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

We report on 2 patients who uncommonly developed isolated limb myorhythmia in association with inferior olive hypertrophy (IOH) after an acute stroke in the brain stem. A slow tremor presented in the proximal upper limbs predominantly when at rest. It was aggravated by outstretched arms and by active hand movements. The surface electromyogram (EMG) recorded simultaneous activities over the agonist and antagonist muscles with a rate of 3.5 Hz and 2.5 Hz in 2 patients respectively. In the first patient, bilateral limb myorhythmia presented 12 months after the brain stem stroke, and both inferior olives were hypertrophic. In the second patient, unilateral limb myorhythmia developed in the left hand 7 months after right pontine hemorrhage, and only the right inferior olive was hypertrophic. These findings indicate that limb myorhythmia commencing after brain stem insult is anatomically and temporally related to hypertrophy of the contralateral inferior olive. Based on our 2 patients and previously reported cases, we propose that a possible causal relationship exists between limb myorhythmia and contralateral IOH, although its pathophysiological mechanisms remain to be established. We suggest that, similar to palatal myoclonus, isolated limb myorhythmia is within the clinical spectrum of IOH.
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PMID:Limb myorhythmia in association with hypertrophy of the inferior olive: report of two cases. 1112 56

Although occurrence of involuntary movements after thalamic stroke has occasionally been reported, studies using a sufficiently large number of patients and a control population are not available. Between 1995 and 1999, the author prospectively identified 35 patients with post-thalamic stroke delayed-onset involuntary movements, which included all or some degree of dystonia-athetosis-chorea-action tremor, occasionally associated with jerky, myoclonic components. A control group included 58 patients examined by the author during the same period who had lateral thalamic stroke but no involuntary movements. Demography, clinical features and imaging study results were compared. There were no differences in gender, age, risk factors, side of the lesion and follow-up periods. During the acute stage of stroke, the patients who had involuntary movements significantly more often had severe (< or = III/V) hemiparesis (50 versus 20%, P < 0.05) and severe sensory loss (in all modalities, P < 0.01) than the control group. At the time of assessment of involuntary movements, the patients with involuntary movements significantly more often had severe sensory deficit (in all modalities, P < 0.01) and severe limb ataxia (60 versus 5%, P < 0.01) than the control patients, but neither more severe motor dysfunction (7 versus 0%) nor more painful sensory symptoms (57 versus 57%). The patients with involuntary movements had a higher frequency of haemorrhagic (versus ischaemic) stroke (63 versus 31%, P < 0.05). Further analysis showed that dystonia-athetosis-chorea was closely associated with position sensory loss, whereas the tremor/myoclonic movements were related to cerebellar ataxia. Recovery of severe limb weakness seemed to augment the instability of the involuntary movements. Persistent failure of the proprioceptive sensory and cerebellar inputs in addition to successful, but unbalanced, recovery of the motor dysfunction seemed to result in a pathological motor integrative system and consequent involuntary movements in patients with relatively severe lateral-posterior thalamic strokes simultaneously damaging the lemniscal sensory pathway, the cerebellar-rubrothalamic tract and, relatively less severely, the pyramidal tract.
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PMID:Delayed onset mixed involuntary movements after thalamic stroke: clinical, radiological and pathophysiological findings. 1115 57

Peripheral pain and ataxic tremor can appear suddenly following thalamic stroke and can significantly alter a patient's psychological, social, and physical functioning. The present paper reports the case of a 70-year-old Caucasian female who sustained an acute left posterior cerebral artery infarction involving the thalamus and left mesiotemporal regions. She subsequently developed Central Poststroke Pain and ataxic movement of her right arm and hand in addition to a significant right-side claudication. She was treated over 16 weeks (6 weeks of EMG biofeedback and 10 weeks of psychotherapy) with a combination of EMG biofeedback, progressive muscle relaxation, behavioral pain coping skills training, Forced Use Therapy, and Cognitive Behavioral Therapy 7 years after her initial cerebral accident. The case demonstrates the utility of biofeedback when combined as part of a comprehensive treatment program to address the multiple complications associated with thalamic stroke.
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PMID:Electromyographic (EMG) biofeedback in the comprehensive treatment of central pain and ataxic tremor following thalamic stroke. 1121 24

