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Motor Phenomena (motor + phenomenon)
Selected AbstractsThe spectrum of benign myoclonus of early infancy: Clinical and neurophysiologic features in 102 patientsEPILEPSIA, Issue 5 2009Roberto H. Caraballo Summary Purpose:, To redefine benign myoclonus of early infancy (BMEI) through analysis of clinical and neurophysiologic features in 102 patients with the aim to widen the spectrum of the syndrome, including a number of different clinical expressions of transient nonepileptic paroxysmal movements occurring in normal infants. Methods:, We recruited patients from one center in Argentina and two in Italy, including infants with normal neurologic and psychomotor development presenting with brief paroxysmal abnormal movements. Children with motor phenomena occurring only during sleep were excluded. Patients with abnormal interictal or ictal electroencephalography (EEG) findings were also excluded. The follow-up ranged from 2,40 years. Results:, One hundred and two infants (60 male) met the inclusion criteria. Age at onset ranged from 1,12 months, with a median age of 6.2 months. The following nonepileptic paroxysmal motor phenomena were recognized: (1) myoclonus, (2) spasms and brief tonic contractions, (3) shuddering, (4) atonia or negative myoclonus, (5) more than one type of motor phenomenon. In the majority of cases the episodes occurred only while awake and repeated several times a day. In 45 (44.1%) of the 102 cases contractions appeared in clusters. Conclusions:, Based on the analysis of clinical and EMG features in this large series of infants, we postulate that the spectrum of the syndrome is wider than initially suspected, and that the different transient motor manifestations and their correlation with different EMG patterns will allow recognition of this definitely benign condition comprising a variety of episodic motor phenomena in normal babies. [source] Interobserver Reliability of Video Recording in the Diagnosis of Nocturnal Frontal Lobe SeizuresEPILEPSIA, Issue 8 2007Luca Vignatelli Summary:,Background: Nocturnal frontal lobe seizures (NFLS) show one or all of the following semeiological patterns: (1) paroxysmal arousals (PA: brief and sudden recurrent motor paroxysmal behavior); (2) hyperkinetic seizures (HS: motor attacks with complex dyskinetic features); (3) asymmetric bilateral tonic seizures (ATS: motor attacks with dystonic features); (4) epileptic nocturnal wanderings (ENW: stereotyped, prolonged ambulatory behavior). Objective: To estimate the interobserver reliability (IR) of video-recording diagnosis in patients with suspected NFLS among sleep medicine experts, epileptologists, and trainees in sleep medicine. Methods: Sixty-six patients with suspected NFLS were included. All underwent nocturnal video-polysomnographic recording. Six doctors (three experts and three trainees) independently classified each case as "NFLS ascertained" (according to the above specified subtypes: PA, HS, ATS, ENW) or "NFLS excluded". IR was calculated by means of Kappa statistics, and interpreted according to the standard classification (0.0,0.20 = slight agreement; 0.21,0.40 = fair; 0.41,0.60 = moderate; 0.61,0.80 = substantial; 0.81,1.00 = almost perfect). Results: The observed raw agreement ranged from 63% to 79% between each pair of raters; the IR ranged from "moderate" (kappa = 0.50) to "substantial" (kappa = 0.72). A major source of variance was the disagreement in distinguishing between PA and nonepileptic arousals, without differences in the level of agreement between experts and trainees. Conclusions: Among sleep experts and trainees, IR of diagnosis of NFLS, based on videotaped observation of sleep phenomena, is not satisfactory. Explicit video-polysomnographic criteria for the classification of paroxysmal sleep motor phenomena are needed. [source] Ictal Pattern of EEG and Muscular Activation in Symptomatic Infantile Spasms: A Videopolygraphic and Computer AnalysisEPILEPSIA, Issue 12 2002Francesca Bisulli Summary: ,Purpose: To investigate ictal muscular phenomena characterizing symptomatic infantile spasms (ISs) and their relation to ictal EEG. Methods: Four children with severe encephalopathy, neurologic impairment, and refractory ISs related to different dysplastic lesions, underwent videopolygraphic recordings collecting surface electromyogram (EMG) activity from several cranial and limb muscles to evaluate the pattern of muscular recruitment, duration, and side-to-side asymmetry of ISs. Acquired data were stored for off-line analysis by a computerized polygraphic system. Results: Spasms were characterized by a complex