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In yet another group of "myoclonic dementias," the most prominent associated abnormality is a progressive deterioration of intellect. Like the myoclonic epilepsies, the myoclonic dementias may be sporadic or familial and may affect both children and adults. Another type, familial in nature and affecting infants and young children, has been described by Ford, who called it progressive poliodystrophy. On a background of normal birth and development over the first few months or years of life, there occurs a progressive psychomotor deterioration, with spastic quadriplegia, seizures, myoclonus, and blindness. The fundamental pathologic alteration is a destruction of nerve cells in the cerebral and cerebellar cortices with replacement gliosis. Intention or Action (Postanoxic) Myoclonus this type of myoclonus was described by Lance and Adams in 1963 in a group of patients who were recovering from hypoxic encephalopathy. When the patient is relaxed, the limb and other skeletal muscles are quiet (except in the most severe cases); only seldom does the myoclonus appear during slow, smooth (ramp) movements. Only the limb that is moving is involved; hence it is a localized, stimulusevoked myoclonus. Speech may be affected; it is fragmented by the myoclonic jerks, and a syllable or word may be almost compulsively repeated, as in palilalia. Lance and Adams found the irregular discharges to be transmitted via the corticospinal tracts, preceded in some cases by a discharge from the motor cortex. Hallett and colleagues found that a cortical reflex mechanism was operative in some cases and a reticular reflex mechanism in others. Several clinical trials and case reports have suggested that the ex- perimental drug piracetam, and, more persuasively, the anticonvulsant levetiracetam may be useful (Krauss et al). The use of 5hydroxytryptophan alone or in combination with tryptophan or other drugs has been recommended in the past (van Woert et al). Usually, a combination of several of these medications is required to make the patient functional. Spinal or Segmental Myoclonus (See also page 1066) the notion that monophasic restricted myoclonus always emanates from the cerebral cortex, cerebellum, or brainstem cannot be sustained, for there are forms that are traceable to a purely spinal lesion. A subacute spinal myoclonus of obscure origin was described many years ago by Campbell and Garland, and similar cases continue to be cited in the literature. We have seen several such cases where myoclonus was isolated to the musculature of the abdominal or thoracic wall on one side or to the legs; only rarely were we able to establish a cause, and the spinal fluid has been normal. It takes the form of an almost continuous arrhythmic jerking of a group of muscles. This form has been referred to as "propriospinal," particularly when it involves repetitive flexion or extension myoclonus of the torso that is aggravated by stretching or action. A sharply demarcated segmental myoclonus has been induced in animals by the Newcastle disease virus, and examples of myelitis with irregular segmental myoclonic jerks (either rhythmic or arrhythmic) have been reported in humans. In our experience, this type of myelitic myoclonus has occurred following zoster myelitis, postinfectious transverse myelitis, and rarely with multiple sclerosis, epidural compression, or after spinal traumatic injury. When highly ionic contrast media were used for myelography, painful spasms and myoclonus sometimes occurred in segments where the dye was concentrated by a block.

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These drugs are thought to cause neuropathy by their action as inhibitors of the depolymerization of tubulin, thereby promoting excessive microtubule assembly within the axon. The neuropathy is dose-dependent, occurring with doses greater than 200 mg/m2 of paclitaxel and at a wide range of dose levels for docetaxel (generally over this enzymatic inhibitor of protein synthesis is used in the treatment of acute lymphoblastic leukemia. They may occur within a day of onset of treatment and clear quickly when the drug is withdrawn, or they may be delayed in onset, in which case they persist for several weeks. These abnormalities are at least in part attributable to the systemic metabolic derangements induced by L-asparaginase, including liver dysfunction. In recent years, increasing attention has been drawn to cerebrovascular complications of L-asparaginase therapy, including ischemic and hemorrhagic infarction and cerebral venous and dural sinus thrombosis. These cerebrovascular complications are attributable to transient deficiencies in plasma proteins that are important in coagulation and fibrinolysis. A small proportion of patients receiving this drug develop dizziness, cerebellar ataxia of the trunk and the extremities, dysarthria, and nystagmus- symptoms that are much the same as those produced by cytarabine (Ara-C; see below). These abnormalities must be distinguished from metastatic involvement of the cerebellum and paraneoplastic cerebellar degeneration. The drug effects are