We report three members of a family, who exhibited a phenotype similar to 'myoclonus epilepsy with ragged-red fibers' but had a genotype usually associated with 'mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes'. The patients, a 48-year-old female, and her two sons, aged 21 and 19 respectively, presented with photo-reactive syncopal episodes, disturbances of gait and writing, dysarthria and finger tremor since the 3rd and 2nd decade of life, respectively, that were accompanied also by numbness and weakness of the extremities. Subsequently, cerebellar ataxia and myoclonus were also noted. Electromyography revealed both myogenic and neurogenic muscular changes, and nerve conduction studies demonstrated a sensory-motor neuropathy. Biopsy showed ragged-red fibers with strongly stained SDH-positive vessels in skeletal muscles, and a marked loss of myelinated fibers of the sural nerves. Mitochondrial (mt) DNA analyses of peripheral blood, muscles and nerves revealed that all members had a heteroplasmic np3271 (T-C) point mutation in the mitochondrial tRNA-Leu gene (UUR). This family is unique, in that all patients presented with a myoclonus epilepsy with ragged-red fibers-like phenotype and had a distinctive peripheral neuropathy, while the detected mtDNA 327l (T-C) mutation has been reported to date only in rare cases of mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes
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PMID:A mitochondrial encephalo-myo-neuropathy with a nucleotide position 3271 (T-C) point mutation in the mitochondrial DNA. 1140 19

Previous reports in the literature concerning cerebrovascular accident have illustrated cases of post-stroke tremor. Treatments of these studies have varied. Trials of levo-dopa have been reported in two such cases. This case study reports on a case of a patient with a left thalamic, left superior cerebellar artery infarction with a lacunar infarction in the basal ganglia. The patient developed a violent tremor/movement disorder which was unresponsive to haloperidol. With this failure, and with the evidence of a basal ganglion lesion, levo-dopa/carbi-dopa was introduced as an intervention. The amplitude of the tremor was dramatically reduced, with protective devices removed, and with complete cessation of the tremor at rest. The medication was withdrawn and reintroduced with a reduction and subsequent resolution of the symptoms. A discussion of the previous studies of movement disorder with cerebrovascular accident is included.
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PMID:Post-stroke violent adventitial movement responsive to levo-dopa/carbi-dopa therapy. 1159 87

A case of neonatal convulsion reported by Thomas Willis (1621-1675) together with its post mortem findings is quoted as being congenital intracerebral haemorrhage or strongly suggested as being the earliest pathological description of childhood cerebrovascular disease. However these authors only reviewed the incomplete written record left by Willis, describing how this case was the fourth consecutive child that the mother had lost to neonatal convulsions. The medical record is completed by notes taken by John Locke from a lecture delivered by Willis 3 or 4 years before the case was first published. Here, Locke relates how the mother subsequently had three further children who were all treated by Willis soon after birth and all survived uneventfully. Reviewing the post mortem findings and the full case histories modern medical science gives a different interpretation. Instead, I suggest that the case history given and pathological features described are more in keeping with a whiplash shaking injury than with cerebrovascular disease or a stroke. I believe that this is the earliest pathological description of shaking injury in childhood. We can never know why Willis did not publish the full success of his management of the subsequent children but it may have been due to his dramatic experience of a similar mother early on in his medical career.
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PMID:Winner of the young physician's section of the Gowers' prize 2000. Too good to be true? Thomas Willis--neonatal convulsions, childhood stroke and infanticide in seventeenth century England. 1174 3

A patient with thalamic stroke underwent microelectrode-guided stereotactic thalamic exploration during surgery for control of tremor. The results of somatic sensory mapping in this patient were compared with explorations carried out during stereotactic surgery for the control of essential tremor (70 patients). There was evidence both of somatotopic reorganization and of anatomic reorganization of the representation of deep structures in the principal somatic sensory nucleus of the thalamus and the nuclei located anterior to it. This case demonstrates that thalamic reorganization can occur after a thalamic stroke and may play a role in recovery from such a stroke.
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PMID:Reorganization of somatic sensory function in the human thalamus after stroke. 1176 79

