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Long standing polyneuropathy as a form of presentation of primary systemic amyloidosis.

Systemic amyloidosis is a rare disease caused by deposition of a fibrillar protein in immunoglobulin light chains (kappa or lambda) on different tissues. Symptoms depend on the organs affected by the deposits, but may include myocardiopathy, liver disease, kidney failure, lingual hypertrophy, dermatitis, gastro-oesophageal reflux disorder, and polyneuropathy. A 59-year-old male patient was examined due to sensory deficit of the hands and feet associated with very painful paraesthesia which had been developing gradually over the course of a year. Neurological examination showed cortical functions and cranial nerve pairs to be normal. The motor system revealed preserved tone with slight motor weakness in dorsiflexion of the feet and extension of the fingers and intrinsic hand muscles. All other muscle groups were normal. Deep muscle reflexes were hypoactive, except for the Achilles reflex which was absent. There was neither amyotrophy nor fasciculations. Decreased superficial and deep sensitivity in a stocking-and-glove pattern were observed. Autonomic changes in hands and feet were also observed. The coordination was normal. Heel-to-toe gait was somewhat abnormal. The general examination did not reveal relevant changes. We ran a haemogram and complete biochemical analyses; glucose and antinuclear antibodies, proteinogram, tumour markers, and onconeural antibodies were all within normal ranges. The lumbar puncture revealed no relevant biochemical or cytological changes. Serological tests for Borrelia, Brucella, syphilis, HIV, and neurotropic viruses were negative. The thoracic and abdominal CT showed no alterations. The electromyogram showed decreased amplitude of sensory potentials at the sural and superficial peroneal nerve levels, and to a lesser extent, in median and cubital nerves. Sensory nerve conduction velocities and distal latencies were within normal limits. There was a slight decrease in motor evoked potential amplitude at the level of both common peroneal nerves, with normal motor potentials at the median and cubital levels. Data were compatible with predominantly sensory axonal polyneuropathy. Biopsies of the sural nerve on 2 different occasions showed no vasculitic changes or amyloid deposits. The patient was treated with different drug groups such as antiepileptic agents (carbamazepine, topiramate, gabapentin, oxcarbazepine, pregabalin, and clonazepam); antidepressants (amitriptyline, venlafaxine); morphine derivatives, and a cycle of intravenous gamma globulin without symptoms improving.