Central motor conduction studies in hereditary spastic paraplegia.

Schady, W.; Dick, Jeremy; Sheard, Ailish C.; Crampton, S.

doi:10.1136/jnnp.54.9.775

Cited by 48 publications

(22 citation statements)

References 27 publications

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“…Its diagnostic value has been applied to a wide variety of central nervous system disorders, such as amyotrophic lateral sclerosis [10, 11], multiple sclerosis [12], various degenerative diseases [8, 13, 14], and stroke [15]. In pontine infarction, CMCT increased in correlation with the severity of paresis [15].…”

Section: Discussionmentioning

confidence: 99%

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Corticospinal Tract Involvement in a Variant of Guillain-Barré Syndrome

Oshima¹,

Mitsui²,

Endo³

et al. 2001

Eur Neurol

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To determine the involvement of the corticospinal tract in Guillain-Barré syndrome (GBS), we examined central motor conduction in patients with GBS-like symptoms and hyperreflexia using a magnetic stimulation technique. The subjects were 3 patients who exhibited ascending muscle weakness 2–4 weeks after preceding infections. Deep tendon reflexes were exaggerated in all four limbs of the 3 patients. The results of cerebrospinal fluid examinations revealed protein elevation without pleocytosis. The serum anti-GM₁ antibody titer was elevated in 2 patients. The results of nerve conduction study revealed axonal motor neuropathy and normal F-wave conduction. Central motor conduction time (CMCT) in patients with hyperreflexia was significantly delayed compared to that in patients with GBS and areflexia (p < 0.001), and the delayed CMCTs were significantly improved in the recovery periods (p < 0.001). Although hyperreflexia is a controversial symptom in patients with GBS, these findings indicate that there is functional corticospinal tract involvement in patients with a GBS variant.

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Section: Discussionmentioning

confidence: 99%

“…Motor evoked studies were also performed twice in each of 3 control patients with GBS and areflexia within 2 weeks of onset. Central motor conduction time (CMCT) was calculated by subtracting (F + M –1)/2 from that of the corresponding MEP latency [5, 7, 8]. The peripheral component was obtained by recording electrically evoked M and F waves.…”

Section: Methodsmentioning

confidence: 99%

Corticospinal Tract Involvement in a Variant of Guillain-Barré Syndrome

Oshima¹,

Mitsui²,

Endo³

et al. 2001

Eur Neurol

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“…In the case of HSP, the altered neuronal targets are mainly in the spinal cord. Electrophysiological [16] and neuropathological [13] studies have demonstrated maximal axonal degeneration in the terminal portions of the longest corticospinal tract ®bres from the motor cortex pyramidal neurones and fasciculus gracilis from dorsal root ganglia neurones. The bene®cial effects of ITB in HSP could therefore be attributed to GABA B -mediated reduction of afferent excitation of alpha motoneurons in the spinal cord.…”

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confidence: 99%

Effect of intrathecal baclofen on gait control in human hereditary spastic paraparesis

Dan

Bouillot²,

Bengoetxea³

et al. 2000

Neuroscience Letters

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The covariation between thigh, shank and foot elevation angles during locomotion was analysed by means of orthogonal planar regression in a patient with pure hereditary spastic paraparesis before and after an intrathecal bolus of baclofen and in seven healthy subjects. The size, shape and spatial orientation of the loop de®ning patient's planar covariation (thigh angle vs. shank angle vs. foot angle) signi®cantly differed from the controls' before baclofen, whereas these features resumed normal characteristics after baclofen injection. This shows that alteration of the control of phase coupling for the co-ordination of lower limb segments in human gait by increased spinal re¯exes can be reversed by intrathecal baclofen injection. q 2000 Elsevier Science Ireland Ltd. All rights reserved.Keywords: Human; Locomotion; Co-ordination; Planar covariation; Baclofen; Hereditary spastic paraparesis As a GABA B agonist [14], baclofen reduces the release by primary afferent terminals in laminae II and III of excitatory neurotransmitters onto ventral horn motoneurons in the spinal cord [5,17]. Although intrathecal baclofen (ITB) is becoming a standard treatment of spinal origin spasticity [15], its effect on locomotor control is unclear. A recent approach has revealed a speci®c covariation of elevation angles of the lower limb segments along an attractor plane during locomotion in healthy humans [2±4,10]. The plane orientation and the shape of the loop that de®nes it re¯ect the phase relationships between these angles and therefore intersegmental co-ordination, on which postural stability with respect to gravity and dynamic equilibrium for forward progression depend. Recently, the features of this covariation in Parkinson's disease before and after therapeutic intervention gave insights into basal ganglia function [11]. In this study, we analysed this covariation in a patient with uncomplicated autosomal dominant hereditary spastic paraparesis (HSP) [9] before and after an ITB bolus.The studied patient, aged 41, has normal muscle power, increased tone and re¯exes in the lower limbs, extensor plantar responses and a spastic gait. Seven healthy subjects (aged 38.2^4.6) participated as controls.Using the ELITE system [8], four sessions of ten trials of the patient's self-paced locomotion over ten meters were recorded with a 100 Hz sampling rate, respectively before ITB of 75 mg (0.77 mg/kg) via lumbar puncture and 2, 4 and 6 h after it. Ten trials were recorded for each control subject. Markers over the anterior-superior iliac spine, trochanter, lateral knee condyle, lateral malleolus and 5th metatarsal, de®ned the segments of the thigh, shank and foot.Statistical analysis of the angle covariation was based on principal component (PC) analysis (see [2]). PCs were computed by pooling the sample of time-varying angles after subtracting the mean. PCs are linear combinations of variates which are the covariance matrix eigenvectors. The ith PC is given by: PCi u i T a where u i is the eigenvector and a the variates. The norm...

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“…6 The results of electrophysiological investigations vary between studies and have not contributed significantly to the elucidation of possible differences in the aetiology and pathogenesis of the disorder. TMS studies have demonstrated that CMCTs to lower extremities are delayed in most but not all patients [7][8][9][10] ; CMCTs to upper extremities are usually normal but may be prolonged in a minority of patients, 8 11 and intracortical facilitation may be increased. 12 In none of these studies, electrophysiological findings have been combined with genotypes.…”

Section: Discussionmentioning

confidence: 99%