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Biomedical subjects

G Sheean

Publications and source records attributed to G Sheean.

14 recordsLinked to original sources
PubMed2002

The pathophysiology of spasticity.

Spasticity is only one of several components of the upper motor neurone (UMN) syndrome, known collectively as the 'positive' phenomena, that are characterized by muscle overactivity. Other components include tendon hyper-reflexia, clonus, the clasp-knife phenomenon, flexor and extensor spasms, a Babinski sign, and spastic dystonia. Spasticity is a form of hypertonia due to hyperexcitable tonic stretch reflexes. It is distinguished from rigidity by its dependence upon the speed of the muscle stretch and by the presence of other positive UMN signs. Hyperactive spinal reflexes mediate most of these positive phenomena, while others are due to disordered control of voluntary movement or abnormal efferent drive. An UMN lesion disturbs the balance of supraspinal inhibitory and excitatory inputs, producing a state of net disinhibition of the spinal reflexes. These include proprioceptive (stretch) and nociceptive (flexor withdrawal and extensor) reflexes. The clinical syndrome resulting from an UMN lesion depends more upon its location and extent, and the time since it occurred, than on the pathology of the lesion. However, the change in spinal reflex excitability cannot simply be due to an imbalance in supraspinal control. The delayed onset after the lesion and the frequent reduction in reflex excitability over time, suggests plasticity in the central nervous system. Knowledge of the electrophysiology and neurochemistry of spinal reflexes, together with the action of antispasticity drugs, helps us to understand the pathophysiology of spasticity.

Humans↗
PubMed2001

Nerve conduction changes in patients with mitochondrial diseases treated with dichloroacetate.

Serial measurements of nerve conduction velocities and amplitudes were performed in 27 patients with congenital lactic acidemia over 1 year of sodium dichloroacetate (DCA) administration. Patients were treated with oral thiamine (100 mg) and DCA (initial dose of 50 mg/kg) daily. Nerve conduction velocity and response amplitude were measured in the median, radial, tibial, and sural nerves at 0, 3, 6, and 12 months, and plasma DCA pharmacokinetics were measured at 3 and 12 months. Baseline electrophysiologic parameters in this population were generally below normal but as a group were within 2 standard deviations of normal means. Although symptoms of neuropathy were reported by only three patients or their families, nerve conduction declined in 12 patients with normal baseline studies, and worsening of nerve conduction occurred in the two who had abnormalities at baseline. Peripheral neuropathy appears to be a common side effect during chronic DCA treatment, even with coadministration of oral thiamine. Nerve conduction should be monitored during DCA treatment.

Action Potentials↗
PubMed2000

Evaluating the role of botulinum toxin in the management of focal hypertonia in adults.

OBJECTIVES: To investigate the effects of EMG guided botulinum toxin (BTX-A) on impairment and focal disability in adults presenting with focal hypertonia. METHODS: A prospective, randomised, double blind, placebo controlled, parallel group trial was carried out with standardised assessment before and at 3 week intervals until 12 weeks after injection, in patients with focal hypertonia affecting upper or lower limbs. Botulinum toxin or placebo was injected with EMG guidance after multidisciplinary assessment. The modified Ashworth scale of spasticity, percentage passive range of joint motion, subjective rating of problem severity, the Rivermead motor assessment scale, a timed 10 metre walk (lower limb patients), nine hole peg test (upper limb patients), and a modified goal attainment scale were used as outcome measures. The patients were 52 adults; 34 male, 18 female; mean age 40.31, range 16-79 years; mean duration of symptoms 35 months (range 3 months to 22 years). Diagnoses included cerebrovascular accidents (23), head injury (12), incomplete spinal cord injury (six), tumour (five), cerebral palsy (three), and anoxic episodes (three). RESULTS: For each variable an overall score for the treatment period was computed by summing the scores from the 3, 6, 9, and 12 week assessments. These overall scores were significantly better in the treated group for the Ashworth scale, percentage passive range of movement, Rivermead lower limb, and subjective rating of problem severity. The significant treatment effect on the Ashworth scale was seen on analysis of variance (ANOVA) at 3 weeks and the subjective rating of problem severity at 3 and 6 weeks. The goal attainment scale score in both groups was similar at 12 weeks. CONCLUSION: Selective use of botulinum toxin to weaken muscles can lead to a reduction in resistance to passive movement about a distal limb joint. This allows for improvements in passive range of movement and focal disability, particularly in patients presenting with focal spasticity of the lower limb.

Adolescent↗
PubMed1998

Changes of somatosensory evoked potentials preceding rapid voluntary movement in Go/No-go choice reaction time task.

