Possible gluten sensitivity in multiple system atrophy.

pearance of sensory potentials (see the table). No change in clinical and neurophysiologic studies was noted 1 year later (week 48). Discussion. We show for the first time a marked improvement of clinical and neurophysiologic deficits in neuronopathy associated with primary SS. In our patient, the sensory potential reappeared but remained low at 48 weeks. However, the sensory examination was normal. It is known that the sensitivity of sensory potentials to detect neuropathy is higher than that for sensory examination. Our description is striking because at 12 weeks reflexes returned and sensory nerve action potentials reappeared. This raises questions about the mechanism of the neuropathy. The history is suggestive of sensory neuronopathy. The issue that remains to be solved is the mechanism by which reflexes reappeared so quickly. We cannot exclude a component of primary demyelination of large-diameter sensory fibers. Only few data are available concerning toxicity of TNF␣ on the dorsal root ganglia. 5 TNF␣ blockers might reverse the partial in-excitability of the sensory nerves. Our case highlights the potential of TNF␣-blocking agents in treating this disabling disorder. Animal studies strongly support the use of such drugs in peripheral neuropathy. 6,7 This case report warrants further investigation of TNF␣ blockade in sensory neuronopathy. There are no data presented, for instance, for its benefit in the more common distal sensorimotor polyneuropathy. A controlled study is scheduled to confirm our findings. Tumor necrosis factor-␣ regulates nicotinic responses in mixed cultures of sympathetic neurons and nonneuronal cells.toxic effects of combined treatments with cytokines in murine primary mixed neuron/glia cultures. KV. Anti-TNF-neutralizing antibodies reduced pain-related behavior in two different mouse models of painful mononeuropathy.bined epineural therapy with neutralizing antibodies to tumor necrosis factor-alpha and interleukin-1 receptor has a additive effect in reducing neuropathic pain in mice. Celiac disease (CD) is an intestinal syndrome characterized by immunologic intolerance to dietary gluten leading to mucosal atrophy and malabsorption. Neurologic complications occur in 8 to 10% of patients with the disease. 1 Neurologic impairment can be the only manifestation of gluten sensitivity. Gluten sensitivity is indicated by increased levels of circulating antibodies to gliadin. 2 Most patients with gluten sensitivity carry a particular HLA variant , DQ2, or in a few cases HLA DQ8. 3 A high frequency of gluten sensitivity in the absence of signs and symptoms of classic CD has been found in patients with certain neurologic syndromes of unknown etiology, including cerebellar ataxia. …