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Having oriented the above discussion to imply that many cases of chronic fatigue have a psychologic basis, we acknowledge that some previously healthy and nonneurotic individuals have become quite disabled for months or more after a severe febrile viral infection, the best characterized being mononucleosis, but undoubtedly other febrile illnesses are implicated as well These cases, in our experience, have arisen suddenly in adolescents and young men who experience overwhelming fatigue during a well-documented and prolonged viral infection They continue to take pleasure in activities in which they are able to participate, do not show anxiety or major depressive symptoms, and have the best prognosis, although complete recovery may take up to 3 to 5 years Often these patients are able to de ne the date on which the illness began The term postviral fatigue state is most appropriate for this group Impressive in some of our cases have been severe headaches and orthostatic hypotension, with wide swings in blood pressure resulting in syncope as well as intermittent hypertension Alcohol intolerance may develop It would seem that the more ambiguous and less severe cases of chronic fatigue occurring in women, particularly those with bromyalgia, have a different basis, but this cannot be stated with certainty At the present time, the status of the chronic fatigue syndrome is undecided The possibility of an obscure metabolic or immunologic derangement secondary to a viral infection cannot be dismissed, as discussed by Swartz, but it seems unlikely in the majority of cases that lack such a history Certainly, high levels of cytokines, such as occur after many types of illness and with cancer, and some of the numerous endocrine aberrations are capable of causing fatigue and lethargy Treatment is discussed below

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tocks as well as the extremities; sensory ataxia is a common accompaniment There is no weakness but movements may be awkward as a result of a sensory ataxia Motor neuronopathy is essentially the opposite condition, a disorder of the anterior horn cells causing weakness, fasciculations, and atrophy in a widespread distribution and, therefore, not properly a process of the peripheral nerves Mononeuropathy is the most circumscribed form of peripheral nerve disease It is re ected by weakness and sensory loss in the territory of a single peripheral nerve Certain speci c features serve to differentiate mononeuropathy from a radiculopathy for example, weakness in dorsi exion and eversion of the foot is referable to the peroneal nerve or to the L5 nerve root; however, inversion of the foot, innervated by the tibial nerve, is affected, only with L5 root lesions The distribution of sensory loss also aids in distinguishing the two processes; for example, in the aforementioned case the region of sensory change corresponding to the L5 root extends almost up to the knee on the anterior surface of the foreleg, whereas it ends a limited distance above the ankle in the case of a peroneal nerve lesion (see the sensory maps on pages 129, 130, and 132) The cumulation of multiple mononeuropathies, termed mononeuritis multiplex, may at times be dif cult to differentiate from polyneuropathy as discussed further on Plexopathies (brachial or lumbosacral) create the most confusing patterns of motor and sensory involvement; only one limb is affected but the motor, sensory, and re ex loss do not conform to a pattern of several adjacent nerve roots or nerves Knowledge of the innervation of the involved muscles at the level of the plexus usually clari es the situation The apparent complexity of peripheral nerve disease is greatly simpli ed by recognizing that, of the multitude of diseases, each manifests itself by one or another of above-described topographic and sensory-motor patterns for which reason the pattern of neuropathy sets limits on the etiologic possibilities In the analysis of a polyneuropathy it is of further value to determine whether the process is predominantly motor with less sensory involvement (motor-sensory), or the converse (sensorimotor), or purely sensory, motor, or autonomic The time course of the disease is also extremely informative An acute onset (ie, rapid evolution) is nearly always diagnostic of an in ammatory, immunologic, toxic, or vascular etiology The other extreme, a polyneuropathy evolving slowly over many years, is indicative of a hereditary or, rarely, a metabolic disease Most of the toxic, nutritional, and systemic diseases of nerve develop subacutely or are of an early chronic or subacute nature, appearing over several weeks and months In addition to the patient s report of the progress of symptoms, signs such as muscle atrophy signify a process of relatively long-standing, at least several months in duration The etiologic diagnosis of polyneuropathy is further aided by attempting to deduce whether the myelin sheath or the axon is primarily involved (ie, demyelinative or axonal) Sometimes the neurologic examination alone is suf cient to make this distinction, but greater precision is attained from nerve conduction studies and needle examination of muscles [electromyogram (EMG)] The latter test also helps to detect primary disorders of muscle (myopathies) and separate them from neurogenic denervation or neuromuscular block The electrical examinations of nerve and muscle described in Chap 45, therefore, clarify the type of abnormality in each of the main categories of neuropathic disease and greatly reduce the number of possible diagnoses In a few instances, the EMG abnormalities are so characteristic as to virtually de ne a.

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