Journal of neurology, neurosurgery, and psychiatry
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J. Neurol. Neurosurg. Psychiatr. · Nov 1994
Optic nerve sheath decompression for the treatment of visual failure in chronic raised intracranial pressure.
The records of all patients undergoing optic nerve sheath decompression for visual failure in chronic raised intracranial pressure performed over a 15 year period have been reviewed. The aim was to study the visual outcome and relation to any shunting procedures. Fourteen patients (20 eyes) were identified in whom follow up information of at least one year was available. ⋯ It is concluded that optic nerve sheath decompression is a safe and important therapeutic option in the management of chronic raised intracranial pressure complicated by visual loss. Vision can be saved after shunt failure, and in other cases may be maintained without the need for a shunt. Shunts may still be required, however, after optic nerve sheath decompression, especially for persistent headache.
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J. Neurol. Neurosurg. Psychiatr. · Oct 1994
Randomized Controlled Trial Clinical TrialThird occipital nerve headache: a prevalence study.
A consecutive series of 100 patients was studied to determine the prevalence of third occipital nerve headache in patients with chronic neck pain (> three months in duration) after whiplash. Seventy one patients complained of headache associated with their neck pain. Headache was the dominant complaint of 40 patients, but was only a secondary problem for the other 31. ⋯ Those patients with a positive diagnosis, however, were significantly more likely to be tender over the C2-3 zygapophysial joint (p = 0.01). Third occipital nerve headache is a common condition in patients with chronic neck pain and headache after whiplash. Third occipital nerve blocks are essential to make this diagnosis.
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J. Neurol. Neurosurg. Psychiatr. · Aug 1994
Case ReportsCongenital insensitivity to pain: a 20 year follow up.
The exact nosological status of "congenital insensitivity to pain" remains in doubt. Possible pathological correlates of this clinical syndrome include sensory neuropathy, central lesions at the level of the reticular formation or dorsal horn of the spinal cord, or a central indifference to, or asymbolia for, pain. The reassessment of two members of a kindred previously reported more than 20 years ago as having congenital insensitivity to pain indicated that they in fact had an inherited sensory and autonomic neuropathy. Prolonged follow up and morphometric analysis of sequential nerve biopsies may be necessary to definitively establish this diagnosis.
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Twenty three patients with hemiballism and two with biballism were studied. Ischaemic and haemorrhagic strokes were the cause in most patients. Other causes were encephalitis, Sydenham's chorea, systemic lupus erythematosus, basal ganglia calcifications, non-ketotic hyperglycaemia, and tuberous sclerosis. ⋯ Only two patients had "pure" hemiballism. The others had other types of dyskinesias, mainly chorea, which was present in 16 patients. The prognosis was usually good.