Journal of neurology, neurosurgery, and psychiatry
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Five patients with chronic arachnoiditis and syringomyelia were studied. Three patients had early life meningitis and developed symptoms of syringomyelia eight, 21, and 23 years after the acute infection. One patient had a spinal dural thoracic AVM and developed a thoracic syrinx 11 years after spinal subarachnoid haemorrhage and five years after surgery on the AVM. ⋯ Small cystic regions of myelomalacia coalesce to form cavities. In other patients, central cord ischaemia mimics syringomyelia but no cavitation is present. Scar formation with spinal block leads to altered dynamics of cerebrospinal fluid (CSF) flow and contributes to the formation of spinal cord cystic cavities.
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Somatic sensory perception thresholds (warm, cold, hot pain, touch, pinprick, vibration, two-point discrimination), allodynia and skin temperature were assessed in the affected area of 42 patients with unilateral postherpetic neuralgia (PHN) and 20 patients who had had unilateral shingles not followed by PHN (NoPHN), and in the mirror-image area on the other side. There was no difference between the two groups for age or length of time after the acute herpes zoster infection. The PHN group showed significant changes in all sensory threshold measurements when the affected area was compared with the mirror-image area on the unaffected side, while the NoPHN group exhibited no threshold changes. ⋯ No differences in skin temperature were recorded between affected and unaffected regions in either group. Our findings show a deficit of sensory functions mediated by both large and small primary afferent fibres and also suggest major central involvement in the pathophysiology of the condition. If PHN does not occur following acute herpes zoster, recovery of neural functions appears to be good.
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J. Neurol. Neurosurg. Psychiatr. · Jan 1990
EMG responses in leg muscles to postural perturbations in Huntington's disease.
This paper compares leg muscle electromyogram (EMG) responses to sudden toe-up tilts of a moveable platform in patients with Huntington's disease (HD), clinically normal offspring at risk of developing HD (HD risks) and healthy controls. The EMG pattern in standing subjects and patients consisted of short- and middle-latency responses (SL and ML) in the stretched triceps surae muscles and long-latency responses (LL) in the shortened tibialis anterior muscles. The SL response could be further divided into two distinct subcomponents termed SL1 and SL2. ⋯ In the sitting condition, the EMG responses of the HD patients and of the HD risks did not differ from those of controls: in all groups SL1 was reduced and delayed, SL2 slightly enhanced, while ML and LL were absent. Because both afferent and efferent conduction times are normal in HD, the delayed LL onset reflects abnormal supraspinal organisation of postural control in HD, and indicates that basal ganglia may have a modulatory effect on the LL responses. The normal EMG responses in the sitting patients suggest appropriate regulation of these responses according to postural set in HD.