EPIDURAL HEMATOMA Causative factor Laceration of middle cerebral artery or dural sinus lateral cerebral convexities Hours Classically,

lucid interval then coma, but more variable Pupillary dilation with contralateral then bilateral limb weakness; slowly evolving stupor then coma Children, young adults Acute bulging epidural clot bounded by cranial sutures; lenticular in shape Urgent evacuation

ACUTE SUBDURAL HEMATOMA Tearing of bridging pial veins and arteries

Typical location

Lateral cerebral convexities Many hours Drowsiness, coma Pupillary dilation with contralateral then bilateral limb weakness; progressive stupor then coma

Evolution Clinical profile

CHRONIC SUBDURAL HEMATOMA Trauma (may be absent or minimal) Risk factors: coagulopathy and severe brain atrophy Lateral cerebral convexities, may be bilateral Days to weeks Headache, progressive alteration in mental status focal neurologic signs

Age at risk Radiologic features

Any Acute blood rimming broad region of cerebral convexity Urgent evacuation if large enough to cause symptoms

Elderly Hyper- or isodense, unilateral or bilateral

Surgical intervention

Evacuation in some circumstances

Acute Epidural Hemorrhage As a rule, this arises with a temporal or parietal fracture and laceration of the middle meningeal artery or vein. Less often, there is a tear in a dural venous sinus. The injury, even when it fractures the skull, may not have produced coma initially, or it may be part P.758 . A few hours or a day later (exceptionally, with venous bleeding the interval may be several days or a week), headache of increasing severity develops, with vomiting, drowsiness, confusion, aphasia, seizures (which may be one-sided), hemiparesis with slightly increased tendon reflexes, and a Babinski sign. As coma develops, the hemiparesis may give way to bilateral spasticity of the limbs and Babinski signs. The pulse is often slow (below 60 beats per minute) and bounding, with a concomitant rise in systolic blood pressure (Cushing effect). The pupil may dilate on the side of the hematoma. Physicians need not be reminded that lumbar puncture is contraindicated in this setting, particularly now that CT and MRI are available. Death, which is almost invariable if the clot is not removed surgically, comes at the end of a comatose period and is due to respiratory arrest. The visualization of a fracture line across the groove of the middle meningeal artery and knowledge of which side of the head was struck (the clot is usually on that side) are of aid in diagnosis and lateralization of the lesion. However, meningeal vessels may occasionally be torn without fracture. The CT scan reveals a lens-shaped clot with a smooth inner margin (Fig.

35-8). The surgical procedure consists of placement of burr holes in an emergency situation or, preferably, a craniotomy, drainage of the hematoma, and identification and ligation of the bleeding vessel. The operative results are excellent except in cases with extended fractures and laceration of the dural venous sinuses, in which the epidural hematoma may be bilateral rather than unilateral. If coma, bilateral Babinski signs, spasticity, or decerebrate rigidity supervene before operation, it usually means that displacement of central structures and crushing of the midbrain have already occurred; prognosis is then poor. Small epidural hemorrhages, followed by serial CT scanning, will be seen to enlarge gradually for a week or two and then be absorbed. There is always controversy about removing these in a patient who has no symptoms; if the clot is small and there is careful surveillance, they can be left alone.

