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herniation syndrome with downward displacement and bilateral compression of the upper brainstem and the other a unilateral displacement of the medial temporal lobe, including the uncal gyrus, into the tentorial opening Both are types of transtentorial herniation According to these authors, the central syndrome takes the form of a rostral-caudal deterioration of function: there is rst confusion, apathy, and drowsiness and often Cheyne-Stokes respiration (CSR); following this, the pupils become small and react very little to light; doll s-head (oculocephalic) eye movements are still elicitable, as are deviations of the eyes in response to cold-water caloric testing Bilateral Babinski signs can be detected early; later, grasp re exes and decorticate postures appear These signs give way to a downward gradient of brainstem signs coma, central hyperventilation, medium-sized xed pupils, bilateral decerebrate postures, loss of oculovestibular (caloric) responses, slow, irregular breathing, and death The uncal syndrome, considered to be the result of herniation of the medial temporal lobe into the tentorial opening, differs mainly in that drowsiness in the early stages is accompanied or preceded by unilateral pupillary dilatation, most often on the side of the mass, as a result of compression of the third nerve by the advancing uncal gyrus Our own experience does not fully accord with this distinction between the two syndromes, and seldom have we been able to follow such an orderly sequence of neural dysfunction from the diencephalic to the medullary level With lateral shift and uncal herniation, one sometimes observes smallness of the pupils, rather than ipsilateral pupillary dilatation, as drowsiness develops Or, infrequently, the contralateral pupil may dilate before the ipsilateral one Nor is it clear that the dilatation of one pupil is always due to compression of the oculomotor nerve by the herniated uncus, as traditionally taught As often in pathologic material, the third nerve is stretched and angulated over the clivus or compressed under the.

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Creasing of contralateral cerebral peduncle (Kernohan s notch) Lateral attening of midbrain and zones of necrosis and secondary hemorrhages in tegmentum and base of subthalamus, midbrain, and upper pons (Duret hemorrhages)

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The correlation between volatility and the underlying risk to the portfolio is not an issue that can be xed to a point or statistical guideline Common market thinking suggests that as volatility increases on one or more positions in the portfolio, the entire portfolio is at additional risk This is not necessarily true in all cases The risk is dependant on the investment objectives of the portfolio and the current contents of the portfolio Some investments do well in up trending volatility, while others will increase in risk signi cantly If the portfolio has a signi cant percentage of assets like options that have exposure to volatility, then the assets may have to be adjusted or compensated for so that the increased volatility can be neutralized It is important to understand the current trading objectives and risk tolerance of the portfolio in order to create strategies to adjust for volatility If the portfolio is set up for a time-based objective, say a retirement portfolio for a middle-aged person, then short-term

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Strangulation of nerve between herniating tissue and medial petroclinoid ligament; stretching of nerve over clivus from lateral displacement of midbrain; entrapment of nerve between posterior cerebral and superior cerebellar arteries from downward displacement of midbrain Pressure of laterally displaced midbrain against sharp edge of tentorium Crushing of midbrain between herniating temporal lobe and opposite leaf of tentorium and vascular occlusion (hemorrhages around arterioles and veins)

TABLE 1-4

Unilateral or bilateral infarction (hemorrhagic) of occipital lobes Rising intracranial pressure and hydrocephalus

Compression of posterior cerebral artery against the tentorium by herniating temporal lobe Lateral attening of aqueduct and third ventricle and blockage of perimesencephalic subarachnoid space

Hemiplegia ipsilateral to herniation ( false localizing sign) and bilateral corticospinal tract signs Cheyne-Stokes respirations; stupor-coma; bipyramidal signs; decerebration; dilated, xed pupils and alterations of gaze (facilitated oculocephalic re ex movement giving way to loss of all response to head movement and labyrinthine stimulation) Usually none detectable during coma; hemianopia (unilateral or bilateral) with recovery Increasing coma, rising blood pressure, bradycardia

descended posterior cerebral artery Involvement of the third nerve nucleus or its bers of exit may be responsible for the dilatation of the opposite pupil, the usual occurrence after the pupil on the side of the mass has become xed (Ropper 1990) In our serial study of 12 patients with brain edema and lateral diencephalic-mesencephalic shifts due to hemispheral infarcts, 4 patients initially had no ipsilateral pupillary enlargement; in 1 patient, the pupillary enlargement was contralateral; in 3 patients, the pupils were symmetrical when drowsiness gave way to stupor or coma (Ropper and Shafran) Cyclic Cheyne-Stokes breathing was an early sign of deterioration In one patient, the rst motor sign was an ipsilateral decerebrate rigidity rather than decorticate posturing; most of the patients had bilateral Babinski signs by the time they became stuporous Indeed, the appearance of a Babinski sign on the nonhemiparetic side has been one of the best sentinels of secondary brain tissue shift These signs usually progressed to deep coma and decerebration within hours, and they uctuated From our observations of computed tomography (CT) and magnetic resonance imaging (MRI) scans obtained soon after the onset of coma, we have favored a mechanism of predominantly lateral displacement that causes compression of subthalamic and mesencephalic structures This is often, but not invariably associated with temporal lobe herniation The resulting neural dysfunction of deep structures is probably due to ischemia Moreover, the early disturbances of consciousness (drowsiness and stupor) dependably follow the degree of lateral displacement of high brainstem and subthalamic structures (judged by shifts in the position of midline structures such as the pineal body and, with less accuracy, the septum pellucidum), all of which can occur in the absence of transtentorial herniation, which arises later The important elements of secondary compression of the upper brainstem, in fact,

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