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Clinical Director, Indiana Wesleyan University

The genetic errors involve either cytoskeletal or structural proteins of the organ of Corti or the ion channel apparatus spasms calf discount 10mg lioresal amex. It should also be remarked that deafness is a component of over 400 different genetic syndromes spasms nose generic lioresal 10mg amex. The gene errors that give rise to some of these diseases spasms to right side of abdomen order lioresal 25 mg with amex, particularly the Usher syndrome muscle relaxant soma cheap lioresal 10 mg on-line, may also cause non-syndromic congenital deafness. The syndromic forms of genetic deafness have been classified largely on the basis of their associated defects: retinitis pigmentosa, malformations of the external ear; integumentary abnormalities such as hyperkeratosis, hyperplasia or scantiness of eyebrows, albinism, large hyperpigmented or hypopigmented areas, ocular abnormalities such as hypertelorism, severe myopia, optic atrophy, and congenital and juvenile cataracts, and mental deficiency; skeletal abnormalities; and renal, thyroid, or cardiac abnormalities. The association of neurosensory deafness with degenerative neurologic disease is discussed further in Chaps. Also to be mentioned as differing from the degenerations are a group of acoustic aplasias. 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. Hysterical Deafness It is possible to distinguish hysterical and feigned deafness from that due to structural disease in several ways. In the case of bilateral deafness, the distinction can be made by observing a blink (cochleo-orbicular reflex) or an alteration in skin sweating (psychogalvanic skin reflex) in response to loud sound. The elicitation of the first several waves of the brainstem auditory evoked potentials provides indisputable evidence that sounds are reaching the receptive auditory structures and that the patient should be capable of hearing sounds. It should be kept in mind that a brief episode of deafness with fully preserved consciousness may rarely be caused by seizure activity in one temporal lobe (epileptic suppression of hearing). For the most part they are benign, but always there is the possibility that they signal the presence of an important neurologic disorder. Diagnosis of the underlying disease demands that the complaint of dizziness be analyzed correctly- the nature of the disturbance of function being determined first and then its anatomic localization. This classic approach to neurologic diagnosis is nowhere more valuable than in the patient whose main complaint is dizziness. The term dizziness is applied by the patient to a number of different sensory experiences- a feeling of rotation or whirling as well as nonrotatory swaying, weakness, faintness, light-headedness, or unsteadiness. Blurring of vision, feelings of unreality, syncope, and even petit mal or other seizure phenomena may be called "dizzy spells. Essentially, the physician must determine whether the symptoms have the specific qualities of vertigo- which in this chapter refers to all subjective and objective illusions of motion or position- or whether they are more properly categorized as light-headedness or nonrotatory pseudovertigo. The distinction between these two groups of symptoms is elaborated after a brief discussion of the factors involved in the maintenance of equilibrium. Physiologic Considerations Several mechanisms are responsible for the maintenance of a balanced posture and for awareness of the position of the body in relation to its surroundings. Continuous afferent impulses from the eyes, labyrinths, muscles, and joints inform us of the position of different parts of the body. In response to these impulses, the adaptive movements necessary to maintain equilibrium are carried out. Normally we are unaware of these adjustments, since they operate largely at a reflex level. Visual impulses from the retinae and possibly proprioceptive ones from the ocular muscles, which enable us to judge the distance of objects from the body. Impulses from the labyrinths, which function as highly specialized spatial proprioceptors and register changes in the velocity of motion (either acceleration or deceleration) and position of the body. The cristae of the three semicircular canals sense angular acceleration of the head (side-to-side or rotary), and the maculae of the saccule and utricle sense linear acceleration and gravity. In each of these structures, displacement of sensory hair cells is the effective stimulus. In the semicircular canals, this is accomplished by movement of the endolymphatic fluid, which, in turn, is induced by rotation of the head and results in an illusion of rotation. In the utricle and saccule, the hairs are displaced in response to the force of gravity on the otoliths, giving rise to a sensation of linear displacement or tilt. In either case, the movement generates an electrical charge in the hair cells, causing depolarization of the nerve terminals and thereby initiating impulses in the vestibular nerve, with the production of two main reflex responses: the vestibulo-ocular, which stabilizes the eyes, and the vestibulospinal, which stabilizes the position of the head and body. Impulses from the proprioceptors of the joints and muscles are essential to all reflex, postural, and volitional movements. Those from the neck are of special importance in relating the position of the head to the rest of the body. The sense organs listed above are connected with the cerebellum and with certain ganglionic centers and pathways in the brainstem, particularly the vestibular nuclei, and, via the medial longitudinal fasciculi, with the ocular motor nuclei.

