PRINCIPLES OF NEUROLOGY - PART 8 pps

of the severity of intoxication. Their occurrence is not necessarily a pre- dictor for the development of alcohol addiction, as has commonly been assumed. Pathological intoxication (complicated intoxication, alcohol paranoid state, atypical intoxication) The boundaries of this syndrome have never been clearly drawn, as one might gather from its diverse designations. Well known are certain idiosyncratic reactions to alcohol, in which a few drinks predictably evoke behavioral abnormalities seemingly alien to the personality of the subject—argumentativeness, assaultiveness, acute paranoia, indiscriminate sexual advances, or crim- inality. All that can be said is that the disinhibitory effects of alcohol have exposed a latent sociopathic trait. More often the term pathological intoxication designates an outburst of blind fury with assaultive and destructive behavior, the patient being subdued only with difficulty and massive sedation; later the patient has no memory of the episode. This state needs to be distinguished from temporal lobe seizures and sociopathy, which occasionally take the form of explosive outbursts of rage and violence. A similar paradoxic reaction sometimes follows the administration of barbiturates. ABSTINENCE OR WITHDRAWAL SYNDROME This is a symptom complex consisting of tremulousness, hallucinations, seizures, confusion, and psychomotor and autonomic overactivity, which develop within several hours or days after an addictive drinker abstains from alcohol. The parts of the brain upon which alcohol acts and that come to tolerate increasing amounts of the drug appear to be disinhibited and become overactive when alcohol is withdrawn. Clinical Features These are depicted diagrammatically in Fig. 41-1. In effect, there are two syndromes: a minor and a major one. The minor or early syndrome is characterized by tremulousness, nausea and vomiting, insomnia, flushed facies, relatively mild diaphoresis, hallucinations (visual and auditory, rarely tactile and olfactory), and convulsive seizures; disorientation and confusion are minimal or absent altogether. These symptoms have their onset within 7 to 8 h after the cessation of drinking, reach their peak intensity within 24 h, and then subside over several days, usually without sequelae. Exceptionally, an alcohol withdrawal state that begins as an acute auditory hallucinosis fails to recede and settles into a quiet chronic delusional-hallucinatory psychosis, one that may be mistaken for paranoid schizophrenia. In a relatively small number of patients, the early symptoms of alcohol withdrawal (particularly withdrawal seizures) are a prelude to delirium tremens. CHAPTER 41 / ALCOHOL AND ALCOHOLISM 387 4777 Victor Ch 41 p385-392 6/11/01 2:16 PM Page 387 The major withdrawal syndrome, traditionally designated as delirium tremens (DTs), is characterized by profound confusion, gross tremor and myoclonus, delusions and hallucinations, and signs of autonomic nervous system overactivity (fever, tachycardia, dilated pupils, marked diaphoresis). These symptoms have their onset between 48 and 96 h (peak onset, 72 h) after the cessation of drinking. The major syndrome is much less frequent than the minor one but far more serious, ending fatally in approximately 5 percent of cases. Hyperthermia, cir- culatory collapse, infection, and serious injury are the conditions usually associated with a fatal outcome. Pathologic study of the brain in these cases has not disclosed any significant histologic abnormalities attributable to the delirium per se. Withdrawal Seizures (“Rum Fits”) Early in the withdrawal period (7 to 48 h after cessation), there is a marked tendency to convulsion, even in persons with no history or EEG evidence of epilepsy. Stated somewhat differently, alcohol withdrawal is an important cause of convulsive seizures occurring for the first time in adult life. 388 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC DISEASE FIG. 41-1 Relation of acute neurologic disturbances to cessation of drinking. The drinking period is greatly foreshortened and not intended to be quantitative. The periodic notching in the baseline represents the tremulousness, nausea, etc., that occur following a night’s sleep. The time relations of the various groups of symptoms to withdrawal are explained in the text. (From Victor and Adams, 1953.) 