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Celiac Disease: Neurological Manifestations in 2 undiagnosed patients Kogulavadanan Arumaithurai MD, Ashish Kapoor MD, Holli Horak MD, Katalin Scherer.

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Presentation on theme: "Celiac Disease: Neurological Manifestations in 2 undiagnosed patients Kogulavadanan Arumaithurai MD, Ashish Kapoor MD, Holli Horak MD, Katalin Scherer."— Presentation transcript:

1 Celiac Disease: Neurological Manifestations in 2 undiagnosed patients Kogulavadanan Arumaithurai MD, Ashish Kapoor MD, Holli Horak MD, Katalin Scherer MD Department of Neurology, University of Arizona BACKGROUND DISCUSSION RESULTS Celiac disease is a chronic inflammatory enteropathy occurring in genetically susceptible individuals secondary to digestion of gluten. Its mean prevalence is 1% (Sander et al 2003). A spectrum of neurological disorders has been reported with adult celiac disease. Most commonly reported are peripheral neuropathy and ataxia. Case series of two patients with celiac disease and neurologic manifestations that went undiagnosed for years due to atypical presentations. OBJECTIVE REFERENCES. Case 1: A 55 year old woman presented with worsening weight loss, muscle weakness and spasms over three years. Her presentation was complicated by history of complex partial seizures, hyponatremia, seizure medications( keppra, valproate) and statins. Her EMG showed mild myopathic changes without fibrillations in the right deltoid. RNS was normal. SFEMG showed abnormal jitter in the left EDB and frontalis. A muscle biopsy was non-specific. She was treated with pyridostigmine and prednisone with modest improvement. 3 years later she developed worsening myalgia and a repeat trial of prednisone had no significant benefit. In the interim she was also treated unsuccessfully for parkinsonian gait features with sinemet. She had a repeated muscle biopsy which was normal. Years later she developed neuropathic pain in feet, and subjective atrophy of legs, and repeat EMG was normal. Over her 7 year course, there was a mild amount of weight loss, but no frank GI symptomatology. Routine chemistries, ANA, ESR, RF, CK, Aldolase, RPR, paraneoplastic abs, acetylcholine receptor abs and MuSK, and P/Q type VGCC antibodies were normal. Anti-endomysial IgA (142U) and transglutaminase IgA (900U) were elevated at an outside institution and celiac disease was confirmed with a small bowel biopsy. She started improving gradually months after initiating a gluten free diet, and tapered off pyridostigmine. Prednisone may have been partially masking her celiac symptoms, and was successfully tapered after her diet change. Case 2: A 64 year old woman with a 10-year history of ataxia, memory loss, weight loss, GI distress and diagnosis of IBS, presented for acute burning pain and numbness in the feet. EMG showed an axonal sensorimotor peripheral polyneuropathy. Routine chemistries and extensive work up including ANA, ESR, RF, CK, Aldolase, RPR, paraneoplastic abs, acetylcholine receptor abs, MuSK, and P/Q type VGCC antibodies were normal. Elevated anti-gliadin antibodies were demonstrated on further testing. Her symptoms improved after starting a gluten free diet Untreated celiac disease may underlie neurological symptoms and cause neuropathy, myalgias or ataxia. Our cases empsize the challenge in diagnosing celiac disease given its varied presentation. Celiac patients who lack prominent gastrointestinal symptoms may remain undiagnosed for years. It is important for physicians to consider celiac disease in patients present with subtle signs of malabsorption associated with unexplained neurological complaints. Gluten-related neurologic dysfunction.Hadjivassiliou M1, Duker AP2, Sanders DS3. Gluten ataxia in perspective: epidemiology, genetic susceptibility and clinical characteristics. Hadjivassiliou M1, Grünewald R, Sharrack B, Sanders D, Lobo A, Williamson C, Woodroofe N, Wood. A primary care cross-sectional study of undiagnosed adult coeliac disease. Sanders DS1, Patel D, Stephenson TJ, Ward AM, McCloskey EV, Hadjivassiliou M, Lobo AJ.


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