Acta neurochirurgica
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Acta neurochirurgica · Aug 2002
Decompressive craniectomy for the management of patients with refractory hypertension: should it be reconsidered?
The management of refractory post-traumatic cerebral oedema remains a frustrating endeavor for the neurosurgeon and the intensivist. Mortality and morbidity rates remain high, despite refinements in medical and pharmacological means of controlling intracranial hypertension. ⋯ Patients with STBI, developing delayed intracranial hypertension caused by diffuse cerebral oedema, definitely benefit from craniectomy when current medical treatment has failed. The encouraging results of outcome in this and more recent studies, indicate the need for a multi-institutional randomized prospective study evaluating early indicators of raised ICP, timing, efficacy of treatment, operative technique and complications of decompressive craniectomy.
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Acta neurochirurgica · Aug 2002
Accumulation of PN1 and PN3 sodium channels in painful human neuroma-evidence from immunocytochemistry.
The axolemmal distribution and density of voltage-gated sodium channels largely determines the electrical excitability of sprouting neurites. Recent evidence suggests that accumulation of sodium channels at injured axonal tips may be responsible for ectopic axonal hyperexcitability and the resulting abnormal sensory phenomena of pain and paresthesias. For future improvement in pain management it is necessary to identify structurally significant generators of autorhythmicity. A first step in this regard will be to determine the predominant types of sodium channels in injured axons. The opportunity to test human specimens from painful and non-painful neuroma is of great value. ⋯ Both, PN1 and PN3 seem to be involved in hyperexcitability induced pain. It can be expected that a variety of other highly specific voltage gated sodium channel subtypes will be detected in regenerating peripheral nerve in the near future, which contribute to the development of neuropathic pain states. Thus, in order to therapeutically control hyperexcitability induced neuropathic pain, it might be worthwhile to develop pharmaceuticals that can selectively block different sodium channel subtypes and subunits.A review of the role of sodium channels in neuropathic pain is implemented in the discussion.