The normal intracranial pressure (ICP) is 60-120 mmH2O, which corresponds to 5-15 mmHg. An ICP greater than 30 mmHg impairs cerebral blood flow; an ICP greater than 50 mmHg for more than 30 minutes is fatal; an ICP greater than 80 mmHg for any length of time can cause brain damage. Intracranial hypertension may be either acute (developing in hours to days) or chronic (lasting for weeks or months). Its manifestations are progressively more severe as the ICP rises, but are not specific; thus, the diagnosis cannot be made from the signs of intracranial hypertension alone but requires either the demonstration of a causative lesion (e.g., subdural hematoma, encephalitis, brain tumor, hydrocephalus) or direct measurement ofthe intracranial pressure. Treatment is indicated when the ICP persistently exceeds 20 mmHg, when plateau waves are found, or when the pulse amplitude rises. Individual cases may manifest a variety of different signs of intracranial hypertension, either in slow or rapid alternation, or all at the same time. Compression of the brain stem by a space-occupying lesion (p. 118) has similar clinical manifestations; the diagnostic differentiation of brain stem compression from intracranial hypertension is critical. Lumbar puncture is contraindicated in cases of suspected or documented intracranial hypertension, as the resulting increase in the already high craniospinal pressure gradient may lead to brain herniation.
Headache due to intracranial hypertension ranges in intensity from mild to unbearable. Patients typically report a pressing, bifrontal headache that is most severe upon awakening in the morning or after naps in the daytime. It is exacerbated by lying flat, coughing, abdominal straining, or bending over, and ameliorated by sitting or standing. It may wake the patient from sleep. Often, both mild daytime headaches and more severe nighttime headaches are present. Nausea due to intracranial hypertension is often independent of movement of the head or of other abdominal complaints, and its intensity is not correlated with that of headache. It may be mild or severe.
Projectile vomiting may occur without warning or after a brief sensation of nausea upon sitting up or moving the head. Initially, vomiting mainly occurs suddenly, in the morning (on an empty stomach).
Eye movements and vision. Compression of CN III or VI causes paresis of extraocular muscles or pupillary dilatation (p. 92). Papilledema often affects the eye on the side of the causative lesion first, and then gradually the other eye as well. The older the patient, the less likely that papilledema will occur as a sign of intracranial hypertension; its absence thus cannot be taken as ruling out in-tracranial hypertension. Early papilledema is characterized by hyperemia, blurred papillary margins, dilated veins, loss of venous pulsations (may be absent normally), and small hemorrhages around the papilla. Full-blown papil-ledema is characterized by disk elevation, engorged veins, tortuous vessels around the papilla, and streaky hemorrhages. If intracranial hypertension persists, chronic papilledema willdevelop in weeks or months, characterized by grayish-white optic nerve atrophy and small vessel caliber. Acute papilledema generally does not affect the visual fields or visual acuity (unlike papillitis, which should be considered in the differential diagnosis); but physical exertion or head movement may cause transient amblyopic attacks lasting several seconds (foggy or blurred vision, or blindness). Chronic papilledema, on the other hand, can cause an impairment visual acuity, concentric visual field defects, and even blindness. Gait disturbances. An unsteady, slow, hesitant, gait with small steps and swaying from sided to side is sometimes seen.
Behavioral changes. Impairment of memory, attention, concentration, and planning ability, confusion, slowed reactions, and changes in personal habits are often observed by relatives and friends.
Mild disk elevation (0.5 diopters), ill-defined margins r\
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