Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sudden and brief involuntary movements of central nervous system (CNS) origin called myoclonus may be cortical (motor strip), thalamocortical (thalamocortical loop) or reticular (caudal reticular formation). Epileptic, cortical and thalamocortical myoclonus are combined with a spike which, when it is focal, needs back-averaging to be demonstrated. Negative myoclonus due to lapse of tone can only be demonstrated during antigravidic posture and may be combined with either a slow wave or the second, positive component of a polyspike-wave. Epileptic myoclonus must be distinguished from epileptic spasms and tonic seizures, and from non-epileptic myoclonus, tics, tremor and chorea. Myoclonus may occur in partial symptomatic (mainly Rasmussen and dysplasia), cryptogenic (frontal) or idiopathic (negative myoclonus in CSWS) epilepsy. Generalized myoclonus is part of inborn errors of metabolism, non-progressive encephalopathy (mainly Angelman) and idiopathic epilepsy (juvenile and infantile benign and severe forms, and myoclonic-astatic epilepsy). Carbamazepine, vigabatrin and eventually lamotrigine may worsen myoclonus whereas it may be improved by benzodiazepines, valproate, lamotrigine, zonisamide and piracetam according to etiology. Pathophysiology must take in account maturation processes, lesions and genetic predisposition. However, precise mechanisms remain unknown and only hypotheses can be proposed, that could clarify the age-related EEG and clinical expression of the various syndromes.
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PMID:Myoclonus and epilepsy in childhood: 1996 Royaumont meeting. 960 May 41

Two seventeen year-old women, developed acute onset left choreic movements following two months and two weeks use of oral contraceptives. Left hemiparesia appeared a few days later, while involuntary movements discontinued. Cranial CT scan and MRI showed bilateral ischemic lesion in the frontal region for the first case and isolated lesion in the right centrum ovale for the second. Angiography showed nearly complete obstruction of the terminal portion of the internal carotid artery with an outline Moya-Moya network. After discontinuing oral contraceptives, there has been no relapse of neurologic dysfunction for more than three years for the first case and twelve months for the second one. The role of perfusion insufficiency in limb-shaking carotid transient ischemic attack is discussed and the possible relations between oral contraceptives, chorea and angiographic features resembling Moya-Moya disease are evaluated.
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PMID:[Angiodysplasia of moya-moya type disclosed by choreic unvoluntary abnormal movements during oral contraception. Apropos of 2 cases]. 968 5

We report a case of dystonia with a partial deletion of the short arm (p) of chromosome 18 and androgen insensitivity. Neurologic findings in the 18p syndrome are reported to include mental retardation, seizures, incoordination, tremor, and chorea. A 15-year-old girl with a denovo 18p deletion [karyotype 46, XY, del (18)(p11.1)] developed progressive asymmetric dystonia. She had oromotor apraxia and partial expressive aphasia since childhood, and she was able to partially communicate through elementary sign language. At the age of 15 years, she developed subacute and progressive choreic movements of the right arm, severe dystonic posturing of the left arm, and spastic dystonia in both legs. Her response to parenteral or oral benzodiazepines, oral trihexyphenidyl, benztropine mesylate, baclofen, and L-dopa were brief and inadequate. The response to intrathecal baclofen has been sustained over 18 months. In all likelihood, the 18p deletion syndrome affecting this patient is significant in the pathogenesis of her acquired dystonia. Chronic intrathecal baclofen therapy via pump has been effective in this case and should be considered as a treatment modality in carefully selected patients with dystonia.
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PMID:Progressive dystonia in a child with chromosome 18p deletion, treated with intrathecal baclofen. 1007 26

Levofloxacin-induced-neurological adverse events such as convulsion, involuntary movement (tremor, myoclonus and chorea-like) and visual hallucination in two elderly patients are reported. A 67-year-old man with minor alcoholism and a past-history of gastrectomy and cholecystectomy was given 300 mg/day of oral levofloxacin and fulfenamic acid for an upper respiratory infection. On the 4th day, he reported gradual exacerbation of hand tremor which resembled chorea-like involuntary movement and gait disturbance. He also experienced visual hallucinations. On the 7th day, he suffered generalized convulsions and was admitted. Serum concentration of levofloxacin at this time (3 hours after last administration of a 100 mg tablet of levofloxacin) was 3.6 micrograms/ml. Cessation of the agents promoted complete recovery of these neurological adverse effects within a week. Another 85-year-old man with chronic bronchitis and slight renal impairment received long term administration of 200 mg/day of levofloxacin. On the 68th day of administration, gradual exacerbation of gait disturbance, dysarthria and chorea-like involuntary movement occurred. On the day of admission, 76 days after the start of administration, the serum level of levofloxacin was 2.55 micrograms/ml and that of spinal fluid was 1.12 micrograms/ml (3 hours after the last administration of a 100 mg tablet of levofloxacin). Cessation of the agents promoted complete recovery of these neurological adverse effects within the next two weeks. Both patients had no apparent neurological disorders except age-related brain atrophy. Age-related renal and brain impairment might have contributed to the neurological adverse effects of levofloxacin.
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PMID:[Levofloxacin-induced neurological adverse effects such as convulsion, involuntary movement (tremor, myoclonus and chorea like), visual hallucination in two elderly patients]. 1038 31

Movement disorders in children encompass disorders of motor control--both hyperkinetic (excessive movement) and hypokinetic (decreased movement). This article focuses on the hyperkinetic movement disorders, particularly tremor, Wilson's disease, dystonia, tics and Tourette syndrome, chorea, myoclonus, neuroleptic-induced movement disorders, and psychogenic movement disorders. Phenomenology of the disorders as well as clinical presentation, basic pathophysiology, genetics, and treatment are discussed.
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PMID:Pediatric movement disorders. 1055 1

