Journal of the neurological sciences
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The pathophysiology of lumbar puncture headache (LPH) is still unclear. There is evidence that leakage of cerebrospinal fluid (CSF) leads to CSF hypotension, which causes dilation of intracranial veins, resulting in LPH. However, CSF leaks at the skull base are not associated with orthostatic headache; there is poor correlation between recumbent CSF pressure and LPH; and there has been no satisfactory explanation of how venous dilation causes orthostatic headache. ⋯ We are, thus, able to explain the orthostatic character of LPH, the fact that spinal but not cranial sites of leakage produce orthostatic headache and the imperfect correlations both between recumbent CSF pressure and LPH and between reduced CSF volume and LPH. The near absence of LPH in the very young and in the elderly relates to the relative stiffness of the epidural space at these ages. Epidural injections of blood or saline give immediate relief by reducing epidural distensibility.
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Brain ischemia and reperfusion engage multiple independently-fatal terminal pathways involving loss of membrane integrity in partitioning ions, progressive proteolysis, and inability to check these processes because of loss of general translation competence and reduced survival signal-transduction. Ischemia results in rapid loss of high-energy phosphate compounds and generalized depolarization, which induces release of glutamate and, in selectively vulnerable neurons (SVNs), opening of both voltage-dependent and glutamate-regulated calcium channels. This allows a large increase in cytosolic Ca(2+) associated with activation of mu-calpain, calcineurin, and phospholipases with consequent proteolysis of calpain substrates (including spectrin and eIF4G), activation of NOS and potentially of Bad, and accumulation of free arachidonic acid, which can induce depletion of Ca(2+) from the ER lumen. ⋯ This picture argues powerfully that, for therapy of brain ischemia and reperfusion, the concept of single drug intervention (which has characterized the approaches of basic research, the pharmaceutical industry, and clinical trials) cannot be effective. Although rigorous study of multi-drug protocols is very demanding, effective therapy is likely to require (1) peptide growth factors for early activation of survival-signaling pathways and recovery of translation competence, (2) inhibition of lipid peroxidation, (3) inhibition of calpain, and (4) caspase inhibition. Examination of such protocols will require not only characterization of functional and histopathologic outcome, but also study of biochemical markers of the injury processes to establish the role of each drug.
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Imaging considerations for the diagnosis and differential diagnosis of MS are based primarily on results of MR studies of the brain. Recent studies suggest that with current technology, MR imaging of the spinal cord can make important contributions, particularly in cases with equivocal or negative brain MRI studies. Spinal cord MRI may also assume an important role in early diagnosis.
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Stereotaxtic surgery is an effective therapeutic maneuver in the management of advanced Parkinson's disease (PD). Thalamotomy is an effective measure to control tremor but other PD symptoms are not changed. Bilateral operations are associated with a risk of severe speech impairment. ⋯ This procedure may control all PD symptoms, and the dose of levodopa can often be dramatically reduced. Neurotransplantation is a promising surgical approach to PD. However, further investigation is needed to optimize this approach.
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The objective of this review is a summary of the clinical and electrographic findings in those forms of epilepsy to which the term 'extratemporal' (ExT) can be applied. They form a group that differs in many ways from the better known temporal lobe epilepsies. ⋯ The concept of 'dual pathology' implies the coexistence of two or more distinct lesions, typically mesial temporal sclerosis and cortical dysplasia. Electroencephalography (EEG) and electrocorticography (ECoG) are valuable tests in the definition of the epileptogenic area beyond the structural lesion, and surgical removal must be guided by the nature of the lesion and the extent of the epileptogenic zone.