4777 Victor Ch 41 p385-392 6/11/01 2:16 PM Page 388 During the period of seizure activity, the EEG may be abnormal and the patient may be unusually sensitive to stroboscopic stimulation, but these abnormalities subside in a few days, even in patients who go on to develop DTs. (This sequence occurs in almost 30 percent of patients with withdrawal seizures.) As a rule, such seizures are grand mal in type; they may occur singly or, more often, there may be several seizures over a period of several hours; rarely, the seizures take the form of grand mal status epilepticus. A focal seizure occurring in this setting indicates the presence of a focal cerebral lesion (most often traumatic), in addition to the effects of alcohol withdrawal. In patients with idiopathic or posttraumatic epilepsy, seizures may be precipitated by a short period (one evening or a weekend) of drinking, but here also the seizures occur not when the patient is intoxicated but in the “sobering-up” period. Treatment of Alcohol Withdrawal Symptoms Minor withdrawal symptoms The main considerations are replace- ment of fluids and electrolytes and the judicious administration of sedative drugs. In depleted alcoholics, the use of parenteral glucose solutions carries a special danger, namely the precipitation of Wer- nicke disease, and should always be supplemented by B vitamins. A variety of sedative drugs are equally useful in allaying tremor, ner- vousness, and insomnia. In general, phenothiazine drugs should be avoided because they reduce the threshold to seizures. Chlordiazepox- ide (Librium), lorazepam (Ativan), and diazepam (Valium) are cur- rently the most popular for this purpose. Paraldehyde, for many years a favored drug, is no longer available. Delirium tremens Treatment of this condition is a more compelling matter than treatment of the minor withdrawal syndrome. It begins with a careful search for an associated injury or infection, particularly cerebral contusions, subdural hematoma, cervical spine injury, pneumonia, and meningitis. A chest film, CT scan or MRI of head and cervical spine, and liver function tests should be obtained routinely and a lumbar puncture performed if there is the slightest suspicion of meningitis. The cornerstones of treatment are the administration of fluids and correction of electrolyte abnormalities. Severe diaphoresis requires the administration of as much as 10 L of fluid daily, of which about one- quarter should be normal saline. The importance of adding B vitamins has been mentioned above. The amounts of glucose and electrolyte to be added are governed by the laboratory findings. Low Na concen- trations should be corrected with caution, for the reasons given in Chap. 39. In severe forms of DTs, vital signs need to be recorded frequently, in anticipation of shock and hyperthermia. Shock requires the urgent use CHAPTER 41 / ALCOHOL AND ALCOHOLISM 389 4777 Victor Ch 41 p385-392 6/11/01 2:16 PM Page 389 of fluids and vasopressor drugs, and hyperthermia requires the use of a cooling mattress in addition to the specific treatment of any infection that may be present. Drugs must be used circumspectly. The objective is not the absolute suppression of agitation and tremor, which could seriously depress respiration, but simply the blunting of symptoms to the point of facilitat- ing nursing care. Medication usually needs to be given parenterally— diazepam, 10 mg IV and repeated once or twice at 20- to 30-min intervals until the patient is calm but awake; or phenobarbital (120 mg) or haloperidal (1 to 2 mg) may be given at 3- to 4-h intervals. Propranolol and other beta-blocking agents may be useful, but corticosteroids have no place in the treatment of withdrawal symptoms. Withdrawal seizures In most cases, anticonvulsant drugs are not re- quired, since the seizures occupy only a brief circumscribed period in the early stages of withdrawal and often have ceased by the time the patient is seen by the physician. The parenteral administration of phenobarbital or chlordiazepoxide early in the withdrawal period might prevent seizures, but phenytoin is ineffective in this respect. Also, the long-term administration of anticonvulsants is impractical. If the patient remains abstinent, he will suffer no further seizures; if he resumes drinking, he usually abandons his medications. Status epilepticus due to alcohol withdrawal should be managed like status of any other cause. Focal seizures need to be investigated and managed along the lines indicated in Chap. 16. In patients with idiopathic or posttraumatic epilepsy, drinking