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

A 52-year-old man has slowly developed a non-flapping tremor during 30 years. He also had suffered from poor concentration for two years. He had, however, no history of episodic disturbance of consciousness. He had no other neurological symptoms except for tremor and hyperreflexia. The tremor was postural and intentional, and extremely increased at the end point. The factor of intentional tremor and hyperkinesia volitionnelle seems to be present in the tremor. Laboratory examination disclosed a hyperammonemia, reduction in Fisher ratio, and poor excretion of ICG. Selective abdominal angiography visualized a large shunt vessel between the left gastric vein and the left renal vein. The normal liver scintigram with 99mTc excluded the dysfunction of liver, and we conclude that the shunt vessel might be congenital. Tremor markedly improved after normalizing blood ammonia level by resection of the shunt vessel. The present case suggests that tremor, even without episodic disturbance of consciousness, could be based on the portal-systemic encephalopathy.
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PMID:[A case of portal-systemic encephalopathy with slowly progressive, non-flapping tremor]. 866 32

A 59-year-old woman presented with consciousness disturbance with flapping tremor. Laboratory examinations revealed normal liver functions, and imaging studies, ultrasonography, magnetic resonance imaging, and angiography, showed portal vein aneurysm communicating from the portal vein to the hepatic vein, splenomegaly, and splenic artery aneurysm. These examinations confirmed porto-systemic shunt leading to hepatic encephalopathy. Porto-hepatic venous shunt via portal vein aneurysm is extremely rare, and there are few reports that it causes encephalopathy; therefore, little is known about the entity and this association. The literature in English is reviewed and the etiology, clinical features, and prognosis discussed.
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PMID:Porto-hepatic venous shunt via portal vein aneurysm with splenomegaly. 896

Portal-systemic encephalopathy may be seen with hyperammonemia that complicates chronic liver disease. We report an unusual case of reversible parkinsonism associated with hyperammonemia and portal vein thrombosis. An active 90-year-old male developed motor slowing and resting hand tremor over 6 months. Examination showed asterixis, bradykinesia, cogwheel rigidity, rest tremor, and a parkinsonian gait. Serum venous ammonia was elevated at 145 microM. The next day, the patient became comatose and serum ammonia was 178 microM. With lactulose therapy, serum ammonia level normalized and examination showed only minimal parkinsonism after 1 week. An abdominal CT scan identified portal vein thrombosis with porto-systemic shunting that reversed after 7 months of treatment. Examination 2 years later showed no signs of parkinsonism. Parkinsonism can dominate the clinical picture of patients with hyperammonemia before the onset of encephalopathy.
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PMID:Reversible parkinsonism and hyperammonemia associated with portal vein thrombosis. 1124 May 69

The authors investigated 12 patients with cirrhosis who had hepatic encephalopathy (HE): six with continuous mini-asterixis and six with subclinical HE without asterixis. They studied the coupling between hand-muscle electromyography (EMG) recordings and brain activity recorded by magnetoencephalography. On forearm elevation, patients with tremor developed excessive coupling between activity in the motor cortex (M1) and contralateral hand-muscle EMG recordings at the frequency of mini-asterixis, which was not found in controls. The corticomuscular coupling demonstrates the involvement of M1 in asterixis and may reflect a pathologically slowed and synchronized motor cortical drive.
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PMID:Cortical origin of mini-asterixis in hepatic encephalopathy. 1180 39

Hepatic encephalopathy is a frequent and serious complication of liver cirrhosis. Usually it is treated by non-absorbable disaccharides or antibiotics and its treatment is often difficult and associated with undesirable effects. The objective of our investigation was to evaluate the safety and effectiveness of a new antibiotic used in this indication--rifaximine. With rifaximine, 400 mg three times per day, a total of 25 patients were treated for a 10-day period. Significant improvement of the manifestations of encephalopathy occurred (evaluated by the grade of encephalopathy, test of combining numerals, the degree of flapping tremor and the arterial ammonia level). None of the patients developed undesirable effects. Rifaximine seems an effective, safe drug for hepatic encephalopathy.
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PMID:[Rifaximin in the treatment of hepatic encephalopathy]. 1213 65

