Monday, December 22, 2014

Gluten and the Brain, Protein Diseases

Celiac disease is the best studied form of delayed pattern food allergy caused by eating wheat and other cereal grains. A surprising range of disease is triggered by the proteins in these foods, collectively referred to as gluten. Celiac disease may present as a vague illness, even a mental illness.

Patients often complain of dysphoria with fatigue, difficulty in concentration, loss of recent memory, irritability, loss of pleasure and interests, often with sleep disturbances. Sleep and dreaming are influenced by food problems. Most people eat their major meal in the evening and snack at night. This food is digested and absorbed during the night and symptoms often emerge as you sleep. Some allergenic effects tend to peak at night - asthma, migraine, body pains, and itching are often at their worst. Sleep disturbances include difficulty falling asleep, frequent waking and nightmares.

Luostarinen et al suggested: It is well known that coeliac disease may be associated with various neurological manifestations. We have had a high index of suspicion of coeliac disease during recent years in our neurological clinic. As a result 10 (7%) out of 144 of our new coeliac patients were detected because of neurological symptoms. The most common neurological manifestations were neuropathy, memory impairment and cerebellar ataxia. In these patient groups screening for coeliac disease with serological antibody tests helps to find patients who may suffer from this disease.

Wills suggested A number of neurological syndromes have been described in association with coeliac disease. These include disorders of the central nervous system encompassing epilepsy, myoclonus, ataxia, internuclear opthalmoplegia, multifocal leukoencephalopathy and dementia. Most of these associated conditions show a poor response to gluten restriction. Peripheral neuropathies, of axonal and demyelinating types, have also been reported and may respond to elimination of gluten from the diet. The mechanism underlying these processes remains obscure but may be immunological or related to trace vitamin deficiencies. Controversially, it has also been claimed that occult coeliac disease accounts for a substantial proportion of patients with neurological dysfunction of unknown cause. Some authorities recommend that cryptogenic ataxias and neuropathies should be routinely screened for the presence of gluten-sensitivity but this remains contentious and has not been universally accepted.

Gluten and Cerebellar Ataxia

One example of specific brain injury from eating gluten is cerebellar ataxia. The cerebellum looks after the coordination and smoothing of movements so that problems here show up as movement disorders. Gluten sensitivity, with or without classical celiac disease symptoms and intestinal pathology, is a treatable cause of cerebellar ataxia.

Bushara et al reported: We investigated the prevalence of abnormally high serum immunoglobulin A (IgA) and IgG anti-gliadin antibody titers and typical human lymphocyte antigen (HLA) genotypes in 50 patients presenting with cerebellar ataxia who were tested for molecularly characterized hereditary ataxias. A high prevalence of gluten sensitivity was found in patients with sporadic (7/26; 27%) and autosomal dominant (9/24; 37%) ataxias, including patients with known ataxia. Patients with hereditary ataxia (including asymptomatic patients with known ataxia genotype) should be considered for screening for gluten sensitivity and gluten-free diet trials.

Hadjivassiliouet al reported that patients with gluten ataxia have antibodies against Purkinje cells. Antigliadin antibodies cross-react with epitopes on Purkinje cells. Burk et al reported the symptoms of gluten ataxia: The clinical syndrome was dominated by progressive cerebellar ataxia with ataxia of stance and gait (100%), dysarthria (100%) and limb ataxia (97%). Oculomotor abnormalities were gaze-evoked nystagmus (66.7%), spontaneous nystagmus (33.3%), saccade slowing (25%) and upward gaze palsy (16.7%). Extracerebellar features also included deep sensory loss (58.3%), bladder dysfunction (33.3%) and reduced ankle reflexes (33.3%).

From The Human Brain by Stephen Gislason MD