is interdicted, and such patients need to be maintained on their anticonvulsant regimen. Nutritional Diseases of the Nervous System Secondary to Alcoholism These do not differ in any particular from nutritional diseases in which alcohol plays no part. They have been described in Chap. 40. Alcoholic Dementia (Alcoholic Deteriorated State) These terms are used to designate a supposedly distinctive form of dementia that is attributable to the long-standing toxic effects of alcohol on the brain. However, the clinical picture has been anything but clear, and the descriptions in current textbooks of psychiatry lack con- sistency. More important, no distinctive neuropathologic changes have ever been described. Such clinical changes as have been attributed to the toxic effects of alcohol are completely reversible. In our experience and that of others, most of the cases that come to autopsy with the label of alcoholic dementia or deteriorated state prove 390 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC DISEASE 4777 Victor Ch 41 p385-392 6/11/01 2:16 PM Page 390 to have the lesions of the Wernicke-Korsakoff syndrome. Traumatic lesions are commonly added, as are the lesions of hepatic or anoxic encephalopathy, normal pressure hydrocephalus, or a variety of diseases unrelated to alcoholism. Practically always, the clinical state can be accounted for by one or a combination of these diseases, and there has been no need to invoke a hypothetical toxic effect of alcohol on the brain. “Alcoholic Cerebral Atrophy” This disorder also does not constitute a clinicopathologic entity. The diagnosis is essentially a radiologic one: the lateral ventricles are enlarged and the sulci are widened. The clinical correlates of these findings are quite unpredictable. About 25 percent of patients with the Wer- nicke-Korsakoff syndrome show dilated lateral and third ventricles and widened sulci, but we have not been able to find a histopathologic basis for these abnormalities. In other alcoholics, the radiologic findings are not associated with any signs of neuropsychiatric disease. Moreover, in alcoholics who remain sober for a protracted period, the radiologic abnormalities are to a large extent reversible, suggesting that a shift of fluids occurred in the brain rather than a true loss of tissue (atrophy). Thus it would be more appropriate to refer to the asymptomatic ven- tricular enlargement and sulcal widening as such rather than as cerebral atrophy, at least until a consistent pathologic basis for this condition has been established. Fetal Alcohol Syndrome Infants born of severely alcoholic mothers who drink throughout pregnancy are often smaller than expected for the duration of pregnancy, are slightly microcephalic, and have short palpebral fissures, epicanthal folds, heart abnormalities, micrognathia, and at times cleft palate. At birth, such infants suck and sleep poorly and are irritable and hyperactive. Later in life, at school age, there are signs of psychomotor back- wardness and learning difficulty. Developmental anomalies have been found in the brain. Since alcohol readily crosses the placental barrier, it is generally assumed to be the factor that damages the brain. However, the possible toxic effects of acetaldehyde (a breakdown product in the metabolism of alcohol), opiates, smoking, or the contributory role of nutritional deficiency, have not been totally excluded. The condition is several times more frequent in blacks and Native Americans than in whites. It is doubtful that alcoholic fathers produce infants with this syndrome. A genetic predisposition has been suspected, but no clear hereditary pat- tern or offending gene has been identified. CHAPTER 41 / ALCOHOL AND ALCOHOLISM 391 4777 Victor Ch 41 p385-392 6/11/01 2:16 PM Page 391 Treatment of Alcohol Addiction Following recovery from the acute medical and neurologic complications of alcoholism, the underlying problem of alcohol dependency remains. To discharge the patient at this point and to leave him to his own devices practically assures that he will resume drinking, with a predictable recurrence of medical illness. At a minimum, the physician must inform the patient and his family of the medical and social conse- quences of continued drinking and of the fact that total abstinence represents the only permanent solution to the problem. To achieve these ends the patient must assume responsibility for his actions. The patient and family must be made aware