To elucidate the sensorimotor mechanisms in preparation of voluntary movement, we examined the changes of the somatosensory evoked potentials (SEPs) following median nerve stimulation in Go/No-go choice-reaction time task. Eleven normal subjects performed extension of the middle finger according to the Go signal while they did not make any movement and relaxed on the No-go and Control signals, respectively. Each signal was randomly presented on a computer screen in front of the subject. Single pulse stimulation was applied to the right median nerve at 150 ms after the response signal in each Go/No-go and Control sequence so as to be just before the voluntary movement in the Go sequence. The SEPs were recorded from F3, C3' (midpoint between P3 and C3) and P3 on the left hemisphere. In comparison with the Control sequence, the amplitude of N20 and P25 recorded from C3' and P3 was significantly attenuated before movement in the Go sequence (P<0.02, ANOVA with Bonferroni-Dunn post hoc procedure). On the other hand, the parietal N33 and frontal N30 were attenuated in both Go and No-go sequences (P<0.02). None of the SEP components were changed when the stimulus was delivered before the response signal. We speculate that the attenuation of N20 was linked with the activation of the motor cortex followed by the actual movement. The attenuation of other components up to 33 ms after stimulus were considered to be more related to the preparation or the attention to the voluntary movement than to the movement itself.

Adult↗
PubMed1997

Botulinum toxin does not reverse the cortical dysfunction associated with writer's cramp. A PET study.

Previous H2(15)O PET activation studies on patients with idiopathic torsion dystonia (ITD) have shown overactive striatum and frontal accessory areas and underactivity of the primary motor cortex and caudal supplementary motor area (SMA) during volitional movement. We have now examined activation of the motor system in healthy control subjects and patients with writer's cramp while they write a stereotyped word repetitively at a paced rate before and after treatment with botulinum toxin to see if these patients showed a similar pattern of abnormalities and whether they were reversible. As in ITD, our patients with writer's cramp showed impaired activation of the contralateral primary motor cortex, but enhanced activation of frontal association cortex. Botulinum-toxin treatment improved writing and increased activation in parietal cortex and caudal SMA. This may represent either a change in movement strategy or associated cortical reorganization secondary to deefferentation of alpha motor neurons. However, botulinum toxin failed to improve the impaired activation of the primary motor cortex. We conclude that, while botulinum toxin is clinically effective in writer's cramp, it does not reverse the associated dysfunction of primary motor and premotor cortex.

Adult↗
PubMed1996

A double-blind, placebo-controlled crossover study of vigabatrin 2 g/day and 3 g/day in uncontrolled partial seizures.

The efficacy and tolerability of vigabatrin as add-on therapy was assessed in patients with uncontrolled partial seizures. Ninety-seven patients entered this seven-centre, double-blind, placebo-crossover study. Vigabatrin (2 g or 3 g) or placebo was administered daily. Vigabatrin was well-tolerated and did not cause clinically significant adverse drug effects when added to established anticonvulsant therapy. No significant differences were observed between dose groups for the overall incidence of adverse events, although drowsiness and visual disturbances (diplopia, ataxia, visual abnormalities) showed a dose-related increase with vigabatrin treatment. The results of this study indicate that vigabatrin, given in a daily dose of either 2 g or 3 g is significantly more effective than placebo in reducing seizure frequency among patients with partial seizures.

Adolescent↗
PubMed1995

Changes in the balance between motor cortical excitation and inhibition in focal, task specific dystonia.

Transcranial magnetic stimulation has been used in a double pulse paradigm to investigate the excitability of intrinsic motor cortical circuits in 15 patients with focal task specific dystonia of the right hand and a group of eight age matched controls. The left hemisphere was examined in five patients; in the remainder, both hemispheres were tested. There was no significant difference in stimulation threshold between patients and controls nor between the left and right hemispheres in the patients. There was a significant decrease in early corticocortical suppression when comparing stimulation of the left hemisphere in the patients and controls at interstimulus intervals of 1-15 ms (P < 0.01). There was no difference in the amount of suppression in the right and left hemispheres of the patients. It is concluded that in focal task specific dystonia there is shift in the balance between excitation and inhibition in local circuits of the motor cortex which leads to a net decrease in the amount of short latency suppression. These changes reflect disturbed basal ganglia input to the motor cortex. Reduced excitability of cortical inhibitory circuits may be one factor which contributes to the excessive and inappropriate muscle contraction which occurs during fine motor tasks in patients with focal dystonia.

Adult↗
PubMed1992

Vigabatrin--plasma enantiomer concentrations and clinical effects.

Plasma concentrations of the [R]- and [S]- enantiomers of the new anticonvulsant vigabatrin were measured by an enantiospecific gas-liquid chromatographic assay in a group of therapy-resistant epileptic patients in whom racemic vigabatrin was added to their existing antiepileptic drug regimens. The peak plasma concentrations of the biologically active [S]-enantiomer of vigabatrin were correlated with those of the [R]-enantiomer, with drug dose, seizure frequency and change in score on various tests of psychological function administered prior to and when the subjects were under steady-state conditions following vigabatrin therapy. Plasma [S]-vigabatrin concentrations correlated with drug dose, [R]-vigabatrin concentration and change in score of certain psychological tests reflecting verbal memory, recall and speed of information processing. No definite pharmacokinetic interactions were detected, though plasma phenobarbitone concentrations tended to fall during vigabatrin administration. There were too few data to assess the relation between [S]-vigabatrin concentrations and seizure frequency.

Adolescent↗