Acute and Chronic Subdural Hematomas The problems created by acute and chronic subdural hematomas are so different that they must be discussed separately. In acute subdural hematoma, which may be unilateral or bilateral, there may be a brief lucid interval between the blow to the head and the advent of coma. Or, more often, the patient is comatose from the time of the injury and the coma deepens progressively. Frequently the acute subdural hematoma is combined with epidural hemorrhage, cerebral contusion, or laceration. The clinical effects of these several lesions are difficult to distinguish; there are some patients in whom it is impossible to state before operation whether the clot is epidural or subdural in location. Subdural clots more than 5 mm thick can be accurately visualized by the CT scan in more than 90 percent of cases (Fig. 35-9). A large acute clot causes a pineal shift as well as marked compression of one lateral ventricle; but if the clots are bilateral, there may be no shift and the ventricles appear symmetrical. Acute, rapidly evolving subdural hematomas are due to tearing of bridging veins, and symptoms are caused by compression of the brain by an expanding clot of fresh blood. Unlike epidural arterial hemorrhage, which is steadily progressive, venous bleeding is usually arrested by the rising intracranial pressure. Exceptionally, the subdural hematoma forms in the posterior fossa and gives rise to headache, vomiting, pupillary inequality, dysphagia, cranial nerve palsies, and, rarely, stiff neck and ataxia of the trunk and gait if the patient is well enough to be tested for these functions. Because of their apposition to bone or their axial orientation along the tentorial dura, posterior fossa clots are more likely than clots over the cerebral convexities to be missed in CT scans. In chronic subdural hematoma, the traumatic etiology is often P.759 less clear. The head injury, especially in elderly persons and in those taking anticoagulant drugs, may have been trivial and may even have been forgotten. A period of weeks then follows when headaches (not invariable), light-headedness, slowness in thinking, apathy and drowsiness, unsteady gait, and occasionally a seizure or two are the main symptoms. The initial impression may be that the patient has a vascular lesion or brain tumor or is suffering from drug intoxication, a depressive illness, or Alzheimer disease. A gradual expansion of the hematoma is believed to cause the progression of symptoms. As with acute subdural hematoma, the disturbances of mentation and consciousness (drowsiness, inattentiveness, incoherence of

thinking, and confusion) are more prominent than focal or lateralizing signs, and they may fluctuate. The focal signs usually consist of hemiparesis and rarely of an aphasic disturbance. Homonymous hemianopia is seldom observed, probably because the geniculocalcarine pathway is deep and not easily compressed; similarly, hemiplegia, i.e., complete paralysis of one arm and leg, is usually indicative of a lesion within the cerebral hemisphere rather than a compressive lesion on its surface. An important feature of the hemiparesis from subdural hematoma, when it occurs, is that it may sometimes be ipsilateral to the clot, as a result of compression of the contralateral cerebral peduncle against the free edge of the tentorium by horizontal displacement of the midbrain (Kernohan-Woltman false localizing sign; see page 310). If the condition progresses, the patient becomes stuporous or comatose, but this course is often interrupted by striking fluctuations of awareness. With both large acute and chronic hematomas, dilatation of the ipsilateral pupil is a fairly reliable indicator of the side of the hematoma, though this sign may be misleading (occurring on the opposite side in 10 percent of cases, according to Pevehouse and coworkers). Convulsions are seen occasionally, most often in alcoholics or in patients with cerebral contusions, but they cannot be regarded as a cardinal sign of subdural hematoma. Rare cases of internuclear ophthalmoplegia and of chorea have been reported but have not occurred in our material. Presumably they are a result of distortion of deep structures. Also, transient disturbances of neurologic function simulating transient ischemic attacks (TIAs) may occur. In infants and children, enlargement of the head, vomiting, and convulsions are prominent manifestations of subdural hematoma. CT scanning with contrast infusion and MRI are the most reliable diagnostic procedures. On CT scans, the acute clot is initially hyperdense but becomes isodense after a period of time (Fig. 3510), during which it may be difficult to detect except by the tissue shifts it causes. It then becomes progressively hypodense (with respect to the cortex) over 2 to 6 weeks. The evolution of signal changes in the MRI is similar to the sequential imaging changes found with parenchymal hematomas. The acute clot is hypointense on T2-weighted images, reflecting the presence of deoxyhemoglobin. Over the subsequent weeks, all image sequences show it as hyperintense as a result of methemoglobin formation. Eventually the chronic clot again becomes hypointense on the T1-weighted images. With contrast infusion, both imaging procedures usually reveal the vascular and reactive border surrounding the clot. Usually, by the fourth week, sometimes later, the hematoma becomes hypodense, typical of a chronic subdural hygroma. Other formerly used investigative measures are seldom necessary but are mentioned here for completeness and in the event that the diagnosis is made in the course of evaluating some other neurologic problem. Skull films are helpful when there is calcification surrounding a chronic hematoma, a calcified pineal that is shifted to one side, or an unexpected fracture line is found. The EEG is usually abnormal bilaterally, sometimes with reduced voltage over the hematoma and high-voltage slow waves over the opposite side. In an arteriogram, the cortical branches of the middle cerebral artery are separated from the inner surface of the skull, and the anterior cerebral artery may be displaced contralaterally. The CSF may be clear and acellular but more often is bloody or xanthochromic depending on the presence or absence of recent or old contusions and subarachnoid hemorrhage; the pressure may be elevated or normal. A