pattern of muscular activation. A constant or rostrocaudal propagation pattern was lacking in all patients. Intervals between the onset of EMG activity in different muscles in each spasm were very long: ,100,200 ms. Two patients, with hemispheric cortical dysplasia and agenesis of the corpus callosum, had asymmetric and asynchronous spasms in which the EMG onset of the muscles contralateral to the affected hemisphere constantly anticipated that of the ipsilateral ones. Backaveraging of EEG activity disclosed a high-amplitude EEG complex on the same side as the dysplastic lesion, preceding or succeeding the contralateral muscle activity onset. In the other two patients with diffuse cortical dysplasia, no EEG transient was related to EMG activity onset. Conclusions: Despite clinical similarity between spasms in the same patient, our data demonstrate the complexity and heterogeneity of these motor phenomena. Our findings cannot be explained simply in terms of cortical or reticular generators like other motor phenomena such as cortical myoclonus or startle reflex. [source] Movement-Induced Focal Motor Seizures and Choreoathetosis As- sociated with Nonketotic Hyperglycemia: A Case ReportEPILEPSIA, Issue 2000Hisashi Tanaka Case Report: We report the case of a diabetic woman who developed right-sided reflex seizures and bilateral choreoathetosis during an episode of nonketotic hyperglycemia. The patient was a 67-year-old woman with a 14-year history of HCV-related liver cirrhosis who experienced polydipsia and polyuria in January 1998. She began to have episodes of abnormal hyperkinetic movements of the right upper extremity and tonic-clonic seizures in the right arm triggered by voluntary movements of right or bilateral arms in the beginning of March 1998. The seizures increased in frequency and consequently left her disabled. She was admitted to our hospital with complaints of these abnormal motor phenomena on March 9, 1998. Neurological examinations revealed that she was alert, well-oriented, and that cranial nerve functions were normal. Slight motor weakness of the right upper limb and deep tendon hyporeflexes were observed in all extremities. Sensations and cerebellar functions were intact. Choreic or athetotic involuntary movements were seen in the bilateral upper limbs and neck. These involuntary movements were increased by voluntary movement or posturing of the upper limbs. The focal tonic-clonic seizures were easily triggered by voluntary movements such as knotting a cord. This seizure suddenly began by tonic movements in the right upper limb and gradually progressed to the right hemi-face and neck without loss of consciousness. The average duration of seizures was about one minute. The laboratory data demonstrated mild leukocytopenia, thrombocytopenia, hepatic dysfunction, and hyperglycemia without ketosis. Fasting blood glucose was 41 I mg/dl, and HbAlc was 14.5%. Blood ammonia was within normal levels. Cranial CT revealed no abnormalities. Brain MRI on T I-weighted images demonstrated bilateral high signal intensity in the putamen. An interictal EEG revealed a symmetrical slow background activity of 7,8 Hz. An ictal EEG recording showed a 2.5 4 Hz irregular sharp and slow wave discharge in the bilateral frontal-central regions. Treatment with carbamazepine was ineffective for the seizures. However, the seizures completely disappeared after the administration of insulin on March 17. Under good control of the hyperglycemia, the abnormal involuntary movements decreased gradually and then completely disappeared; the patient became neurologically asymptomatic by March 30. The follow-tip EEG demonstrated 9-Hz alpha background activity without any epileptic discharges. Conclusions: Nonketotic hyperglycemia has been rarely reported to cause stimulus-induced seizures or hyperkinetic involuntary movements such as hemichorea-ballism. To our knowledge, this is the first reported case of both induced seizures and involuntary movements simultaneously caused by hyperglycemia. Movement-induced seizures and choreoathetoid movements in this patient can be considered to result from transiently-increased activity in the basal ganglia and/or cerebral cortex associated with metaholic disorders. [source] Topographic electroencephalogram in children during mask induction of anaesthesia with sevofluraneACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 1 2009E. SONKAJÄRVI Background: Epileptiform patterns, spikes, polyspikes and periodic epileptiform discharges (PED) have been reported in electroencephalograms (EEGs) during anaesthesia induction with sevoflurane in healthy adults and children. Published