Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014547 (focal epilepsy)
 1,627 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a review of 45 patients with ankylosing spondylitis 10 had neurological symptoms and signs and three of them had two separate neuropathological disorders. The neurological profiles fell into five main categories-multiple sclerosis, the cauda equina syndrome, focal epilepsy, vertebrobasilar insufficiency, and peripheral nerve lesions. An association between ankylosing spondylitis and multiple sclerosis is suggested, possibly due to an immunological defect or to one being a complication of the other.
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PMID:Nervous system involvement in ankylosing spondylitis. 435 25

Recurrent transient ischemic attacks, migraine and dementia represent the principal symptoms of cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL). During the course of the disease, about 10% of patients may experience epileptic seizures, mainly related to the presence of an ischemic stroke. We present a 30-year-old woman with new-onset focal epilepsy leading to the diagnosis of CADASIL. The neuropsychological testing revealed no cognitive impairment. Interictal EEG demonstrated spikes and polyspikes with low amplitude over the right occipital region during NREM sleep. MRI showed white-matter hyperintensities on both hemispheres with confluent lesions at the right parieto-occipital junction, with juxtacortical components. Like in multiple sclerosis, we can suppose that this type of white matter lesions, close to the cortex, may be causative of seizures.
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PMID:Focal epilepsy as first symptom in CADASIL. 2141 9

Structural cerebral MRI analysis in patients with neurological diseases usually requires T1-weighted datasets for tissue segmentation. For this purpose, synthetic T1-weighted images which are constructed from quantitative maps of the underlying tissue parameters such as the T1 relaxation time and the proton density (PD) may provide advantages over conventional datasets. However, in some cases synthetic images may suffer from specific artifacts, hampering accurate tissue segmentation. The goal was to improve a previously described method for the calculation of synthetic magnetization-prepared rapid gradient-echo (MP-RAGE) datasets from quantitative T1 and PD maps. Improvements comprise a B0-correction for the water-selective excitation pulses employed in T1-mapping and the use of T1-based pseudo-PD maps. Synthetic T1-weighted MP-RAGE datasets were calculated, using the standard and the improved algorithm, for 10 patients with focal epilepsy (caused by focal cortical dysplasia in 9), 10 patients with multiple sclerosis and 10 healthy control subjects and segmented with the Freesurfer toolbox. Visual inspection disclosed that segmentation of the standard synthetic datasets was inaccurate in 6 out of 10 patients with epilepsy, 7 out of 10 patients with multiple sclerosis and 7 out of 10 healthy control subjects, while the improved synthetic datasets resulted in adequate segmentation outcomes in the majority of cases. Only for one patient with multiple sclerosis and one with epilepsy, segmentation in basal temporal regions was not sufficient. Furthermore, data based on the standard algorithm showed strong signal non-uniformities in basal regions. This effect was not present in the improved synthetic datasets.
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PMID:Improved synthetic T1-weighted images for cerebral tissue segmentation in neurological diseases. 3107 21

A 45-year-old Italian woman, affected by relapsing-remitting multiple sclerosis (RR-MS) starting from 2011, started treatment with alemtuzumab in July 2016. Nine months after the second infusion, she had an immune thrombocytopenic purpura (ITP) with complete recovery after steroid treatment. Three months after the ITP, the patient presented with transient aphasia, cognitive deficits, and focal epilepsy. Serial brain magnetic resonance imaging showed a pattern compatible with encephalitis. Autoantibodies to glutamate receptor 3 peptide A and B were detected in cerebrospinal fluid and serum, in the absence of any other diagnostic cues. After three courses of intravenous immunoglobulin (0.4 mg/kg/day for 5 days, 1 month apart), followed by boosters (0.4 mg/kg/day) every 4-6 weeks, her neurological status improved and is currently comparable with that preceding the encephalitis. Autoimmune complications of the central nervous system during alemtuzumab therapy are relatively rare: only one previous case of autoimmune encephalitis following alemtuzumab treatment has been reported to date.
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PMID:Autoimmune Encephalitis and CSF Anti-GluR3 Antibodies in an MS Patient after Alemtuzumab Treatment. 3167 19