Adams and Victor's Principles of Neurology / Edition 7

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You know it as the masterwork in its field. . . and now,you can own the newest,most up-to-date version of this classic text: Adams and Victor's PRINCIPLES OF NEUROLOGY,7th Edition. This remarkable volume now incorporates the latest findings in the growing areas of neurology even as it retains its authority,comprehensive scope,and popular,easy-use format.

Approaches neurologic disease just as you would approach the patient!

Adams and Victor's PRINCIPLES OF NEUROLOGY,7th Edition,begins with a detailed exposition of the symptoms and signs of disordered nervous function,just as you would begin with symptoms as presented by a patient. The text logically proceeds to syndromes and then to a description of all the main categories and types of disease that express themselves by each syndrome.

The book contains black-and-white illustrations.

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Editorial Reviews

From The Critics
Reviewer: Charles C Wang, MD, MS (University of Illinois at Chicago College of Medicine)
Description: This book covers the most updated knowledge in clinical neurology. The new edition continues its elegant written style. The principles of neurology are extensively illustrated in this book from basic neurosciences to pathophysiology and clinical aspects.
Purpose: The purpose is to provide information that is essential not only to the practice of neurology and neurosugery, but also to the practice of internal medicine, pediatrics, and psychiatry. The authors' purpose is clearly achieved.
Audience: The audience includes neurologists, neurosurgeons, internists, pediatricians, psychiatrists, emergency and intensive care physicians, primary care physicians, neuropathologists, and orthopedists at all levels from attending physicians to resident physicians. The authors are highly credible authorities in this field.
Features: This book covers broad aspects of clinical neurology necessary fro clinical practice. The organization is unique, starting from patient approach, cardinal manifestations of neurological disease, to specific neruological diseases. New develpments in neurology, such as molecular neurology and genetics, are incorporated in this edition. The inherited metabolic, congenital, developmental, and psychiatric disorders are largely emphasized.
Assessment: This edition inherits the tradition of elegant writing from its previous editions and expands on the information presented. The authors are highly respected authorities in the field, although Dr. Adams is no longer the official author. This book is still the "bible" of neurology.

4 Stars! from Doody
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Product Details

  • ISBN-13: 9780071163330
  • Publisher: McGraw-Hill Medical Publishing Division
  • Publication date: 1/1/2001
  • Edition description: 7TH
  • Edition number: 7
  • Pages: 1692
  • Product dimensions: 8.50 (w) x 11.00 (h) x 0.01 (d)

Meet the Author

Maurice Victor, M. D., Professor of Medicine and Neurology, Dartmouth Medical School, Hanover, New Hampshire, Distinguished Physician of the Veterans Administration, White River Junction, Vermont

Allan H. Ropper, M.D., Professor and Chairman of Neurology, Tufts University School of Medicine, Chief, Neurology Service, St. Elizabeth's Medical Center, Boston, Massachusetts

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Read an Excerpt

Part II: Cardinal Manifestations of Neurologic Disease

Complex auditory hallucinations may occur as part of temporal-lobe seizures, arising from a variety of temporal-lobe lesions. Conversely, seizures may be induced by musical sounds as well as by other auditory stimuli. These topics are discussed in Chaps. 16 and 22. Paracusis, a condition in which a sound, tune, or voice is repeated for several seconds, is also a cerebral auditory phenomenon similar in a sense to the visual phenomenon of palinopsia. The precise anatomy is unknown.

Causes of Middle Ear Deafness

The common causes are otosclerosis, otitis media, and trauma. Of the various types of progressive conductive deafness, otosclerosis is the most frequent, being the cause of about half the cases of bilateral (but not necessarily symmetrical) deafness that have their onset in early adult life (usually in the second or third decade). Otosclerosis is transmitted as an autosomal dominant trait with variable penetrance; pathologically, it is characterized by an overgrowth of labyrinthine capsular bone around the oval window, leading to progressive fixation of the stapes. The remarkable advances in micro-otologic surgery, designed to mobilize or replace the stapes and to reconstruct the ossicular chain, have greatly altered the prognosis in this disease; significant improvement in hearing can now be achieved in the majority of such patients.

