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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Whole-head MEG-systems and modern spatial-filter-based analysis tools recently provided new possibilities to analyze non-invasively cerebral networks of human tremor syndromes. We compared tremor syndromes in Parkinsonian patients with a typical resting tremor as well as in patients with hepatic encephalopathy (HE) with a postural tremor called "mini-asterixis". In 6 patients with idiopathic Parkinson's disease (PD) we found strong coherence between the electromyography (EMG) of forearm muscles and activity in the contralateral primary motor cortex (M1) at tremor frequency but also at double tremor frequency. Furthermore, significant coherences were observed between M1 and medial wall areas (CMA/SMA), lateral premotor cortex, diencephalon, SII cortex, posterior parietal cortex and the contralateral cerebellum at tremor and, stronger, at double tremor frequency. In contrast, in 6 patients with "mini-asterixis" and HE due to chronic liver cirrhosis excessive corticomuscular coherence occurred at the individual tremor frequency between EMG and M1 activity. Interestingly, thalamus-M1 coupling was significantly altered towards lower frequencies matching the individual frequency of the mini-asterixis. Cerebro-muscular or cerebro-cerebral coupling at double tremor frequency was not observed. Therefore, "mini-asterixis" reflects most likely a pathologically decelerated and augmented synchronized rhythmical motor cortical output. This could be due to functional alterations in the M1-basal-ganglia-thalamo-cortical loops in severe HE. In summary, tremor syndromes in PD as well as in patients with HE and "mini-asterixis" are characterized by pathological oscillatory activity within cerebral networks of motor areas. However, the present study shows different mechanisms of tremor generation in PD and HE patients.
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PMID:Pathological oscillatory coupling within the human motor system in different tremor syndromes as revealed by magnetoencephalography. 1601 24

Hepatic encephalopathy (HE) is clinically characterized by a large variety of symptoms including motor symptoms, cognitive deficits, as well as changes in the level of alertness up to hepatic coma. A number of pathological processes affecting glial and neuronal function have been identified, including hyper-ammonia, changes within the excitatory and inhibitory transmitter systems, as well as osmolytic changes with consecutive cell swelling. One explanation how these pathological processes result in neurological deficits in HE is the concept of pathologically synchronized oscillations within and between relevant brain regions. A number of studies suggest that the cognitive deficits and the reduced level of alertness in patients with HE can be attributed to a significantly slowed and pathologically synchronized spontaneous oscillatory brain activity, depending on the grade of HE. Moreover, HE motor symptoms, like postural tremor called"mini asterixis," have recently been shown to be associated with abnormal thalamo-cortical and cortico-muscular synchronization. Indirect evidence exists from studies of processing and recognition of flicker stimuli that in HE slowing of oscillations also occurs in the visual system. Taken together, pathological synchronization of neuronal activity may turn out to be a promising pathophysiological concept for linking neuronal dysfunction to the diversity of clinical deficits in HE.
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PMID:Neural synchronization in hepatic encephalopathy. 1638 44

