The Experts below are selected from a list of 222 Experts worldwide ranked by ideXlab platform
Hideyuki Sawada - One of the best experts on this subject based on the ideXlab platform.
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transient myoclonic state with Asterixis presenting as persistent hyperperfusion on single photon emission computed tomography a case report
Neurology and Clinical Neuroscience, 2015Co-Authors: Atsushi Umemura, Tomoko Oeda, Hideyuki SawadaAbstract:Transient myoclonic state with Asterixis is characterized by sudden onset generalized myoclonus and Asterixis without consciousness impairment. Electrophysiological studies have shown that myoclonus correlates with cortical hyperexcitability localized in the primary motor cortex during the symptomatic period. However, it is unclear whether this excitability remains in the asymptomatic period. Here, we report a 79-year-old Japanese man who presented with transient myoclonic state with Asterixis. He had been diagnosed with progressive non-fluent aphasia and he suffered from rhythmic myoclonus; predominantly in the neck, shoulders and upper extremities. Asterixis was observed in the forearms. Brain 123I-iodoamphetamine single-photon emission computed tomography showed focal hyperperfusion in the bilateral precentral gyri even at 3 months after remission of the myoclonus. These data suggest that cortical hyperactivity was persistent without symptoms and led to transient myoclonic state with Asterixis, which could have been due to the underlying neurodegenerative disorder of progressive non-fluent aphasia.
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Transient myoclonic state with Asterixis presenting as persistent hyperperfusion on single‐photon emission computed tomography: A case report
Neurology and Clinical Neuroscience, 2014Co-Authors: Atsushi Umemura, Tomoko Oeda, Hideyuki SawadaAbstract:Transient myoclonic state with Asterixis is characterized by sudden onset generalized myoclonus and Asterixis without consciousness impairment. Electrophysiological studies have shown that myoclonus correlates with cortical hyperexcitability localized in the primary motor cortex during the symptomatic period. However, it is unclear whether this excitability remains in the asymptomatic period. Here, we report a 79-year-old Japanese man who presented with transient myoclonic state with Asterixis. He had been diagnosed with progressive non-fluent aphasia and he suffered from rhythmic myoclonus; predominantly in the neck, shoulders and upper extremities. Asterixis was observed in the forearms. Brain 123I-iodoamphetamine single-photon emission computed tomography showed focal hyperperfusion in the bilateral precentral gyri even at 3 months after remission of the myoclonus. These data suggest that cortical hyperactivity was persistent without symptoms and led to transient myoclonic state with Asterixis, which could have been due to the underlying neurodegenerative disorder of progressive non-fluent aphasia.
W M Carroll - One of the best experts on this subject based on the ideXlab platform.
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unilateral Asterixis duetoalesion ofthe ventrolateral thalamus
1994Co-Authors: R Stell, W M CarrollAbstract:A caseofunilateral Asterixis ina man withafocal ischaemic lesion ofthecontralateral ventral thalamus ispresented. Atypically, themovementswerepresent atrestandhada pattern ofactivation thatresulted inaninitial misdiagnosis of epilepsia partialis continua. Thiscase emphasisesthe importanceof electromyographic analysis in establishing the correctdiagnosis of involuntary movementsbefore starting specific treatment. (JNeurol Neurosurg Psychiatry 1994;57:878-880)
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unilateral Asterixis due to a lesion of the ventrolateral thalamus
Journal of Neurology Neurosurgery and Psychiatry, 1994Co-Authors: R Stell, S Davis, W M CarrollAbstract:A case of unilateral Asterixis in a man with a focal ischaemic lesion of the contralateral ventral thalamus is presented. Atypically, the movements were present at rest and had a pattern of activation that resulted in an initial misdiagnosis of epilepsia partialis continua. This case emphasises the importance of electromyographic analysis in establishing the correct diagnosis of involuntary movements before starting specific treatment.
Toshihiko Suenaga - One of the best experts on this subject based on the ideXlab platform.
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transient myoclonic state with Asterixis in elderly patients a new syndrome
Journal of the Neurological Sciences, 1992Co-Authors: Shuji Hashimoto, Junichiro Kawamura, Toru Yamamoto, Ayae Kinoshita, Yoshiaki Segawa, Yuzuru Harada, Toshihiko SuenagaAbstract:Abstract We report 7 patients who developed acute co-occurences of fragmentary generalized myoclonus and Asterixis. All patients were elderly and had other chronic diseases. This condition appeared acutely, progressed over several hours and then disappeared in 2–3 days with diazepam administration. No sequelae were noted, although most cases developed recurrences. The myoclonus occured spontaneously and was slightly enhanced by action. The myoclonus was widely distributed but predominated in the neck, shoulder girdle, and upper extremities. Opsoclonus was not noted. Clinically apparent myoclonus was not evoked by sensory stimuli. Asterixis was observed in the upper extremities in all cases. Asterixis-like movements of the protruded tongue were also observed. Neurological findings other than the myoclonus and Asterixis were unremarkable. Neither metabolic nor organic abnormalities clearly responsible for this condition were identified. Cerebral potentials preceding the myoclonic jerks recorded in one case suggested that the myoclonus may have been a spontaneous cortical myoclonus. We named this condition a transient myoclonic state with Asterixis (TMA). Awareness of this syndrome is clinically important because of its benign nature, although it can recur.
