Clinical manifestations
1.Hypertensive cerebral hemorrhage
It usually occurs in 50-70 years old, slightly more in men, and is prone to occur in winter and spring, and usually develops during activity and emotional excitement.
Clinical symptoms often peak in a few minutes to a few hours. Clinical signs and symptoms vary depending on the site of the hemorrhage and the hemorrhage, and mild hemiparesis due to hemorrhage in the basal ganglia, thalamus and internal capsule is a common early symptom; epileptic seizures occur in about 10% of cases.
They are often focal; in severe cases, they rapidly turn into confusion or coma.
2. Common clinical types and characteristics
(1) Hemorrhage in the basal ganglia region: the nucleus accumbens and the thalamus are the two most common sites of hypertensive cerebral hemorrhage; they are separated by the posterior limb of the internal capsule, with inferior motor fibers, superior sensory fibers, and visual radiation penetrating them.
Compression of these fibers by a dilated hematoma in the lateral (nucleus accumbens) or medial (thalamus) side produces contralateral motor and sensory dysfunction, typically seen as triple hemiplegia (hemiparesis contralateral to the lesion.
The hemorrhage can also penetrate the brain tissue into the ventricles and produce bloody CSF, but direct penetration of the cortex is uncommon.
(1) Shell nucleus hemorrhage: mainly rupture of the lateral branch of the ductus arteriosus, which usually causes more severe motor deficits, persistent isotropic hemianopia, inability of both eyes to gaze to the opposite side of the lesion, and aphasia in the main hemisphere.
(2) Thalamic hemorrhage: caused by rupture of the thalamic geniculate artery and thalamic penetrating artery, producing transient isotropic hemianopia with more pronounced sensory deficits; the hemorrhagic foci compressing the cortical language center may produce aphasia.
Thalamic focal hemorrhage may present as an independent aphasia syndrome with a good prognosis. Thalamic hemorrhage is characterized by more equal paralysis of the upper and lower extremities, with more prominent deep sensory deficits; massive hemorrhage causes damage to the superior midbrain visual center and downward deviation of the eyes.
If the nasal tip is gazed at, the disturbance of consciousness is common and heavy, and if the hemorrhage reaches the lower thalamus or breaks into the third ventricle, the coma deepens and the pupils narrow.
If the hemorrhage involves both the nucleus accumbens and the thalamus, it is difficult to distinguish the starting site of the hemorrhage, which is called hemorrhage in the basal nucleus.
(3) Caudate nucleus head hemorrhage: less common, manifesting headache, vomiting and mild meningeal irritation signs, without obvious paralysis, rather like subarachnoid space hemorrhage, sometimes seen contralateral central facial tongue palsy, often easy to ignore clinically.
(2) Lobar hemorrhage: often caused by cerebral arteriovenous malformation, Moyamoya disease, vascular amyloidosis and tumor, etc. Headache, vomiting, aphasia, visual field abnormalities and meningeal irritation signs are often seen, and seizures are more common.
Coma is less common. Parietal hemorrhage is the most common and is seen as hemiplegia, spatial conformation disorder; frontal lobe is seen as hemiplegia, Broca’s aphasia, groping, etc.; temporal lobe is seen as Wernicke’s aphasia and psychiatric symptoms; occipital lobe appears as contralateral hemianopia.
(3) Cerebral bridge hemorrhage: mostly caused by the rupture of the cerebral bridge branch of the basilar artery, the hemorrhage foci are located between the base of the cerebral bridge and the periaqueductal part, with massive hemorrhage (hematoma >5ml) involving the cerebral bridge bilaterally.
It often breaks into the fourth ventricle or extends dorsally to the midbrain. The patient falls into coma within seconds to minutes, with tetraplegia and decortication tonic seizures; bilateral pinpoint pupils and fixation in the median position, vomiting of coffee-like gastric contents, and central hyperthermia are seen.
Central respiratory disturbances and eye floaters (downward jumping movements of both eyes at intervals of about 5 s), etc. Death usually occurs within 48 h. Small hemorrhages show crossed paralysis or ataxic mild hemiparesis, gaze paralysis of both eyes toward the side of the lesion or inter-nuclear eye muscle paralysis.
Midbrain hemorrhage is rare, with mild manifestations of one-sided or bilateral incomplete articulatory nerve paresis or Weber syndrome, and severe manifestations of deep coma, flaccid paralysis of the limbs, and rapid death; the diagnosis can be confirmed by CT.
