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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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cPtr = c; for ( i=0; i<kMaxArraySize; i++ ) cPtr++ = 0;

created, notice the ActionScript in the actions layer, the size of the movie, and the publish settings are all the same as when you set them up From now on, you can just create a new file from this template instead of changing those settings each time Cool!

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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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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

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