Manabu Inoue - One of the best experts on this subject based on the ideXlab platform.
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pathophysiology of unilateral Asterixis due to thalamic lesion
Clinical Neurophysiology, 2012Co-Authors: Manabu Inoue, Yasuhiro Kojima, Tatsuya Mima, Nobukatsu Sawamoto, Masao Matsuhashi, Tomoyuki Fumuro, Masato Kinboshi, Satoko Koganemaru, M KandaAbstract:Abstract Objective Unilateral Asterixis has been reported in patients with thalamic lesion. This study aims at elucidating the pathophysiology of the thalamic Asterixis. Methods Two cases with unilateral Asterixis caused by an infarction in the lateral thalamus were studied by analysing the Asterixis-related cortical activities, transcranial magnetic stimulation (TMS) for motor cortex excitability and probabilistic diffusion tractography for the thalamo-cortical connectivity. Results Averaging of electroencephalogram (EEG) time-locked to the Asterixis revealed rhythmic oscillations of a beta band at the central area contralateral to the affected hand. TMS revealed a decrease in the motor evoked potential (MEP) amplitude and a prolongation of the silent period (SP). The anatomical mapping of connections between the thalamus and cortical areas using a diffusion-weighted image (DWI) showed that the lateral thalamus involved by the infarction was connected to the premotor cortex, the primary motor cortex (M1) and the primary somatosensory cortex (S1) of the corresponding hemisphere. Conclusions The thalamic Asterixis is mediated by the sensorimotor cortex, which is subjected to excessive inhibition as a result of the thalamic lesion involving the ventral lateral nucleus. Significance This is the first demonstration of participation of the sensorimotor cortex in the generation of Asterixis due to the lateral thalamic lesion.
H Rittmannsberger - One of the best experts on this subject based on the ideXlab platform.
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medikamentos ausgeloste Asterixis
Deutsche Medizinische Wochenschrift, 2008Co-Authors: H Rittmannsberger, F LeblhuberAbstract:: A 54-year-old woman with acute schizoaffective psychosis was treated with lithium carbonate (1,350 mg daily) and zuclopenthixol. On admission, clozapine was added (250 mg daily). Because extrapyramidal symptoms (rigor, akinesia) developed, she was additionally given biperiden retard (4 mg daily) from the fourth hospital day onwards. Eleven days after admission she began to complain of "unsteadiness" and "tremors" in her arms and she had Asterixis (flapping tremor) on holding up her arms. The electromyogram showed electrical pauses of 60-120 ms, typical for Asterixis. There were no significant metabolic or organic cerebral changes that could have accounted for the symptoms which presumably had been induced by the drugs even though their dosage was not unusual. The symptoms in fact regressed completely after the clozapine dose had been reduced, at first to 125 mg then to 50 mg. Previous experience has suggested that the risk of Asterixis is particularly high when lithium and clozapine are taken together.
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Asterixis induced by psychotropic drug treatment
Clinical Neuropharmacology, 1996Co-Authors: H RittmannsbergerAbstract:Summary:Asterixis (flapping tremor) can be induced by treatment with psychopharmacologic agents. We observed 10 cases of Asterixis in psychiatric inpatients, most with affective spectrum disorders being treated with combination therapy. The drugs most often used were clozapine (eight cases), lithium
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Asterixis induced by carbamazepine therapy
Biological Psychiatry, 1992Co-Authors: H Rittmannsberger, F LeblhuberAbstract:Abstract There are very few reports about Asterixis as a side effect of treatment with psychopharmacologic agents. In this report we present four patients treated with a combination of different psychotropic drugs, in whom Asterixis was triggered either by adding carbamazepine (CBZ) to a treatment regimen, or by increasing its dosage. Neither dosage nor serum levels of CBZ were in a higher range. We consider Asterixis to be an easily overlooked sign of neurotoxicity, which may occur even at low or moderate dosage levels, if certain drugs as lithium or clozapine are used in combination with CBZ.
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Asterixis as a side effect of carbamazepine therapy
Journal of Molecular Medicine, 1991Co-Authors: H Rittmannsberger, F Leblhuber, R SommerAbstract:A patient developed Asterixis 13 weeks after starting a therapy with carbamazepine. Serum concentration of carbamazepine was within the therapeutic levels. Further factors which might have provoked Asterixis were an impairment of pulmonary function and the combination with a neuroleptic and lithium. Since the latter risk factors had already been present for a long time, it may be assumed that the addition of carbamzepine triggered the development of Asterixis.
