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Brain/Nerve Damage
See also Links
to Neurological Studies.
See also “Neurological
complications of coeliac disease”
See also Developmental Disorders.
Contents:
Clippings: Gluten and Alzheimer's
Clippings: Gluten and Neuropathy
Clippings:
Gluten and Neurological Illnesses
Ataxia
“The word ataxia is often used to describe a symptom of incoordination which can be associated with infections, injuries, other diseases, or degenerative changes in the central nervous system. Ataxia is also used to denote a group of specific degenerative diseases of the nervous system called the hereditary and sporadic ataxias.” -- National Ataxia Foundation
Ataxia is commonly associated with injury or deterioration of the cerebellum. The Purkinje cells are particularly susceptible to attack from anti-gliadin antibodies developed by some people in response to gluten in the diet. (Anomalies of the cerebellum may affect perception and are also associated with Autism, Asperger’s Syndrome, ADHD, and schizophrenia).
“Gluten ataxia is an immune mediated disease, part of the spectrum of gluten sensitivity, and accounts for up to 40% of cases of idiopathic sporadic ataxia.”[1] (and perhaps some portion of other forms of ataxia due to overlapping conditions or misdiagnosis.)
“Gluten ataxia responds to a strict gluten-free diet even in the absence of an enteropathy. The diagnosis of gluten ataxia is vital as it is one of the very few treatable causes of sporadic ataxia.” [2]
“Gluten ataxia is therefore the single most common cause of sporadic idiopathic ataxia. Antigliadin antibody testing is essential at first presentation of patients with sporadic ataxia.”[3]
“The studies on gluten ataxia have revealed a significant statistic. In patients who had clearly measurable antibodies that are diagnostic of celiac disease and were suffering from gluten ataxia, only 13% had any gastrointestinal complaints. In other words, the hallmark symptoms of poor digestion we associate with celiac disease and use to diagnose the condition may be absent in 87% of patients with gluten related problems! This suggests that celiac may be way under diagnosed.” [4]
See also Clippings: Ataxia and Gluten.
Lupus
Gluten sensitivity may be misdiagnosed as Lupus:
“Case reports: Three patients are described whose original presentation and immunological profile led to the erroneous diagnosis of systemic lupus erythematosus. The correct diagnosis of gluten sensitivity was made after years of treatment with steroids and other immunosuppressive drugs.
Conclusions: The immunological profile of IgA deficiency and/or raised double stranded DNA in the absence of antinuclear factor together with raised inflammatory markers and symptoms suggestive of an immune diathesis should alert the physician to the possibility of gluten sensitivity. The presence of an enteropathy is no longer a prerequisite for the diagnosis of gluten sensitivity, which can solely present with extraintestinal symptoms and signs. Knowledge of the diverse manifestations of gluten sensitivity is essential in avoiding such misdiagnosis.”[5]
Multiple Sclerosis (MS)
I have several dear friends who are doctors other states. One, a non-primary care specialist, tells me of watching a patient whom several doctors had diagnosed with Multiple Sclerosis. For 15 years, my friend had seen this patient "die by inches", while treating an unrelated problem. Recently, another primary care doctor took over this patient's case. This new doctor managed to convince the patient that she actually had Celiac Disease rather than MS. So, this patient tried the Gluten Free Diet and had a large positive reversal in her health. The patient was, however unable to convince other symptomatic relatives to try the diet cure.
This story brings up two subjects. First, Celiac Disease has in the recent past been so hard to diagnose that even those doctors familiar with CD can still misdiagnose it. Second, Multiple Sclerosis is closely associated with CD in at least some cases.
Celiac Disease is very common in cases of Multiple Sclerosis. One drug used to treat MS allegedly reduces gluten damage to the gut even if the patient is eating wheat. Research is underway to determine how much Multiple Sclerosis is really caused or worsened by wheat gluten.
Links to studies to appear here….
Huntington's Disease
“The authors found high antigliadin antibody [blood levels] in 23 of 52 (44%) patients with Huntington's disease (HD), suggesting a previously unrecognized association between HD and gluten sensitivity.” [6]
Alzheimer's Disease
Because of the commonalities between Alzheimer's Disease and Celiac Disease, and because presently over 99% of Celiac cases are misdiagnosed (see Prevalence Essay), there is a real possibilities of misdiagnosis of Celiac Disease as Alzheimer's Disease. One such case is described below (Clippings: Gluten and Alzheimer's).