A huge number of neurological disorders are associated with myoclonus. This paper describes these disorders whose diagnosis partly relies on the presence of myoclonus. The diagnostic approach is related to certain clinical features of myoclonus, which, after their integration in the clinical context, help orientate towards diagnosis. Myoclonus is frequent during dementia. Although its presence is well-known to take part in the diagnosis of Creutzfeldt-Jakob disease (CJD), myoclonus can also be present to a significant degree in Alzheimer's disease and Lewy body dementia (LBD), which raises a diagnostic issue. Both its clinical and electrophysiological features may help differential diagnosis, given that myoclonus with fast-evolving dementia and focal neurological signs should favor the diagnosis of CJD. Myoclonus in a context of progressive ataxia suggests one clinical form of the Ramsay-Hunt syndrome (progressive myoclonic ataxia, PMA), whose most frequent causes are: coeliac disease, mitochondriopathies, some spino-cerebellar degenerations, and some late metabolic disorders. In addition to ataxia and myoclonus, the presence of opsoclonus directs diagnosis toward the opsoclonus-myoclonus syndrome (OMS), whose origin, in adult, is idiopathic or paraneoplastic. Palatal tremor (myoclonus) with ataxia may represent either a sporadic pattern, which often reflects the evolution of degenerative or lesional disorders, or a familial pattern in some degenerative affections or metabolic diseases. Of more recent knowledge is the association of progressive ataxia, myoclonus, and renal failure, which corresponds to a recessive autosomic disease. In a context of encephalopathy, myoclonus is frequent in metabolic or hydro-electrolytic disorders, and in brain anoxia. One should distinguish these various forms of myoclonus which may occur in the acute post-anoxic phase, from those occurring as sequels at a later stage, i.e. the Lance and Adams syndrome whose clinical aspects are also multiple. Myoclonus is less frequent during toxic or drug exposures. Irrespective of its acute or insidious onset, Hashimoto's encephalopathy is accompanied by myoclonus and tremor. Myoclonus may also be present during encephalic and/or spinal infectious disorders. Myoclonus with focal neurological signs may be observed in thalamic lesions, responsible for unilateral asterixis or unilateral myoclonus superimposed on dystonic posture. Segmental spinal myoclonus or propriospinal myoclonus may be associated with several spinal-cord disorders. Myoclonus associated with peripheral nerve lesions is exceptional or even questionable for some of these.
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PMID:Symptomatic myoclonus. 1733 75

Dyskinesias are infrequent presentations in acute stroke (1%). They can be found more frequently as delayed presentations after a stroke, but the prevalence is not available from the literature. The full spectrum of hyper- and hypo-akinetic syndromes has been described, but three main pictures are rather specific of an acute stroke: limb shaking, hemichorea-hemiballism and unilateral asterixis. Besides limb shaking, that seems to reflect a transient diffuse ischemia of the frontosubcortical motor pathway, lesions are described at all levels of the frontosubcortical motor circuit including the sensorimotor frontoparietal cortex, the striatum, the pallidum, the thalamic nuclei, the subthalamic nucleus, the substantia nigra, the cerebellum, the brainstem and their interconnecting pathways, as ischemic or hemorrhagic strokes. The preferentially late development of dyskinesia could reflect the return to a more ancestral motor control level, the most functional possible with the remaining configuration of structures, elaborated by brain plasticity after stroke.
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PMID:[Movement disorders in stroke]. 1876 Apr 32

An array of movement disorders is associated with ethanol, illicit drugs, and tobacco. Heavy ethanol users experience withdrawal tremor and, less often, withdrawal parkinsonism, chorea, and myoclonus. Asterixis is a feature of hepatic failure. On the other hand, ethanol can ameliorate essential tremor and myoclonus-dystonia. Among opioid drugs, meperidine can precipitate myoclonus. Severe parkinsonism affected users of a synthetic meperidine analog contaminated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Spongiform leukoencephalopathy, sometimes with chorea and myoclonus, occurred in inhalers of heroin vapor (chasing the dragon). Psychostimulants including cocaine acutely cause stereotypies and dyskinesias. Phencyclidine toxicity causes myoclonus. Tobacco use, on the other hand, protects against Parkinson's disease. Clinicians need to consider substance abuse in patients with unexplained movement disorders.
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PMID:Substance abuse and movement disorders. 2072 28

The aim of this study was to investigate the presence of movement disorders associated with ifosfamide toxicity. One of the most common adverse events of ifosfamide treatment is central nervous system toxicity. However, little is known about the occurrence of movement disorders associated with ifosfamide toxicity. We performed a retrospective computer search of the electronic medical records database of the Mayo Clinic, Rochester, MN from 1 January 1997-30 June 2010, using a series of search terms to identify all patients that had been treated with ifosfamide for systemic cancer. Among 400 patients that have ever used ifosfamide, we selected those patients that had any neurological complication in their medical records after the use of ifosfamide. Fifty-two had a neurological complication after ifosfamide administration. The most common neurological complication was encephalopathy that was present in 11 cases (21%). The presence of a movement disorder time locked to the administration of ifosfamide was reported in seven cases (13%). Generalized myoclonus was most common, occurring in four patients while postural tremor was documented in the other three. All patients with myoclonus had asterixis. Four of the patients also had encephalopathy. In six patients the movement disorders resolved within 48 h, spontaneously, after the discontinuation of ifosfamide, while in one case resolved in 24 h after the treatment with methylene blue. Our study demonstrates that although encephalopathy is the most common adverse neurological event associated with ifosfamide toxicity, movement disorders, including generalized myoclonus, asterixis, and postural tremors may also occur. Treatment with methylene blue may be further considered as useful to ameliorate the movement disorders.
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PMID:Ifosfamide associated myoclonus-encephalopathy syndrome. 2139 85