Neuropathic pain, whether of peripheral or central origin, is characterized by a neuronal hyperexcitability in damaged areas of the nervous system. In peripheral neuropathic pain, damaged nerve endings exhibit abnormal spontaneous and increased evoked activity, partly due to an increased and novel expression of sodium channels. In central pain, although not explored in detail, the spontaneous pain and evoked allodynia are also best explained by a neuronal hyperexcitability. The peripheral hyperexcitability is due to a series of molecular changes at the level of the peripheral nociceptor, in dorsal root ganglia, in the dorsal horn of the spinal cord, and in the brain. These changes include abnormal expression of sodium channels, increased activity at glutamate receptor sites, changes in gamma-aminobutyric acid (GABA-ergic) inhibition, and an alteration of calcium influx into cells. The neuronal hyperexcitability and corresponding molecular changes in neuropathic pain have many features in common with the cellular changes in certain forms of epilepsy. This has led to the use of anticonvulsant drugs for the treatment of neuropathic pain. Carbamazepine and phenytoin were the first anticonvulsants to be used in controlled clinical trials. Studies have shown these agents to relieve painful diabetic neuropathy and paroxysmal attacks in trigeminal neuralgia. Subsequent studies have shown the anticonvulsant gabapentin to be effective in painful diabetic neuropathy, mixed neuropathies, and postherpetic neuralgia. Lamotrigine, a new anticonvulsant, is effective in trigeminal neuralgia, painful peripheral neuropathy, and post-stroke pain. Other anticonvulsants, both new and old, are currently undergoing controlled clinical testing. The most common adverse effects of anticonvulsants are sedation and cerebellar symptoms (nystagmus, tremor and incoordination). Less common side-effects include haematological changes and cardiac arrhythmia with phenytoin and carbamazepine. The introduction of a mechanism-based classification of neuropathic pain, together with new anticonvulsants with a more specific pharmacological action, may lead to more rational treatment for the individual patient with neuropathic pain.
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PMID:Anticonvulsants in neuropathic pain: rationale and clinical evidence. 1188 43

This study sought an operational definition of parkinsonism in elderly people (n = 2,914) who underwent a clinical examination in the Canadian Study of Health and Aging (CSHA). Parkinsonism was defined as having two of the following features: (1) bradykinesia of face or limbs, (2) resting tremor, (3) rigidity, and (4) abnormality of gait and posture. The association of parkinsonism with other parkinsonian-related features (prior diagnosis of Parkinson's disease, use of drugs with extrapyramidal side effects, and use of antiparkinsonian medications) and variables not expected to be related to parkinsonism (stroke and Hachinski score > 5) was determined. Parkinsonism was identified in 337 people (11.6%). It was significantly more likely with other parkinsonian-related characteristics, and was not associated with a history of stroke, but was slightly higher among those subjects with a Hachinski score > 5. Posture and gait abnormalities were significantly associated with other parkinsonian-related variables, but were also more common among subjects with stroke-related features. When the gait and posture disturbance category was excluded as a parkinsonian sign, the narrower definition was more specific but less sensitive in detecting cases with a clinical diagnosis of Parkinson's disease. Despite limitations, the approach presented in this article is a valid method to operationalize parkinsonism from the dataset.
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PMID:Defining parkinsonism in the Canadian Study of Health and Aging. 1189 57

Migraine may be comorbid with several other neurologic and psychiatric conditions, including mood disorders (eg, depression, anxiety, panic disorder), epilepsy, stroke, and essential tremor. Comorbidity presents physicians with opportunities and challenges for both diagnosis and treatment. All diseases must be considered, and therapeutic strategies may need to be modified to avoid potential drug interactions. Comorbidities also may provide clues to the pathophysiologies and any shared mechanisms of the two disorders. Longitudinal studies have demonstrated a bidirectional influence between migraine and major depression, but not between migraine and other severe headache. Migraine is strongly and consistently associated with panic disorder. The risk of migraine in epilepsy is increased particularly in individuals with head trauma, partial seizures, and a positive family history of migraine. The influence is bidirectional. There is also growing evidence of an association between migraine and stroke, particularly among women of childbearing age and individuals who experience migraine with aura. Lastly, a bidirectional association between migraine and essential tremor also exists. These findings suggest that migraine, major depression, epilepsy, and essential tremor share one or more common etiologies. Clinicians should be mindful of them as they design treatment strategies, and also should consider the use of a single pharmacologic agent that is effective for all conditions.
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PMID:Shared mechanisms and comorbidities in neurologic and psychiatric disorders. 1190 35


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