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place eg, tingling, burning, stabbing pain, or just an uncomfortable dysesthesia is induced by tactile stimuli Under these conditions, a given stimulus induces not only an aberrant sensation but also one that radiates and persists after the stimulus is withdrawn As remarked on pages 118 and 133, the patient s reaction may seem to indicate a hypersensitivity ( hyperesthesia ), but more often the sensory threshold is actually raised and it is the sensory experience or response that is exaggerated (hyperpathia) Painful paresthesias and dysesthesias are particularly common in certain types of diabetic, alcoholic-nutritional, and amyloid neuropathies Mainly they affect the feet ( burning feet ) and less often the hands In herpes zoster they are con ned to limited regions of the body They may be a prominent feature in some cases of diabetic and other types of vascular neuropathy, and in a fairly common sensory neuropathy of obscure nature in elderly individuals A particularly intense form of burning pain typi es the causalgia of a partial nerve lesion (usually traumatic) of the ulnar, median, posterior tibial, peroneal, or occasionally some other nerve (pages 120 and 1172) The mechanism of thermal and painful dysesthesias is not fully understood It has been theorized that a loss of large touchpressure bers disinhibits the pain-receiving nerve cells in the posterior horns of the spinal cord An argument against this explanation is the lack of pain in Friedreich ataxia, in which the larger neurons degenerate, and also in certain purely sensory polyneuropathies, where only the perception of tactile stimuli (large bers) is lost A more likely explanation, supported by microneurographic recordings is that dysesthetic pain results from autogenic ectopic discharges arising at many sites along surviving intact or regenerating nociceptive nerve bers or their terminal receptors In contrast to dysesthetic pain, it has been postulated, on uncertain grounds, that the deep, aching neuropathic pain of sciatica or brachial neuritis (nerve trunk pain) arises from irritation of the normal endings (nervi nervorum) in the sheaths of the nerve trunks themselves (Asbury and Fields) These considerations are discussed in Chap 8 Sensory Ataxia and Tremor Proprioceptive deafferentation with retention of a reasonable degree of motor function may give rise to ataxia of gait and of limb movement, as discussed in Chap 9 Probably, dysfunction of the spinocerebellar bers of the peripheral nerves is the source of the ataxia Some of the most severe ataxias of this type occur with sensory ganglionopathy, as commented further on Ataxia without weakness is characteristic of tabes dorsalis, a purely posterior root affection, but this syndrome can be essentially duplicated by diabetic polyneuropathy, which affects posterior roots as well as nerves (diabetic pseudotabes), and by a variant of the GBS (Fisher syndrome) as well as by certain sensory neuronopathies (ganglionopathies) While the ataxia in some instances is indistinguishable from that caused by cerebellar disease, other features of cerebellar dysfunction such as dysarthria and nystagmus are, of course, lacking In the chronic sensory neuropathies with ataxic features, all movements, though strong, are rendered ineffective by virtue of the deep sensory loss Characteristic of the sensory (tabetic) ataxic gait are brusque, inging, slapping movements of the legs Loss of proprioception may also give rise to small wavering, uctuating movements of the outstretched ngers called pseudoathetotic, or dancing ngers An action tremor of fast-frequency type may also appear during certain phases of a polyneuropathy Shahani and coworkers had the impression that it is due to loss of input from the muscle-spindle.

Quarter Calendar Year 12003 Billed Quantity Net Sales Planned Sales 170,250,32 742,34430 756,136 22003 171,406,182 747,32980 762,019 32003 172,765,649 753,02196 754,590 42003 171,685,760 748,07847 744,2760

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