There are some theories that gluten intolerance may contribute to Alzheimer's Disease. Further weight is added to these theories is the new knowledge that gluten sensitivity is at least twice as common as Alzheimer's Disease.
Human Tissue Transglutaminase
Theory:
Aberrant human tissue transglutaminase enzyme (TGM) activity is believed to play a role in neurological disorders such as Alzheimer's, Parkinson's and Huntington's diseases. [7][8][9] The presences of anti-bodies to TGM in the blood is generally considered to be very specific to celiac disease (but not all that sensitive to alternative or less advance forms of gluten sensitivity). These anti-TGM anti-bodies bind to TGM to trigger an immune response in that location.
TGM is known to be present in neuronal tissues![10] So an autoimmune condition triggered by chronic inflammation in the small intestine may cross-attack the brain.
Malabsorption Theories:
Long term, low grade to severe B-vitamin deficiencies are a consequence of malabsorption, which gluten intolerance commonly causes, often without obvious symptoms.
“People who get enough niacin [vitamin B3] in their diet cut their risk of Alzheimer's disease by 70%, ….” [11]
It follows that B-vitamin deficiency from gluten intolerance could contribute to Alzheimer's disease.
“Alternatively exorphins and peptides from foods may suppress prostaglandin E1 synthesis, or food sensitivities may alter toxic metal absorption mechanisms, which are thought to play a role in the development of Alzheimer's disease.”[12]
See also Clippings: Gluten and Alzheimer's, which includes a report of the reversal of a case of a case of Alzheimer's.
There is some argument that there is no evidence of higher rates of celiac disease among Alzheimer's cases, however, celiac disease is a minority symptom of gliadin sensitivity. The only valid statement could only come from the results of applying the GFD to Alzheimer's cases. Furthermore, there is now knowledge that trials of the gluten free diet for nerve and brain conditions must be conducted for at least one year.
Clippings: Gluten and Neuropathy
Excerpts
of articles on Neuropathy and Gluten. Bold highlights and [italicized]
comments are added by Harold G. Kraus.
Summary:
Celiac Disease (or gluten sensitivity) is commonly associated with sensory
neuropathy and should be considered even in the absence of gastrointestinal
symptoms.
Excerpted
from Brain, Vol. 126, No. 3, 685-691, March 2003
Neurology. 2003 May 27;60(10):1581-5.
Celiac neuropathy.
Chin RL, Sander HW, Brannagan TH, Green
PH, Hays AP, Alaedini A, Latov N.
Department of Neurology and Neuroscience
(Drs. Chin, Sander, Brannagan, Alaedini, and Latov), Weill Medical College of
Cornell University, New York, NY.
BACKGROUND: Celiac disease (CD) is a
chronic inflammatory enteropathy resulting from sensitivity to ingested gluten.
Neurologic complications are estimated to occur in 10% of affected patients,
with ataxia and peripheral neuropathy being the most common problems. The
incidence and clinical presentation of patients with CD-associated peripheral
neuropathy have not previously been investigated. OBJECTIVE: To determine the
incidence of CD in patients with neuropathy and to characterize the clinical
presentation. METHODS: The records of 20 patients with neuropathy and
biopsy-confirmed CD were reviewed. RESULTS: Six of the 20 patients had
neuropathic symptoms alone without gastrointestinal involvement, and
neuropathic symptoms preceded other CD symptoms in another 3 patients. All
patients had burning, tingling, and numbness in their hands and feet, with
distal sensory loss, and nine had diffuse paresthesias involving the face,
trunk, or lumbosacral region. Only two had weakness. Results of
electrophysiologic studies were normal or mildly abnormal in 18 (90%) of the
patients. Sural nerve biopsies, obtained from three patients, revealed mild to
severe axonopathy. Using the agglutination assay, 13 (65%) of the patients were
positive for ganglioside antibodies. Excluding patients who were referred with
the diagnosis of celiac neuropathy, CD was seen in approximately 2.5% of all
neuropathy patients and in 8% of patients with neuropathy and normal
electrophysiologic studies seen at our center. CONCLUSION: CD is commonly
associated with sensory neuropathy and should be considered even in the absence
of gastrointestinal symptoms.
Excerpted
from http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=P12640070&dopt=Abstract
1: J Neurol Neurosurg Psychiatry. 2003
Apr;74(4):490-4. Related Articles,
Links
Neuromuscular and sensory disturbances in
patients with well treated coeliac disease.
Luostarinen L, Himanen SL, Luostarinen M,
Collin P, Pirttila T.