Central cannabinoid receptors are densely located in the output nuclei of the basal ganglia (globus pallidus, substantia nigra pars reticulata), suggesting their involvement in the regulation of motor activity. Furthermore, there is evidence that endogenous cannabinoid transmission plays a role in the manipulation of other transmitter systems within the basal ganglia by increasing GABAergic transmission, inhibiting glutamate release and affecting dopaminergic uptake. Most hyperkinetic and hypokinetic movement disorders are caused by a dysfunction of basal ganglia-thalamo-cortical loops. It has been suggested that an endogenous cannabinoid tone participates in the control of movements and, therefore, the central cannabinoid system might play a role in the pathophysiology of these diseases. During the last years in humans a limited number of clinical trials demonstrated that cannabinoids might be useful in the treatment of movement disorders. Despite the lack of controlled studies there is evidence that cannabinoids are of therapeutic value in the treatment of tics in Tourette syndrome, the reduction of levodopa-induced dyskinesia in Parkinson s disease and some forms of tremor and dystonia. It can be speculated that cannabinoid antagonists might be useful in the treatment of chorea in Huntington s disease and hypokinetic parkinsonian syndromes.
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PMID:Cannabis in movement disorders. 1062 63

The paper reports 4-years results of a pilot study concerning the influence of a stereotactic pallidotomy on somatosensory evoked potentials in idiopathic Parkinson's disease. Potentials were recorded through the scalp surface from sensorimotor cortex of both hemispheres. Amplitudes and latencies of early and late waves were compared before and after the surgery. The surgery was recommended after 4 years of L-dopa therapy when bradykinesia and rigidity of right leg led to gait difficulty and postural instability. The dominant features of the syndrome were accompanied by tremor, micrography, chorea and lower responsiveness to L-dopa. Following the surgery a clear improvement of motor activity was observed. Increase of 20-90 ms waves amplitudes and P45 latency prolongation of 6-11 ms appeared due to the attenuation of pallidal inhibition exerted upon the thalamo-cortical transmission and a new arrangement of a cortical motor program. These electrophysiological changes, correlated with a clinical amelioration, may indicate as a favourable prognosis for a patient. Five months after pallidotomy a slight decrease of amplitudes occurred in relation to the previous examinations. Four years after surgery increase of most amplitudes and latencies and reconfiguration of later waves were related to deterioration of clinical course and worsening of left-side signs. We believe that somatosensory evoked potentials change may be a sensible indicator of motor state in Parkinson's disease. As far as we know the present study is one of the first presentation of somatosensory evoked potentials after pallidotomy.
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PMID:[Cryopallidotomy in Parkinson disease. Effect on somatosensory potentials]. 1096 25

We describe an autopsy case of parkinsonism with bradykinesia, muscle rigidity, and dementia as major symptoms. The patient had developed bradykinesia at the age of 62, and then muscle rigidity, a parkinsonian posture, bradylalia, and dementia gradually appeared. Neurological examination revealed rigidity in the neck and limbs, with motion and speech being generally slow. He lacked involuntary movements including alien hand, tremor, chorea, and dystonia. Vertical gaze palsy, both upward and downward was noted, but other cranial nerves were intact. He was diagnosed as suffering from PSP clinically based on vertical gaze palsy, bradykinesia, instability on standing and gait, and dementia. Levodopa was only transiently effective. Within three years he became bed-ridden and in a state of akinetic mutism. At age 65 he died from pneumonia. Neuropathology revealed severe neuronal degeneration and gliosis in the substantia nigra. Because atrophy of the tegmentum of brainstem, dentate nuclei, inferior olivary nuclei was very mild and Alzheimer neurofibrillary tangles in the brainstem were relatively few, PSP was ruled out. Cortical neuronal degeneration was not apparent, but in the deep layer of cingulate gyrus, frontal lobe, and insula, there were several ballooned neurons. Gallyas-Braak silver staining showed no tuft-shaped astrocytes, specific for PSP, but it disclosed astrocytic plaques in the basal ganglia and the cerebral cortex. At present, astrocytic plaques are recognized as a hallmark of corticobasal degeneration (CBD), along with ballooned neurons in the cerebral cortex. The present case thus illustrates that CBD has a wide spectrum and may include cases in which degeneration of cerebral cortex is very mild.
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PMID:[An autopsy case of corticobasal degeneration without prominent cortical pathology--an imitator of progressive supranuclear palsy]. 1096 56

Tremor is the most common involuntary movement disorder. It is differentiated from other involuntary movement disorders, such as chorea, athetosis, ballismus, tics, and myoclonus, by its repetitive, stereotyped, movements of a regular amplitude and frequency. Tremor can be defined as an involuntary, rhythmic, periodic, mechanical oscillation of a body part. Since small-amplitude tremors may not be visible to the naked eye and may only be detectable by sensitive recording devices, amplitude of the tremor is therefore not critical to the definition. Accurate diagnosis of tremor is important because appropriate treatment depends on the accuracy of the clinical diagnosis. This article reviews the classification and management of tremor.
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PMID:Diagnosis and management of tremor. 1097 54

We have studied the function of inhibitory interneurons within the motor cortex in several movement disorders using a paired-pulse magnetic stimulation technique. Their function was disturbed in patients with dystonia or focal lesions of the basal ganglia. On the other hand, the inhibition was normal in patients with chorea or essential tremor. The inhibitory circuit in the motor cortex must be functionally involved in some movement disorders probably because of changes of the inputs from basal ganglia to motor cortices, but not involved in the others. This difference in the functional involvement of inhibitory interneurons of the motor cortex may reflect different pathogenesis of these movement disorders.
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PMID:Intracortical inhibition of the motor cortex in movement disorders. 1098 74


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