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Found 6 results

  1. Celiac.com 10/01/2018 - A team of researchers recently set out to establish the rates of epilepsy in patients with celiac disease or gluten sensitivity and vice versa and to characterize aspects of the epileptic syndromes presented by these patients. The research team included Thomas Julian, Marios Hadjivassiliou, and Panagiotis Zis. They are variously affiliated with the Sheffield Institute for Translational Neuroscience University of Sheffield in Sheffield, UK; and the Academic Department of Neurosciences Sheffield Teaching Hospitals NHS Trust Sheffield, UK. The team conducted a systematic computer-based literature search on the PubMed database, and gathered information on rates, demographics and epilepsy phenomenology. Patients with celiac disease are nearly twice as likely to have epilepsy as the general population. Celiac disease is twice as common in epilepsy patients as in the general population. Researchers still need to do more studies to assess rates of gluten sensitivity in epilepsy patients. The data indicate that the prevalence of celiac disease or gluten sensitivity is higher for certain epilepsy scenarios, including childhood partial epilepsy with occipital paroxysms, adult patients with fixation off sensitivity (FOS) and those with temporal lobe epilepsy (TLE) with hippocampal sclerosis. Epilepsy in the context of gluten-related disorders is a syndrome of celiac disease, epilepsy and cerebral calcification (CEC syndrome), which is frequently described in the literature. The good news is that gluten-free diet helps to control epilepsy in 53% of cases, either reducing seizure frequency, enabling reduced doses or even termination of anti-epileptic drugs. Patients with epilepsy of unknown cause should receive blood tests for markers of gluten sensitivity, and may benefit from a gluten-free diet. Read more at: Springer.com
  2. Celiac.com 10/03/2016 - It's hard for researchers to figure out the exact rate of celiac disease, in part because the disease so often presents a range of atypical symptoms. Most people with celiac disease suffer from classic gastrointestinal symptoms, but many patients may also be asymptomatic or have extra intestinal symptoms. A team of researchers recently set out to assess celiac disease rates in patients with epilepsy, align with determining the effect of a gluten-free diet on seizure control in these patients. The research team included Homayoon Bashiri, Darioush Afshari, Nosrat Babaei, and Mohammad R. Ghadami. They are variously affiliated with the Department of Internal Medicine, and the Sleep Disorders Research Center at Kermanshah University of Medical Sciences in Kermanshah, Iran. For their study, the team assessed patients with epilepsy in Imam Reza and Farabi Hospitals, Kermanshah, Iran. The team first screened patients screened based on results of immunoglobulin A antiendomysial (IgA) antibodies. In patients with positive screens for IgA antibodies, the team took 2–3 endoscopic small bowel biopsies from the distal duodenum to confirm celiac-related changes. People with celiac disease received a gluten-free diet for 5 months, during which time the researchers regularly recorded patient seizure activity. Of the 113 patients with epilepsy, the team diagnosed seven patients (6%) with celiac disease. After 5 months of instituting a gluten-free diet, 6 patients had their seizures completely under control, and were able to discontinue anti-epileptic drugs. In one patient, dosage of anticonvulsant drugs was cut in half, seizures were also controlled. These results showed that about 6% of epileptic patients were positive for celiac disease, and that these patients see significant improvement in seizure control on a gluten-free diet. Source: Adv Clin Exp Med 2016, 25, 4, 751–754
  3. Celiac.com 06/11/2014 - A new study provides strong evidence for an autoimmune cause for a significant number of epilepsy cases, and that screening autoimmune patients for epilepsy and vice versa may be helpful in making more complete diagnosis. The team used insurance claims data from more than 2.5 million members of a national health insurance provider to examine the relationship between epilepsy and 12 autoimmune diseases: type 1 diabetes mellitus, psoriasis, rheumatoid arthritis, Graves' disease, Hashimoto's thyroiditis, Crohn's disease, ulcerative colitis, systemic lupus erythematosus, antiphospholipid syndrome, Sjögren syndrome, myasthenia gravis, and celiac disease. Patients with an autoimmune disease faced a nearly four-fold higher risk for epilepsy (odds ratio [OR], 3.8; 95% confidence interval [CI], 3.6 - 4.0; P < .001). The elevated risk was consistently observed across all 12 autoimmune diseases, and was especially high in children (OR, 5.2; 95% CI, 4.1 - 6.5; P < .001). The data showed that 17.5% of patients with epilepsy also had an autoimmune disease. In about 70% of epilepsy patients, the autoimmune diagnosis came first. Seizures tended to occur within the first 1 to 2 years after diagnosis of an autoimmune disease. The results of the study prompted lead investigator Kenneth Mandl, MD, MPH, from Intelligent Health Laboratory, Harvard Medical School and Boston Children's Hospital, Boston, Massachusetts, to remark that health professionals “need to expand our thinking when it comes to clinical management of these conditions.” The research team further added that the “potential role of autoimmunity must be given due consideration in refractory epilepsy” so that they do not overlook treatable causes for epilepsy Source: JAMA Neurology, March 31, 2014.
