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)

Somatosensory evoked potentials (SEPs) of the median nerve were recorded in 40 patients suffering from cervical dystonia and in 40 healthy volunteers as a control. Before recording the median nerve SEPs, polymyographic recordings were performed in all patients with cervical dystonia. The activity of cervical muscles was recorded, and the leading muscle of cervical dystonia was determined. Patients were divided into two groups according to the results of polymyography. The leading muscle was sternocleidomastoid in the first group and the splenius capitis in the second group. Patient SEPs were recorded during abnormal head rotation. SEPs in 20 healthy volunteers were recorded with the head in the middle position. SEPs of another 20 healthy volunteers were recorded with the head rotated 60 degrees to the right. The mean peak-to-peak amplitude values of the precentral P22/N30 complex and the mean ratio of the P22/N30 amplitudes between both hemispheres were calculated in the F3 (F4) and C3' (C4') electrode positions in all four groups. No significant lateralization of the precentral P22/ N30 component was found in either group of healthy volunteers. In dystonic patients in whom the sternocleidomastoid was determined as the leading muscle of dystonia, a statistically significant lateralization of the P22/N30 component toward the ipsilateral side of the leading muscle was found. In the group with the splenius capitis determined as the leading muscle of dystonia, a statistically significant lateralization of the P22/N30 component toward the contralateral side of the leading muscle was found. The possibility that the precentral cortex is activated differently in cervical dystonia patients who have different muscle patterns of dystonia is discussed.
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PMID:Lateralization of the P22/N30 component of somatosensory evoked potentials of the median nerve in patients with cervical dystonia. 925 Oct 74

The precentral P22/N30 cortical component of the median nerve somatosensory evoked potentials (SEPs) was recorded in 16 patients (11 women and five men) suffering from cervical dystonia before and after botulinum toxin therapy. Cervical dystonia was diagnosed as idiopathic in all patients: 13 patients suffered from right-sided torticollis, and three suffered from left-sided torticollis. The amplitude of the P22/N30 component and the side-to-side ratio of amplitude values were measured. Normal values were obtained by acquiring measurements in two groups of healthy volunteers (n1 = 20 and n2 = 20). The recordings in the first control group were done with the patient's head in a normal position, whereas, in the second control group, the patient kept the head intentionally rotated 60 degrees to the right. Patients were treated with local injections of botulinum toxin A (BTX-A). The mean duration of treatment was 8.3 months, and the mean total amount of BTX injected was 295 U. The P22/N30 precentral component was repeatedly recorded in patients after head posture had been corrected to the normal plane by BTX-A treatment. The recordings showed that the amplitude of the P22/N30 precentral component recorded contralaterally to the direction of head deviation was significantly higher in patients before treatment than after treatment. Contralateral pretreatment amplitudes were also significantly higher (p < 0.01 and p < 0.05, respectively) than amplitudes in both groups of healthy volunteers. The mean side-to-side ratio of precentral P22/N30 component amplitudes was significantly higher in patients before treatment compared with after treatment and also compared with both control groups. These changes in dystonic patients probably reflect the direction of head rotation, the muscle pattern of torticollis, and the change in force of dystonic contraction after the treatment. The changes presumably could be the result of higher excitability of the precentral cortex contralateral to head rotation in patients with cervical dystonia and its change after successful BTX-A treatment.
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PMID:Change in lateralization of the P22/N30 cortical component of median nerve somatosensory evoked potentials in patients with cervical dystonia after successful treatment with botulinum toxin A. 945 35