Department of Neurology, Tampere
University Hospital and Medical School, University of Tampere, Lahti, Finland.
liisa.luostarinen@phks.fi
OBJECTIVES: A body of evidence shows that
coeliac disease is associated with protean manifestations outside the
intestine, and neurological disorders are well recognised. However, it remains
obscure whether there are signs of clinical or subclinical nervous system
involvement even in patients adopting an adequate gluten free diet. The aim of
this study was to assess in a controlled study whether patients with treated
coeliac disease carry an increased risk for neuropathy and characterise the
type of possible neuropathy. METHODS: Electroneuromyographic findings and
vibration, thermal, and tactile thresholds of 26 patients with coeliac disease
and 23 patients with reflux disease were analysed. RESULTS: Six (23.1 %)
coeliac disease patients and one (4.3 %) reflux disease patient showed findings
of chronic axonal neuropathy in quantitative needle EMG. In addition, two
coeliac disease patients showed findings suggestive for myopathy. There were no
significant differences in warm, cold, or vibration thresholds between the
groups but means of heat pain thresholds and tactile thresholds were
significantly higher in coeliac patients than in controls. CONCLUSION: An
increased occurrence of axonal neuropathy was observed in well treated coeliac
disease. This further indicates that neurological manifestations occur even in
patients without overt malabsorption.
Clippings: Gluten and Neurological Illnesses
Search on Springer link for “Celiac”
Criteria: celiac 1 to 3 of 3
1. Clinical and neurological abnormalities in adult celiac disease
Publication: Neurological Sciences
Authors: G. Cicarelli, G. Della Rocca, M. Amboni, et al.
Publisher: Springer-Verlag Italia Srl
Recency: Volume 24, Number 5
Relevancy: 19.2%
Excerpt: We assessed the occurrence of neurological signs and symptoms in adult patients with celiac disease and evaluated the correlation between neurological features and diet. A total of 176 patients and 52 age-matched controls underwent a semistructural interview ...
2. Migraine, cortical blindness, multiple cerebral infarctions and hypocoagulopathy in celiac disease
Publication: Neurological Sciences
Authors: F. Morello, G. Ronzani, F. Cappellari
Publisher: Springer-Verlag Italia Srl
Recency: Volume 24, Number 2
Relevancy: 12.8%
Excerpt: Abstract. We describe the case of a female patient affected by migraine and untreated adult celiac disease who presented with a state of acute migraine accompanied by multiple neurological deficits, including transient cortical blindness with ischemic CT and MRI ...
Publication: Neurological Sciences
Authors: A. Ghezzi, M. Zaffaroni
Publisher: Springer-Verlag Italia Srl
Recency: Volume 22, Number 8
Relevancy: 3.8%
Excerpt: Abstract. Neurological manifestations of gastrointestinal disorders are described, with particular reference to those resembling multiple sclerosis (MS) on clinical or MRI grounds. Patients with celiac disease can present cerebellar ataxia, progressive ...
Search on Springer link for “Celiac”
Neurol Sci. 2001 Nov;22 Suppl 2:S117-22.
Neurological manifestations of gastrointestinal
disorders, with particular reference to the differential diagnosis of multiple
sclerosis.
Ghezzi A, Zaffaroni
M.
Centro Studi Sclerosi Multipla, Ospedale di Gallarate, Universita di Milano,
Gallarate, Varese, Italy.
Neurological manifestations of gastrointestinal disorders are described, with
particular reference to those resembling multiple sclerosis (MS) on clinical or
MRI grounds. Patients with celiac disease can present cerebellar ataxia,
progressive myoclonic ataxia, myelopathy, or cerebral, brainstem and peripheral
nerve involvement. Antigliadin antibodies can be found in subjects with
neurological dysfunction of unknown cause, particularly in sporadic cerebellar
ataxia ("gluten ataxia"). Patients with Whipple's disease can develop
mental and psychiatric changes, supranuclear gaze palsy, upper motoneuron
signs, hypothalamic dysfunction, cranial nerve abnormalities, seizures, ataxia,
myorhythmia and sensory deficits. Neurological manifestations can complicate
inflammatory bowel disease (e.g. ulcerative colitis and Crohn's disease) due to
vascular or vasculitic mechanisms. Cases with both Crohn's disease and MS or
cerebral vasculitis are described. Epilepsy, chronic inflammatory
polyneuropathy, muscle involvement and myasthenia gravis are also reported. The
central nervous system can be affected in patients with hepatitis C virus (HCV)
infection because of vasculitis associated with HCV-related cryoglobulinemia.