  4. Ok, quick overview of myself and my family... My sister has epilepsy, my brother has down syndrome, my mother has digestive issues, thyroid disease, has had a miscarriage and has mood swings, her mother (my grandmother) has schizophrenia and chronic depression and debilitating arthritis and her brother (my great uncle) has parkinsons. All of these can be linked to celiac/GI correct? Now for my symptoms- I have medication controlled epilepsy, regular pain in my shoulder, hip, knees and wrists and occasionally unexplained upper abdominal pain, heartburn, mild eczema on the back of my arms, constantly battling with cold sores/fever blisters (when I did not just have a cold or fever) and acne, occasional digestive issues(foul odor, inconsistancy), bloating and bad pms symptoms/ irregular cycles and the WORST sugar cravings. The eczema didn't start until this past year, I've had knee pain since I was 17 from volleyball injuries and knee surgury. I also wasn't eating regularly until this year, I was on a medication called topamax which drastically reduced my appitite, I probably wasn't eating enough of anything to have a problem. With this kind of family history how likely is it that my mother's side of the family is a carrier of celiac or GI? I went on the ketogenic diet (high fat mod. protein, low carbs) last week to see if it may be an alternative to dropping off of my last epilepsy medication, within 4 days my joint pain completely disapperared, acne started clearing up, eczema disappeared, I felt normal. Over this past weekend I skimped on my diet and had wheat twice- a bite of danish and a flour tortilla, By Tuesday my eczema was back, acne on my face, knee pain. I initally thought it was because it also follows along the guidelines of an anti-inflammitory diet, but after running across article after article about celiac and gluten intolerance and these same symptoms I started wondering if that could be it. I'm back on the keto diet as I just feel better overall when I'm on it. Thoughts, questions, comments? I'll be perusing the forum for answers but for those knowledgeable and experienced I'd LOVE to hear from you!
  5. Celiac.com 10/29/2012 - Celiac disease with epilepsy and cerebral calcifications, also known as CEC, is a rare form of celiac disease that is accompanied by occipital epilepsy. Past studies have suggested that the neurological symptoms could be the result of a folate deficiency, as folate levels are typically low in patients suffering from CEC. However, a recent case report indicates that as with other neurological gluten-related diseases (such as gluten ataxia), there may be some correlation between CEC and TG6 autoantibodies, indicating that the disease is autoimmune in nature. The case study focuses on a four year old boy who suffered from 30+ minute long complex partial seizures every two to three days. He was given antiepileptic drugs (carbamazepine, sodium valproate, levetiracetam), but these only slightly helped reduce seizure frequency. After one year, MRI and CT scans revealed bilateral occipital calcifications over parieto-occipital regions of the brain. The patient also suffered from chronic diarrhea: endoscopy and biopsy confirmed villous atrophy and patient tested positive for antibodies associated with celiac disease. His folate levels were also markedly low. After being placed on a gluten-free diet, the patient's symptoms, including seizures, cleared within two weeks. After the seizures had ceased, the patient was given folate supplements, and taken off antiepileptic drugs. Gluten challenge caused a relapse of all symptoms. At the time of the report, the patient had been gluten-free and seizure-free for 18 months, and showed improved behavior and reading and writing abilities. Because the patient responded so well to gluten-free diet treatment before being given folate supplements and all symptoms resumed during gluten challenge, it would seem that the neurological symptoms of CEC are the result of immune mechanisms rather than vitamin deficiencies or malabsorption. Most CEC patients have low folate levels; folate deficiency was previously thought to play a causative role in the disease, but this case study brings that conclusion into question. Furthermore, the patient tested positive for TG6 autoantibodies, which are associated with gluten ataxia (another gluten-related disease with neurological symptoms, which are an autoimmune response). More studies are required, but this case study suggests that gluten ataxia is not the only gluten-related disease with autoimmune neurological manifestations. Source: http://www.ncbi.nlm.nih.gov/pubmed/22845673