Somatosensory evoked potentials (SEPs) of the median nerve were recorded in 40 patients with the tonic and tremulous form of torticollis and in 40 healthy volunteers. Polymyographic recordings of the activity of cervical muscles were performed in all patients with cervical dystonia to determine the dystonic and antagonistic muscles. Patient SEPs were recorded during abnormal head movement. SEPs in 20 healthy volunteers were recorded with the head in the middle position. SEPs in another 20 healthy volunteers were recorded with the head rotated 60 degrees to the right. The mean peak-to-peak amplitude values of the precentral P22/N30 and the postcentral N20/P25 complexes and their mean side-to-side ratios were calculated in the F3 (F4), C3' (C4'), and C3+ (C4+) electrode positions in all four groups. In patients with the tonic form of torticollis (group I), an apparent mean P22/N30 amplitude increase was found above the hemisphere contralateral to the direction of head deviation in both precentral electrode positions, F3(4) and C3(4)'. A statistically significant difference was observed between group I and other patient and control groups. In patients with the tremulous form of torticollis (group II), an increase in the mean P22/N30 amplitude was found above both hemispheres in both precentral electrode positions F3(4) and C3(4)'; a significant difference was found between group II and both control groups. Lateralization of the P22/N30 component was found only in patients with the tonic form of torticollis. The mean side-to-side ratio of the precentral P22/N30 component amplitude was significantly different when group I was compared with either group II or control groups. No significant difference between group II and either control group was found. No significant abnormalities in the postcentral N20/P25 component were found in either the dystonic patients or in healthy control subjects. These results might indicate a different pattern of cortex excitability in patients with tonic versus tremulous forms of torticollis and therefore may implicate different underlying pathophysiological mechanisms in these two forms of disorder.
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PMID:Lateralization of the P22/N30 precentral cortical component of the median nerve somatosensory evoked potentials is different in patients with a tonic or tremulous form of cervical dystonia. 1043 2

We report a 66-year-old woman clinically diagnosed as having a corticobasal degeneration (CBD), who showed electrophysiologically cortical reflex myoclonus. She developed a clumsiness and action myoclonus on the right extremities, and aphasia. The extrapyramidal signs such as dystonia and rigidity were also noted on the right side. Sequential MR images showed a progressive brain atrophy in the left frontoparietal area, where a blood perfusion was reduced on single photon emission computed tomography (SPECT). The median nerve stimulation on the affected right side, but not left side, elicited an enhanced long-loop reflex. The onset latency of the long-loop reflex (43.8msec) was similar to that of the reported cases of CBD (Thompson et al, 1994); but, significantly shorter than that reported in the patients with typical cortical reflex myoclonus. The right median nerve stimulation also elicited so-called giant somatosensory evoked potentials (SEPs). On the basis of the scalp topography of the giant SEPs, we found the high amplitude central P22-N30 components to reflect a radial dipole. We also recorded the myoclonus-related cortical spike by jerk-locked back averaging. Both the giant SEP and myoclonus-related cortical spike were recorded only on the left scalp. We therefore suggest that these two cortical activities are similar in terms of wave form, scalp topography and time relationship to either the long-loop reflex or myoclonus and may be located in the precentral area. This is the first report of a patient with CBD presenting both the giant SEP and myoclonus-related cortical spike.
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PMID:[A case of clinically diagnosed corticobasal degeneration with unilateral cortical reflex myoclonus showing so-called giant SEP]. 1054 7

One characteristic of focal dystonia is the sensory trick, by which sensory input to a certain area of the body can reduce abnormal contractions in muscles nearby. This suggests that adjusting the link between sensory input and movement allows motor commands to be issued more effectively from the brain. To explore this sensorimotor link, we studied the attenuation (gating) of somatosensory evoked potentials (SEPs) before and during hand movements in patients with writer's cramp. For premovement gating, 10 patients and 11 age-matched normal subjects were given a warning sound followed 1s later by an electric stimulus to the right median nerve at the wrist. The latter served both as a reaction signal to start a finger extension task and as the input to evoke SEPs over the scalp. Because reaction times always exceeded 70 ms, short-latency SEPs thus obtained were unaffected by the afferents activated by the movement. The amplitudes of frontal N30 components were significantly decreased over the frontal leads compared with SEPs elicited at rest (P: < 0.002) in the normal group, whereas significant gating was found not for N30 but for frontal P22 (P: = 0. 002) in the patient group. For midmovement gating studies, SEPs to the right median nerve stimulation were recorded in 16 patients and 12 age-matched normal subjects at rest, and during active and passive finger extension-flexion movements. In contrast to the premovement SEPs, the frontal N30 was equally gated during active and passive movements both in the patient (P: < or = 0.002) and the normal group (P: < or = 0.003). These findings indicate that in writer's cramp the sensitivity of sensory input channels from the hand is wrongly set by the central command to move. Perhaps the sensory trick, by supplying additional input not usually present during unobstructed movement, is a manoeuvre to correct this imbalance. Dystonia may result not only from abnormalities in the central motor command but also from disturbed central processing of sensory input.
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PMID:Abnormal premovement gating of somatosensory input in writer's cramp. 1096 45

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