Mitochondrial neurogastrointestinal encephalopathy (MNGIE) is a disease caused
by multiple deletions of mitochondrial DNA. It is characterized by peripheral
neuropathy, ophthalmoplegia, deafness, leukoencephalopathy, and
gastrointestinal symptoms due to visceral neuropathy. Neurological
manifestations can be the consequence of vitamin B1, nicotinamide, vitamin B12,
vitamin D, or vitamin E deficiency and from nutritional deficiency states
following gastric surgery.
Clippings: Gluten and Alzheimer's
Excerpts
of articles on Alzheimer's and Gluten.
Bold highlights and italicized comments are added by Harold G. Kraus.
Summary:
TBD
Excerpted
from http://www.drhoffman.com/page.cfm/89
or
http://www.mental-health-matters.com/articles/article.php?artID=298
...
Even
hidden food intolerances may contribute to the development of Alzheimer's
Disease, for example, atypical presentation of coeliac disease in the absence
of classic intestinal manifestations. Recent research has demonstrated a high
prevalence of antigliadin antibodies (IgG, IgA or both) in patients with
neurological dysfunction of obscure etiology (57 percent versus 5 percent in
neurological controls and 12 percent in normal controls). There was a nearly
tenfold increase in neurological dysfunction or dementia in gluten-sensitive
individuals compared to those not gluten-sensitive. Detection was made more
elusive by the fact that only 35 percent of patients who developed
neurological problems had histological evidence of celiac disease.
Two-thirds had no clinical signs of celiac disease. [Celiac disease is only the tip of the gluten intolerance
iceberg - HGK.]
....
[There
follows a Hoffman Center case study of a73 year old woman with a neurologist
rendered a diagnosis of Alzheimer's dementia.
The woman was placed on a gluten-free diet with B12 injections and other
targeted supplementation. After 2
years, her memory and capabilities had improved and stabilized to the point she
was re-diagnosed as “... having minimal dementia in the order of Age Related
Memory Loss." - HGK]
[There
follows a Hoffman Center case study of a73 year old woman with a neurologist
rendered a diagnosis of Alzheimer's dementia.
The woman was placed on a gluten-free diet with B12 injections and other
targeted supplementation. After 2
years, her memory and capabilities had improved and stabilized to the point she
was re-diagnosed as “... having minimal dementia in the order of Age Related
Memory Loss." - HGK]
Excerpted from http://www.drbobmartin.com/2004k_01_16news10.html
Vitamin
E, C supplements may prevent Alzheimer's disease
...
Currently,
the recommended daily allowance for vitamin E is 22 IU (15 mg) and for vitamin
C, 75 to 90 mg, the team points out.
Although multivitamin preparations typically contain approximately these
levels, individual supplements commonly contain doses up to 1000 IU of vitamin
E and 500 to 1000 mg or more of vitamin C.
...
SOURCE:
Archives of Neurology, January 2004
[Even
if gliadin does not directly cause Alzheimer's disease, the widespread
intestinal or even systemic inflammation caused by gluten can certainly consume
the anti-oxidant capacities of nominal intakes of vitamins E and C. Furthermore, any intestinal damage and sprue
caused by gluten would reduce update of vitamins E and C, further reducing any
anti-oxidant capacities. - HGK]
Clippings: Ataxia and Gluten
Excerpts
of articles on Ataxia and Gluten. Bold highlights and [italicized]
comments are added by Harold G. Kraus.
Summary:
Much of the reference below is to the research of Marios Hadjivassiliou,
Richard Grünewald, et al, at Royal Hallamshire Hospital in Sheffield, U.K. Identifying gluten sensitivity by
serological tests, they have determined high rates of gluten sensitivity in
idiopathic sporadic ataxia. They
achieved a very high success rate in treating that form of otherwise untreatable
ataxia with the Gluten Free Diet.
Classic symptoms of Celiac Sprue were absent in some of these
cases. Later research indicates that
hereditary ataxia is probably the same condition as idiopathic sporadic
ataxia. Given that the GFD stops and
even reverses these forms of ataxia, it is suggested that gluten intolerance is
the main cause of these forms. However,
others suggest that some other factor may be the common root of both gluten
intolerance and these ataxias. I can
then imagine that the GFD possibly permits other body systems to relieve the
ataxia conditions.
