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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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neuropathy, eg, chronic demyelinative motor neuropathy with multifocal conduction block Other useful laboratory procedures are (1) biochemical tests to identify metabolic, nutritional, or toxic states; (2) CSF examination (increase in protein and in cells that indicate radicular or meningeal involvement); (3) nerve and muscle biopsy; (4) measurement of immunoglobulins and antineural antibodies that relate to immune-mediated neuropathies; (5) genetic testing for several of the inherited neuropathies; and (6) nerve biopsy Once having established that the patient has a disease of the peripheral nerves and having ascertained its clinical and electrophysiologic pattern and time course, one is usually able to determine its nature This is accomplished most readily by allocating the case in question to one of the categories in Table 46-2, wherein the peripheral nerve diseases are classi ed syndromically according to their mode of evolution and clinical presentation Again, by categorizing the neuropathic syndrome in this way by topography and time course and by motor or sensory predominance, only a limited number of diagnoses are possible These are discussed in the sections that follow Our use of the terms acute, subacute, and chronic neuropathy must be explained By acute we mean evolution in terms of days and by subacute, weeks Chronic is divided into two groups: one in which the neuropathy has progressed for a period of several months to a few years, and another in which progression is over several years, most of which prove to have a genetic cause It can be restated that these temporal properties are, with the topographic pattern, the main determinants in the categorization of neuropathy Diseases of the peripheral nerves are considered in a more comprehensive fashion in the two-volume monograph Peripheral Neuropathy, edited by Dyck and colleagues Also recommended are more concise monographs on this subject by Schaumburg and associates and by Asbury and Thomas and the atlas on the pathology of peripheral nerve by King
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