Hyperkinetic movement disorders are characterized by excess movement, and include chorea, akathesia, asterixis, dystonia, tremor, myoclonus, and tics. A wide variety of pharmacologic agents may induce or exacerbate these disorders. Neuroleptic-induced tardive dyskinesia and levodopa-induced hyperkinesia are the most common causes of medication-induced chorea. However, several nonneuroleptic agents, including antidepressants and antiepileptic medications, may also worsen hyperkinetic movement disorders. Over-the-counter medications, such as analgesics and antiheartburn medications, have also occasionally been implicated as causing hyperkinetic movement disorders. Most information regarding drug-induced hyperkinetic disorders comes from case reports and anecdotes, rather than controlled clinical trials. Further research with larger controlled trials needs to verify many of these findings.
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PMID:Drug-induced hyperkinetic movement disorders by nonneuroleptic agents. 2149 94

Although rare, many different types of hyperkinetic and hypokinetic movement disorders have been described after both ischemic and hemorrhagic stroke in children and in adults. Current knowledge about these disorders comes from single case reports or small series of cases compiled from retrospective studies. Data from hospital-based studies suggest a prevalence of poststroke movement disorders ranging from 1.1 to 3.9%. However, despite the development of emergency care for stroke, these clinical syndromes remain insufficiently recognized. Poststroke movement disorders take place in the acute phase or following a variable delay after stroke onset, and could be transient or persistent. Dystonia is the most frequent movement disorder, occurring after a delay of several months, while chorea and hemiballism are most frequent in the acute stages. Amongst transient movement disorders, limb shaking is associated with high-grade stenosis or occlusion of the internal carotid artery, while myoclonus and asterixis are rare. From a pathophysiological point of view, most of these symptoms are induced by a lesion involving the basal ganglia, the thalamus, or the frontal subcortical pathways. In this article, we updated the clinical spectrum, neuropathophysiological mechanisms, and prognosis of stroke-induced movement disorders in adults and children.
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PMID:Clinical spectrum of movement disorders after stroke in childhood and adulthood. 2273 57

Asterixis as limb-shaking transient ischemic attack (TIA) is rare and poorly understood. Bilateral asymmetrical asterixis as limb-shaking TIA has not been reported in carotid stenosis. A 69-year-old gentleman presented with a TIA episode (dysarthria, right-arm weakness, and numbness). Bilateral asterixis was observed and was more severe on the right side. No prior infarcts were noted in the thalamus. Liver function was normal. A computerized tomography angiogram revealed 85%stenosis of the right internal carotid artery (ICA) and 65% stenosis of the left ICA. Three days after left ICA endarterectomy, the patient had complete disappearance of bilateral asterixis, with the right side showing initial improvement. The bilateral asterixis observed is proposed to be secondary to hemodynamic impairment and hypoperfusion of certain brain territory with resolution on revascularization.
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PMID:Bilateral asymmetrical asterixis as limb-shaking transient ischemic attack in bilateral carotid stenosis. 2544 Mar 34

Cerebellar circuitry is important to controlling and modifying motor activity. It conducts the coordination and correction of errors in muscle contractions during active movements. Therefore, cerebrovascular lesions of the cerebellum or its pathways can cause diverse movement disorders, such as action tremor, Holmes' tremor, palatal tremor, asterixis, and dystonia. The pathophysiology of abnormal movements after stroke remains poorly understood. However, due to the current advances in functional neuroimaging, it has recently been described as changes in functional brain networks. This review describes the clinical features and pathophysiological mechanisms in different types of movement disorders following cerebrovascular lesions in the cerebellar circuits.
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PMID:Movement Disorders Following Cerebrovascular Lesions in Cerebellar Circuits. 2724 Aug 9


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