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)

[Case records of Epileptic Disorders. Anatomo-electro clinical correlations. Case 01-2009]. Tuberous sclerosis complex (TSC) is a multisystem genetic disorder with variable phenotypic expression, caused by mutations in one of the two tumor suppressor genes, TSC1 or TSC2. Epilepsy is the most common neurological presentation and seizures are often medically intractable. Definition of the epileptogenic zone during presurgical evaluation is challenging given the multiple potentially epileptogenic lesions visible on MRI. However, TSC patients may nevertheless achieve seizure freedom, when preoperative evaluation yields concordant results. The strategies used in these patients vary substantially among different epilepsy surgery centres. We present a 21-year-old right-handed, intellectually not impaired woman with TSC and medically intractable seizures since the age of 15 years. Careful multi-stage presurgical evaluation, including prolonged video-EEG-monitoring, cerebral high resolution MRI, ictal and interictal [99m Tc]HMPAO-SPECT, [18 F]FDG-PET and further invasive recordings with subdural and depth electrodes led to the identification of an epileptogenic tuber with concordant seizure onset zone in the right neocortical temporal lobe. A tailored resection was performed leading to excellent surgical outcome (follow-up 12 months, Engel class I).
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PMID:Successful surgery in late onset epilepsy with tuberous sclerosis complex. 1934 55

We present a case with intractable partial complex seizures in a 14-year-old girl who was found to have brain heterotopia on MRI and PET-CT. The patient presented with intractable partial complex seizures and a normal electroencephalogram. Her brain magnetic resonance imaging showed heterotopic gray matter lining the ventricular margin of the right occipital horn. Subsequent PET-CT demonstrated moderate tracer localization in the heterotopic gray matter surrounding the ventricular margin of the right occipital horn. Heterotopia may demonstrate normal or increased FDG uptake on PET, therefore its appearance may be deceiving when other pathologies are being considered.
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PMID:Brain heterotopia. 1935 76

A part of patients with the therapy resistant epilepsy can be cured by surgical interventions. The more concordant the presurgical evaluation data, the better prognosis the patient has postoperatively. In case of discordant examination data, multimodal evaluation or case-specific decision might be successful. We report on a five-year-old boy with bilateral (left-dominated) cortical dysplasia and therapy resistant epilepsy. The ictal EEG did not help to localize the seizure onset zone, semiology had little lateralization value; however, FDG-PET showed left hemispheric hypermetabolism. The child became almost seizure-free and showed improved development after left-sided hemispherotomy.
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PMID:[Surgical treatment of resistant epilepsy, caused by hemispherical dysgenesis--case report]. 1957 68

We present a male infant with hemifacial seizures refractory to antiepileptic medication. Hemifacial spasms around the left eye were frequent during wakefulness and sleep since birth. He also had mild psychomotor retardation. Magnetic resonance imaging (MRI) revealed a large tumor in the left middle cerebellar peduncle. Ictal single photon emission computed tomography (SPECT) and ictal (18)F-fluorodeoxyglucose [(18)F-FDG] positron emission tomography (PET) revealed hyperperfusion and hyper glucose metabolism at the tumor. Total removal of the tumor resulted in complete disappearance of hemifacial seizures and improved psychomotor development, indicating that the cerebellar tumor caused hemifacial seizures. A histopathological study confirmed that the tumor was a ganglioglioma. This case and the literature on similar cases indicated that this was a new epileptic syndrome originating in the cerebellum. Early diagnosis and early complete removal of the epileptogenic lesion should be recommended for this syndrome.
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PMID:Hemifacial seizures due to ganglioglioma of cerebellum. 1962 47

The spatial relationship between an intracranial EEG-defined epileptic focus and cortical hypometabolism on glucose PET has not been precisely described. In order to quantitatively evaluate the hypothesis that ictal seizure onset and/or rapid seizure propagation, detected by subdural EEG monitoring, commonly involves normometabolic cortex adjacent to hypometabolic cortical regions, we applied a novel, landmark-constrained conformal mapping approach in 14 children with refractory neocortical epilepsy. The 3D brain surface was parcellated into finite cortical elements (FCEs), and hypometabolism was defined using lobe- and side-specific asymmetry indices derived from normal adult controls. The severity and location of hypometabolic areas vs. ictal intracranial EEG abnormalities were compared on the 3D brain surface. Hypometabolism was more severe in the seizure onset zone than in cortical areas covered by non-onset electrodes. However, similar proportions of the onset electrodes were located over and adjacent to (within 2 cm) hypometabolic regions (46% vs. 41%, respectively), whereas rapid seizure spread electrodes preferred these "adjacent areas" rather than the hypometabolic area itself (51% vs. 22%). On average, 58% of the hypometabolic regions had no early seizure involvement. These findings strongly support that the seizure onset zone often extends from hypometabolic to adjacent normometabolic cortex, while large portions of hypometabolic cortex are not involved in seizure onset or early propagation. The clinical utility of FDG PET in guiding subdural electrode placement in neocortical epilepsy could be greatly enhanced by extending grid coverage to at least 2 cm beyond hypometabolic cortex, when feasible.
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PMID:Quantitative brain surface mapping of an electrophysiologic/metabolic mismatch in human neocortical epilepsy. 1973 12