of the many community resources that are available, including special clinics, “detoxification” centers, hospi- tal units, mental health clinics, and particularly Alcoholics Anony- mous—the informal fellowship of recovering alcoholics that has proved to be the single most effective force in the rehabilitation of alcoholic patients. For a more detailed discussion of this topic, see Adams, Victor, and Ropper: Principles of Neurology, 6th ed, pp 1166–1185. ADDITIONAL READING Goldstein DB: Pharmacology of Alcohol. New York, Oxford University, 1983. Grove WM, Cadoret RJ: Genetic factors in alcoholism, in Kissin B, Begleiter H (eds): The Biology of Alcoholism, vol 7: The Pathogenesis of Alcoholism. New York, Plenum, 1983, pp 31–56. Isbell H, Fraser HF, Wikler A, et al: An experimental study of etiology of “rum fits” and delirium tremens. Q J Stud Alcohol 16:1, 1955. Schenker S, Becker HC, Randall CL, et al: Fetal alcohol syndrome: Current status of pathogenesis. Alcoholism: Clinical and Experimental Research 14:635, 1990. Victor M: Neurologic disorders due to alcoholism and malnutrition, in Joynt RJ, Griggs RC (eds): Clinical Neurology. Philadelphia, Lippincott, 1986, chap 61. Victor M: Alcohol withdrawal seizures: An overview, in Porter RJ, Mattson RH, Cramer JA, Diamond I (eds): Alcohol and Seizures. Basic Mechanisms and Clinical Concepts. Philadelphia, Davis, 1990, pp 148–161. Victor M: Alcoholic dementia. Can J Neurol Sci 21:88, 1994. Victor M, Adams RD: The effect of alcohol on the nervous system. Res Publ Assoc Res Nerv Ment Dis 32:526, 1953. Victor M, Adams RD, Collins GH: The Wernicke-Korsakoff Syndrome and Other Disorders Due to Alcoholism and Malnutrition. Philadelphia, Davis, 1989. 392 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC DISEASE 4777 Victor Ch 41 p385-392 6/11/01 2:16 PM Page 392 42 Disorders of the Nervous System due to Drugs and Other Chemical Agents Drugs and other injurious or poisonous substances, customarily designated as toxins, exist in great number. Many of them affect the nervous system directly; some produce their effects secondarily through damage to other organs. The scope of neurotoxicology is vast, and obviously one cannot do justice to it in a few pages. The most that can be done here is to draw attention to the major categories of neurotoxic agents and the manner in which they affect the nervous system. OPIATES AND RELATED SYNTHETIC ANALGESICS Opiates refer to the naturally occurring alkaloids of opium; morphine and codeine are the ones used most often. Opioids designate all drugs with actions similar to those of opium: (1) chemical modifications of morphine or (2) purely synthetic analgesics. Compounds of the first group include diacetylmorphine or heroin (the most regularly abused opioid), hydromorphone (Dilaudid), hydrocodone (Hycodan), and oxycodone (Percodan). The best-known synthetic analgesics are meperidine (Demerol), methadone (Dolophine or Amidone), and pro- poxyphene (Darvon). All these drugs have been assigned a “controlled” status because of their highly addictive properties. Apart from analgesia, the opioids produce a sense of well-being, a state conventionally referred to as morphine euphoria or a “high.” For this reason, they are sought to allay boredom and misery. Once intro- duced to the drug, the victim discovers that euphoria is soon followed by dysphoric symptoms—faintness, nausea, and vomiting—which can be alleviated only by repeated self-administration of the drug. This is the genesis of addiction, and the need becomes so compelling that crimes will be committed to obtain the drug. Opioid poisoning, the result of a miscalculation of dosage or a suici- dal attempt, results in varying degrees of unresponsiveness, slow and shallow or periodic breathing, pinpoint pupils, bradycardia, and hypo- thermia. In the most advanced stage of coma, the pupils are dilated, the skin and mucous membranes are cyanotic, and circulation fails. Death results from respiratory depression and asphyxia. Survivors may show the effects of hypoxic encephalopathy. 