Cerebral hemorrhage, commonly known as cerebral hemorrhage, is a hemorrhage that originates in the brain parenchyma and is therefore called spontaneous cerebral hemorrhage; hypertensive small artery sclerosis and rupture are the most common causes of this disease and are therefore also called hypertensive cerebral hemorrhage. Cerebral amyloid angiopathy, arteriovenous malformations, aneurysms, hematologic diseases, coagulation abnormalities, cerebral arteritis, drug abuse, and tumors and cerebral infarction are other causes of intracerebral hemorrhage. The site of hemorrhage in spontaneous cerebral hemorrhage is most common in the nucleus accumbens, followed by the thalamus, caudate nucleus, white matter of the hemispheres, cerebral bridge, cerebellum, and ventricles.
General symptoms.
1. Acute onset and limited neurological deficits, which can generally reach a peak within a few hours. In individual patients, the clinical symptoms are progressively aggravated by continued hemorrhage and hematoma expansion and last for 6-12 hours.
2. Except for small amount of cerebral hemorrhage, most patients have varying degrees of impaired consciousness. The degree of impaired consciousness is an important indicator to judge the severity of the disease and prognosis.
3.Headache and vomiting are the most common symptoms of cerebral hemorrhage, which can occur alone or in combination. Headache is the most severe in lobar and cerebellar hemorrhage, while a small amount of hemorrhage can be without headache. The simultaneous appearance of headache and vomiting is one of the indications of increased intracranial pressure.
4. Increased blood pressure is a common cause and co-morbidity of cerebral hemorrhage. The coexistence of increased blood pressure and slow heartbeat and pulse is often an important indication of high cranial pressure.
5. Seizures can occur in people with cerebral hemorrhage, and they are mostly focal and secondary to generalized seizures. Lobar hemorrhage and deep hemorrhage are most common.
Focal signs and symptoms.
Focal symptoms correlate with the site of the hematoma, but the accuracy of localization and diagnosis is not as good as the results of neuroimaging.
1. Shell nucleus hemorrhage.
It is the most common type of hypertensive cerebral hemorrhage. Most of them are caused by rupture of the lateral pulsatile artery. The hematoma may be confined to the nucleus accumbens itself, or may extend to involve the internal capsule, corona radiata, centrum semiovale, temporal lobe, or break into the ventricles. The typical clinical manifestations of a hematoma compressing the internal capsule inward are contralateral mild hemiparesis or hemiparesis, sensory disturbance, and hemianopia. The acute phase is accompanied by gaze of both eyes to the side of the hematoma, and aphasia may occur when located in the dominant hemisphere; non-dominant hemisphere may show loss of use and recognition, visual field neglect and structural loss.
2. Thalamic hemorrhage.
In thalamic hemorrhage, if the hemorrhage volume is large, different clinical syndromes appear according to the direction of hematoma expansion: outward expansion invading the internal capsule; inward breaking into the ventricles; downward invasion of the hypothalamus and dorsal aspect of the midbrain; and upward expansion invading the parietal white matter, and thus the respective corresponding symptoms and signs appear.
However, the common clinical manifestations in order of magnitude are.
Mild hemiparesis or hemiparesis, hemianesthesia, superior gaze palsy, pupillary abnormalities (pupil narrowing and loss of light reflex), aphasia, absence of disease sense, eye gaze to the side of the lesion (same as in case of shell nucleus hemorrhage), hemianopia and muteness. If the hematoma is less than 2 cm in diameter and confined to the thalamus itself, different clinical manifestations occur depending on the localization of the hematoma within the thalamus.
The different clinical manifestations depending on the localization of the hematoma within the thalamus are.
(1) Anterolateral type: mild prefrontal symptoms, mild sensory and motor deficits.
(2) Postero-lateral type: severe motor and sensory deficits, as well as pupillary constriction and superior gaze palsy, with a poor prognosis.
(3) Ortholateral type: Impaired consciousness in the acute phase, followed by prefrontal signs after the acute phase, such as reduced initiative and impaired attention and memory. (4) Dorsolateral type: manifesting as parieto-occipital signs, aphasia may appear in the dominant hemisphere, and graphic memory impairment may appear in the non-dominant hemisphere.
3. Caudate nucleus hemorrhage.
Hemorrhage in the caudate nucleus region, mostly seen in the head of the caudate nucleus, is very easy to break into the ventricles, so the most common clinical manifestations are acute onset of headache, vomiting, neck stiffness and other signs of meningeal irritation, accompanied by a certain degree of impaired consciousness and transient near-memory impairment, which is clinically difficult to distinguish from subarachnoid hemorrhage. In addition, transient contralateral gaze palsy, contralateral mild hemiparesis and transient hemianesthesia may also occur. Ipsilateral Horner’s syndrome is occasionally seen, and these symptoms are more common when the hemorrhage extends downward and outward. Occasionally, hemorrhage is seen to extend from the head of the caudate nucleus to the anterior thalamus, with prominent transient near-memory impairment.
4, Lobar hemorrhage (Lobar hemorrhage).
Lobar hemorrhage is a hemorrhage in the subcortical white matter. Unlike other types of cerebral hemorrhage, in addition to chronic hypertension as its main cause, the most common causes are cerebral amyloid angiopathy and arteriovenous malformations and other disorders. The clinical presentation of lobar hemorrhage is often indistinguishable from thromboembolic cerebral infarction. The neurological deficits in lobar hemorrhage vary depending on the site of hemorrhage.
(1) Frontal lobe hemorrhage: frontal lobe hemorrhage may present with forehead pain, more severe on the hematoma side, contralateral hemiparesis, bilateral eye gaze to the hematoma side, diaphoresis, impaired consciousness and epilepsy.
(2) Parietal hemorrhage: It can cause contralateral hemianopsia and contralateral visual field neglect, also contralateral isotropic hemianopia or quadrant blindness, mild hemiparesis and disease sense deficit.
(3) Temporal lobe hemorrhage: may cause contralateral 1/4 quadrant visual field loss. Predominantly anterior or peri-auricular headache on the side of the hematoma may occur, and occasionally agitated delirium may occur. Wernicke’s aphasia may result in the dominant hemisphere. Hematoma to the left temporal-parietal region may cause conductive aphasia or complete aphasia; non-dominant hemisphere hemorrhage may result in confusion and cognitive impairment.
(4) Occipital hemorrhage: pain in the orbital region ipsilateral to the hematoma and contralateral ipsilateral partial blindness, transient blackness and visual deformation, sometimes sensory loss and writing impairment, etc.
5. Cerebral bridge hemorrhage.
Cerebral bridge hemorrhage is the most frequent site of brainstem hemorrhage and is caused by rupture of the paramedian branch of the basilar artery. The clinical symptoms and signs of cerebral bridge hemorrhage vary greatly depending on the size and localization of the hematoma, whether it has broken into the ventricles or not, and whether there is hydrocephalus. A small amount of cerebral bridge hemorrhage has mild symptoms and is easily confused with lacunar infarction.