  6. November 1993. European Journal of Pediatrics. Authors Hilhorst MI. Brink M. Wauters EA. Houwen RH. Institution: Department of gastro-enterology, Wilhelmina Childrens Hospital, Utrecht, The Netherlands. Among 783 patients referred to our institute with different types of seizures as presenting symptom, systematic evaluation of antigliadin and antiendomysial antibodies in the serum has identified nine in whom jejunal biopsy has subsequently confirmed the diagnosis of celiac disease (celiac disease). In three of them brain imaging showed the presence of calcified areas in the occipital region. They had complex partial seizures (CPS), associated in two with transient episodes of blindness. In another patient with CPS and generalized tonic-clonic seizures (GTCS) progressive multifocal cerebral calcifications were noted. In the other six patients with CPS and/or GTCS cerebral calcifications were absent. Symptoms of celiac disease in all these cases were either not previously taken into account, or they were very mild or completely absent. In a group of 36 patients with clinically manifest celiac disease, regular follow-up, and good compliance with the dietary regimen, no clinical seizures were reported. The pathogenic mechanism and the relationship between epilepsy and an early diagnosis and treatment of celiac disease are discussed (Footnote #1). Bilateral occipital calcifications, occurring in celiac disease, are factors coming under a particular cerebral syndrome, which also includes epilepsy, migraine-like headache, visual troubles and mental deterioration. They seem to arise from hypofolatemia following gluten-induced enteropathy (Footnote #2). There have been anecdotal reports of an association between celiac disease and epilepsy with cerebral calcifications that resemble those of the Sturge-Weber syndrome. A series of patients who had epilepsy with calcifications, in whom celiac disease (celiac disease) was incidentally observed, prompted us to study this association. 43 patients (15 male, age range 4.6-30.7 years) were selected from two series. 31 patients with cerebral calcifications of unexplained origin and epilepsy (series A) underwent intestinal biopsy. 12 patients with celiac disease and epilepsy (series underwent computed tomography. Antibodies to gluten, folic acid serum concentrations, were measured, and HLA typing was done in most patients. 24 of the series A patients were identified as having celiac disease on the basis of a flat intestinal mucosa (15/22 with a high concentration of serum antigluten), and 5 series B patients showed cerebral calcifications, giving a total of 29 cases with the combination of celiac disease, epilepsy, and cerebral calcifications (CEC). In 27 of these CEC patients, calcifications were located in the parieto-occipital regions. Only 2 of the series A patients had gastrointestinal symptoms at the time of intestinal biopsy; most patients had recurrent diarrhea, anemia, and other symptoms suggestive of celiac disease in the first 3 years of life. The epilepsy in CEC patients was poorly responsive to antiepileptic drugs. Gluten-free diet beneficially affected the course of epilepsy only when started soon after epilepsy onset. Cases of atypical Sturge-Weber syndrome (characterized by serpiginous cerebral calcifications and epilepsy without facial port-wine naevus) should be reviewed, and celiac disease should be ruled out in all cases of epilepsy and cerebral calcifications of unexplained origin (Footnote #3). 