393 4777 Victor Ch 42 p393-404 6/11/01 2:17 PM Page 393 Copyright 1998 The McGraw-Hill Companies, Inc. Click Here for Terms of Use. Treatment of opioid poisoning consists of gastric lavage if the intake was oral, maintenance of an adequate airway with a cuffed endotracheal tube, oxygenation, and the administration of naloxone (Narcan), the specific antidote to both opiates and synthetic analgesics. Naloxone is given IV in a dose of 0.01 mg/kg, repeated once or twice at 5-min intervals if necessary. If an adequate respiratory response is obtained, 1.0 mg of naloxone IM may then be given and repeated as needed. In cases of minor overdose, however, respiratory support is all that is necessary, thus avoiding the withdrawal reaction that may be precipitated by naloxone (see below). Addiction to opiates or opioids afflicts more than 600,000 people in the United Stated, half of them adolescents and young adults in New York City alone. It is characterized by a striking degree of tolerance to increasing doses and the development of typical symptoms and signs when the drug is withdrawn (abstinence syndrome). The latter appear within 8 to 16 h after the last dose of morphine (later with other opioids) and consist of yawning, rhinorrhea, sweating, lacrimation, diffuse pain, dilatation of pupils, waves of gooseflesh, muscle twitching, nausea and vomiting, diarrhea, insomnia, and an increase in temperature, respiratory rate, and blood pressure. These physical changes subside gradually over a period of 7 to 10 days but persist in mild form for several more weeks. The diagnosis of opiate addiction, if history is not available, should be suspected from needle marks on the skin and the finding of opiate derivatives in the urine and can be confirmed by the administration of naloxone (0.4 mg IV, repeated once if necessary), which induces some of the abstinence symptoms. Clonidine (5 mg/kg bid for a week) coun- teracts most of the noradrenergic withdrawal symptoms. An alternative method is to stabilize the patient on methadone for 3 to 5 days (10 to 20 mg bid orally) and then to withdraw the latter drug over a similar period. SEDATIVE-HYPNOTIC DRUGS There are three main groups: (1) barbiturates, bromides, and chloral hy- drate; (2) carbonic acid derivatives (meprobamate is the best known); and (3) the benzodiazepines, the most important of which are chlordiazepoxide (Librium), lorazepam (Ativan), and diazepam (Valium). Barbiturates Clinically, these drugs are now used very little. However, their non- medical and illicit uses are still important causes of suicide, accidental death, and addiction. Pentobarbital (Nembutal), secobarbital (Seconal), amobarbital (Amytal), thiopental (Pentothal), and phenobarbital (Lumi- nal) are the only barbiturates encountered with any regularity, and the first three are the ones most commonly abused. 394 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC DISEASE 4777 Victor Ch 42 p393-404 6/11/01 2:17 PM Page 394 Acute barbiturate coma Ingestion of 15 to 20 times the oral hypnotic dose of barbiturate induces coma, slow and shallow respiration, and flaccidity of the limbs with diminished or absent tendon reflexes; ocu- locephalic and oculovestibular reflexes are also muted; however, pu- pillary light and corneal reflexes are retained (unless asphyxia has occurred). In the early hours of coma, a phase of decerebrate rigidity with hyperactive tendon reflexes and Babinski signs may be present. The pupils become small in extreme overdoses. The diagnosis, if history is not available, is established by measurement of barbiturate levels in the blood or by urine toxicology. Treatment is directed along the lines indicated in Chap. 17—maintenance of respiration, prevention of atelectasis and infection, and, if coma is profound, hemodialysis. Chronic barbiturate intoxication This resembles alcohol intoxication, and the symptoms fluctuate with the time of self-administration of the drug. Withdrawal from the barbiturate is followed by insomnia, gener- alized convulsions, and a confusional state—symptoms similar to those of the alcohol withdrawal syndrome, including seizures. Anxiety states and depression, for which patients may have taken barbiturates, may be uncovered and require psychiatric treatment. Sometimes patients will have abused both alcohol and barbiturates or opioids and barbiturates. Meprobamate (Miltown) This drug is approved only for the treatment of anxiety but has been used widely as a nighttime sedative. Overdose causes hypotension, respiratory depression, and coma. Withdrawal symptoms are similar to those of barbiturates. Benzodiazepines These are among the most commonly prescribed drugs in the world. Chlordiazepoxide, lorazepam, alprazolam, diazepam, and related mem- bers of this group are particularly effective in the treatment of anxiety, insomnia, and (given parenterally) delirium, status