Cases reported "Myoclonus"

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1/81. Facial dyskinesia induced by auditory stimulation: a report of four cases.

    INTRODUCTION: The Vibroacoustic disease (VAD) is an occupational pathology induced by long-term (>10 yr) exposure to large pressure amplitude (> or = 90 dB SPL) and low frequency (< or = 500 Hz) noise. During studies contributing to the characterization of VAD, abnormal facial movements induced by repetitive auditory stimuli were observed in one individual employed as an aeronautical mechanic. The goal of this study was to investigate the existence of movement disorders triggered by auditory stimuli in a group of VAD-diagnosed patients. methods: Sixty VAD patients received auditory and median nerve stimulation. Simultaneously, EEG monitoring was performed. RESULTS: Abnormal myoclonus movements were triggered by auditory stimuli in four patients. EEG recordings were normal in all 60 patients. Stimulation of the median nerves did not trigger any abnormal movements. CONCLUSION: These data suggest that this facial dyskinesia has a subcortical origin.
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2/81. Idiopathic rolandic epilepsy with "interictal" facial myoclonia and oromotor deficit: a longitudinal EEG and PET study.

    PURPOSE: The prognosis of benign epilepsy with centrotemporal spikes (BECTS) is always favorable as far as the epilepsy is concerned. However, some data suggest that affected children may be at risk for minor cognitive impairment. We report here the longitudinal study of a young girl demonstrating that BECTS also may be associated with severe motor disturbances. methods: BECTS (rare left oromotor seizures, right rolandic spike-waves activated during sleep) started at the age of 3 years 6 months in a girl with normal initial psychomotor development. Her clinical, neuropsychological, and EEG status was assessed every 3-6 months. Regional cerebral glucose metabolism was measured by using the [18F]fluorodeoxyglucose-positron emission tomography (FDG-PET) method. RESULTS: Between the age of 5 and 6 years, the girl had (a) increased seizure frequency; (b) brief perioral and palpebral myoclonic jerks, concomitant with the spike component of interictal spike-waves, and (c) persistent but fluctuating oromotor deficits (drooling, dysarthria, dysphagia). The EEG showed a marked increase in abundance and amplitude of wake and sleep interictal abnormalities, which became bilateral. Awake FDG-PET revealed a bilateral increase of glucose metabolism in opercular regions. A complete and definitive EEG and clinical remission occurred at age 5 years 11 months and has persisted since (present age, 7 years 9 months). CONCLUSIONS: This case confirms that during BECTS, epileptiform dysfunctions within rolandic areas may induce "interictal" positive or negative oromotor symptoms, independent of classic seizures.
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3/81. Facial reflex myoclonus induced by language: a neuropsychological and neurophysiological study.

    We studied a 53 year old right-handed patient who presented isolated myoclonus of right facial muscles induced exclusively by language. Twitching significantly hindered speaking and reading performance. MRI and CT-scan revealed no brain lesion. Conventional EEG showed a few spike-waves predominantly in the left hemisphere. Spike-waves increased during drowsiness. An EEG-EMG polygraphic study was performed during stimulation tests which included linguistic tasks and non-verbal/non-linguistic tests. myoclonus was triggered by speaking and writing but not by non-linguistic tasks. The severity of myoclonus was dependent on the complexity of the language task. back-averaging of right facial EMG bursts failed to show a reliable EEG-EMG correlation. However, the facial reflex myoclonus might have originated from the left rolandicopercular cortex, as it was triggered by complex language activities. Findings in this case are compared with those reported for other forms of reflex seizure and myoclonus.
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4/81. Cortical reflex myoclonus studied with cortical electrodes.