Excerpted
from Brain, Vol. 126, No. 3, 685-691, March 2003
http://brain.oupjournals.org/cgi/content/abstract/126/3/685
Gluten
Ataxia In Perspective: Epidemiology, Genetic Susceptibility And Clinical
Characteristics
Marios
Hadjivassiliou, Richard Grünewald, Basil Sharrack, David Sanders, Alan Lobo, Clare
Williamson, Nicola Woodroofe, Nicholas Wood and Aelwyn Davies-Jones
We
previously have described a group of patients with gluten sensitivity
presenting with ataxia (gluten ataxia) and suggested that this disease entity
may account for a large number of patients with sporadic idiopathic ataxia. We
have therefore investigated the prevalence of gluten sensitivity amongst a
large cohort of patients with sporadic and familial ataxia and looked at
possible genetic predisposition to gluten sensitivity amongst these groups. Two
hundred and twenty-four patients with various causes of ataxia from North Trent
(59 familial and/or positive testing for spinocerebellar ataxias 1, 2, 3, 6 and
7, and Friedreich’s ataxia, 132 sporadic idiopathic and 33 clinically probable
cerebellar variant of multiple system atrophy MSA-C) and 44 patients with
sporadic idiopathic ataxia from The Institute of Neurology, London, were
screened for the presence of antigliadin antibodies. A total of 1200 volunteers
were screened as normal controls. The prevalence of antigliadin antibodies[*]
in the familial group was eight out of 59 (14%), 54 out of 132 (41%) in the
sporadic idiopathic group, five out of 33 (15%) in the MSA-C group and 149
out of 1200 (12%) in the normal controls. The prevalence in the sporadic
idiopathic group from London was 14 out of 44 (32%). The difference in
prevalence between the idiopathic sporadic groups and the other groups was
highly significant (P < 0.0001 and P < 0.003, respectively). The clinical
characteristics of 68 patients with gluten ataxia were as follows: the mean age
at onset of the ataxia was 48 years (range 14–81 years) with a mean duration of
the ataxia of 9.7 years (range 1–40 years). Ocular signs were observed in 84%
and dysarthria in 66%. Upper limb ataxia was evident in 75%, lower limb ataxia
in 90% and gait ataxia in 100% of patients. Gastrointestinal symptoms were
present in only 13%. MRI revealed atrophy of the cerebellum in 79% and white
matter hyperintensities in 19%. Forty-five percent of patients had
neurophysiological evidence of a sensorimotor axonal neuropathy.
Gluten-sensitive enteropathy was found in 24%. HLA DQ2 was present in 72% of
patients. Gluten ataxia is therefore the single most common cause of
sporadic idiopathic ataxia. Antigliadin antibody testing is essential at first
presentation of patients with sporadic ataxia.
[*]
By the less sensitive serum test? See
Dr. Fine’s fecal test at www.enterolab.com -- HGK
Excerpted from http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12933922&dopt=Abstract
J Neurol Neurosurg Psychiatry. 2003 Sep;74(9):1221-4. Related Articles, Links
Dietary treatment of gluten ataxia.
Hadjivassiliou M, Davies-Jones GA, Sanders DS, Grunewald RA.
Department of Clinical Neurology, The Royal Hallamshire
Hospital, Sheffield, UK. m.hadjivassiliou@sheffield.ac.uk
BACKGROUND:
Gluten ataxia is an immune mediated disease, part of the spectrum of
gluten sensitivity, and accounts for up to 40% of cases of idiopathic sporadic
ataxia. No systematic study of the effect of gluten-free diet on gluten ataxia
has ever been undertaken. OBJECTIVE: To study the effect of gluten-free diet on
patients presenting with ataxia caused by gluten sensitivity. METHODS: 43
patients with gluten ataxia were studied. All were offered a gluten-free diet
and monitored every six months. All patients underwent a battery of tests to
assess their ataxia at baseline and after one year on diet. Twenty six patients
(treatment group) adhered to the gluten-free diet and had evidence of
elimination of antigliadin antibodies by one year. Fourteen patients refused
the diet (control group). Three patients had persistently raised antigliadin
antibodies despite adherence to the diet and were therefore excluded from the
analysis. RESULTS: After one year there was improvement in ataxia
reflected in all of the ataxia tests in the treatment group. This was significant when
compared with the control group. The diet associated improvement
was apparent irrespective of the presence of an enteropathy. CONCLUSIONS: Gluten ataxia
responds to a strict gluten-free diet even in the absence of an enteropathy. The
diagnosis of gluten ataxia is vital as it is one of the very few treatable
causes of sporadic ataxia.