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Treatment Alkalinization of the urine by ingestion or infusion of sodium bicarbonate is said to protect the kidneys by preventing myoglobin casts spasms mid back generic lioresal 10 mg, but in severe cases it is of doubtful value spasms while going to sleep purchase generic lioresal canada, and the sodium may actually be harmful if anuria has already developed muscle relaxer z discount lioresal 10mg with visa. Diuresis induced by mannitol or by loop diuretics such as furosemide and by the administration of intravenous fluids also reduces the chances of anuric renal failure if given in time muscle spasms 9 weeks pregnant discount lioresal 25mg on line. Statin-Induced Myopathy With the widespread use of these lipid-lowering medications, myotoxicity has become a welldescribed but probably overrated problem. The first generation of these drugs were fungal metabolites (lovastatin, paravastatin, simvastatin) and were infrequently implicated in muscle damage, but the new synthetic ones (atorvastatin, fluvastatin, cerivastatin) are more frequently toxic, especially when given with gemfibrizil. The mechanism of muscle damage is not well understood but it is likely that inherent enzymatic defects are present in a proportion of the severe cases (see the brief review by Farmer). As mentioned, the combination of one of these medications with gemfibrizil is particularly likely to result in muscle damage. Drugs in the statin class with higher lipid solubility appear to have a greater potential for toxicity as a result of their increased muscle penetration. Noted on page 1134 is a polyneuropathy in which statin drugs have been tentatively implicated. Colchicine Myoneuropathy this condition is included here as much for its clinical interest as for its curious histopathologic features. The drug, used widely in the treatment of gout, often gives rise to a mild subacute proximal muscular weakness, but has also produced an acute necrotizing myopathy. Most instances of the latter have occurred in patients with a degree of renal failure, which allows accumulation of the drug (even though the drug is metabolized predominantly by the liver). Many cases also show clinical or electrophysiologic evidence of a polyneuropathy as pointed out by Kuncl and colleagues, leading to the term colchicine myoneuropathy. Rare cases of colchicine-induced hypokalemic periodic paralysis and also of myotonia have been reported. Proximal atrophy, weakness Weakness may be periodic, reflexes may be depressed or absent, rarely severe myoglobinuria Proximal muscle pain and weakness, sensorimotor neuropathy, cardiomyopathy 1. Weakness resolves in a matter of days or weeks when the drug is discontinued but the neuropathic features may remain. Alcoholic Toxic Myopathy Several forms of muscle weakness have been ascribed to alcoholism. In one type, a painless and predominantly proximal weakness develops over a period of several days or weeks in the course of a prolonged drinking bout and is associated with severe degrees of hypokalemia (serum levels 2 meq/L). The urinary excretion of potassium is not significantly increased; depletion is probably the result of vomiting and diarrhea, which usually precede the onset of muscular weakness. Biopsies from severely weakened muscles show single-fiber necrosis and vacuolation. Treatment consists of the administration of potassium chloride intravenously (about 120 meq daily for several days), after which oral administration suffices. Strength returns gradually in 7 to 14 days, and enzyme levels return to normal concomitantly. A more dramatic myopathic syndrome, occurring acutely at the height of a prolonged drinking bout, and appropriately termed acute alcoholic myopathy, is manifest by severe pain, tenderness, and edema of the muscles of the limbs and trunk, accompanied in severe cases by renal damage (see Hed et al). The muscle affection is generalized in some patients and remarkably focal in others. A swollen, painful, tender limb or part of a limb may give the appearance of a deep venous thrombosis or lymphatic obstruction. Indeed, in a general hospital alcoholism is one of the most common causes of rhabdomyolysis and myoglobinuria rivaled only by status epilepticus and trauma. Some patients recover within a few weeks, but others require several months, and relapse during another drinking spree occurs frequently. Restoration of motor power is attendant upon muscle regeneration but may be complicated by polyneuropathy and other syndromes of neuromuscular disability associated with alcoholism. Perkoff and his associates described what is presumably a third form of acute muscular disorder in alcoholics, characterized by severe muscular cramps and diffuse weakness, occurring in the course of a sustained drinking bout. In distinction to the latter, however, myophosphorylase levels were not consistently reduced in the alcoholic patients. From time to time one observes in alcoholics the subacute or chronic evolution of painless weakness and atrophy of the proximal muscles of the limbs, especially of the legs, with only minimal signs of neuropathy in the distal segments of the legs and feet.

