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Attention was drawn to this entity by Sterman and colleagues in a report of three adult patients with rapidly evolving sensory ataxia, are exia, numbness, and pain, beginning in the face and spreading to involve the entire body In each instance, the symptoms began within 4 to 12 days following the institution of penicillin therapy for a febrile illness (antibiotics were subsequently shown not to be the cause) Proprioception was profoundly reduced, but there was no weakness or muscle atrophy, despite generalized are exia The sensory de cit attained its maximum severity within a week, after which it stabilized and improved very little Electrophysiologic studies showed absent or slowed sensory conduction but there were no abnormalities of motor nerve conduction or signs of denervation In two of these patients, the CSF protein content was elevated to 126 and 175 mg/dL Follow-up observations (for up to 5 years) disclosed no neoplastic or immunologic disorder, the usual causes of such a sensory neuronopathy Lacking pathology, it was assumed, from the permanence of the condition, that sensory neurons were destroyed (sensory neuronopathy) In all likelihood, these cases were postinfectious and immune mediated A subsequent series of 42 patients reported by Windebank and colleagues emphasized an asymmetrical and brachial pattern of symptoms in some patients and an initial affection of the face in others In contrast to Sterman s cases, the CSF was usually normal and most patients had some improvement or a spontaneous resolution of symptoms These authors viewed the process as a sensory neuropathy In this and subsequent reports, as mentioned, antibiotics were not implicated At present, this clinical pattern should be viewed as a syndrome rather than as a disease Probably, some instances are immune-postinfectious in nature The same pattern of sensory loss evolving in a subacute or chronic manner is well known to occur as a paraneoplastic illness, described further on in this chapter, or in association with the Sjogren syndrome, scleroderma, lupus erythematosus, paraproteinemia, and HTLV-I infection Certain drugs and other agents, especially cisplatin and excessive intake of pyridoxine, are also causes of a sensory neuronopathy Also to be distinguished from sensory neuronopathy is a rare form of GBS that involves solely the large sensory bers and produces ataxia In the latter, there is usually some degree of proximal weakness, and the sensory changes do not normally extend to the face and trunk. rdlc ean 13 EAN - 13 Client Report RDLC Generator | Using free sample for EAN ...
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