usually mild and subside within 1 to 6 weeks after discontinuation of therapy. Cytarabine (Ara-C) this drug, long used in the treatment of acute nonlymphocytic leukemia, is not neurotoxic when given in the usual systemic daily doses of 100 to 200 mg/m2. The administration of very high doses (up to 30 times the usual dose) has been shown to induce remissions in patients refractory to conventional treatments. It also may produce, however, a severe degree of cerebellar degeneration in a considerable proportion of cases (4 of 24 reported by Winkelman and Hines). Ataxia of gait and limbs, dysarthria, and nystagmus develop as early as 5 to 7 days after the beginning of high-dose treatment and worsen rapidly. Postmortem examination has disclosed a diffuse degeneration of Purkinje cells, most marked in the depths of the folia, as well as a patchy degeneration of other elements of the cerebellar cortex. Other patients receiving high-dose Ara-C have developed a mild, reversible cerebellar syndrome with the same clinical features. Patients more than 50 years of age are said to be far more likely to develop cerebellar degeneration than those younger than 50; therefore the former should be treated with a lower dosage (Herzig et al). Very rarely, probably as an idiosyncratic response to the drug, intrathecal administration results in an acute paraplegia that may be permanent. The full-blown syndrome consists of the insidious evolution of dementia, pseudobulbar palsy, ataxia, focal cerebral cortical deficits, or paraplegia. Milder cases show only radiographic evidence of a change in signal intensity in the posterior cerebral white matter ("posterior leukoencephalopathy") that is similar to the imaging findings that follow cyclosporine use (see further on) and hypertensive encephalopathy (see. The present authors have the impression that the severe necrotic lesions possess features comparable to (and therefore maybe the result of) the coagulative necrosis of radiation encephalopathy. Tremor is perhaps the most frequent side effect, particularly of tacrolimus, and myoclonus may be added.

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Symptoms may begin 1 to 3 days following the first dose and affect the feet and hands simultaneously. The neuropathy is axonal in type, with secondary demyelination, and is at least partially reversible after discontinuation of the drug. Compare to the similar conditions of hypertensive encephalopathy and toxemia shown in. It has also proved to be especially effective in the treatment of oligodendrogliomas. Neural complications are infrequent and usually take the form of somnolence, confusion, agitation, and depression. Diffuse aching pain in proximal muscles of the limbs and mild symptoms and signs of polyneuropathy occur in 10 to 15 percent of patients treated with relatively high doses. Procarbazine, taken in conjunction with phenothiazines, barbiturates, narcotics, or alcohol, may produce serious degrees of oversedation. This toxic manifestation appears to be related to the total amount of drug administered, and it usually improves slowly after it has been discontinued. Approximately one-third of patients receiving this drug also experience tinnitus or high-frequency hearing loss or both. Seizures associated with drug-induced hyponatremia and hypomagnesemia have been reported. Paclitaxel and Docetaxel Taxol (paclitaxel) and Taxotere (docetaxel) are newer anticancer drugs derived from the bark of the western yew. Both are particularly useful in the treatment of ovarian and breast cancer, but they have a wide range of antineoplastic activities. Seizures may be a manifestation of toxicity, but the cause may lie with the other complications of organ transplantation and immunosuppression. As already noted, a posterior leukoencephalopathy syndrome resembling hypertensive encephalopathy- headache, vomiting, confusion, seizures, and visual loss (cortical blindness)-may follow the use of either drug (see Table 43-1). Interferon treatment for malignant melanoma and a number of other chemotherapeutic agents have been associated with the same condition. Hinchey and colleagues have described several such cases and suggested that cyclosporin alters the blood-brain barrier and that the fluid overload and hypertension which accompanies the use of cyclosporin underlies the radiologic changes. A variety of psychotic syndromes with delusions, paranoia, and visual hallucinations have also been ascribed to the use of these drugs (see Wijdicks). A dose-dependent sensory neuropathy is the limiting factor in its use, and serial electrophysiologic testing is recommended if the medication is to be prescribed for protracted periods. Antibiotics and Other Medications Numerous antibiotics, cardioactive medications, and other drugs may have adverse effects on the central or peripheral nervous system. Here we mention mainly that penicillin and its derivatives such as imipenem, and to a lesser degree, cephalosporins are capable of causing seizures when high serum concentrations are attained. During the 1960s, more than 10,000 cases of this disease were collected in Japan by Tsubaki et al.