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Asking the patient to give his own interpretation of the possible meaning of symptoms may sometimes expose unnatural concern spasms left shoulder blade buy lioresal 25mg free shipping, anxiety muscle relaxant lodine purchase 25 mg lioresal with visa, suspiciousness infantile spasms youtube discount lioresal 10 mg, or even delusional thinking spasms medicine discount 25 mg lioresal visa. Errors and inconsistencies in the recorded history are as often the fault of the physician as of the patient. As a corollary, the patient should be discouraged from framing his symptom(s) in terms of a diagnosis that he may have heard; rather, he should be urged to give as accurate a description of the symptom as possible- being asked, for example, to choose a single word that best describes his pain and to describe precisely what he means by a particular term, such as dizziness, imbalance, or vertigo. The patient who is given to highly circumstantial and rambling accounts can be kept on the subject of his illness by discreet questions that draw out essential points. The setting in which the illness occurred, its mode of onset and evolution, and its course are of paramount importance. If such information cannot be supplied by the patient or his family, it may be necessary to judge the course of the illness by what the patient was able to do at different times. This is followed by an assessment of the function of sphincters and the autonomic nervous system and suppleness of the neck and spine (meningeal irritation). Gait and station (standing position) should be observed before or after the rest of the examination. In addition, it is often instructive to observe the patient in the course of his natural activities, such as walking or dressing; this may disclose subtle abnormalities of gait and movement that might not be evident in formal testing. When an abnormal finding is detected, whether cognitive, motor, or sensory, it becomes necessary to analyze the problem in a more elaborate fashion. Details of these more extensive examinations are to be found in appropriate chapters of the book (motor, Chaps. The neurologic examination is ideally performed and recorded in a sequential and uniform manner in order to avoid omissions and facilitate the subsequent analysis of case records. Some variation in the precise order of examination from physician to physician is permissible, but each examiner establishes an accustomed pattern. The thoroughness of the neurologic examination must of necessity be governed by the type of clinical problem presented by the patient. To spend a half hour or more testing cerebral, cerebellar, cranial nerve, and sensorimotor function in a patient seeking treatment for a simple compression palsy of an ulnar nerve is pointless and uneconomical. Obviously many parts of the examination cannot be carried out in a comatose patient; also, infants and small children as well as patients with psychiatric disease must be examined in special ways. Not to be neglected are certain portions of the general physical examination that may be particularly informative in the patient with neurologic disease. For example, examination of the pulse and blood pressure as well as carotid and cardiac auscultation are essential in a patient with stroke; likewise, the skin can reveal a number of conditions that pertain to congenital, metabolic, and infectious causes of neurologic disease; and so on. Attention, speed of response, ability to give relevant answers to simple questions, and the capacity for sustained and coherent mental effort all lend themselves to straightforward observation. Useful bedside tests of attention, concentration, memory, and clarity of thinking include the repetition of a series of digits in forward and reverse order, serial subtraction of 3s or 7s from 100, recall of three items of information or a short story after an interval of 3 min, and naming the last six presidents or prime ministers. In addition, his ability to read, write, and spell, execute spoken commands, repeat words and phrases spoken by the examiner, name objects and parts of objects, and solve simple arithmetical problems should be assessed. The ability to carry out commanded tasks (praxis) has great salience in the evaluation of several aspects of cortical function. The testing of language, cognition, and other aspects of higher cerebral function are considered in Chaps. For a full account of the methods, the reader is referred to the monographs of DeMyer, Ross, Mancall, Bickerstaff and Spillane, Glick, Haerer, and of the staff members of the Mayo Clinic, each of which approaches the subject from a somewhat different point of view. An inordinately large number of tests of neurologic function have been devised, and it is not proposed to review all of them here. Some are described in subsequent chapters dealing with disorders of mentation, cranial nerves, and motor, sensory, and autonomic functions. Many tests are of doubtful value or are repetitions of simpler tests and should therefore not be taught to students of neurology. Merely to perform all of them on one patient would require several hours and probably, in most instances, would not make the examiner any the wiser. The danger with all clinical tests is to regard them as indisputable indicators of disease rather than as ways of uncovering disordered functioning of the nervous system. The fol- Testing of Cranial Nerves the function of the cranial nerves must be investigated more fully in patients who have neurologic symptoms than in those who do not.

