apraxias/seizures

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Negative motor seizure arising from the negative motor area: is it ictal apraxia?

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OBJECTIVE Seizure manifesting motor arrest, that is, negative motor seizure (NMS), is a rare epileptic condition in which only inability to conduct voluntary movements or praxis is produced, although consciousness is preserved. The negative motor area (NMA) seems to be responsible, but its generator

Obstructive sleep apnea, seizures, and childhood apraxia of speech.

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Associations between obstructive sleep apnea and motor speech disorders in adults have been suggested, though little has been written about possible effects of sleep apnea on speech acquisition in children with motor speech disorders. This report details the medical and speech history of a nonverbal

[A 78-year-old female patient with dizziness, apraxia and seizure under proton pump inhibitor therapy].

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We report about a female patient with severe hypomagnesemia under therapy with proton pump inhibitors (PPI) who presented with a cerebral seizure. Chronic use of PPIs can cause hypomagnesemia. Because of mostly unspecific symptoms which become symptomatic only with severe deficiency, the disease

Newly recognized overgrowth syndrome with macrosomia, macrocrania, hyperostosis of the cranial vault, mental deficiency, seizures, poor motor control, and orofacial dyspraxia.

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Two patients with PNKP mutations presenting with microcephaly, seizure, and oculomotor apraxia.

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[Language regression of the anarthric-dyspraxic type with innervation apraxia and prolonged tonic seizures; notes on a case].

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Syndrome of dyspraxia and multifocal seizures associated with chronic hemodialysis.

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Diagnostic outcome of surgical revision of intracranial electrode placements for seizure localization.

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OBJECTIVE We aimed to determine the yield of revising intracranially implanted electrodes and the factors contributing to the yield. METHODS Patients were identified from the Mayo Clinic Epilepsy Surgery Database between 1997 and 2010. Twenty patients had revision of intracranial electrode

[Variants of Todd's paralysis: postictal apraxia and prolonged postictal hemineglect].

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Todd's post-epileptic paralysis is a well-known complication after focal or generalized epileptic seizures. The underlying pathophysiology, however, is still unknown. Commonly, it is associated with a hemiparesis, usually lasting minutes or hours, rarely as long as two days, with subsequent complete

Carbamazepine responsive epileptic oral motor and ocular motor apraxia.

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We evaluated seven patients with oral motor apraxia and ocular motor apraxia. Apraxia in three patients (Group 1) with new-onset partial seizures and epileptiform discharges on EEG improved with carbamazepine. Four patients (Group 2) without seizures and nonepileptiform EEG findings had no change in

Nonlesional central lobule seizures: use of awake cortical mapping and subdural grid monitoring for resection of seizure focus.

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OBJECTIVE Surgical treatment options for intractable seizures caused by a nonlesional epileptogenic focus located in the central sulcus region are limited. The authors describe an alternative surgical approach for treating medically refractory nonlesional perirolandic epilepsy. METHODS Five

New X-linked syndrome with apraxia, ataxia, and mental deficiency: clinical, cytogenetic and neuropsychological studies in two Danish families.

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In 2 unrelated families 9 males presented with ataxia, apraxia, and neuropsychological abnormalities or mental deficiency, inherited as an X-linked recessive syndrome with partial clinical expression in obligate female carriers. The symptoms were present in early childhood and were non-progressive.

[Bifocal atypical rolandic epilepsy with speech dyspraxia].

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Clinical and neurophysiological analysis of a case of a 7 year old patient with typical benign partial seizures with rolandic spikes and speech disorder, differing from those in Landau-Kleffner syndrome and in typical benign partial epilepsy of childhood presenting as speech dyspraxia. Two

Ictal Phase Perfusion SPECT of Nonketotic Hyperglycemia-Induced Parieto-occipital Seizure.

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A 68-year-old man with diabetes mellitus type 2 presented himself with visual distortion and apraxia. Nonketotic hyperglycemic seizure with both motor and sensory components was suspected. Tc-ECD perfusion SPECT demonstrated hyperperfusion at right parieto-occipital lobe during ictal phase.

Expanding the ataxia with oculomotor apraxia type 4 phenotype.

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Ataxia with oculomotor apraxia type 4 (AOA4) is an autosomal recessive (AR) disorder recently delineated in a Portuguese cohort and caused by mutations in the PNKP (polynucleotide kinase 3'-phosphatase) gene.(1) AOA4 is a progressive, complex movement disorder that includes hyperkinetic features,

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