    OBJECTIVE: To study the mechanism of cortical reflex myoclonus. methods: A patient with stimulus sensitive myoclonus of the left foot had an array of subdural electrodes placed over the right sensorimotor cortex. RESULTS: Stimulation through one of the electrodes (contact 13) facilitated leg muscles with the shortest latency and was presumed to lie over the motor cortex. tibial nerve stimulation evoked a potential with the shortest latency 1 cm further posteriorly (contacts 11-12). These contacts were presumed to lie over the sensory cortex. The potential at 11-12 was followed by a much larger potential that reversed polarity at contact 13. back averaging from spontaneous myoclonic jerks showed a cortical premovement potential which reversed polarity at contact 13. The threshold for the motor evoked potential in leg muscles evoked by transcranial magnetic stimulation was lower on the affected side. Electrical stimulation through contact 13 produced cortical potentials that could be recorded at adjacent contacts. The combination of a positive potential followed by a negative potential recurred at approximately 35-40 ms intervals, each positive potential generating a myoclonic jerk. Additional waves resembling I waves accompanied only the first positive potential. Surgical removal of the cortex under electrode 13 abolished the myoclonus. CONCLUSIONS: The myoclonic jerks arose in the motor cortex. We postulate that there is increased excitability or synchronization of the cortical neurons at that site. The spontaneous, peripherally induced and recurrent cortical potentials and myoclonic jerks can occur without participation of the circuitry of the presumed I waves.
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5/81. Segmental facial myoclonus in moebius syndrome.

    Moebius syndrome is characterized by sixth and seventh nerve palsy and is usually the result of bilateral hypoplasia or aplasia of the respective brain stem nuclei. There have been no reports of involuntary facial movements associated with this malformative complex. We report on a 6-year-old boy affected by Moebius syndrome with asymmetric involvement and segmental facial myoclonus with onset at age 2 years, affecting the side with partially conserved motility. Clinical presentation included congenital peripheral palsy of the right seventh cranial nerve and left-sided rhythmic rising of the upper lip and eyebrow. Surface-electromyography (EMG) of the left levator labii and frontalis muscles showed rhythmic bursting (duration: 150-450 ms; frequency: 1-3 Hz). Electroencephalographic (EEG)-polygraphic recordings and burst-locked EEG averaging failed to show any consistent EEG activity preceding the EMG bursts. Study of the blink reflex, somatosensory and motor-evoked potentials showed findings consistent with pontine pathology. Segmental facial myoclonus, although extremely rare in children, must be differentiated from several other paroxysmal motor manifestations associated with structural lesions involving the brain stem. Segmental facial myoclonus stem-Structural lesion.
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6/81. Postural and action myoclonus in patients with parkinsonian type multiple system atrophy.

    patients with a parkinsonian syndrome and features of multisystem atrophy (pMSA) may exhibit abnormal movements of the hands and fingers, which are reported in the literature either as "jerky" tremor or myoclonus. We studied clinically and electrophysiologically these movements in 11 consecutive patients with pMSA. No abnormal movements were observed when the patients were at complete rest, except for a characteristic parkinsonian "pill-rolling" tremor in one patient. Abnormal small-amplitude, nonrhythmic movements involving just one or a few fingers, or more rarely the whole hand, were observed in nine patients when holding a posture or at the beginning of an action. Accelerometric recordings showed small-amplitude irregular oscillations which, contrary to those of patients with tremor, had no predominant peak in the Fast Fourier frequency spectrum analysis. Electromyographic recordings in the forearm and hand muscles showed brief jerks of less than 100 ms duration which were synchronous in antagonist muscles of the forearm and alternated with brief periods of silence. Electrical stimulation of the digital nerves evoked consistent reflex responses in the wrist flexor and extensor muscles at a latency of 55.3 /-4.1 ms (range, 50-63 ms). Routine electroencephalographic (EEG) and somatosensory evoked potentials to median nerve stimulation were normal. back-averaging of the EEG activity time-locked to the jerks was performed in two patients with no evidence of abnormal cortical activity. Two patients had episodes of transient respiratory failure related to pneumonia. This caused a long-lasting enhancement of the abnormal hand and finger movements, which became larger and more widespread, with features of posthypoxic myoclonus. We conclude that the abnormal hand and finger movements of patients with pMSA are a form of postural and action myoclonus, and can be described as mini-polymyoclonus.
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7/81. Irregular jerky tremor, myoclonus, and thalamus: a study using low-frequency stimulation.