xanthochromic fluid with relatively low protein content should always raise the suspicion of chronic subdural hematoma. The chronic subdural hematoma becomes gradually encysted by fibrous membranes (pseudomembranes) that grow from the dura. Some hematomasprobably those in which the initial bleeding was slight (see below)resorb spontaneously. Others expand slowly and act as space-occupying masses (Fig. 35-11). Gardner, in 1932, first postulated that the gradual enlargement of the hematoma was due to the accession of fluid, particularly CSF, which was drawn into the hemorrhagic cyst by its increasing osmotic tension as red blood cells (RBCs) hemolyzed and protein was liberated. This hypothesis, which came to be widely accepted, is not supported by the available data. Rabe and colleagues demonstrated that the breakdown of RBCs contributes little if at all to the accumulation of fluid in the subdural space. According to the latter authors, the most important factor in the accumulation of subdural fluid is a pathologic permeability of the developing capillaries in the outer pseudomembrane of the hematoma. The CSF plays no discernible role in this process, contrary to the original view of Munro and Merritt. In any event, as the hematoma enlarges, the compressive effects increase gradually. Severe cerebral compression and displacement with temporal lobetentorial herniation are the usual causes of death.
Why somewhat less than one-half of all subdural hematomas remain solid and nonenlarging and the remainder liquefy and then enlarge is not known. The experimental observations of Labadie and Glover suggest that the volume of the original clot is a critical factor: the larger its initial size, the more likely it will be to enlarge. An inflammatory reaction, triggered by the breakdown products of blood elements in the clot, appears to be an additional stimulus for growth as well as for neomembrane formation and its vascularization

Clinical Signs of Increased Intracranial Pressure A history of headache before the onset of coma, vomiting, severe hypertension beyond the patient's static level, unexplained bradycardia, and subhyaloid retinal hemorrhages are immediate clues to the presence of increased intracranial pressure, usually from one of the types of cerebral hemorrhage. Papilledema develops within 12 to 24 h in cases of brain trauma and hemorrhage, but if it is pronounced, it usually signifies brain tumor or abscessi.e., a lesion of longer duration. Increased intracranial pressure produces coma by impeding global cerebral blood flow; but this occurs only at extremely high levels of pressure. High pressure within one compartment produces shifts of central structures and a series of false localizing signs due to lateral displacements and herniations, as noted in the above discussion of herniation. The syndrome of acute hydrocephalus, most often from subarachnoid hemorrhage or from rapid obstruction of the ventricular system by a tumor in the posterior fossa, induces a state of abulia (page 359) followed by stupor and then coma with bilateral Babinski signs The pupils are small and tone in the legs is increased. These signs may be accompanied by headache and systemic hypertension. This subject is discussed further in Chap Hemisphere hemorhage A lesion in a cerebral hemisphere can usually be detected, even though the patient is comatose, by careful observation of the patient's spontaneous movements, responses to stimulation, prevailing postures, respiratory rate and rhythm, and by examination of the cranial nerves. A hemiplegia is revealed by a lack of restless movements of the limbs and by inadequate protective

movements in response to painful stimuli on only one side. The paralyzed limbs are usually slack; they tend to remain in passive positions and, if lifted from the bed, they fall flail. The hemiplegic leg lies in a position of external rotation (this may also be due to a fractured femur), and the affected thigh may appear wider and flatter than the nonhemiplegic one. In expiration, the cheek and lips puff out on the paralyzed side. With hemispheric lesions, the eyes are often turned away from the paralyzed side (toward the lesion, as described below); the opposite may occur with brainstem lesions. In most cases, a hemiplegia and an accompanying Babinski sign are indicative of a contralateral hemispheral lesion; but with lateral mass effect and compression of the opposite cerebral peduncle against the tentorium, extensor rigidity, a Babinski sign, and weakness of arm and leg may also occur ipsilateral to the lesion (the above described Kernohan-Woltman sign). A moan or grimace may be provoked by painful stimuli on one side but not on the other, reflecting the presence of a hemianesthesia; also during grimacing, facial weakness may be noted. Of the various indicators of brainstem function, the most useful are pupillary size and reactivity, ocular movements, oculovestibular reflexes, and, to a lesser extent, the pattern of breathing. These functions, like consciousness itself, are to a large extent dependent on the integrity of structures in the midbrain and rostral pons.