Involvement of the central nervous system in chronic inflammatory demyelinating polyneuropathy: A clinical, electrophysiological and magnetic resonance imaging study.

In a consecutive series of 30 patients with chronic inflammatory demyelinating polyneuropathy (CIDP) minor clinical evidence of CNS involvement was found in five. Cranial magnetic resonance imaging (MRI) was performed in 28 and revealed abnormalities consistent with demyelination in nine patients aged less than 50 years and abnormalities in five aged 50 years or over. Measurements of central motor conduction time (CMCT) were obtained in 18 and showed unilateral or bilateral abnormalities in six. It is concluded that subclinical evidence of central nervous system (CNS) involvement is common, at least in patients with CIDP in the United Kingdom, but that clinically evident signs of CNS disease are infrequent. The association of a multiple sclerosis-like syndrome with CIDP is rare

A language-action approach to operational research

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Magnetic resonance imaging in clinically isolated lesions of the brain stem.

Twenty-seven patients with an isolated brain stem syndrome, thought to be due to demyelination, were examined by magnetic resonance imaging (MRI). A brain stem lesion was identified in 25, and clinically silent lesions outside the brain stem were demonstrated in 20. MRI was more sensitive than evoked potentials in detecting brain stem and other lesions. The scan findings were compared with those in 23 patients with multiple sclerosis, who had chronic brain stem dysfunction, with particular reference to the distribution of abnormalities and the MRI characteristics of the lesions. The relaxation times, T1 and T2, of the lesions were measured by MRI. These values were seen to fall in serial studies of acute lesions, but remained unchanged in the chronic lesions. MRI may therefore allow the age of lesions to be assessed

Evolving expectations around early management of multiple sclerosis

Multiple sclerosis is a progressive inflammatory disease of the central nervous system. With prevention or at least delay of disease progression as a key target in the management of multiple sclerosis, current opinion on treatment encourages early intervention with well-tolerated disease-modifying treatments in order to optimize long-term clinical outcomes. Patients presenting with a clinically isolated syndrome (CIS) may progress to clinically definite multiple sclerosis, and clinical trials have demonstrated that early treatment with interferon beta can reduce the conversion rate. Cognitive impairment may already be present in patients with CISs. Today there is evolving evidence that cognitive impairment may be relevant for prognosis and that early treatment with interferon beta may also have a protective effect on the cognitive function. As an accumulation of neuronal loss is now considered to underlie the development of persistent disability in multiple sclerosis, it is crucial that treatment can protect against neuronal damage. In addition to its anti-inflammatory activity, interferon beta may have direct and indirect neuroprotective effects, and several studies have explored the role of interferon beta in regulating neuroprotective factors. With over 15 years of clinical experience as evidence, the long-term safety and efficacy of interferon beta treatment is unquestionable. Results from the CIS studies have demonstrated the high percentage of patients converting to clinically definite multiple sclerosis without treatment and the short- and long-term benefits of an early use of disease-modifying treatments. These findings support starting disease-modifying treatment as soon as the diagnosis of MS is reasonably formulated