Rifaximin has been reported to be effective for the treatment of hepatic encephalopathy (HE) in Europe. However, it is unknown whether Rifaximin is effective for the treatment of HE in Koreans, therefore we conducted a open-label prospective randomized study to evaluate the efficacy of rifaximin versus lactulose in Korean patients. Fifty-four patients with liver cirrhosis and hepatic encephalopathy were enrolled. Thirty-two patients were randomized to receive rifaximin and 22 to receive lactulose both over a 7-day periods. Before and at the end of treatment, gradation of blood ammonia, flapping tremor, mental status, number connection test (NCT) were performed and estimation of HE indexes determined. Both rifaximin and lactulose were effective in the majority of patients (84.4% and 95.4%, respectively, p = 0.315). Blood NH3, flapping tremor, mental status, and NCT was significantly improved by rifaximin and lactulose, and the post- treatment levels of these measures were similar for the rifaximin and lactulose-treated groups, as was the HE index (rifaximin group (10.0 --> 4.2, p = 0.000); lactulose group (11.3 --> 5.0, p = 0.000)). One patient treated with rifaximin complained of abdominal pain, which was easily controlled. There was no episode of renal function impairment in either treatment group. Rifaximin proved to be as safe and as effective as lactulose for the treatment of Korean patients with hepatic encephalopathy.
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PMID:Comparison of rifaximin and lactulose for the treatment of hepatic encephalopathy: a prospective randomized study. 1598 13

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

Human brain functions are heavily contingent on neural interactions both at the single neuron and the neural population or system level. Accumulating evidence from neurophysiological studies strongly suggests that coupling of oscillatory neural activity provides an important mechanism to establish neural interactions. With the availability of whole-head magnetoencephalography (MEG) macroscopic oscillatory activity can be measured non-invasively from the human brain with high temporal and spatial resolution. To localise, quantify and map oscillatory activity and interactions onto individual brain anatomy we have developed the 'dynamic imaging of coherent sources' (DICS) method which allows to identify and analyse cerebral oscillatory networks from MEG recordings. Using this approach we have characterized physiological and pathological oscillatory networks in the human sensorimotor system. Coherent 8 Hz oscillations emerge from a cerebello-thalamo-premotor-motor cortical network and exert an 8 Hz oscillatory drive on the spinal motor neurons which can be observed as a physiological tremulousness of the movement termed movement discontinuities. This network represents the neurophysiological substrate of a discrete mode of motor control. In parkinsonian resting tremor we have identified an extensive cerebral network consisting of primary motor and lateral premotor cortex, supplementary motor cortex, thalamus/basal ganglia, posterior parietal cortex and secondary somatosensory cortex, which are entrained in the tremor or twice the tremor rhythm. This low frequency entrapment of motor areas likely plays an important role in the pathophysiology of parkinsonian motor symptoms. Finally, studies on patients with postural tremor in hepatic encephalopathy revealed that this type of tremor results from a pathologically slow thalamocortical and cortico-muscular coupling during isometric hold tasks. In conclusion, the analysis of oscillatory cerebral networks provides new insights into physiological mechanisms of motor control and pathophysiological mechanisms of tremor disorders.
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PMID:Physiological and pathological oscillatory networks in the human motor system. 1605 47

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

Acquired (non-Wilsonian) hepatocerebral degeneration (AHD) is a chronic brain disorder caused by liver dysfunction and long-standing portal-systemic shunting. It typically presents with dysathria, ataxia, tremor, involuntary movements and altered mental status, and often does not respond to conventional medical therapy for hepatic encephalopathy. There is scarce and conflicting information regarding the clinical course of AHD after liver transplantation (OLT). We present a case of a 47-year-old woman with hepatitis C (HCV) cirrhosis who developed severe manifestations of AHD after multiple bouts of hepatic encephalopathy. Her first OLT was complicated with primary nonfunction requiring immediate retransplantation. The second OLT led to complete clinical and radiological resolution of the AHD. However the patient developed recurrence of AHD 11 months post-transplant due to recurrent HCV and chronic rejection leading to cirrhosis of the graft. The patient developed severe neurological symptoms, despite mild synthetic graft dysfunction. A third OLT led again to disappearance of the clinical and radiological manifestations of AHD. AHD may show complete resolution after OLT; however it may rapidly recur following recurrent liver disease or graft dysfunction.
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PMID:Acquired hepatocerebral degeneration in a patient with HCV cirrhosis: complete resolution with subsequent recurrence after liver transplantation. 1679 48


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