Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although frequently underdiagnosed, several epidemiological studies have estimated the prevalence of restless legs syndrome (RLS) in western countries at 5-15% of the general population. The diagnosis is usually made on a clinical basis, according to the criteria established by the international RLS study group. There are case reports of transient RLS in opiate withdrawal. We describe three opiate (dextropropoxyphene (DPP)) dependent young male patients; two of them had DPP intoxication/withdrawal seizure developing RLS during opiate withdrawal. However, their RLS persisted even after the remission of other withdrawal symptoms. Thyroid function test, hemogram, serum ferritin were normal in all of them. The cases responded well to a treatment with ropinirole. Hence, there might be a causal association, which required further well-designed studies to substantiate. The sleep disturbances and use of benzodiazepines can be minimized by increasing clinician's sensitivity to diagnose RLS.
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PMID:Restless legs syndrome in opioid dependent patients. 2470 Oct 19

Thyroid hormones (TH) play crucial roles in brain maturation and are important for neuronal migration and neocortical lamination. Subcortical band heterotopia (SBH) represent a class of neuronal migration errors in humans that are often associated with childhood epilepsy. We have previously reported the presence of SBH in a rodent model of low level hypothyroidism induced by maternal exposure to the goitrogen, propylthiouracil (PTU). In the present study, we report the dose-response characteristics of this developmental malformation and the connectivity of heterotopic neurones with other brain regions, as well as their functionality. Pregnant rats were exposed to varying concentrations of PTU through the drinking water (0-10 p.p.m.) beginning on gestational day 6 to produce graded levels of TH insufficiency. Dose-dependent increases in the volume of the SBH present in the corpus callosum were documented in the adult offspring, with a clear presence at concentrations of PTU that resulted in minor (< 15%) reductions in maternal serum thyroxine as measured when pups were weaned. SBH contain neurones, oligodendrocytes, astrocytes and microglia. Monoaminergic and cholinergic processes were prevalent and many of the axons were myelinated. Anatomical connectivity of SBH neurones to cortical neurones and the synaptic functionality of these anatomical connections was verified by ex vivo field potential recordings. SBH persisted in adult offspring despite a return to euthyroid status on termination of exposure and these offspring displayed an increased sensitivity to seizures. Features of this model are attractive with respect to the investigation of the molecular mechanisms of cortical development, the effectiveness of therapeutic intervention in hypothyroxinaemia during pregnancy and the impact of the very modest TH imbalance that accompanies exposure to environmental contaminants.
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PMID:Subcortical band heterotopia in rat offspring following maternal hypothyroxinaemia: structural and functional characteristics. 2488 16

The diagnosis of Hashimoto's encephalopathy is made when no other cause is found for an acute encephalopathic illness, in the presence of positive thyroid autoantibodies, and is supported by a response to steroid therapy. A 59-year-woman developed an encephalopathic illness with mixed aphasia, global weakness and generalised seizures requiring intubation and ICU admission. Extensive imaging and laboratory investigations looking for an underlying cause for the encephalopathy were unremarkable. Thyroid autoantibodies were strongly positive, raising the possibility of Hashimoto's encephalopathy. Thyroid function testing showed profound primary hypothyroidism. The patient was commenced on high-dose methyprednisolone, with prompt cessation of seizure activity. Thyroxine replacement was commenced, with the methyprednisolone switched to oral prednisone and slowly weaned. The patient had no further seizures and ultimately made a full recovery.
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PMID:Endocrine encephalopathy. 2492 74

Thyroid hormones (THs) L-thyroxine and L-triiodothyronine, primarily known as metabolism regulators, are tyrosine-derived hormones produced by the thyroid gland. They play an essential role in normal central nervous system development and physiological function. By binding to nuclear receptors and modulating gene expression, THs influence neuronal migration, differentiation, myelination, synaptogenesis and neurogenesis in developing and adult brains. Any uncorrected THs supply deficiency in early life may result in irreversible neurological and motor deficits. The development and function of GABAergic neurons as well as glutamatergic transmission are also affected by THs. Though the underlying molecular mechanisms still remain unknown, the effects of THs on inhibitory and excitatory neurons may affect brain seizure activity. The enduring predisposition of the brain to generate epileptic seizures leads to a complex chronic brain disorder known as epilepsy. Pathologically, epilepsy may be accompanied by mitochondrial dysfunction, oxidative stress and eventually dysregulation of excitatory glutamatergic and inhibitory GABAergic neurotransmission. Based on the latest evidence on the association between THs and epilepsy, we hypothesize that THs abnormalities may contribute to the pathogenesis of epilepsy. We also review gender differences and the presumed underlying mechanisms through which TH abnormalities may affect epilepsy here.
Seizure 2015 Sep
PMID:Thyroid hormones: Possible roles in epilepsy pathology. 2636 94

A 33 yr old man, previously diagnosed with hypothyroidism, presented with decreased level of consciousness and generalized tonic-clonic (GTC) seizure to Namazi hospital, Shiraz, Iran, during April 2015. The patient later referred with another episode of seizure like attack for which he received phenytoin, carbamazepine and levothyroxine and was discharged. During his last admission, the patient was admitted with chief complaints of decreased consciousness and four GTC attacks. On admission, the patients had aphasia, ataxia, loss of verbal communication, eye contact and complete loss of obedience. Thyroid function tests showed low levels of T3 and T4 with high levels of thyroid stimulating hormone. Other blood tests were all either normal or slightly abnormal. Lumbar puncture and CSF analysis had a high titer of Anti-TPO antibodies. With high suspicion of Hashimoto encephalopathy, pulsed methyl prednisolone (10 mg) was administered, however the patient showed little improvement. Therefore, plasmaphresis was started, to which the patient showed dramatic response.
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PMID:Hashimoto Encephalopathy with an Unusual Presentation of Status Epilepticus Seizures: A Case Report. 2795 68

Hashimoto's encephalopathy (HE) is a rare, clinically heterogeneous condition associated with positive thyroid autoantibodies. It is increasingly recognized as an important and treatable cause of autoimmune encephalopathy. Thyroid-associated antibodies such as thyroperoxidase (TPO) antibody, thyroglobulin (TG) antibody, and thyrotropin receptor (TR) antibody were found in HE patients with seizure disorders. Although antithyroid antibodies are required for the diagnosis of HE, their role in the pathogenesis of HE remains uncertain. Instead of playing a key role in the pathophysiology processes of HE, it is suggested that thyroid-associated antibodies are hallmarks of HE. Seizure disorders were found in approximately two-thirds of HE patients, and common anticonvulsant therapy alone is usually ineffective. Some patients did not respond to any antiepileptic drugs. The use of immunotherapy can effectively control seizure disorders. Electroencephalography and imaging findings are not specific to HE patients and can also be seen in other causes of encephalopathies. However, the prognosis in the majority of patients with HE was usually good if it is diagnosed and treated correctly.
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PMID:Hashimoto's Encephalopathy and Seizure Disorders. 3113 60


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