The use of antibiotic drugs has markedly reduced the incidence of suppurative otitis media, both the acute and chronic forms, which in former years were common causes of conductive hearing loss. Repeated attacks of serous otitis media are still an important cause ofthis type of deafness.

Fractures of the temporal bone, particularly those in the long axis of the petrous pyramid, may damage middle ear structures; frequently there is bleeding into the middle ear as well, and a ruptured tympanic membrane. Transverse fractures through the petrous pyramid are more likely to damage both the cochlear-labyrinthine structures and the facial nerve. Other diseases of the temporal bone such as Paget disease, fibrous dysplasia, and osteopetrosis may impair hearing by compression of the cochlear nerve.

Causes of Sensorineural Deafness

This has many causes. Explosions or intense, sustained noise in certain industrial settings or from gun blasts or even rock music may result in a high-tone sensorineural hearing loss. Certain antimicrobial drugs (namely, the aminoglycoside group and vancomycin) damage cochlear hair cells and, after prolonged use, can result in severe hearing loss. If these drugs have been used to treat bacterial meningitis, it may be difficult to determine if the antibiotic or the infection is the cause. A variety of other commonly used drugs have been reported to be ototoxic (see Nadol). Quinine and acetylsalicylic acid may impair sensorineural function transiently. The common high-frequency sensorineural type of hearing loss in the aged (presbycusis) is probably due to neuronal degeneration, i.e., progressive loss of spiral ganglion neurons (Suga and Lindsay).

The cochlea may be damaged by rubella in the pregnant mother. Mumps, acute purulent meningitis (particularly from pneumococcus and Haemophilus), or chronic infection spreading from the middle to the inner ear may cause nerve deafness in childhood. The meningeal infection may spread along the cochlear aqueduct, a structure that connects the cerebrospinal fluid (CSF) space with the perilymph of the cochlea. The inner ear contains melanocytes, and their involvement in VogtKoyanagi-Harada disease adds dysacusis, tinnitus, and sensorineural deafness to the usual manifestations of vitiligo of the eyebrows, iridocyclitis, retinal depigmentation, and recurrent meningitis. Measles vaccination, Mycoplasma pneumoniae infection, and scarlet fever are sometimes associated with acute deafness with or without vestibular symptoms. It is uncertain whether the deafness in these cases is due to direct infection or represents an autoimmune reaction directed to the inner ear. Meningeal hemosiderosis, a rare process that results from repeated bouts of subarachnoid hemorrhage, also causes eighth nerve damage and deafness, presumably as a toxic effect of iron deposition in the meninges.

Of most concern to neurologists is the onset, in an adult, of sudden unilateral hearing loss without vertigo. Many patients can date the onset by noting that they have changed from their customary ear when using the telephone or that they need to turn their head in order to carry on a conversation. Little is known about the pathogenesis of this syndrome. A vascular causation (occlusion of the auditory artery or its cochlear branch or presumed arterial spasm in the course of migraine) has been postulated, on uncertain grounds. A few cases have, complicated herpes zoster and mumps parotitis, but aside from these there is no proven relationship to the usual viral respiratory infections. Episodic deafness in one ear without vertigo proves in most instances to be Wniere disease (see further on). In a prospective study of 88 cases of acute sensorineural hearing loss, two-thirds recovered their hearing completely within a few days or a week or two (Mattox and Simmons). In the remaining patients, recovery was much slower and often incomplete; in this latter group, the hearing loss was predominantly for high tones and in some cases was associated with varying degrees of vertigo and hypoactive caloric responses.

The sudden onset of bilateral sensorineural hearing loss has been reported to follow cardiopulmonary bypass surgery and has been ascribed to microemboli. Less often such an event follows general anesthesia for nonotologic surgery (Evan et al); the pathogenesis is quite obscure. None of the currently popular therapeutic agents-such as histamine, calcium channel blockers, anticoagulants, carbogen inhalation, and steroids-seem to affect the outcome of sudden unilateral or bilateral deafness without vertigo.