    High-frequency thalamic stimulation alleviates tremor in Parkinson's disease (PD) and essential tremor (ET). The origin of thalamic myoclonus is unexplained and the effects of low-frequency thalamic stimulation on movement control are still unknown. We studied the effects of stimulation at a low frequency of 15 Hz in five drug-free patients (3 PD, 2 ET) 6 months after thalamic implantation of quadripolar electrodes (unilateral in four patients, bilateral in one patient). Clinical, electrophysiological, and videotaped assessment, using a monopolar 15 Hz frequency (3 V, 90 micros) stimulation current applied simultaneously through two adjacent contacts of the electrode, was performed. We observed myoclonus and irregular jerky tremor in the upper limb contralateral to the site of stimulation. The jerks lasted less than 200 ms, were irregular and not synchronous with stimulation, were superimposed on rest or postural tremor, and increased in response to tactile, proprioceptive, or vibratory stimuli. The fact that this complex movement disorder can be induced by low-frequency stimulation in the ventral intermediate nucleus (Vim) of the thalamus suggests that it results, at least partly, from dysfunction of the Vim and possibly adjacent nuclei of the thalamus.
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8/81. Phase relationships between cortical and muscle oscillations in cortical myoclonus: electrocorticographic assessment in a single case.

    AIM: To compare voluntary- and sensory-induced myoclonic jerks using spectral analysis in a subject with cortical myoclonus. methods: The coherence, phase and cumulant density estimates were calculated between right electrocorticographic (ECoG) signals and distal left leg muscles in a patient with subdural electrodes inserted over the right sensorimotor cortex. RESULTS: Significant coherence between sensorimotor cortex and muscle was found up to 60 Hz during voluntary induced myoclonic jerks. Additional higher frequency coherence ( approximately 140 and 190 Hz) was found during sensory-induced myoclonic jerks. The cortical signals phase led muscle signals at frequencies >15 Hz by delays consistent with transmission along corticospinal pathways. Below 15 Hz the cortex phase lagged the muscle signals. Polarity reversal of the cumulant density estimate and the ECoG site demonstrating the highest coherence helped to localize the site of the abnormal oscillatory activity to the leg area of the motor cortex. CONCLUSIONS: Oscillations of different frequencies can co-exist at a given location and can both phase lead and lag contralateral muscle. This has implications for cortex-muscle latency measures calculated by back-averaging techniques.
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9/81. Disinhibition of somatosensory and motor cortex in mitochondriopathy without myoclonus.

    OBJECTIVE: To test electrophysiologically, if patients with mitochondriopathy but without evidence of myocloni have subclinical signs of disinhibition in motor and somatosensory cortices. methods: Two patients were studied and compared with age-matched control groups. RESULTS: In both patients, giant somatosensory evoked potentials after median nerve stimulation and a reduced intracortical inhibition tested by transcranial magnetic stimulation in a paired pulse paradigm indicated a dysfunction of inhibitory circuits in the motor as well as the somatosensory cortex. In addition, the somatosensory evoked 600 Hz activity recorded by magnetoencephalography was abolished. CONCLUSIONS: patients with mitochondriopathy may suffer from a subclinical disturbance of inhibition in the sensorimotor cortex. The loss of 600 Hz activity indicates that these high-frequency oscillations could reflect the activity of inhibitory neurons in the somatosensory cortex.
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10/81. Paradoxical lateralization of parasagittal spikes revealed by back averaging of EEG and MEG in a case with epilepsia partialis continua.

    Our aim was to localize the generator site of parasagittal epileptiform discharges in a patient with epilepsia partialis continua (EPC) in the right leg. We examined a 32-year-old woman with EPC whose conventional EEG did not show any epileptic discharge. We performed the jerk-locked back averaging (JLA) of EEG and magnetoencephalography (MEG) to localize the dipole source of sharp transients. The myoclonic discharges in the right soleus muscle were used as a trigger pulse. JLA revealed consistent EEG and MEG sharp transients that coincided consistently and constantly preceded the myoclonic jerks. JLA of EEG demonstrated sharp waves paradoxically distributed over the vertex and right hemisphere. However, the estimated dipoles of MEG were localized in a restricted area in the primary leg motor area in the left hemisphere, which was closely located in the abnormal lesion on the brain MRI. JLA of MEG is considered to be a useful non-invasive method for localizing the epileptogenic area in EPC even when paradoxical lateralization of electroencephalographic discharges was noted.
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