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The relation of this syndrome to acquired aphasia with convulsive disorder in children, described by Landau and Kleffner, is unsettled. As described in the review by Taylor and colleagues, visual hallucinations, while not invariable, are the most common clinical feature; sensations of movements of the eyes, tinnitus, or vertigo are also reported in cases of occipital epilepsy. These authors point out symptomatic causes of the syndrome, such as cortical heterotopias. In both of these types of childhood epilepsy, the observation that spikes are greatly accentuated by sleep is a useful diagnostic aid. Infantile Spasms (West Syndrome) this is the term applied to a particular form of epilepsy of infancy and early childhood. West, in the mid-nineteenth century, described the condition in his son in exquisite detail. This seizure disorder, which in most cases appears during the first year of life, is characterized by recurrent, single or brief episodes of gross flexion movements of the trunk and limbs and, less frequently, by extension movements (hence the alternative terms infantile spasms or salaam or jackknife seizures). However, this pattern, referred to originally by Gibbs and Gibbs as hypsarrhythmia ("mountainous" dysrhythmia), is not specific for infantile spasms, being frequently associated with other developmental or acquired abnormalities of the brain. As the child matures, the seizures diminish; they usually disappear by the fourth to fifth year. However, most patients, even those who were apparently normal when the seizures appeared, are left mentally impaired. Infantile spasms may also be part of the Lennox-Gastaut syndrome, a seizure disorder of early childhood of grave prognosis (see page 274). When patients with both types are lumped together under the rubric of febrile convulsions, it is not surprising that a high percentage are complicated by atypical petit mal, atonic, and astatic spells followed by tonic seizures, mental retardation, and partial complex epilepsy. Falconer, who studied psychomotor seizures in adults, noted retrospectively a high incidence of "febrile seizures" during the infancy and childhood in his cohort of surgical subjects. The present authors believe that he was referring to complicated febrile seizures, i. In a later study of 67 patients with proven medial temporal lobe epilepsy (French et al), 70 percent had a history of complicated febrile seizures during the first 5 years of life, although many did not develop temporal lobe epilepsy until their teens. Bacterial meningitis was another important risk factor; head and birth trauma were less common factors. All of the patients had complex partial seizures and half of them, in addition, had secondarily generalized tonic-clonic seizures. Annegers and colleagues observed a cohort of 687 children for an average of 18 years after their initial febrile convulsion. Overall, these children had a fivefold excess of unprovoked seizures in later life. By contrast, children with what Annegers et al called complex febrile convulsions (focal, prolonged, or repeated episodes of febrile seizures) had a greatly increased risk- 8, 17, or 49 percent, depending on the association of one, two, or three of the complicating features. Reflex Epilepsy For a long time it has been known that seizures could be evoked in certain epileptic individuals by a discrete physiologic or psychologic stimulus. Forster has classified these seizures in accordance with their evocative stimuli into five types: (1) visual- flickering light, visual patterns, and specific colors (especially red), leading to rapid blinking or eye closure; (2) auditory- sudden unexpected noise (startle), specific sounds, musical themes, and voices; (3) somatosensory- either a brisk unexpected tap or sudden movement after sitting or lying still, or a prolonged tactile or thermal stimulus to a certain part of the body; (4) writing or reading of words or numbers; and (5) eating.