4. We report the electroclinical findings of four epileptic patients with clinically asymptomatic celiac disease (celiac disease). Celiac disease diagnosis was suspected by past history and/or computed tomography (CT) findings in all patients and confirmed by laboratory tests and jejunal biopsy. All patients had paroxysmal visual manifestations and ictal EEG discharges arising from the occipital lobe. Epilepsy evolution was favorable in two patients and severe in 2, regardless of CT evidence of occipital corticosubcortical calcifications in 2 patients. Occipital lobe seizures may be characteristic of the epilepsy related to celiac disease, and epileptic patients with these seizures of unknown etiology should be carefully investigated for malabsorption. If past history and/or laboratory tests suggest gastrointestinal (GI) dysfunction they should also undergo small intestinal biopsy even if they do not have GI tract symptoms (Footnote #4). References: Fois A; Vascotto M; Di Bartolo RM; Di Marco V, Celiac disease and epilepsy in pediatric patients,Childs Nerv Syst; 10 (7) p450-4, Sep 1994. Cerebral occipital calcifications in celiac disease, Crosato F; Senter S, Neuropediatrics; 23 (4) p214-7, Aug 1992. Celiac disease, epilepsy, and cerebral calcifications. The Italian Working Group on Celiac Disease and Epilepsy Gobbi G; Bouquet F; Greco L; Lambertini A; Tassinari CA; Ventura A; Zaniboni MG ,Lancet; 340 (8817) p439-43, Aug 22 1992. Ocipital lobe seizures related to clinically asymptomatic celiac disease in adulthood , mbrosetto G; Antonini L; Tassinari CA, Epilepsia; 33 (3) p476-81, May-Jun 1992. A MEDLINE search showed these additional articles on celiac and epilepsy: Convulsive disorder in celiac disease, Cohen O; River Y; Zelinger I, Harefuah; 126 (12) p707-10, 763, Jun 15 1994. Need for follow up in celiac disease, Bardella MT; Molteni N; Prampolini L; Giunta AM; Baldassarri AR, Arch Dis Child; 70 (3) p211-3, Mar 1994. Familial unilateral and bilateral occipital calcifications and epilepsy, Tortorella G; Magaudda A; Mercuri E; Longo M; Guzzetta F, Neuropediatrics; 24 (6) p341-2, Dec 1993. Endocranial calcifications, infantile celiac disease, and epilepsy, Piattella L; Zamponi N; Cardinali C; Porfiri L; Tavoni MA, Childs Nerv Syst; 9 (3) p172-5, Jun 1993. Cortical vascular abnormalities in the syndrome of celiac disease, epilepsy, bilateral occipital calcifications, and folate deficiency, Bye AM; Andermann F; Robitaille Y; Oliver M; Bohane T; Andermann E, Ann Neurol; 34 (3) p399-403, Sep 1993. Progressive cerebral calcifications, epilepsy, and celiac disease, AU- Fois A; Balestri P; Vascotto M; Farnetani MA; Di Bartolo RM; Di Marco V; Vindigni C, Brain Dev; 15 (1) p79-82, Jan-Feb 1993. Celiac disease, posterior cerebral calcifications and epilepsy, Gobbi G; Ambrosetto P; Zaniboni MG; Lambertini A; Ambrosioni G; Tassinari CA, Brain Dev; 14 (1) p23-9, Jan 1992. Intracranial calcifications--seizures--celiac disease: a case presentation, Della Cella G; Beluschi C; Cipollina F, Pediatr Med Chir; 13 (4) p427-30, Jul-Aug 1991. Celiac disease, folic acid deficiency and epilepsy with cerebral calcifications, Ventura A; Bouquet F; Sartorelli C; Barbi E; Torre G; Tommasini G, Acta Paediatr Scand; 80 (5) p559-62, May 1991. Ramsay Hunt syndrome and celiac disease: a new association?, Lu CS; Thompson PD; Quinn NP; Parkes JD; Marsden celiac disease, Mov Disord; 1 (3) p209-19, 1986. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients, Molteni N; Bardella MT; Baldassarri AR; Bianchi PA, Am J Gastroenterol; 83 (9) p992-4, Sep 1988. Bilateral cerebral occipital calcifications and migraine-like headache, Battistella PA; Mattesi P; Casara GL; Carollo C; Condini A; Allegri F; Rigon F Cephalalgia; 7 (2) p125-9, Jun 1987. Blood selenium content and glutathione peroxidase activity in children with cystic fibrosis, celiac disease, asthma, and epilepsy, Ward KP; Arthur JR; Russell G; Aggett PJ, Eur J Pediatr; 142 (1) p21-4, Apr 1984.
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