Neurology
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Randomized Controlled Trial Clinical Trial
Phentolamine sympathetic block in painful polyneuropathies. II. Further questioning of the concept of 'sympathetically maintained pain'.
To test for the presence of "sympathetically maintained pain" (SMP), we administered placebo-controlled phentolamine sympathetic blocks to 14 patients with painful polyneuropathies. Six received i.v. infusion of saline for 30 minutes, followed by phentolamine (35 mg). In eight patients, the saline phase was followed by double-blind infusion of phentolamine or phenylephrine (500 micrograms), a second saline phase, and then the other active drug. ⋯ Five patients reported significant diminution of pain (> 50%), all in response to placebo. Neither phentolamine nor phenylephrine provided relief, although all patients had signs of physiologic abnormalities reputed to be determinants or predictors of SMP. These results complement previous studies demonstrating the nonexistence of SMP among "reflex sympathetic dystrophy" patients and further question the concept of SMP.
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The challenges of treating patients with partial seizures soon will be met, in part, by a number of new additions (felbamate, gabapentin, lamotrigine) to existing treatment options. Gabapentin, has shown significant promise in the treatment of patients with refractory partial seizures and secondarily generalized tonic-clonic seizures. Three large, randomized, multicenter, double-blind, placebo-controlled, parallel-group clinical trials have established its efficacy and safety as add-on therapy in patients with refractory partial seizures. ⋯ To date, serious adverse events have been rare. Long-term safety data are needed. The lack of drug interaction potential between gabapentin and traditional antiepileptic drugs also was confirmed in clinical trials.
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Clinical Trial Controlled Clinical Trial
'Sympathetically maintained pain.' I. Phentolamine block questions the concept.
Patients with "reflex sympathetic dystrophy" or "causalgia" underwent sympathetic blocks. In protocol A (77 patients), we infused placebo (saline) for 30 minutes followed by phentolamine (35 mg). In protocol B (23 patients), the saline phase was followed by double-blind infusion of phentolamine or phenylephrine (500 micrograms), a second phase of saline, and then the other active drug. ⋯ Most patients did not respond significantly to saline or drugs. Thus, pharmacologic manipulation of the alpha-1 adrenergic receptor by either agonist or antagonist drug does not influence neuropathic pains. These results raise questions about the existence of "sympathetically maintained pain," as diagnosed by sympathetic blocks improperly controlled for placebo.
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Significant progress in the classification, diagnosis, and pharmacologic management of epileptic seizures has occurred over the past two decades, but epilepsy remains a therapeutic challenge. Clinical studies show that most patients with epilepsy can have complete or almost complete seizure control with optimally managed monotherapy that employs a traditional antiepileptic drug (AED). About half of the remaining patients can obtain improved seizure control with combination antiepileptic drug therapy, but usually with more adverse effects. ⋯ Advances in understanding the pathogenesis of epilepsy and the mechanisms of action of antiepileptic drugs have provided a basis for the development of new AEDs that hold promise for difficult-to-treat patients. In this decade, a number of new AEDs that may overcome some of the disadvantages of traditional AEDs and offer clinicians and patients added therapeutic options will become clinically available. These will be more fully evaluated for their clinical potential to meet existing challenges of epilepsy treatment.
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We evaluated a simplified method for preparation and analysis of platelet cytochrome c oxidase activity in Alzheimer's disease (AD) and control patients. Mean cytochrome c oxidase activity in controls (n = 17) was 0.233 sec-1/mg whereas mean cytochrome c oxidase activity in Alzheimer patients (n = 19) was 0.193 sec-1/mg, p = 0.033. Complex III (ubiquinol:cytochrome c oxidoreductase), complex II (succinic dehydrogenase), and citrate synthase were all assayed as internal controls and were not significantly different in controls and Alzheimer patients. There is a relatively specific loss of platelet cytochrome c oxidase activity in Alzheimer disease patients.