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Formerly, society accepted this state in responsible individuals and prescribed the obvious cure- a vacation. Even Charcot made time for regular "cures" during the year, in which he retired to a spa without family, colleagues, or the drain of work. Nowadays, the need to contain this type of stress, to which some individuals are more prone than others, has spawned a small industry of meditation, yoga, and similar "therapies. A common error in diagnosis, however, is to ascribe fatigue to overwork when actually it is a manifestation of a neurosis or depression, as described below. It may be difficult to decide whether the fatigue is a primary manifestation of the disease or secondary to a lack of interest. Among chronically fatigued individuals without medical disease, not all deviate enough from normal to justify the diagnosis of neurosis or depression. Many persons, because of circumstances beyond their control, have little or no purpose in life and much idle time. Such circumstances are conducive to fatigue, just as the opposite, a strong emotion or a new enterprise that excites optimism and enthusiasm, will dispel fatigue. As mentioned, one must be aware of striking individual differences in energy potential. Some persons are born low in impulse and energy and become more so at times of stress; they have a lifelong inability to play games vigorously, to compete successfully, to work hard without exhaustion, to withstand illness or recover quickly from it, or to assume a dominant role in a social group- a "constitutional asthenia" (Kahn). Fatigue with Medical Disease Myopathic Fatigue Not unexpectedly, fatigue and intolerance of exercise (i. Even in a disease such as myasthenia gravis, the muscles exhibiting fatigue are usually weak even in the resting state. The classes of myopathic disease in which weakness, inability to sustain effort, and excessive fatigue are notable features include the following: the muscular dystrophies, congenital myopathies, disorders of neuromuscular transmission (myasthenia gravis, Lambert-Eaton syndrome), toxic myopathies. One type of glycogen storage disease- McArdle phosphorylase deficiency- is exceptional in that fatigue and weakness are accompanied by pain and sometimes by cramps and contracture. The first contractions after rest are of near normal strength, but after 20 to 30 contractions, there occurs a deep ache and an increasing firmness and shortening of the contracting muscles. The characteristics of these diseases are presented in the chapters on muscle disease. Another such process- acid maltase deficiency- is at times associated with disproportionate weakness and fatigue of respiratory muscles, which leads to dyspnea and retention of carbon dioxide. Fatigue in Neurologic Diseases Fatigue of varying degree is a regular feature of all diseases that are marked by denervation of muscle and loss of muscle fiber. Fatigue in these cases is due to the excessive work imposed on the intact muscle fibers (overwork fatigue).

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A patient who has also ingested alcohol may be comatose with relatively low blood barbiturate concentrations. Contrariwise, the barbiturate addict may show only mild signs of intoxication with very high blood barbiturate concentrations. In more severe intoxication, the fast waves become less regular and interspersed with 3- to 4-per-second slow activity; in still more advanced cases, there are short periods of suppression of all activity, separated by bursts of slow (delta) waves of variable frequency. Management In mild or moderate intoxication, recovery is the rule and special treatment is not required except to prevent aspiration. If the patient is unresponsive, special measures must be taken to maintain respiration and prevent infection. Any risk of respiratory depression or underventilation requires the use of a positive-pressure respirator. Hemodialysis or hemofiltration with charcoal may be used in comatose patients who have ingested long-acting barbiturates and these treatments are particularly advisable if anuria or uremia has developed. Occasionally, in the case of a barbiturate addict who has taken an overdose of the drug, recovery from coma is followed by the development of abstinence symptoms, as described later. Barbiturate Addiction (Chronic Barbiturate Intoxication) Chronic barbiturate intoxication, like other drug addictions, tends to develop on a background of some psychiatric disorder, most commonly a depressive illness with symptoms of anxiety and insomnia. Alcoholics find that barbiturates effectively relieve their nervousness and tremor. As with other drug addictions, the incidence of barbiturism is particularly high in individuals with ready access to drugs, such as physicians, pharmacists, and nurses. The easy availability through the internet of medications that contain barbituates may increase dependence on these drugs (Romero et al). The manifestations of barbiturism are much the same as those of alcohol intoxication. The barbiturate addict thinks slowly, exhibits increased emotional lability, and becomes untidy in dress and personal habits. The neurologic signs include dysarthria, nystagmus, and cerebellar incoordination. If the dosage is elevated rapidly, the signs of moderate or severe intoxication, as described earlier, become manifest. A characteristic feature of chronic barbiturate intoxication is the development of a striking degree of tolerance. Barbiturate Abstinence, or Withdrawal, Syndrome Immediately following withdrawal, the patient seemingly improves over a period of 8 to 12 h, as the symptoms of intoxication diminish. Then a new group of symptoms develops, consisting of nervousness, tremor, insomnia, postural hypotension, and weakness.