To investigate the metabolic behavior of different disease processes and pathology in epilepsy, fluorodeoxyglucose-positron emission tomography (FDG-PET) images of 280 patients with refractory epilepsy who had been surgically treated were retrospectively analyzed. The image findings were compared with the surgical pathology report. For all the pathology types reported, the major manifestations were regional hypometabolism. Of patients with sclerosis 92.1% (153/166) demonstrated FDG hypometabolism; 5.4% (9/166) were normometabolic and 2.4% (4/166) had increased FDG uptake (hypermetabolism). Of patients with malformation of cortical development, 84.5% (60/71) demonstrated hypometabolism, 8.4% (6/71) hypermetabolism, and 7% (5/71) showed normal metabolism. All of the neoplasms (24/24) and inflammatory processes (25/25) showed regional hypometabolism. The study suggests that although the major findings on FDG-PET in patients with refractory epilepsy are hypometabolic, attention should also be paid to patients with regional hypermetabolism, which might sufficiently localize the seizure origin. It might be worthwhile to repeat the study if no regions of hypometabolism are found and the electroencephalography suggests frequent spiking activity.
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PMID:PET manifestation in different types of pathology in epilepsy. 1989 98

A fluorescent analog to 2-deoxy-2 [(18)F] fluoro-D-glucose position emission tomography (FDG-PET) would allow for the introduction of metabolic imaging into intraoperative and minimally invasive settings. We present through in vitro and in vivo experimentation an evaluation of 2-(N-(7-nitrobenz-2-oxa-1,3-diazol-4-yl)amino)-2-deoxyglucose (2-NBDG), a fluorescently labeled glucose molecule, as a molecular beacon of glucose utilization. The competitive inhibition of 2-NBDG uptake by excess free glucose is directly compared against FDG uptake inhibition in cultured cells. 2-NBDG uptake in the brain of a mouse experiencing a generalized seizure is measured, as well as in subcutaneously implanted tumors in mice during fed and fasting states. Localization of 2-NBDG into malignant tissues is studied by laser scanning microscopy. The clinical relevance of 2-NBDG imaging is examined by performing fluorescence colonoscopy, and by correlating preoperative FDG-PET with intraoperative fluorescence imaging. 2-NBDG exhibits a similar uptake inhibition to FDG by excess glucose in the growth media. Uptake is significantly increased in the brain of an animal experiencing seizures versus control, and in subcutaneous tumors after the animals are kept nil per os (NPO) for 24 h versus ad libitum feeding. The clinical utility of 2-NBDG is confirmed by the demonstration of very high target-to-background ratios in minimally invasive and intraoperative imaging of malignant lesions. We present an optical analog of FDG-PET to extend the applicability of metabolic imaging to minimally invasive and intraoperative settings.
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PMID:Evaluation and clinically relevant applications of a fluorescent imaging analog to fluorodeoxyglucose positron emission tomography. 2005 52

Establishing an early diagnosis of Lafora disease (LD) is often challenging. We describe two cases of LD presenting as myoclonus and tonic-clonic seizures, initially suggesting idiopathic generalized epilepsy. The subsequent course of the disease was characterized by drug-resistant myoclonic epilepsy, cognitive decline, and visual symptoms, which oriented the diagnosis toward progressive myoclonic epilepsy and, more specifically, LD. Early in the evolution in the first case, and before histopathologic and genetic confirmation of LD in both cases, [18]Fluorodeoxyglucose positron emission tomography (FDG-PET) revealed posterior hypometabolism, consistent with the well-known posterior impairment in this disease. This suggests that FDG-PET could help to differentiate LD in early stages from other progressive myoclonic epilepsies, but confirmation is required by a longitudinal study of FDG-PET in progressive myoclonic epilepsy.
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PMID:Posterior glucose hypometabolism in Lafora disease: early and late FDG-PET assessment. 2016 46

We describe a 61-year-old patient with clinical evidence of limbic encephalitis who improved with anticonvulsant treatment only, that is, without the use of immunosuppressive agents. Three years following occurrence of anosmia, increasing memory deficits, and emotional disturbances, he presented with new-onset temporal lobe epilepsy, with antibodies binding to neuronal voltage-gated potassium channels and bitemporal hypometabolism on FDG-PET scan; the MRI scan was normal. This is most likely a case of spontaneous remission, illustrating that immunosuppressive therapy might be suspended in milder courses of limbic encephalitis. It remains open whether treatment with anticonvulsant drugs played an additional beneficiary role through the direct suppression of seizures or, additionally, through indirect immunomodulatory side effects.
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PMID:Improvement of non-paraneoplastic voltage-gated potassium channel antibody-associated limbic encephalitis without immunosuppressive therapy. 2016 92

We describe the ictal [(18)F]FDG-PET study of a case of absence status showing bilateral thalamic hypermetabolism and frontal cortex hypometabolism. This is the first ictal assessment of absence status by [(18)F]FDG-PET reporting this particular cortical and subcortical involvement. Our findings support the theory of corticothalamic circuitry involvement in the pathophysiology of absence seizures and stress the similarities of the clinical and metabolic pattern observed during absences with the pattern of task-induced interruption of the default state of brain function.
Seizure 2010 Apr
PMID:Thalamic activation and cortical deactivation during typical absence status monitored using [18F]FDG-PET: a case report. 2016 11


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