epilepticus, and the muscle spasms of tetanus and the “stiff-man” syndrome. Flurazepam and triazolam are widely used in the management of insomnia (Chap. 19), and clonazepam, in the treatment of tremor and certain types of seizures (Chap 16). Midazolam (Versed) is used for conscious sedation before surgical and other procedures and for treatment of status epilepticus (Chap. 16). The advantages of the benzodiazepines are their relatively low hypnotic effects and low addictive potential and their minimal interactions with other drugs. Despite these attributes, the benzodiazepines are far from ideal. In large doses, they cause drowsiness, unsteadiness of gait, and at times, hypotension and syncope, confusion, and impairment of memory, especially in the elderly. Flumazenil partially reverses the effects of diazepines. Also, these drugs can be addictive, and when discontinued, they sometimes give rise to a withdrawal syndrome and seizures much like those due to barbiturates. CHAPTER 42 / DISORDERS DUE TO DRUGS AND OTHER AGENTS 395 4777 Victor Ch 42 p393-404 6/11/01 2:17 PM Page 395 ANTIPSYCHOSIS DRUGS This heterogeneous group of drugs, called neuroleptics, includes the phenothiazines, thioxanthines, butyrophenones, rauwolfia alkaloids, molindine, a dibenzoxazepine (loxapine), and the newer agents cloza- pine, olanzepine and risperidone. The phenothiazines are the most popular and are recognized by their trade names—Thorazine, Sparine, Compazine, Trilafon, Mellaril, Stelazine, and Prolixin. The most famil- iar of the butyrophenones is haloperidol (Haldol). All these drugs are in common use for the control of psychotic behavior in schizophrenia, manic-depressive disease, and confusional-agitated states that compli- cate other diseases of the brain (see Chap. 20). The side effects of the phenothiazines and butyrophenones are common and serious: parkinsonian syndrome, buccolingual and oromas- ticatory dystonia, akathisia, choreoathetosis, the so-called rabbit syndrome (repetitive pouting movements), and other dyskinesias. Some of the dyskinesias begin after the drug is discontinued (tardive dyskinesia). A severe and often fatal neuroleptic malignant syndrome (cata- tonic rigidity, stupor, unstable blood pressure, high fever, diaphoresis and other signs of autonomic dysfunction, and high creatine kinase levels) may also occur. Dantrolene and the dopamine agonist bromo- criptine have been used with some success (see Chap. 53). The antipsychosis drugs must be given with great caution because some of the side effects are worse than the disease for which they are given. One uses the lowest possible dose for the shortest time, interspersing chronic administration with vacation periods. Neuroleptic drugs must be discontinued as soon as the adverse effects are recognized. The parkinsonian syndrome usually resolves under the influence of anticholinergic drugs, but tardive dyskinesia may persist for months or years. The latter is unresponsive to drug therapy but tends to wane in time. Olanzepine and rispiridone have found special use because of their minimal extrapyramidal side effects. ANTIDEPRESSION DRUGS These are monoamine oxidase (MAO) inhibitors such as isocarboxizide (Marplan), tranylcypromine (Parnate), and phenelzine (Nardil); tri- cyclic dibenzazepine derivatives such as imipramine (Tofranil), desipramine (Norpramin), and amitriptyline (Elavil); the newer sero- tonin reuptake inhibitors such as fluoxetine (Prozac), sertraline (Zoloft), and paroxetine (Paxil); and lithium. The MAO inhibitors need to be dispensed cautiously and with constant awareness of their poten- tially serious side effects—restlessness and agitation, insomnia, anxiety, and occasionally muscle twitching, mania, and convulsions. Also, sympathomimetic amines and tyramine (in over-the-counter cold med- icines, cheeses, beer, and wine) may induce hypertension, cardiac arrhythmias, pulmonary edema, and even death. Either the serotoniner- 396 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC DISEASE 4777 Victor Ch 42 p393-404 6/11/01 2:17 PM Page 396 [...]