Otologists have described a progressive sensorineural type of hearing loss as a late manifestation of congenital syphilis, allegedly occurring despite prior treatment with adequate doses of penicillin. It has been claimed that the long-term administration of steroids may be useful in such cases. The pathologic basis of the hearing loss has not been determined and the causal relationship to congenital syphilis remains to be established.

The auditory nerve may be involved by tumors of the cerebellopontine angle or by mycotic, lymphomatous, carcinomatous, tuberculous, or other types of chronic meningitis. Lymphomatous meningitis appears particularly liable to cause unilateral hearing loss, and we have seen several such cases in which no other cranial nerves were infiltrated. Of the solid tumors, the ones that involve the auditory nerve most frequently are neurofibromas (schwannomas), meningiomas, dermoids, and metastatic carcinoma. In central neurofibromatosis (type II) the involvement by acoustic neuromas is often bilateral. Unilateral deafness may also result from demyelinative plaques, infarction, or tumor involving the cochlear nerve fibers or nuclei in the brainstem. Rarely, deafness is the result of bilateral lesions of the temporal lobes (Chap. 22). The condition called pure word deafness is also due to temporal lobe disease; despite normal pure-tone perception and audiometry and normal brainstem auditory evoked potentials, spoken words cannot be understood. This condition is discussed in Chap. 23.

A large number of genetically determined syndromes that feature a neural or conductive type of deafness-some congenital and others having their onset in childhood or early adult life-have come to light (see articles by Konigsmark and by Proctor and Proctor). About 70 percent of cases of congenital deafness are inherited as an autosomal recessive trait. In most of the remainder, inheritance is autosomal dominant in type and in 2 percent it is sex-linked (Sank and Kallman). The most important advance in this field has been the identification in recessive nonsyndromic deafness of a mutation of the connexin-26 gene on chromosome 13. This mutation is found in half of recessive familial cases and, what is more striking, the same gene abnormality occurs in 37 percent of cases of apparently sporadic congenital deafness (Estivill et al, and Morell et al). The connexin protein is a component of gap junctions and the mutation is theorized to interfere with the recycling of potassium from the cochlear hair cells to the endolymph. There are few complete histopathologic studies of congenital and hereditary deafness. From available data, two groups can be recognized-aplasias and degenerations. Four types of inner ear aplasia have been described: (1) Michel defect, a complete absence of the otic capsule and eighth nerve; (2) Mondini defect, an incomplete development of the bony and membranous labyrinths and the spiral ganglion; (3) Scheibe defect, a membranous cochleosaccular dysplasia with atrophy of the vestibular and cochlear nerves; and (4) rare chromosomal aberrations (trisomies) characterized by abnormality of the end organ and absence of the spiral ganglion.

In addition to these more or less pure aplasias of the peripheral auditory system, cochleovestibular atrophies and degenerations occur as part of many other developmental and heredodegenerative syndromes. Konigsmark has classified these hereditary forms of deafness on the basis of associated defects caused by the same gene: malformations of the external ear; integumentary abnormalities such as hyperkeratosis, hyperplasia or scantiness of eyebrows, albinism, large hyperpigmented or hypopigmented areas, brittle twisted hair, and coniform and missing teeth; ocular abnormalities such as hypertelorism, severe myopia, optic atrophy, congenital and juvenile cataracts, and retinitis pigmentosa; neurologic abnormalities such as polyneuropathy and sensory ataxia (Refsum disease), progressive ophthalmoplegia and cerebellar ataxia, bilateral acoustic neuromas, photomyoclonic seizures, and mental deficiency; skeletal abnormalities; and renal, thyroid, or cardiac abnormalities. Deafness is also a feature of several mitochondrial disorders, particularly the Keams-Sayre syndrome and occasionally the MELAS syndrome (page 1042). The Wolfram syndrome can have either a nuclear or mitochondrial genetic origin. This and other hereditary syndromes are summarized in Table 15-1, and the mitochondrial causes of deafness have recently been summarized by Chinnery et al...

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Table of Contents

Preface                                                     ix
Index 1645
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