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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 uctuate 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, ie, 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 uctuations 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 35-10), during which it may be dif cult 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, re ecting 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 T1weighted 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 lms are helpful when there is calci cation surrounding a chronic hematoma, a calci ed pineal that is.

Figure 35-10 Subacute subdural hematoma on the left (reader s right) CT scans after administration of intravenous contrast material The lesion is isodense to the adjacent brain tissue, but its margin can be appreciated with contrast enhancement Note displacement of cerebral structures

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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 uid with relatively low protein content should always raise the suspicion of chronic subdural hematoma The chronic subdural hematoma becomes gradually encysted by brous membranes (pseudomembranes) that grow from the dura Some hematomas probably 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, rst postulated that the gradual enlargement of the hematoma was due to the accession of uid, 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 uid in the subdural space According to the latter authors, the most important factor in the accumulation of subdural uid 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 lobe tentorial herniation are the usual causes of death.

This command should create a new MBR on the boot drive Be aware that using it can produce unexpected results and cause unrecoverable damage, and that FDISK/ MBR may not work if you have used the manufacturer s tools to partition the hard drive As a last resort, use the drive manufacturer s program to completely initialize the drive You can usually find this on their website If the problem persists, it could be a hardware problem That is, the BIOS might not be able to communicate with the boot drive itself If this is the case, use the hardware troubleshooting procedures discussed in 3

index, the write could invalidate the column values if that new value falls outside the high and low boundaries for the column Storage indexes are memory structures that are built the first time a Smart Scan query hits the storage region If a cell has to be rebooted, the storage index for that cell has to be rebuilt Whether a column s storage index values have been invalidated or the entire storage index is gone, the new values are calculated whenever a Smart Scan query accesses data in the storage region Successive Smart Scan queries also refine the values kept for a storage region by only tracking for those columns whose high and low values allow for effective selectivity for the storage region Because of the potential for invalidation or destruction, you should think of a storage index as an evolving entity You don t have to do anything to aid in the periodic recovery of the storage index or its values the natural operation of Smart Scans will take care of this for you You can see how much value a storage index is providing by looking for the

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