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ABSTRACT: In the 1840s Brown-Séquard described the motor and sensory effects of sectioning half of the spinal cord. Penetrating injuries can cause Brown-Séquard or, more frequently, Brown-Séquard-plus syndromes.
To report the case of a 25-year-old man who developed left-sided Brown-Séquard syndrome at the C8 level and left-sided Horner syndrome plus urinary retention and bilateral extensor responses following a stab wound in the right side of the neck.
Magnetic resonance imaging demonstrated a low cervical lesion and somatosensory evoked potentials confirmed the clinical finding of left-side dorsal column disturbance. At follow-up, the patient's mobility and bladder function had returned to normal.
This patient recovered well after a penetrating neck injury that disturbed function in more than half the lower cervical spinal cord (Brown-Séquard-plus syndrome).
Archives of Neurology 10/2001; 58(9):1470-2. · 7.58 Impact Factor
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Journal of Telemedicine and Telecare 02/1999; 5(2):134-6. · 1.21 Impact Factor
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F V Elmslie,
M Rees,
M P Williamson,
M Kerr,
M J Kjeldsen, K A Pang,
A Sundqvist,
M L Friis,
D Chadwick,
A Richens,
A Covanis,
M Santos,
A Arzimanoglou,
C P Panayiotopoulos,
D Curtis,
W P Whitehouse,
R M Gardiner
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ABSTRACT: The epilepsies are a group of disorders characterised by recurrent seizures caused by episodes of abnormal neuronal hyperexcitability involving the brain. Up to 60 million people are affected worldwide and genetic factors may contribute to the aetiology in up to 40% of patients. The most common human genetic epilepsies display a complex pattern of inheritance. These are categorised as idiopathic in the absence of detectable structural or metabolic abnormalities. Juvenile myoclonic epilepsy (JME) is a distinctive and common variety of familial idiopathic generalised epilepsy (IGE) with a prevalence of 0.5-1.0 per 1000 and a ratio of sibling risk to population prevalence (lambda(s)) of 42. The molecular genetic basis of these familial idiopathic epilepsies is entirely unknown, but a mutation in the gene CHRNA4, encoding the alpha4 subunit of the neuronal nicotinic acetylcholine receptor (nAChR), was recently identified in a rare Mendelian variety of idiopathic epilepsy. Chromosomal regions harbouring genes for nAChR subunits were therefore tested for linkage to the JME trait in 34 pedigrees. Significant evidence for linkage with heterogeneity was found to polymorphic loci encompassing the region in which the gene encoding the alpha7 subunit of nAChR (CHRNA7) maps on chromosome 15q14 (HLOD = 4.4 at alpha = 0.65; Z(all) = 2.94, P = 0.0005). This major locus contributes to genetic susceptibility to JME in a majority of the families studied.
Human Molecular Genetics 09/1997; 6(8):1329-34. · 7.64 Impact Factor
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The Lancet 03/1997; 349(9050):470. · 38.28 Impact Factor
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F V Elmslie,
M P Williamson,
M Rees,
M Kerr,
M J Kjeldsen, K A Pang,
A Sundqvist,
M L Friis,
A Richens,
D Chadwick,
W P Whitehouse,
R M Gardiner
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ABSTRACT: Linkage analysis in separately ascertained families of probands with juvenile myoclonic epilepsy (JME) has previously provided evidence both for and against the existence of a locus (designated "EJM1"), on chromosome 6p, predisposing to a trait defined as either clinical JME, its associated electroencephalographic abnormality, or idiopathic generalized epilepsy. Linkage analysis was performed in 19 families in which a proband and at least one first- or two second-degree relatives have clinical JME. Family members were typed for seven highly polymorphic microsatellite markers on chromosome 6p: D6S260, D6S276, D6S291, D6S271, D6S465, D6S257, and D6S254. Pairwise and multipoint linkage analysis was carried out under the assumptions of autosomal dominant inheritance at 70% and 50% penetrance and autosomal recessive inheritance at 70% and 50% penetrance. No significant evidence in favor of linkage to the clinical trait of JME was obtained for any locus. The region formally excluded (LOD score < -2) by using multipoint analysis varies depending on the assumptions made concerning inheritance parameters and the proportion of linked families, alpha-that is, the degree of locus heterogeneity. Further analysis either classifying all unaffected individuals as unknown or excluding a subset of four families in which pyknoleptic absence seizures were present in one or more individuals did not alter these conclusions.
The American Journal of Human Genetics 10/1996; 59(3):653-63. · 10.60 Impact Factor
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ABSTRACT: Conventional treatment for painful peripheral diabetic neuropathy is largely symptomatic and often ineffective, with unacceptable side-effects. We tested electrical spinal-cord stimulation for the management of chronic neuropathic pain.
Ten diabetic patients who did not respond to conventional treatment (mean age 51 [SD 9.3] years, six with type II diabetes, mean duration of diabetes 12 [6.3] years, mean duration of neuropathy 5 [2.1] years) were studied. The electrode was implanted in the thoracic/lumbar epidural space. Immediate neuropathic pain relief was assessed by visual analogue scale (VAS) after connecting the electrode, in a random order, to a percutaneous electrical stimulator or to a placebo stimulator. Exercise tolerance was assessed on a treadmill.
Eight subjects had statistically significant pain relief with the electrical stimulator (p < 0.02) and were therefore converted to a permanent system. Statistically significant relief of both background and peak neuropathic pain was achieved at 3 months (n = 7, p = 0.016), at 6 months (n = 7, p = 0.03), and at the end of the study (14 months, n = 7, background pain p = 0.06, peak pain p = 0.03). One patient died 2 months after the start of the study of unrelated cause while continuing to benefit from treatment and another patient ceased to benefit at 4 months. McGill pain questionnaire scores with the stimulator turned off did not change significantly from baseline scores, indicating that the severity of the underlying pain was unaltered. However, with the stimulator turned on, there was a statistically significant (p < 0.05) improvement in all four components of the score, by the end of the study. At the end of the study, six patients continued to gain significant pain relief and used the stimulator as the sole treatment for their neuropathic pain. For example, median background and peak pain scores at the end of study, were, respectively, 77 and 81 with the stimulator off and 23 and 20 with the stimulator on. Exercise tolerance significantly improved at 3 months (n = 7, median % increase 85 [IQR, 62-360], p = 0.015) and at 6 months (n = 6, 163 [61-425], p = 0.0007). Electrophysiological tests, vibration perception-threshold, and glycaemic control were unchanged.
Electrical spinal-cord stimulation offers a new and effective way of relieving chronic diabetic neuropathic pain and improves exercise tolerance. The technique should be considered in patients with neuropathic pain who do not respond to conventional treatment.
The Lancet 348(9043):1698-701. · 38.28 Impact Factor
