barcode scanner java api THE PATHOPHYSIOLOGY OF NERVE INJURY ELECTRODIAGNOSTIC AND CLINICAL CORRELATES in Objective-C

Creation Data Matrix 2d barcode in Objective-C THE PATHOPHYSIOLOGY OF NERVE INJURY ELECTRODIAGNOSTIC AND CLINICAL CORRELATES

THE PATHOPHYSIOLOGY OF NERVE INJURY ELECTRODIAGNOSTIC AND CLINICAL CORRELATES
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The pathophysiology of peripheral nerve lesions can be inferred from EDX data, as can the clinical symptoms that the pathophysiological process produces Four different pathophysiologies can be considered from an EDX perspective, axon loss, and three forms of demyelination The latter have been referred to as focal or uniform slowing, differential slowing also known as temporal dispersion, and conduction block More than one of these mechanisms may coexist with any given disease or injury There is a fth pathophysiology of nerve to consider from at least a theoretical if not a practical basis, that being disordered function of ion channels Certain marine toxins and potentially some drugs such as phenytoin may affect peripheral nerve adversely by this mechanism Loss of CMAP and SNAP amplitudes are the primary nerve conduction manifestations of axon loss With axon loss, conduction slowing may occur if the largest, fastest
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TESTING IN NEUROMUSCULAR DISEASE
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conducting axons degenerate Conduction slowing tends to be modest in primarily axon loss disorders In pure axon loss, focal conduction abnormalities do not occur The needle examination in axon loss is characterized by abnormal spontaneous activity within 1 3 weeks of disease-onset, reduced motor unit recruitment immediately and enlarged, reinnervated MUPs within a matter of months Axon loss leads to muscle atrophy and weakness, loss of all sensory modalities, and loss of deep tendon re exes within the territories of nerves that are affected Demyelination may cause uniform slowing of nerve conduction Conceptually, in uniform slowing, conduction is slowed equally in all bers within the affected segment of nerve As all impulses traverse the affected portion of nerve synchronously, the only clinical consequence of such a lesion is paresthesia, with or without pain Uniform slowing may occur in a focal segment of nerve as a consequence of mechanical injury It is a common EDX signature of carpal tunnel syndrome and some ulnar neuropathies It may occur along the entire
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course of multiple nerves in the hereditary demyelinating and dysmyelinating disorders It may occur as a consequence of disordered ion channel function as well Historically phenytoin, a sodium channel blocker, was identi ed as the cause of peripheral neuropathy This association seems to be based predominantly, if not solely, on the basis of slowed nerve conduction velocities Clinical neuropathy associated with phenytoin use seems to be a rare event Differential slowing and demyelinating conduction block are always associated with acquired nerve disease and occur in either a focal or a multifocal distribution Conceptually, differential slowing results from different degrees of slowing within different nerve bers within the same segment of nerve Again, all impulses traverse the damaged segment of nerve successfully As a result, the CMAP waveform broadens and becomes dispersed, with a resulting loss of amplitude and lengthening of duration Typically, the waveform takes on a serrated rather than smooth contour (Fig 2 16) Theoretically, as all axons are conducting and all muscle bers
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2 1 3 4 5 Wrist 1 50ms 10mV
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2 1 34 5 Axilla3 50ms 10mV
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Figure 2 16 Motor nerve conduction with differential slowing (temporal dispersion) in patient with multifocal motor neuropathy
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SECTION I
APPROACH TO PATIENTS WITH NEUROMUSCULAR DISEASE
activated, the area under the curve remains the same Differential slowing may occur either from mechanical nerve injury in a mononeuropathy or in a multifocal fashion in the acquired demyelinating polyradiculoneuropathies such as GBS and chronic in ammatory demyelinating polyradiculoneuropathy (CIDP) Clinically, differential slowing primarily affects modalities that require synchronous impulse transmission, notably deep tendon re exes and vibratory perception Conduction block usually implies demyelination affecting consecutive myelin internodes to the extent that impulse transmission is actually blocked in a variable population of bers within a given nerve It is most accurately recognized when stimuli can be delivered sequentially over short segments of nerve When a nerve is stimulated below the affected area, the CMAP amplitude is normal as the nerve distal to the lesion remains unaffected as long as the pathology is exclusively demyelinating Above the block, the CMAP amplitude drops off proportionate to the number of bers affected (Figure 2 2) This same phenomenon may also occur prior to overt demyelination, presumably on the basis of immune-mediated ion channel dysfunction, as most ion channels exist at internodes Clinically, conduction block produces neither signi cant muscle atrophy, loss of the so-called small ber modalities including autonomic functions, nor perception of pain and temperature Signi cant atrophy does not occur as the trophic in uence of preserved axons remains The latter functions are preserved as small poorly myelinated or unmyelinated bers remain relatively unscathed, as demyelinating lesions have little or no in uence on these ber types Conduction block is the only type of demyelinating pathology that results in muscle weakness
EDX examination is fairly sensitive and can provide support for most neuromuscular disorders, there are notable exceptions One of these is the increasingly accepted concept of small ber peripheral neuropathy, typically presenting with burning, hypersensitive feet Conventional EDX techniques exclusively test large myelinated bers and do not adequately assess disorders that exclusively affect small myelinated or unmyelinated bers producing distortions in perception of pain and thermal sense with or without impaired autonomic function Other tests, described later in this chapter and in the subsequent chapter on histological testing, have been used in attempts to assess small ber integrity Another arena in which EDX is inadequately sensitive is in certain muscle disorders Myopathies in which the pathology consists solely of myo ber atrophy or nondestructive internal changes of myo ber architecture can be particularly dif cult Certain endocrine, congenital, and mitochondrial myopathies are examples of this In the myopathy of excessive corticosteroid use characterized by type II myo ber atrophy, the abnormal type II MUPs are not detectable, as these are obscured by their initially recruited type I counterparts As previously mentioned, an additional drawback of EDX is the time required for the full complement of EDX abnormalities to develop following nerve injury In addition with traumatic injuries, EDX cannot adequately distinguish between complete severance of axons with preservation of the connective tissue sheath and complete nerve transaction This is of pragmatic importance as the current standard of care would be to attempt primary nerve reanastomosis acutely if complete nerve transaction had occurred
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