Journal of neurology, neurosurgery, and psychiatry
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J. Neurol. Neurosurg. Psychiatr. · Oct 1999
Bacterial meningitis associated with lumbar drains: a retrospective cohort study.
The infective potential of lumbar drainage is an important topic deserving particular study. The aetiology, incidence, and clinical findings associated with bacterial meningitis are described in patients having continuous lumbar CSF drainage to treat communicating hydrocephalus after subarachnoid haemorrhage or CSF leaks after traumatic dural rents. ⋯ External lumbar drainage seems to carry a low risk of infectious meningitis and offers a safe alternative to ventriculostomy or serial lumbar punctures. Antibiotics do not seem to protect completely against developing the infection. The infection happens most often with skin organisms. The meningitis often appears within 24 hours after lumbar drain placement. Daily CSF samples should include bacterial cultures but cell counts may not offer any additional useful information in diagnosing the complication. Lumbar drain insertion and management need not be confined to the intensive care unit.
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J. Neurol. Neurosurg. Psychiatr. · Oct 1999
Night time versus daytime transient ischaemic attack and ischaemic stroke: a prospective study of 110 patients.
Ischaemic stroke occurs only in 20%-40% of patients at night. The aim of the study was to compare sleep and stroke characteristics of patients with and without night time onset of acute ischaemic cerebrovascular events. ⋯ Patients with night time and daytime transient ischaemic attack/stroke are similar in sleep and stroke characteristics. Diastolic hypotension may predispose to night time cerebrovascular events. Factors not assessed in this study probably account for the circadian variation in the frequency of transient ischaemic attack and acute ischaemic stroke.
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J. Neurol. Neurosurg. Psychiatr. · Sep 1999
Anti-Hu antibody titre and brain metastases before and after treatment for small cell lung cancer.
To follow up the level of anti-Hu antibody titres during chemotherapy and to compare the pattern of metastases and other neurological complications before and after chemotherapy in patients with small cell lung cancer (SCLC) with and without low titre anti-Hu antibodies. Seventeen per cent of patients with SCLC without paraneoplastic syndromes have a low titre of anti-Hu antibodies in their serum. Previous studies suggested that these antibodies correlate with a more indolent tumour growth. ⋯ No anti-Hu antibody positive serum, as tested by western blot, became negative during chemotherapy. Anti-Hu positive and anti-Hu negative patients had similar survival, but anti-Hu positive patients tended to be women, had limited disease at the time of tumour diagnosis, and initially metastases seemed to spare the nervous system.
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J. Neurol. Neurosurg. Psychiatr. · Sep 1999
Improvement of levodopa induced dyskinesias by thalamic deep brain stimulation is related to slight variation in electrode placement: possible involvement of the centre median and parafascicularis complex.
To define the reason why two teams using the same procedure and the same target for deep brain stimulation (DBS) obtained different results on levodopa induced dyskinesias, whereas in both, parkinsonian tremor was improved or totally suppressed. ⋯ The retrospective analysis of patients treated with DBS using comparable methodologies provides important information concerning electrode position and therapeutic outcome. The position of the electrode is related to the therapeutic effects of DBS. The results support the hypothesis that patients experiencing an improvement of dyskinesias under DBS are actually stimulated in a structure which is more posterior, more internal, and deeper than the VIM, very close to the CM-Pf. These results are consistent with neuroanatomical and neurophysiological data showing that the CM-Pf is included in the motor circuits of the basal ganglia system and receives an important input from the internal pallidum. This suggests that the CM-Pf could be involved specifically in the pathophysiology of levodopa peak dose dyskinesias.