... resultant tearing of spinal ligaments permits the dislocation of an upper vertebra anteriorly on the one below, often with fracture of the vertebral body or pedicles The spinal cord is liter405 Copyright 19 98 The McGraw-Hill Companies, Inc Click Here for Terms of Use 4777 Victor Ch 43 p40 5-4 14 406 6/11/01 2:19 PM Page 406 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC DISEASE ally crushed In cases of cervical... affect the nervous system adversely, often requiring discontinuation of the drug or modification in its usage This is also true for several antibiotic and immunosuppressant drugs Tables 4 2-2 and 4 2-3 summarize the most predictable of these complications For a more detailed discussion of this topic, see Adams, Victor, and Ropper: Principles of Neurology, 6th ed, pp 1 186 –1223 ADDITIONAL READING Brust JCM:... may be a saltatory progression of symptoms, probably due to thrombotic occlusions of parts of the malformation Arteriovenous angiomas tend to involve the posterior parts of the lower thoracic and upper lumbar segments or the anterior parts of the cervical enlargement The patients are often younger, and the sexes are equally affected The clinical syndrome may take the form of a slow spinal cord compression,... by the exclusion of other spinal cord diseases The main differential diagnostic considerations are demyelinative disease and subacute combined degeneration and there is a superficial resembance to amyotrophic lateral sclerosis 4777 Victor Ch 43 p40 5-4 14 4 08 6/11/01 2:19 PM Page 4 08 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC DISEASE In the early stages of the disease, the use of a soft collar may be... epidemic of cocaine use; in the United States, an estimated 7 to 8 million people use the drug regularly Cocaine induces a state of well-being, euphoria, restlessness, and loquacity Psychologic dependence or habituation—i.e., an inability to abstain from frequent compulsive use (“craving”)—develops readily 4777 Victor Ch 42 p39 3-4 04 3 98 6/11/01 2:17 PM Page 3 98 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC... Neurol 8: 361, 1 980 Herrick M, Mills PE Jr: Infarction of spinal cord Arch Neurol 24:2 28, 1971 Petito CK, Navia BA, Cho ES, et al: Vacuolar myelopathy pathologically resembling subacute combined degeneration in patients with AIDS New Engl J Med 312:374, 1 985 4777 Victor Ch 43 p40 5-4 14 414 6/11/01 2:19 PM Page 414 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC DISEASE Rossier AB, Foo D, Shillito J: Post-traumatic... discussion of this topic, see Adams, Victor, and Ropper: Principles of Neurology, 6th ed, pp 12 78 1301 ADDITIONAL READING Aminoff MJ: Electrodiagnosis in Clinical Neurology, 3rd ed New York, Churchill Livingstone, 1992 Asbury AK, Thomas PK (eds): Peripheral Nerve Disorders 2nd ed Boston, Butterworth-Heinemann, 1995 Brown WF, Bolton CF (eds): Clinical Electromyography, 2nd ed Boston, Butterworth-Heinemann,... intoxication), the most important of the heavy-metal poisonings, will be described here; the pathogenic properties of the others are summarized in Table 4 2-1 Restrictions of space preclude consideration of the toxic effects of other heavy metals (iron, antimony, zinc, silver, gold, platinum, etc.), certain nonmetallic elements (phosphorus), and industrial toxins (see suggested reading at end of chapter) Lead poisoning... Pharmacological Basis of Therapeutics, 9th ed New York, McGraw-Hill, 1996 Hollister LE: Clinical Pharmacology of Psychotherapeutic Drugs, 3rd ed New York, Churchill Livingstone, 1990 Johnson MV, MacDonald RL, Young AB (eds): Principles of Drug Therapy in Neurology Philadelphia, Davis, 1992 Klaassen CD (ed): Casarett and Doull’s Toxicology: The Basic Science of Poisons, 5th ed New York, McGraw-Hill, 1995 LeQuesne... cavitation of the spinal cord, predominantly cervical, and often of undetermined cause Rarely, it is associated with spinal cord tumor (especially 4777 Victor Ch 43 p40 5-4 14 412 6/11/01 2:19 PM Page 412 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC DISEASE hemangioblastoma) or occurs as a late complication of spinal cord trauma Clinically, syringomyelia is distinguished by segmental weakness and atrophy of . cause of convulsive seizures occurring for the first time in adult life. 388 PART IV / THE MAJOR CATEGORIES OF NEUROLOGIC DISEASE FIG. 4 1-1 Relation of acute neurologic disturbances to cessation of drinking Tables 4 2-2 and 4 2-3 summarize the most predictable of these complications. For a more detailed discussion of this topic, see Adams, Victor, and Ropper: Principles of Neurology, 6th ed, pp 1 186 –1223. ADDITIONAL. force in the rehabilitation of alcoholic patients. For a more detailed discussion of this topic, see Adams, Victor, and Ropper: Principles of Neurology, 6th ed, pp 1166–1 185 . ADDITIONAL READING Goldstein

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