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I./4.3.: Symptomatology of intracerebral hemorrhage by localisation
I./4.3.1.: Putaminal hemorrhage
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Lateral striatocapsular – referring to the origin of the bleeding- or lateral putaminal hemorrhages are the most common. Symptoms are the results of posterior two-third of the internal capsule injury: contralateral severe hemiparesis or often hemiplegia without predominance, contralateral facial- and body hypaesthesia for all qualities of sensation and horizontal gaze palsy result in conjugated deviation of the eyeballs towards the lesion. Extremities are hypotonic due to the diaschisis phenomenon initially, and become spastic later.
Dominant hemisphere lesions frequently accompany with transortical expressive aphasia , or visual neglect and constructive apraxia in non-dominant hemorrhage. Cortical symptoms explained by disconnection of the referred cortical areas. This specific location also called middle putaminal hemorrhage.
Anterior portion of the internal capsule injured in anterior putaminal hemorrhages; result in less severe lesion of the corticospinal tract and no sensory disturbance. Posterior putaminal hemorrhage, damage to the posterior third of the internal capsule, represented with severe sensory symptoms, homonymous quadrant- or hemianopsy and fluent aphasia in dominant hemisphere lesions. Severity of the focal symptoms depends on localization and size of the hematoma. Large hemorrhages tend to propagate into the ventricles. This complication brings high lethality.
I./4.3.2.: Caudate hemorrhage
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Account for 7% of hypertensive intracerebral hemorrhage, but ruptured arteriovenous malformation also occur in this region. Intraventricular propagation is common, since the frontal horn of the lateral ventricle is near to the site of bleeding. Damage to the anterior arm of the internal capsule (lateral spread), dysfunction of the prefrontal circuits result in disorientation, confusion and memory disturbance. Downward propagation, hematoma growth causes hypothalamic lesion with ipsilateral Horner-syndrome. Despite the more common intraventricular propagation, prognosis of the caudate hemorrhages is better then putaminal bleedings of same size.
I./4.3.3.: Thalamic hemorrhage
Four pairs of penetrating arteries from the vertebrobasilar artery (except one) supply the thalamus. Tuberothalamic artery, branch of the posterior communicating artery supply the anterior nuclei with blood. Thalamoperforate (paramedian), thalamogeniculate and posterior choroid arteries originate from posterior cerebral artery. Thalamoperforate artery supplies midline and intralaminar nuclei, while thalamogeniculate supplies posterolateral, and posterior choroid supplies the dorsolateral/pulvinar region.
Hemorrhages occur in different areas present with characteristic symptoms similar to ischemic strokes. In the case of thalamic hemorrhage focal symptoms, common intraventricular propagation and hydrocephalus because of the proximity of the third ventricle have prognostic value. In case of smaller hemorrhage, „drainage” to the ventricular system might be beneficial. A large thalamic hemorrhage could spread caudal towards the oculomotor nerve nucleus result in the common findings of bilateral ptosis, ventricular gaze palsy or conjugated downwards gaze.
Hemorrhages in the region of the thalamogeniculate artery – posterolateral thalamus - are the largest, implicitly with sensory predominant symptoms. In anterior and medial thalamic hemorrhage, hypnoid unconsciousness is a common finding, later followed by poor initiative and severe memory disturbance.
Thalamic injuries could accompany with „cortical” symptoms such as aphasia, visual neglect, anosognosia or visuospatial dysfunction because of the disconnection from the cortex. Thalamic hemorrhages usually present with worse prognosis then similar size putaminal bleeding because of the more severe hypnoid unconsciousness.
I./4.3.4.: Pontine hemorrhage
Predilection site of the hypertensive brainstem hemorrhages is the pons, because of the corresponding pattern of the blood supply with the basal ganglia region. Most hypertensive pontine hemorrhages from the ruptured paramedian arterioles located in the basis-tegmentum area. Large hemorrhages tend to spread to the mesencephalon. Pontine hemorrhages frequently rupture into the IV. ventricle and cause triventricular occlusive hydrocephalus. Outcome of the pontine hemorrhage is poor because of the severe motor symptoms (tetraparesis or plegia), common severe hypnoid unconsciousness and the above-mentioned hydrocephalus.
Miotic, reactive pupils because of bilateral sympathetic pathway damage, horizontal gaze palsy and downward nystagmus are also characteristic and common. Hemiparesis, ataxic hemiparesis, dysarthria-clumsy hand syndrome or one-and-a-half syndrome may be caused by lateral pontine hemorrhages. Outcome is better then midline bleedings. Secondary pontine hemorrhage as a consequence of increased intracranial pressure is well-known.
I./4.3.5.: Lobar haemorrhage
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Lobar haemorrhages arise from the cortical-subcortical white matter junction. Spread defined by the orientation of the white matter fibres, because the location of the blood clot is between them, growth is perpendicular. Usually, slit-like cavity in line with the axis of the hemisphere will remain after resorption of blood. Since the blood clot disconnects the cortex , lobar haemorrhages frequently associated with epilepsy. Outcome after lobar haemorrhage is better then basal ganglia hemorrhages, because hypnoid unconsciousness seldom associated, since lobar bleedings are far away from the ascending reticular activating system. Hypnoid unconsciousness only occurs in case of severe increase of intracranial pressure or upper brain stem compression. Lobar haemorrhage consequent of anticoagulant therapy is the only exception with high mortality .
Most lobar haemorrhages originate from arteriovenous malformations or ruptured cavernomas in the young, and from amyloid angiopathy in older patients. Hypertension might cause lobar bleeding, but infrequently. Frequency of location of lobar haemorrhages is as follows: parietal, occipital, frontal, temporal.
I./4.3.6.: Intraventricular haemorrhage
Most of the intraventricular haemorrhages are complication of large caudate, putaminal or thalamic bleedings: these are secondary ventricular haemorrhages. Primary intraventricular bleedings originate from the subependymal germinal matrix in infants. While vascular malformations near to ventricles or ruptured choroid plexus angiomas are the main causes in adulthood, symptomatology is similar to subarachnoid haemorrhage: ictal thunderclap headache and later neck stiffness and clinical signs of increased intracranial pressure develop. Intraventricular bleedings frequently result in occlusive hydrocephalus.
I./4.3.7.: Cerebellar haemorrhage
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10% of intracerebral hemorrhages are cerebellar. Rupture of the terminal branch of the inferior posterior cerebellar artery or rarely the superior cerebellar artery in the region of the dentate nucleus is responsible. The bleeding spreads between the fibres of the white matter similarly to supratentorial hemorrhages, and frequently ruptures to the fourth ventricle. Cerebellar hemorrhages can cause tonsillar herniation without any alarming sign, which make the extremely malignant. The earliest and most severe focal sign is gait disturbance. Patients tend to fall towards the lesion and frequently unable to sit. It often accompanied with vomiting and severe occipital or frontal headache.
Some more of the possible symptoms are horizontal gaze palsy towards the lesion, narrowed pupils and ipsilateral Holmes-sing. Limb ataxia and intention tremor less often found then the previous symptoms. Large cerebellar hematomas may compress the brain stem with the clinical sings of deepening hypnoid unconsciousness, horizontal gaze palsy and bilateral pyramidal signs. By the time, brain stem compression occurs; fourth ventricle compression and occlusive hydrocephalus develop as well. Cerebellar hemorrhages larger then 3 cm should be neurosurgically treated; if the fourth ventricle is open and the patient is alert or does not have cranial nerve lesion: operation could be delayed. Operated cerebellar hemorrhages tend to have good prognosis, since the hematoma could easily reached, but surgical intervention should take place before severe hypnoid unconsciousness develop.
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