Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology
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Randomized Controlled Trial Clinical Trial
A randomised, double-blind, dose-ranging study to evaluate efficacy and safety of three doses of botulinum toxin type A (Botox) for the treatment of spastic foot.
Botulinum toxin A (BTX) injections have been used successfully in the treatment of post-stroke foot spasticity, but the optimal dose-response relationship for selected muscles has yet to be established. The aim of this study was to outline beneficial and unwanted effects of three different doses of BTX in the treatment of spastic foot. In this randomised, double-blind, dose-ranging study, 45 spastic feet were randomly allocated to one of three groups, each of which was treated with a different dosage of BTX. ⋯ Group III showed the highest rate of adverse effects 4 weeks post-treatment. BTX injections constitute a useful and safe method of improving post-stroke foot spasticity, associated pain, gait speed and function. In particular, the medium BTX dosages (320 UI spread over 2-5 muscles) were found to be both safe and effective in producing long-lasting improvement of spastic foot dysfunction.
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Current antispastic medications are unsatisfactory for spasticity treatment, but botulinum toxin type A (BTX-A) shows promise as a new therapeutic option. This open-label, prospective study aimed to assess the effectiveness of BTX-A in improving functional mobility in the early post-stroke population using an individualised, flexible range of doses and targeted muscle groups. Twenty-one stroke patients (13 male, 8 female) were enrolled and injected with BTX-A (Botox, Allergan, mean dose: 255 U; range: 185-300) according to individual spasticity patterns. ⋯ Pain was present only in 11 patients and did not significantly improve following treatment. Individualised BTX-A injection regimens may be an effective, reversible and safe new treatment option for patients with spasticity. Nevertheless, functional improvement may be reached only in selected patients.
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Cranial subdural haematoma formation following spinal anaesthesia is exceptionally rare. A 38-year-old male developed headache two days after testicular surgery under spinal anaesthesia. ⋯ The pathogenesis of subdural haematoma formation after dural puncture is discussed and the literature briefly reviewed. Prolonged and severe post-dural puncture headache should be viewed with suspicion and investigated promptly to rule out any intracranial complication.
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Multiple sclerosis (MS) is characterized by multiple demyelinated inflammatory lesions disseminated in the central nervous system (CNS). Additional features of MS pathology include axonal loss and gliosis. Remyelination may take place predominantly in the early stages of lesion formation. ⋯ Devic's neuromyelitis optica may represent the prototypical disease with antibody/complement-mediated demyelination, whereas cases with Balò's concentric sclerosis show oligodendrocyte dystrophy. Acute disseminated encephalomyelitis (ADEM) may be regarded as a related condition lacking extensive demyelination. Thus, atypical MS forms may help to elucidate pathogenic mechanisms in MS.
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We investigated if, in patients with vascular lesions, the variable that best discriminated demented from non-demented patients was the severity of the vascular pathology or the degree of hippocampal atrophy. A total of 39 patients multiple subcortical infarcts, who could be considered as possible vascular dementia with small vessel pathology, with underwent a neuropsychological study and brain magnetic resonance imaging (MRI) DSM IV criteria supported by neuropsychological data were used to distinguish demented from non-demented patients. ⋯ The distribution of lesions and a factor analysis showed that hippocampal atrophy is a better predictor of dementia than the number of brain infarcts. Multiple subcortical infarcts alone are probably not able to cause clinical dementia but the presence of vascular lesions increases the expression of concomitant Alzheimer's disease.