Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013421 (dystonia)
 8,418 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A single case study of a 58 year-old male with right asymmetric apraxia and akinetic-rigid syndrome is described. Brainimaging scans (MRI, SPECT) indicated asymmetric cortical atrophy compatible with the diagnosis of Corticobasal Degeneration. Reflex myoclonus was absent and myoclonic discharges only appeared in response to pharmacological treatment of limb dystonia and rigidity. Electromyographic evidence of jerky movements was recorded only in the affected right hand and forearm after muscle relaxation, and myoclonus was not preceded by an EEG paroxysm. The cortical components of the correspondent SEPs were not increased in amplitude while LLRs recordings showed a late response over the muscles of the affected side. Furthermore, the duration of post MEP silent period was bilaterally reduced. This single case study report points out that sometimes myoclonus in Corticobasal Degeneration can be masked by the presence of increased muscle tone.
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PMID:Masked myoclonus in corticobasal degeneration: neurophysiological study of a case. 1185 Oct 11

Cortical excitability and cortico-cortical inhibition were examined in twenty-one patients suffering from idiopathic rotational cervical dystonia. Polymyography of cervical muscles, somatosensory evoked potential recordings, and paired transcranial magnetic stimulation were used to assess the dystonic disorder. The results were compared with those obtained in a group of sixteen healthy age-matched volunteers. Statistically significant differences between the patient group and the control group were found when the amplitude values of the mean P22/N30 component measured at F [3, 4] and C[3, 4]' electrode positions were compared. The mean amplitude of P22/N30 in both of these electrode positions contralaterally to the direction of head deviation was significantly higher in the patient group (p <or= 0.05). The mean side-to-side P22/N30 amplitude ratio was calculated in both groups in the F[3, 4] and C[3, 4]' electrode positions: there was a significant difference between the two groups. The mean ratio (calculated contralaterally/ipsilaterally in the patient group and left/right side in the control group) was significantly higher in the patient group (p <or= 0.05). There were statistically significant differences between the two groups when the mean values of MEP amplitudes following paired stimuli at short and medium interstimulus intervals (ISI)) were compared. The percentage of amplitude reduction registered at short ISI was significantly lower in the patient group when both 3 ms ISI and 5 ms ISI were considered, and when the hemisphere contralateral to the direction of head deviation was stimulated. There was also a difference (with the short ISI) when the hemisphere ipsilateral to the direction of head deviation was stimulated, but this difference was not significant (p < 0.5). Almost all of the amplitude changes following the paired stimulus at the longer ISI, i. e. 10, 15, and 20 ms were significantly different when the patient group was compared with control group: when the ipsilateral hemisphere was stimulated, the amplitude of conditioned responses was significantly higher following all three paired stimuli (with 10, 15, and 20 ms ISI) at the p <or= 0.05 significance level; when the contralateral hemisphere was stimulated, they were significantly higher following the 10 and 20 ms ISI paired stimuli (significance level p <or= 0.05). The interhemispheric difference in the patient group was significant only for the paired stimuli using 3 and 5 ms (short) ISI and 15 and 20 ms (medium) ISI. There was a significantly decreased inhibition at 3 and 5 ms ISI when the hemisphere contralateral to the direction of head deviation was stimulated, as compared with the hemisphere ipsilateral (p <or= 0.05). Similarly, there was a significantly increased facilitation at 15 and 20 ms when the hemisphere contralateral to the direction of head deviation was stimulated, as compared with the hemisphere ipsilateral (p <or= 0.05). The results indicate that a disorder of both cortical excitability and intracortical inhibition exists in patients with cervical dystonia, and that this disorder is lateralized, i. e. it is located within the hemisphere contralateral to the direction of head deviation.
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PMID:Abnormalities of cortical excitability and cortical inhibition in cervical dystonia Evidence from somatosensory evoked potentials and paired transcranial magnetic stimulation recordings. 1252 91

Recent evidence suggests a role for cerebellum in pathophysiology of dystonia. Here we explored, the cerebellar modulation of motor cortex in patients with focal upper limb dystonia. Eight patients and eight controls underwent a transcranial magnetic stimulation protocol to study the cerebellar-brain-inhibition (CBI): a conditioning cerebellar stimulus (CCS) was followed 5 ms after by the contralateral motor cortex stimulation (test stimulus: TS). We explored the effects of CBI on MEP amplitude, short intracortical inhibition (SICI) and intracortical facilitation (ICF) measures. At baseline no differences in TS-MEP amplitude, SICI or ICF were found between patients and controls. Cerebellar-conditioning significantly reduced TS-MEP amplitude, increased ICF, and decreased SICI in control subjects. In contrast, no changes in these neurophysiological measures were observed in the motor cortex of patients, regardless of which side was tested. If further confirmed, these findings suggest a reduced cerebellar modulation of motor cortex excitability in patients with focal dystonia.
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PMID:Effects of cerebellar TMS on motor cortex of patients with focal dystonia: a preliminary report. 1881 75

This article reports a patient with spinal cord injury who was treated with conventional rehabilitation therapy plus repeated transcranial magnetic stimulation (rTMS) during the postoperative rehabilitation, and to observe the effects of rTMS on dystonia. A 66-year-old male patient fell from the bed 8 months ago. At that time, he felt pain in his neck, dysfunction in limbs movement, and loss of sensation in trunk and limbs. Magnetic resonance imaging (MRI) revealed spinal cord injury. Under general anesthesia, anterior cervical decompression and bone graft fusion (ACDF) and cervical spine internal fixation of C 3-C 6 were performed. Postoperative hyperbaric oxygen chamber and conventional rehabilitation treatment were performed. Eight months after surgery, he was admitted to the hospital due to motor function, balance dysfunction, neurogenic bladder/rectal dysfunction. After admission, the patient was treated with rTMS plus rehabilitation treatment, once per day, 5 times/week, for 4 weeks. rTMS worked by wearing a positioning cap for transcranial magnetic stimulation (80% resting motor threshold, 1 Hz, 30 min), and then conduct walking, balance proprioception, muscle strength training, and coordination training. After 4 weeks, MEP, sEMG and H reflex were improved. Therefore, rTMS on the premotor cortex to improve the dystonia after spinal cord injury is effective in this case, which can be further studied.
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PMID:[Improvement of Dystonia after Spinal Cord Injury by Applying Repetitive Transcranial Magnetic Stimulation on the Premotor Cortex: Case Report]. 3297 74