recordings have been performed with a limited number of channels, and therefore the topographic distributions of these patterns are not known. Methods: Twenty ASA I children aged 4,10 years undergoing routine operations were anaesthetized with 8% sevoflurane in 50%/50% oxygen and nitrous oxide using mask induction with controlled normoventilation. An EEG was recorded with a full 10,20 electrode system including orbitofrontal and ear electrodes, and a recording band of 0.016,70 Hz. Beat-to-beat heart rate (HR) was calculated off-line. Results: Nineteen out of 20 children developed multifocal spikes and polyspikes with a maximum over the frontal lobes. Four patients developed suppression, which was almost continuous and lasted several minutes, and thereafter a continuous EEG resumed, a few spikes were seen and then a nonepileptiform pattern. In three children a couple of PED waves were seen at the onset of a continuous EEG. HR increased maximally before the onset of spikes. No motor phenomena were seen. Conclusion: These recordings confirm the epileptogenic property of sevoflurane in mask induction. The spikes and polyspikes had frontal multifocal maxima and may be missed in recordings from frontopolar electrodes used by depth-of-anaesthesia monitors. PED and burst suppression were synchronous over the whole cortex. Epileptiform activity was indiscernible from epileptiform waveforms without anaesthesia, such as the patterns seen in status epilepticus. [source] Sleep-related stridor due to dystonic vocal cord motion and neurogenic tachypnea/tachycardia in multiple system atrophyMOVEMENT DISORDERS, Issue 5 2007Roberto Vetrugno MD Abstract Sleep-disordered breathing and sleep-related motor phenomena are part of the clinical spectrum of multiple system atrophy (MSA). Stridor has been attributed to denervation of laryngeal muscles or instead to dystonic vocal cord motion. We studied 3 patients with nocturnal stridor in the setting of MSA. All patients underwent nocturnal videopolysomnography (VPSG) with breathing and heart rate, O2 saturation and intra-esophageal pressure recordings, and simultaneous EMG recordings of the posterior cricoarytenoid, cricothyroid, and thyroarytenoid muscles and continuous vocal cord motion evaluation by means of fiberoptic laryngoscopy. VPSG/EMG and fiberoptic laryngoscopy documented normal vocal cord motion without denervation during wake and stridor only during sleep when hyperactivation of vocal cords adductors appeared in the absence of significant O2 desaturation. All patients had tachycardia and tachypnea and paradoxical breathing during sleep, erratic intercostalis and diaphragmatic EMG activity and Rem sleep behavior disorder. One of the patients had restless legs syndrome with periodic limb movement during sleep and excessive fragmentary hypnic myoclonus. In conclusion, our patients with MSA had nocturnal stridor due to sleep-related laryngeal dystonia. Stridor was associated with other abnormal sleep-related respiratory and motor disorders, suggesting an impairment of homeostatic brainstem integration in MSA. © 2007 Movement Disorder Society [source] Misdiagnosis of epileptic and non-epileptic seizures in a neurological intensive care unitACTA NEUROLOGICA SCANDINAVICA, Issue 3 2010F. Boesebeck Boesebeck F, Freermann S, Kellinghaus C, Evers S. Misdiagnosis of epileptic and non-epileptic seizures in a neurological intensive care unit. Acta Neurol Scand: 122: 189,195. © 2009 The Authors Journal compilation © 2009 Blackwell Munksgaard. Objective,,, The etiological misinterpretation of paroxysmal neurological symptoms frequently causes a delayed treatment or an inappropriate utilization of ICU-capacities. Methods,,, In this study, the data of 208 patients admitted to a neurological ICU because of acute transient neurological deficits, loss of consciousness or unclear motor phenomena were retrospectively analyzed. The initial emergency room diagnosis was compared to the final diagnosis and the rate of misdiagnosis was related to the patients' history and diagnostic data. Results,,, In 13.9%, the emergency room diagnosis of epileptic seizures turned out to be incorrect, whereas in 15.6%, the final diagnosis of epileptic seizures was missed in the emergency room. Factors that were significantly correlated to missing the seizure diagnosis were (i) no prior history of epilepsy, (ii) old age, (iii) multi-morbidity, (iv) pathologic CT-scans demonstrating cerebrovascular lesions, (v) seizure description by non-professionals, (vi) predominantly negative seizure phenomena (aphasia, loss of consciousness, paresis), (vii) lack of tongue-bite lesions. [source] | ||||||||||