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indicates that the corresponding corticospinal pathway is intact With massive destruction of a cerebral hemisphere, as occurs in hypertensive hemorrhage or internal carotid middle cerebral artery occlusion, focal seizures are seldom seen on the paralyzed side, however, seizure activity may be manifest solely in the ipsilateral limbs, the contralateral limbs being prevented from participating by the hemiplegia Often, elaborate forms of semivoluntary movement are present on the good side in patients with extensive disease in one hemisphere; they probably represent some type of disequilibrium or disinhibition of cortical and subcortical movement patterns De nite choreic, athetotic, or hemiballistic movements indicate a disorder of the basal ganglionic and subthalamic structures, just as they do in the alert patient Posturing in the Comatose Patient One of these abnormal postures is decerebrate rigidity, which in its fully developed form consists of opisthotonos, clenching of the jaws, and stiff extension of the limbs, with internal rotation of the arms and plantar exion of the feet (see Chap 3) This postural pattern was rst described by Sherrington, who produced it in cats and monkeys by transecting the brainstem at the intercollicular level The decerebrate pattern was noted to be ipsilateral to a one-sided lesion, hence not due to involvement of the corticospinal tracts Such a precise correlation is rarely possible in patients who develop stereotyped extensor posturing since it arises in a variety of settings with midbrain compression due to a hemispheral mass; with cerebellar or other posterior fossa lesions; with certain metabolic disorders, such as anoxia and hypoglycemia; and rarely with hepatic coma and profound intoxication Patients with an acute lesion of one cerebral hemisphere may show a similar type of extensor posturing of the contralateral and sometimes ipsilateral limbs, and this may coexist with the ability to make purposeful movements of the same limbs Extensor postures, unilateral or bilateral, may seemingly occur spontaneously, but more often they are in response to manipulation of the limbs or a tactile or noxious stimulus Another pattern is the extensor posturing of arm and leg on one side and exion and abduction of the opposite arm This reaction is analogous to the tonic re exes described by Magnus in decerebrate animals In some patients with the foregoing postural changes the lesions are clearly in the cerebral white matter or basal ganglia, which is dif cult to reconcile with the classic physiologic explanation of decerebrate posturing; presumably there is a functional derangement of structures in the midbrain Decerebrate posturing, either in experimental preparations or in humans, is usually not a persistent steady state but an intermittent and transient one Hence the term decerebrate state, as suggested by Feldman, is preferable to decerebrate rigidity, which implies a xed, tonic extensor attitude Decorticate rigidity, with arm or arms in exion and adduction and leg(s) extended, signi es lesions at a higher level in the cerebral white matter or internal capsule and thalamus Bilateral decorticate rigidity is essentially a bilateral spastic hemiplegia Diagonal postures, eg, exion of one arm and extension of the opposite arm and leg, usually indicate a supratentorial lesion Forceful extensor postures of the arms and weak exor responses of the legs are probably due to lesions at about the level of the vestibular nuclei Lesions below this level lead to accidity and abolition of all postures and movements The coma is then usually profound and often progresses to brain death Only in the most advanced forms of intoxication and metabolic coma, as might occur with anoxic necrosis of neurons throughout the entire brain, are coughing, swallowing, hiccoughing, and spontaneous respiration all abolished Further, the tendon.

As indicated above, PSVER is especially valuable in proving the existence of active or residual disease of an optic nerve Examinations of large numbers of patients who were known to have had retrobulbar (optic) neuritis has shown that only a small proportion will have normal latencies Furthermore, similar abnormalities of PSVER are found in about one-third of multiple sclerosis patients who have no history or clinical evidence of optic nerve involvement This acquires signi cance in that the nding of abnormal PSVER in a patient with a clinically apparent lesion elsewhere in the CNS may usually be taken as evidence of multiple sclerosis A compressive lesion of an optic nerve will have the same effect as a demyelinative one Many other diseases of the optic nerves including toxic and nutritional amblyopias, ischemic optic neuropathy, and the Leber type of hereditary optic neuropathy show abnormalities of the PSVER Glaucoma and other diseases involving structures anterior to the retinal ganglion cells may also produce increased latencies Impaired visual acuity has little effect on the latency but does correlate well with the amplitude of the PSVER (a property that is exploited in computerized testing for visual acuity) By presenting the pattern-shift stimulus to one hem-

i eld, it is sometimes possible to isolate a lesion to an optic tract or radiation, or one occipital lobe, but with less precision than that provided by the usual monocular test Brainstem Auditory Evoked Potentials The effects of auditory stimuli can be studied in the same way as visual ones by a procedure called brainstem auditory evoked responses or potentials (BAERs or BAEPs) Between 1000 and 2000 clicks, delivered rst to one ear and then to the other, are recorded through scalp electrodes and maximized by computer A series of seven waves appears at the scalp within 10 ms after each stimulus On the basis of depth recordings and the study of lesions produced in cats as well as pathologic studies of the brainstem in humans, it has been determined that each of the rst ve waves is generated by the brainstem structures indicated in Fig 2-5 The generators of waves VI and VII are uncertain Clinical interpretations of BAERs are based mainly on latency measurements of waves I, III, and V The most important are the interwave latencies between I and III and III and V (see Table 2-4) The presence of wave I and its absolute latency are of particular value in testing the integrity of the auditory nerve A lesion that affects one of the relay stations or its immediate

The second wizard available in the Settings area, the Condition Wizard, has only four steps The first step is to set the condition type either Ranked List Criterion, Threshold Value Condition, or Mixed Condition These condition types cover most of the common filters required by business users and can be very useful to focus the business users attention on the critical list of values Table 1-5 provides the description and functionality of each setting As in the Exception Wizard, depending on the setting in this step, other information will change For example, Step 2, Set Condition Parameter, will change to fit the requirements The following illustration shows Step 1 of the Condition Wizard, with Ranked List Criterion being chosen The second illustration shows Step 2, with the condition set to the top 10 based on incoming orders

II Cochlear nuclei (pons)

V Inferior colliculus (midbrain)

VI Medal geniculate( )

VII Auditory radiations( )

1:

Figure 2-5 Short-latency brainstem auditory evoked responses (BAERs) Diagram of the proposed electrophysiologic-anatomic correlations in human subjects Waves I through V are the ones measured in clinical practice

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