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This is difficult to understand, since a majority of the cochlear-superior olivary-lateral lemniscal-medial geniculate fibers cross to the opposite side. It is also surprising that a severe lesion of one relay station would allow impulses, even though delayed, to continue their ascent and be recordable in the cerebral cortex. The impulses generated in large touch fibers by 500 or more stimuli and averaged by computer can be traced through the peripheral nerves, spinal roots, and posterior columns to the nuclei of Burdach and Goll in the lower medulla, through the medial lemniscus to the contralateral thalamus, and thence to the sensory cortex of the parietal lobe. The normal waveforms are designated by the symbols P (positive) and N (negative), with a number indicating the interval of time in milliseconds from stimulus to recording. The corresponding cortical wave after tibial or peroneal nerve stimulation is called N/P 37. Recordings with pathologically verified lesions at these levels are to be found in the monograph by Chiappa. The central counterpart also pertains- namely, that obliteration of the cortical waves (assuming that all preceding waves are unaltered) reflects profound damage to the somatosensory pathways in the hemisphere or to the cortex itself. As corollaries, the bilateral absence of cortical somatosensory waves after cardiac arrest is a powerful predictor of a poor clinical outcome; the persistent absence of a cortical potential after stroke usually indicates such profound damage that only a limited clinical recovery is to be expected. Evoked potential techniques have also been used in the experimental study of olfactory sensation (see Chap. Transcranial Motor Cortex Stimulation It is now possible, by using single-pulse high-voltage magnetic stimulation, to directly activate the motor cortex and cervical spine segments and to detect delays or lack of conduction in descending motor pathways. This technique, introduced by Marsden and associates, painlessly stimulates only the largest motor neurons (presumably Betz cells) and the fastest-conducting axons. Berardelli and colleagues, who have applied the technique to 20 hemiplegic patients with cerebrovascular lesions, found that in 15 there was no descending influence in comparison with the normal side. Although the degree of functional deficit does not correlate with the degree of electrophysiologic change, one expects that refinements of this technique will be useful in evaluating the status of the corticospinal motor system as well as other cortically based functions. Endogenous Event-Related Evoked Potentials Among the very late brain electrical potentials ( 100-ms latency), which can be extracted from background activity by computer methods, are a group that cannot be classified as sensory or motor but rather as psychophysical responses to environmental stimuli. These responses are of very low voltage, often fleeting and inconsistent, and of unknown anatomic origin. The most studied types occur approximately 300 ms (P 300) after an attentive subject identifies an unexpected or novel stimulus that has been inserted into a regular train of stimuli.

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If the patient is unobservant or imprecise in his descriptions, a helpful tactic is to provoke a number of dissimilar sensations by rotating him rapidly, irrigating his ears with warm and cold water, and then asking him to stoop for a minute and straighten up; having him stand relaxed for 3 min and checking his blood pressure for orthostatic effect; and particularly, having him hyperventilate for 3 min. Should the patient be unable to distinguish among these several types of induced dizziness or to ascertain the similarity of one of the types to his own condition, the history is probably too inaccurate for purposes of diagnosis. At the other end of the scale are attacks of such abruptness and severity as to virtually throw the patient to the ground. On the other hand, a dizzy sensation that is not made worse markedly by vigorous shaking of the head is unlikely to relate to vertigo. All but the mildest forms of vertigo are accompanied by some degree of nausea, vomiting, pallor, perspiration, and some difficulty with walking. The patient may simply be disinclined to walk or may walk unsteadily and veer to one side, or he may be unable to walk at all if the vertigo is intense. One common form of vertigo, benign positional vertigo (see further on), occurs only with the repositioning that accompanies lying down, sitting up, or turning. The source of the gait ataxia associated with vertigo (vertiginous ataxia) is recognized by the patient as being "in the head," not in the control of the legs and trunk. It is noteworthy that the coordination of individual movements of the limbs is not impaired in these circumstances- a point of difference from most instances of cerebellar disease. Loss of consciousness as part of a vertiginous attack nearly always signifies another type of disorder (seizure or faint). Pseudovertigo To be distinguished from true vertigo are symptoms of giddiness and other types of pseudovertigo. The patient, who may complain only of dizziness, will, on closer questioning, describe his symptoms as a feeling of swaying, light-headedness, a swimming sensation, or, less often, a feeling of uncertainty or imbalance, "walking on air," faintness, or some other unnatural sensation in the head. These sensory experiences are particularly common in states characterized by anxiety or panic attacks- namely, anxiety neurosis, hysteria, and depression. They are in part reproduced by hyperventilation, and then it may be appreciated that varying degrees of apprehension, palpitation, breathlessness, trembling, and sweating are concurrent. This constellation of nonvertiginous symptoms has been loosely referred to as "phobic," "functional," and " psychogenic" vertigo. He relates the disorder to anxiety and panic spells but finds that it exists more often as an independent entity that is subject to improvement after careful explanation and reassurance. We agree with Furman and Jacobs that the term psychiatric dizziness, if used at all, should be restricted to dizziness that occurs as part of a recognized psychiatric syndrome, notably anxiety disorder.


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