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In these areas and well beyond them spasms left side buy 25 mg lioresal with amex, Purkinje cells were lost and the granule cell layer was somewhat thinned muscle relaxant non sedating buy 10mg lioresal overnight delivery. The neurofibrillary changes were scattered diffusely through the cerebral cortex and brainstem but were most prominent in the mediotemporal gray matter back spasms x ray 25 mg lioresal free shipping. Noteworthy was the absence of discrete senile plaques in this material; however spasms with stretching cheap 10mg lioresal otc, all cases showed extensive immunoreactive deposits of -amyloid ("diffuse plaques"). In three boxers who developed a parkinsonian syndrome, Davie and colleagues found a reduction of N-acetylaspartate in the putamen and pallidum by protein magnetic resonance spectroscopy. This probably reflected a loss of neurons in these regions and was said by these authors to differentiate it from idiopathic Parkinson disease. Posttraumatic Hydrocephalus this is an uncommon complication of severe head injury. Intermittent headaches, vomiting, confusion, and drowsiness are the initial manifestations. Since a similar syndrome is observed occasionally after the rupture of a saccular aneurysm with subarachnoid hemorrhage, the same mechanisms, i. Zander and Foroglou have had extensive experience with this condition and have written informatively about it. Posttraumatic Nervous Instability (Postconcussion Syndrome) this troublesome and frequent sequela of head injury has been mentioned above as well as in the chapter on headache (page 158). When the syndrome is protracted, neurologists are vexed by the condition- a problem intensified by worried patients and family. It has also been called the posttraumatic or postconcussion syndrome, posttraumatic headache, traumatic neurasthenia (Symonds), and traumatic psychasthenia, among many other names. Headache is the central symptom, either generalized or localized to the part that had been struck. The headache is variously described as aching, throbbing, pounding, stabbing, pressing, or band-like and is remarkable for its variability. The intensification of the headache and other symptoms by mental and physical effort, straining, stooping, and emotional excitement has been mentioned earlier; rest and quiet tend to relieve it. Dizziness, another prominent symptom, is usually not a true vertigo but a giddiness or lightheadedness. However, a certain number of patients describe symptoms that are consonant with labyrinthine disorder. They report that objects in the environment move momentarily, and that looking upward or to the side may cause a sense of unbalance; labyrinthine tests may show hyporeactivity; far more often they disclose no abnormalities. McHugh found a high incidence of minor abnormalities by electronystagmography both in concussed patients and in those suffering from whiplash injuries of the neck; but we find some of the data difficult to interpret. Exceptionally, vertigo is accompanied by diminished excitability of both the labyrinth and the cochlea (deafness), and one may assume the existence of direct injury to the eighth nerve or end organ. When the symptoms persist, however, the patient is intolerant of noise, emotional excitement, and crowds. Tenseness, restlessness, fragmentation of sleep, inability to concentrate, feelings of nervousness, fatigue, worry, apprehension, and an inability to tolerate the usual amount of alcohol complete the clinical picture. The resemblance of these symptoms to those of anxiety and depression and to other forms of "posttraumatic stress disorder" is quite apparent. In contrast to this multiplicity of subjective symptoms, memory and other intellectual functions show little or no impairment, although this has been disputed. Leininger et al, for example, found that most of their 53 patients who suffered minor head injury in traffic accidents performed less well than controls on psychologic tests (category test, auditory verbal learning, copying of complex figures). The fact that those who were merely dazed did as poorly as those who were concussed and that litigation was involved in some cases would lead one to question these results. The syndrome of posttraumatic nervous instability complicates all types of head injury, mild and severe. Once established, it may persist for months or even years, and it tends to resist all varieties of treatment.

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