(4) Cerebellar hemorrhage: caused by rupture of the cerebellar dentate nucleus artery, sudden onset, headache, vertigo, frequent vomiting, severe occipital headache and balance disorder within a few minutes, but no limb paralysis, clear consciousness at the beginning of the disease or mildly blurred consciousness.
In mild cases, one limb is clumsy, unstable, ataxic and nystagmus, and massive hemorrhage can lead to coma and brainstem compression signs within 12-24 h, such as peripheral facial nerve palsy, two eyes gazing at the opposite side of the lesion (compression of the visual center on the side of the brain bridge).
The pupils are narrowed while the light response exists, limb paresis and pathological reflexes; late pupil dilatation, central respiratory impairment, death may occur due to occipital foramen herniation, fulminant onset of immediate coma, which is not easily distinguished from cerebral bridge hemorrhage.
(5) Primary ventricular hemorrhage: accounting for 3% to 5% of cerebral hemorrhage, caused by ruptured intraventricular choroid plexus artery or subventricular artery hemorrhage, most cases are small amount of ventricular hemorrhage, visible headache, vomiting.
Meningeal irritation signs and bloody cerebrospinal fluid, no impairment of consciousness and focal neurological signs, cool subarachnoid space hemorrhage, complete recovery and good prognosis.
Massive ventricular hemorrhage has an acute onset and rapidly falls into coma, quad. Flaccid paralysis and decortical tonic seizures, frequent vomiting, pinpoint pupils, separated strabismus or floating eyes, etc. The condition is critical and death is mostly rapid.
Diagnosis
Since the introduction of CT, the clinical diagnosis of cerebral hemorrhage has not been difficult.
1.The main basis for diagnosis of cerebral hemorrhage
(1) Most of the patients are over 50 years old and have a long history of hypertensive arteriosclerosis.
(2) Sudden onset during physical activity or emotional excitement, with symptoms such as headache, vomiting, and impaired consciousness.
(3) The onset is rapid, with symptoms of limb dysfunction and increased intracranial pressure appearing within minutes or hours.
(4) There are neurological localization signs on physical examination.
(5) Brain CT scan examination: intracerebral hematoma is a high-density area, which can accurately show hematomas larger than 1,5 cm in diameter, and can determine the site of bleeding, the size of the hematoma, and whether it has broken into the ventricles.
It can determine the site of hemorrhage, the size of the hematoma, whether it has broken into the ventricle, whether there is cerebral edema and brain herniation, and the diagnosis is confirmed by the hemorrhagic lesion seen on CT scan of the brain.
(6) Blood cerebrospinal fluid can be seen by lumbar puncture, but nowadays, cerebral hemorrhage is rarely diagnosed based on cerebrospinal fluid.
2.Etiology diagnosis
For patients with cerebral hemorrhage not only. There is a diagnosis of cerebral hemorrhage, but also must find the cause for treatment and prevention. Most causes of cerebral hemorrhage are due to hypertensive atherosclerosis but there are many other uncommon causes that can cause cerebral hemorrhage, such as simple arteriosclerosis, arteriovenous malformation, blood disorders and activity status, defecation, emotional excitement, etc. In particular, the following etiologies should be considered comprehensively in young and middle-aged patients with onset under 50 years of age
(1) Rupture of small arteriovenous malformation or congenital aneurysm in the brain parenchyma. After rupture, a hematoma is formed and the malformed vessel or aneurysm disappears on its own, which is difficult to show even by cerebral angiography.
(2) Periarteritis nodosa, virus, rickettsial infection, etc. can cause arteritis, resulting in necrosis and rupture of the canal wall.
(3) Vitamin C and B deficiency, necrosis of the intima of small blood vessels in the brain, punctate hemorrhage may occur or fuse into hematoma.
(4) Blood diseases: such as leukemia, platelet deficiency purpura, hemophilia, etc.
(5) Cerebral hemorrhage may occur during anticoagulation therapy.
(6) Intracranial tumor hemorrhage: tumor can erode blood vessels causing cerebral hemorrhage, rupture and bleeding of neovascularization within the tumor.
(7) Amyloid angiopathy: mostly seen in the elderly, with recurrent and/or multiple lobar hemorrhages as the main clinical manifestation, with the frontal and parietal lobes of the cortex being the most obvious.
(8) Allergic reactions: can produce punctate hemorrhage in the brain.
(9) Dehydration, cerebral venous thrombosis due to sepsis and hyperemesis, etc., can sometimes cause cerebral hemorrhage.