow; spasm of the arteries of the brain in response to acute vascular accident. The most frequently observed headache, nausea, vomiting, depression of consciousness, sometimes to the level of coma. However, the cerebral symptoms usually tend to devolution within a few hours, especially fast, the less Ambrosiana artery. In cases of lesions of small arteries cerebral symptoms may not be, and alopecia – accept character pnmc.

The pathogenesis of this variant of stroke associated with the presence of narrowing of the artery and subcommentaries hemodynamics in her pool. Then on the background of the emergence or strengthening of systemic factors there is a further deterioration of blood flow (slow flow – a current) at the site, leading to decompensation and the appearance of focal symptoms. Further development of the situation due to such factors as the degree and size of the ischemic area of the brain, the change in the severity of systemic factor.

Clinical picture. The onset is in most cases gradual, often at night; waking up the patient detects focal symptoms corresponding to a certain vascular pool. Most often it is the hemiparesis and hemihypesthesia with a predominance in the hand, that is, the basin of the internal carotid artery. Further development of a state depends on the above factors. At a favorable outcome the symptoms can almost completely regressed, however, if the area of ischemia transformirovalsya in necrosis, there is a deepening of focal manifestations and the appearance of 2-3 days cerebral syndrome.

3.Thrombotic type.

The pathogenesis of the disease is associated with progressive thrombosis and rapidly progressive deterioration of blood flow in this artery and distal to it. Usually thrombotic stroke is more severe than stenotic, as it has due to the rapid development of occlusive process is not time to place a compensatory vascular tissue changes.

Clinical picture. It is believed that the appearance of focal symptoms, vollsynthetisches for several days preceded by precursors: malaise, avestapolarit dizziness, headache, fatigue, etc. Then almost the same as when the option appears stenotic focal symptoms, which however tends to increase and the appearance after 2-3 days cerebral manifestations.

29. Subarachnoid hemorrhage.

20% of all intracranial nontraumatic hemorrhage. Most suffering from age 35-55 years. The reason more than half of the cases is the rupture of arterial aneurysms rarely arterio-venous malformations and altered atheromatous arteries. Blood from the burst artery flows into the subarachnoid space by stimulating receptors of the membranes and causing the elements of aseptic inflammation.

Clinical picture. Is composed mainly of two syndromes: cerebral and meningeal. Acute beginning with the appearance of a severe headache a blow to the head , some of the patients said that the felt like something burst and flowed inside his head. Immediately increase cerebral manifestations: nausea, vomiting, stupor, coma, often with psychomotor agitation. Meningeal syndrome in the first hours is not characteristic, and develops a few hours of the day.

Enough of great practical importance grading of subarachnoid haemorrhage severity on the basis of the clinical picture suggested Hunt RC, Hess RN, 1968

Stage 1 – asymptomatic or minimal headache and easy rigidity of the neck muscles.

Stage 2 – severe headache, severe muscle stiffness of the neck.

Grade 3 – drowsiness or confusion and possible mild hemiparesis.

Degree 4 – stupor, moderate or rough hemiparesis, decerebration signs.

Stage 5 – deep coma.

Treatment. Bed rest for 4 weeks. Mandatory diagnostic lumbar puncture. Repeated puncture may relieve severe headache, however, their conduct carries a risk. In the acute stage is a vigorous dehydrating therapy: mannitol, glycerol, corticosteroids (dexamethasone 10-16 mg / day with reduced dose to 2 weeks), and all other activities carried out in the treatment of hemorrhagic strokes.

30. Coming cerebrovascular accident.

This group includes disorders of cerebral circulation, manifested focal neurologic symptoms for a period of one day, in real life, typically in 2-15 minutes. If focal symptoms persisted for several hours, dramatically increases the probability of finding at CT of the zone of infarction. In addition, the TIA is characterized by rapid development of symptoms from the appearance to the maximum, no more than 5 minutes, usually less than 2 minutes. The mechanism of TIA is a temporary ishemizatsii area of the brain which ceases to work, but not destroyed. The reasons for this situation are most frequently the deterioration of blood flow in the stenosis of major arteries due to systemic hemodynamic disturbances and microemboli particles of atheromatous plaque or microthrombuses.

Non-focal neurological symptoms not typical for pnmc, unless it is the cause of focal symptoms.

TIA in carotid manifest.

· Movement disorders (dysarthria, weakness, or clumsiness in the limbs and/or face.

· Loss of vision in one eye (amaurosis fugas) and significantly less hemianopsia.

· Sensory disorders (numbness or paresthesia in the arm and/or leg and/ or face.

· Aphasia in lesions of the right carotid artery.

TIAS in the vertebral-basilar pool.

· Motor dysfunction (weakness or clumsiness) in any combination of arms, legs, face, both from the right and from the left.

· Impaired sensation (numbness or paresthesias) involving the right, left or both sides.

· Loss of vision on one or both halves of the visual fields.

· Impaired balance, dizziness, double vision, dysphagia, or dysarthria characteristic, but none of these symptoms cannot be considered sufficient for the diagnosis of TIA if it occurs in isolation.

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