Article

Bushara KO. Neurologic presentation of celiac disease

Neurology Department, Minneapolis VA Medical Center, University of Minnesota, Minneapolis, Minnesota, USA.
Gastroenterology (Impact Factor: 13.93). 05/2005; 128(4 Suppl 1):S92-7. DOI: 10.1053/j.gastro.2005.02.018
Source: PubMed

ABSTRACT Celiac disease (CD) long has been associated with neurologic and psychiatric disorders including cerebellar ataxia, peripheral neuropathy, epilepsy, dementia, and depression. Earlier reports mainly have documented the involvement of the nervous system as a complication of prediagnosed CD. However, more recent studies have emphasized that a wider spectrum of neurologic syndromes may be the presenting extraintestinal manifestation of gluten sensitivity with or without intestinal pathology. These include migraine, encephalopathy, chorea, brain stem dysfunction, myelopathy, mononeuritis multiplex, Guillain-Barre-like syndrome, and neuropathy with positive antiganglioside antibodies. The association between most neurologic syndromes described and gluten sensitivity remains to be confirmed by larger epidemiologic studies. It further has been suggested that gluten sensitivity (as evidenced by high antigliadin antibodies) is a common cause of neurologic syndromes (notably cerebellar ataxia) of otherwise unknown cause. Additional studies showed high prevalence of gluten sensitivity in genetic neurodegenerative disorders such as hereditary spinocerebellar ataxia and Huntington's disease. It remains unclear whether gluten sensitivity contributes to the pathogenesis of these disorders or whether it represents an epiphenomenon. Studies of gluten-free diet in patients with gluten sensitivity and neurologic syndromes have shown variable results. Diet trials also have been inconclusive in autism and schizophrenia, 2 diseases in which sensitivity to dietary gluten has been implicated. Further studies clearly are needed to assess the efficacy of gluten-free diet and to address the underlying mechanisms of nervous system pathology in gluten sensitivity.

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    • "Entre las causas no psiquiátricas de depresión que muchas veces el clínico no las relaciona con esta destacan: ACV [1] , Artritis, Cáncer, Consumo de aspartame [2] , Diabetes [3] [4] , Dolor crónico, Enfermedad celíaca [5] , Epilepsia [6] , Fibromialgia, SIDA, Lesiones dérmicas, Lupus , Menopausia [7] [8] , Polifarmacia [9] , Psoariasis [10] , Quemaduras severas, Síndrome de Terson [1] . "
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    • "Several neurological and psychiatric disorders have also been widely described in CD patients [8] [9]; in 7% of newly-diagnosed cases, such disorders have been reported to precede the diagnosis of CD [10]. They include migraine, febrile seizures, encephalopathy, chorea, brainstem dysfunction, autism, myopathy, neuropathy with positive antiganglioside antibodies, cerebellar ataxia, dementia , white matter lesions, depression and, lastly, epilepsy, which is the most frequent disorder associated with CD [11] [12]. "
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    ABSTRACT: Although a range of neurological and psychiatric disorders are widely reported to be associated with coeliac patients, their pathogenesis remains unclear. Some such disorders are believed to be secondary to vitamin deficiency due to malabsorption, others to immune mechanisms. We hypothesise that hyperhomocysteinemia might, by damaging the blood-brain barrier, expose neuronal tissue to all neuro-irritative metabolites, such as homocysteine itself, a neurotoxic excitatory and proconvulsant amino acid. Neurons respond to these stimuli through hyperexcitability, thereby predisposing subjects to neurological disorders such as epilepsy and headache. Furthermore, persisting endothelial damage may cause blood extravasation and subsequent deposition of calcium salts. We suggest that this might be the pathogenesis of the CEC syndrome, which is characterized by the association of coeliac disease, epilepsy and cerebral calcifications. Indeed, homocysteine plays a well-known role in cardiovascular endothelial dysfunction, with high serum and cerebrospinal fluid levels often being reported in coeliac patients. Moreover, data in the literature show a strong, growing association of homocysteine with epilepsy and migraine in non-coeliac subjects.
    Medical Hypotheses 07/2013; 81(4). DOI:10.1016/j.mehy.2013.06.025 · 1.07 Impact Factor
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    • "The increased risk of depressive symptoms in CD patients could be explained by several mechanisms. Firstly, dietary non-compliance and sustained malabsorption may play a role [18], which could lead to sustained nutritional deficiencies (e.g. of vitamin B6, vitamin B12, and folic acid) which in turn may have increased the risk of depression [21]. Secondly, nutritional deficiencies may be a consequence of the strict restrictive GFD. "
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    ABSTRACT: OBJECTIVES: We aimed to investigate whether long-term adherence to a gluten-free diet is related to depressive symptoms in coeliac disease (CD) patients. METHODS: A cross-sectional survey was performed in 2265 adult CD patients recruited through the Dutch Coeliac Association. Self-reported diet adherence was compared among groups based on self-reported depressive symptoms (categorized into current [1-month], remitted, and never). RESULTS: The life-time prevalence rate of self-reported depressive symptoms was 39.0% (n=883), of whom 270 (11.9%) suffered from current depressive symptoms. Adherence to gluten-free diet was strict in 50.2% of patients, sufficient in 46.3%, and insufficient in 3.6%. Insufficient adherence was not associated with current depressive symptoms (odds ratio [OR] 0.95; 95% confidence interval [CI]: 0.48-1.92). Keeping a gluten-free diet for longer than five years was associated with lower OR of current depressive symptoms compared to being on a diet for less than two years (OR 0.69; 95% CI: 0.50-0.95). CONCLUSIONS: Lifetime depressive symptoms may be present in one third of the CD patients who adhere to gluten-free diet. Long-term adherence to the gluten-free diet may reduce the risk of current depressive symptoms.
    Journal of psychosomatic research 02/2013; 74(2):155-160. DOI:10.1016/j.jpsychores.2012.11.007 · 2.84 Impact Factor
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