Spontaneous intracranial hemorrhage
Cerebral hematomas. The most common cause of cerebral hemorrhage is hypertensive vascular damage. Prolonged hypertension results in arteriosclerosis and in the development of small microaneurysms, which predispose to vessel rupture, resulting in a hematoma. The common sites for hypertensive intracerebral hematoma are those supplied by fine perforating vessels (basal ganglia, internal capsule, thalamus, cerebellum and pons).
In patients over the age of 70 years, the cerebral hemorrhages may be caused by the presence of cerebral artery amyloid. This causes hematomas, seen in the periphery of cerebral hemispheres (lobar hemorrhages). Less common causes of a cerebral hematoma are bleeding into a tumour, rupture of vascular malformations, cerebral vasculitis, bleeding associated with disordered coagulation, and bleeding occurring in association with leukemias.
Macroscopically, hematomas appear as a large blood clot, causing compression and damage to adjacent brain. Large hematomas in the basal ganglia or thalamus often rupture into the ventricular system. If the patient survives a bleed, the hematoma is removed by phagocytic cells; astrocytic gliosis takes place, leaving a cavity stained yellow-brown with hemosiderin. Large bleeds that cause raised intracranial pressure, and those that rupture into the ventricular system, are usually fatal.
Subarachnoid hemorrhage is the bleeding into the subarachnoid space (between the arachnoid and the pia).
In most cases, the cause of subarachnoid bleeding is rupture of a berry aneurysm; less common causes are rupture of an intracerebral hematoma into the subarachnoid space or rupture of a vascular malformation.
Macroscopically a layer of blood is present over the brain surface in the subarachnoid space. Blood is
therefore present in the cerebrospinal fluid (CSF) and can be detected on lumbar puncture. There are two effects of subarachnoid hemorrhage: 1. Blood around vessels causes vascular spasm and leads to widespread cerebral ischemia and brain swelling. 2. There may be blockage of CSF resorption, causing acute hydrocephalus.
Outcome: about 30% of patients die immediately; others who present with headache and signs of meningeal irritation may have surgical intervention and clipping of the aneurysm. In the absence of operative intervention, 30% of patients have a re-bleed within one year, most within one month of their first bleed. A long-term complication is development of hydrocephalus caused by blockage and fibrosis in the CSF pathways.
Head injuries are divided into two types:
1. Non-missile trauma (closed head injury) is the result of acceleration or deceleration forces to the head.
2. Missile trauma (open head injury) is caused by penetration of the skull or brain by an external object such as a bullet.
Brain pathology from head injury may be primary (i.e. the immediate consequence of impact damage) or secondary (i.e. occurring later from brain swelling, bleeding and hypoxia).
There are two main patterns of primary brain damage in non-missile head injury, cerebral contusions and diffuse axonal injury.
Cerebral contusions occur when the brain moves within the cranial cavity, causing parts of the brain to be crushed by violent contact with the skull or dural membranes. For the most part, these occur adjacent to the site of impact (coup lesions) and diagonally opposite (contrecoup lesions). The most common sites for this pattern of damage are the underside of the frontal lobes, the tips and inferior aspects of the temporal lobes, the occipital poles, and the cerebellum. Early contusions appear as petechial hemorrhage into cortical grey matter and underlying white matter. Over a period of several hours there is oozing of blood, and contusions become hemorrhagic, with severe swelling of the brain. Severe contusions may be associated with extensive intracerebral, subarachnoid and subdural hemorrhage. Contusions heal by gliosis, which is associated with brown hemosiderin deposition (caused by associated hemorrhage).
Diffuse axonal injury is the result of shearing of axons due to acceleration or deceleration or torsional forces, leading to severe damage to white matter tracts. Patients with this pattern of damage who survive are generally severely disabled. Most of the changes are seen histologically only, consisting of axonal tearing visible as swellings of the torn ends of nerve fibres (axonal retraction balls). Petechial hemorrhages may
also occur in the corpus callosum and brain stem, and their detection at these sites is a useful indicator of this type of severe head injury.
Secondary brain damage occurs after the immediate impact. Head injury is often associated with widespread trauma, which leads to problems maintaining blood oxygenation and blood pressure. As a consequence, head injury is often complicated by the development of secondary hypoxic brain damage and cerebral edema.
There are four main types of cerebral hemorrhage: intracerebral hematoma, subarachnoid hemorrhage, subdural hemorrhage, and extradural hemorrhage.
Extradural hemorrhage causes hematoma in the potential extradural space between the skull and the dura and is almost always the result of skull fracture, which tears an artery or a main venous sinus running outside the dura. The vessel most commonly involved is the middle meningeal artery (associated with fracture of the temporal bone). The extradural hematoma appears as a gelatinous layer of blood clot outside the dura. This accumulation causes compression of the brain and development of transtentorial herniation. In many cases, high-pressure arterial blood accumulates rapidly, leading to an acute decline in conscious level with raised intracranial pressure. In other cases, blood accumulates over a period of hours and it is not uncommon to have a history of head trauma followed by gradual development of drowsiness, leading to coma and death.
Subdural hemorrhage results in a hematoma developing in the subdural space between the dura and the arachnoid. It is caused by traumatic tearing of venous vessels that traverse the subdural space. Two patterns exist.
1. Acute subdural hematomas are usually seen after a severe head injury and are associated with other types of brain injury. They cause rapid accumulation of blood, leading to acute neurological deterioration as a result of raised intracranial pressure.
2. Chronic subdural hematomas usually occur as a result of minimal trauma and are mainly seen in the very young (including childhood non-accidental injury) and the elderly. Blood typically accumulates slowly over a period of days or weeks, becoming localized by a membrane of fibrovascular granulation tissue. In addition to the osmotic effects of degenerating blood clot drawing in fluid from the CSF, increase in the size of the hematoma occurs with further bleeding. Clinical symptoms and signs may only become obvious weeks after an apparently trivial injury, as a result of raised intracranial pressure.
Macroscopically a subdural hematoma is seen as a layer of gelatinous blood clot (acute type) or as an organized layer of dark liquefied clot surrounded by membranes (chronic type), which flattens and compresses the underlying brain, staining the outside of the arachnoid with hemosiderin.
Excess CSF in the intracranial cavity is termed hydrocephalus. The term «hydrocephalus» is used to describe conditions in which there is increase in the CSF volume within the brain, with expansion of the cerebral ventricles. The most common type, which is termed non-communicating hydrocephalus or obstructive hydrocephalus, is caused by blockage of the CSF pathway from the ventricles to the subarachnoid space. A less common type is communicating hydrocephalus, in which there is impairment of resorption of CSF at the arachnoid villi along the dural venous sinuses, usually precipitated by previous infection or bleeding into the subarachnoid space.
Causes: congenital stenosis of the aqueduct, tumours, meningitis and subarachnoid hemorrhage.
Macroscopically, there is dilatation of the ventricular cavities of the brain proximal to the site of obstruction. The effects of hydrocephalus depend on the speed of development of disease and age of the patient.
In acute hydrocephalus, swelling of the brain may be rapid and may cause death due to cerebral herniation.
In chronic hydrocephalus, signs and symptoms develop slowly and there are clinical features of raised intracranial pressure. When hydrocephalus develops in children, before fusion of the skull bones, there is
progressive enlargement of the head circumference. In adults, in whom the skull is rigidly fused, prolonged disease causes thinning of the skull vault. In the absence of treatment, long-standing disease causes axonal damage and gliosis in the white matter. In children this leads to mental subnormality and in adults can lead to the development of a dementia syndrome, with gait disturbance and incontinence as prominent features.
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