basal ganglia hemorrhage

Introduction

Introduction The putamen and thalamus are the two most common sites of hypertensive intracerebral hemorrhage. Typical signs of trigeminal signs (contralateral hemiplegia, partial sensation of eccentricity and hemianopia, etc.), a large number of bleeding may appear disturbance of consciousness, but also can break through the brain tissue into the brain, bloody CSF, direct penetration of the cortex is not common. Other causes include cerebral atherosclerosis, hematological diseases (leukemia, aplastic anemia, thrombocytopenic purpura, hemophilia, cytomegalovirus and sickle cell disease), as well as cerebral amyloid angiopathy, aneurysms , arteriovenous malformation, Moyamoya disease, cerebral arteritis, dural sinus thrombosis, dissecting aneurysm, primary or metastatic tumor, post-infarction cerebral hemorrhage, anticoagulation or thrombolytic therapy.

Cause

Cause

Hypertensive cerebral hemorrhage is the most common cause of non-traumatic intracranial hemorrhage. It is caused by hypertension with cerebral arteriolar disease and sudden increase in blood pressure. Other causes include cerebral atherosclerosis, hematological diseases (leukemia, aplastic anemia, thrombocytopenic purpura, hemophilia, cytomegalovirus and sickle cell disease), as well as cerebral amyloid angiopathy, aneurysms , arteriovenous malformation, Moyamoya disease, cerebral arteritis, dural sinus thrombosis, dissecting aneurysm, primary or metastatic tumor, post-infarction cerebral hemorrhage, anticoagulation or thrombolytic therapy.

Examine

an examination

Related inspection

Magnetic resonance imaging (MRI) CT examination

1, CT examination

CT examination is the first choice for clinical suspected cerebral hemorrhage. It can show a round or oval uniform high-density hematoma. The boundary is clear, and the location, size and shape of the hematoma can be determined, and whether it breaks into the ventricle, the edema around the hematoma and the mass effect. Etc.; a large amount of blood in the ventricle can be seen in high-density casts, and the ventricles expand. After 1 week, a ring-shaped enhancement was observed around the hematoma, and the hematoma became low-density or cystic after absorption. Progressive cerebral hemorrhage can be found by CT dynamic observation.

2, MRI examination

It can be found that CT can not determine the small amount of brainstem or cerebellar hemorrhage, can distinguish the cerebral hemorrhage that can not be recognized by CT after 4-5 weeks, distinguishing old cerebral hemorrhage and cerebral infarction, showing vascular malformation. The bleeding time can be judged according to the dynamic change of the hematoma signal (affected by the change of red blood protein in the hematoma).

1 hyperacute phase (0-2h): hematoma is a high signal of T1 and T2, which is not easy to distinguish from cerebral infarction.

2 acute phase (2-48h): signal such as T1 and low signal of T2.

3 subacute phase (3d-3w): Both T1 and T2 showed high signals.

4 chronic phase (>3w): T1 low signal, T2 high signal.

3. Digital subtraction angiography (DSA)

Brain aneurysms, cerebral arteriovenous malformations, Moyamoya disease and vasculitis were detected.

Diagnosis

Differential diagnosis

Cerebral hemorrhage: refers to the rupture of blood vessels in the brain parenchyma causing bleeding. Hypertension and arteriosclerosis are the main factors of cerebral hemorrhage, and can also be caused by congenital cerebral aneurysms, cerebrovascular malformations, brain tumors, blood diseases, infections, drugs, trauma and poisoning. Awareness of consciousness. Headache is the focus of the lesion side; vomiting is more common, mostly jetting, vomit is the contents of the stomach, most of them are brown, and hiccups are quite common. Go to cerebral rigidity and convulsions. The patient generally breathes faster, and the severely ill person breathes deep and slow. When the condition deteriorates, it turns fast and irregular, or it is tidal breathing, sigh-like breathing, double inhalation, and the like. High blood pressure is not stable. High fever after bleeding. Meningeal irritation.

Thalamic hemorrhage: Obstructive hydrocephalus is prone to occur after breaking into the ventricles. Thalamic hemorrhage caused obstructive hydrocephalus, the patient was comatose at the time of onset, relieved after conservative treatment of internal medicine, obstruction was relieved, and consciousness was restored. Coma at the time of onset leads to death. The amount of thalamic hemorrhage broke into the ventricles, and there were 23 cases with more than 15ml, indicating that the greater the amount of bleeding, the greater the possibility of breaking into the ventricles.

Bridge cerebral hemorrhage: about 10% of cerebral hemorrhage, mostly caused by rupture of the pons of the basilar artery. Clinical manifestations include sudden headache, vomiting, dizziness, diplopia, different axes of the eye, side palsy, cross sputum or hemiplegia, quadriplegia. When the amount of bleeding is small, the patient's consciousness can be expressed as some typical syndromes, such as foville syndrome, millard-gubler syndrome, atresia syndrome, etc., may be accompanied by high fever, sweating, stress ulcers, acute pulmonary edema, Acute myocardial ischemia and even myocardial infarction. When a large amount of hemorrhage occurs, the hematoma spreads to both sides of the pons and the covered part of the pons. The patient quickly enters a coma. The bilateral pupils are needle-like, side-viewing paralysis, quadriplegia, difficulty breathing, and have a brain-strength attack. They can also vomit brown stomach contents. There are midline symptoms such as central hyperthermia, often dying within 48 hours.

Cerebellar hemorrhage: refers to bleeding in the parenchyma of the cerebellum, which is directly related to hypertension. Most of the sudden onset of symptoms of dizziness, frequent vomiting, occipital headache, one side of the upper and lower limbs ataxia without obvious paralysis, may have nystagmus, one side of the facial paralysis. A small number of subacute progressive, similar to cerebellar space-occupying lesions. Severe massive hemorrhage showed rapid progressive intracranial pressure and soon entered a coma. More than 48 hours, the pillow was smashed and died.

Brain stem bleeding: mostly occurs in the pons. CT showed a mass, round or elliptical high-density shadow; CT value was 40-80HU; single or multiple (mostly single); the lesion edge was clear. If the amount of bleeding is large, the brain stem can be thickened, the density is increased, and the bridge pool and the ring pool are narrowed or disappeared. It can also break into the fourth ventricle and back up, causing the third ventricle and the midbrain aqueduct to change into a ventricle. , volume expansion, forward breakthrough, there may be blood in the bridge pool, ring pool, saddle upper pool. When a small amount of bleeding, attention should be paid to the identification of the volumetric effect of the posterior cranial fossa.

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