naloxone and Hemiplegia

We report the repeated improvement in neurological function following naloxone administration in a patient who developed acute hemiplegia after an intracranial neurological procedure. The mechanisms responsible for the neurological deficit and for its reversal by naloxone are discussed. A review of the literature suggests that the beneficial effect of naloxone can result from an improvement in haemodynamic status or from metabolic effects that could be favorable during cerebral ischaemia.

Topics: Arachnoid Cysts; Female; Hemiplegia; Humans; Middle Aged; Naloxone; Postoperative Complications; Sufentanil; Tomography, X-Ray Computed

Topics: Acute Disease; Adult; Aged; Brain Ischemia; Cerebral Infarction; Double-Blind Method; Female; Hemiplegia; Humans; Morphine; Naloxone; Pain

Topics: Cerebrovascular Disorders; Female; Hemiplegia; Humans; Hypesthesia; Infusions, Intravenous; Male; Middle Aged; Naloxone; Palliative Care; Syndrome; Thalamic Diseases

Topics: Aged; Cerebrovascular Disorders; Endorphins; Hemiplegia; Humans; Male; Middle Aged; Naloxone

The effects of an opiate agonist (morphine) and antagonist (naloxone) on neurologic function in conditions of acute and subacute focal cerebral ischemia were tested in a baboon model. Fourteen baboons (Papio papio) underwent unilateral transorbital microsurgical occlusion of the middle cerebral artery (MCA). Blood pressure, heart rate and core temperature were monitored continuously; frequent arterial blood gas measurements were made. Cardiac output, cardiac filling pressures, and regional cerebral blood cross-flow were measured in selected baboons. Naloxone administered intravenously consistently reversed hemiparesis and hemiplegia in all baboons for as long as they lived (4 h to 8 days postocclusion). Morphine administered intravenously converted hemiparesis to hemiplegia; this effect was naloxone-reversible. There were no significant changes in any parameter measured after the administration of either drug. Phenylephrine (used to elevate mean arterial pressure to 20 mm higher than the highest pressure measured after naloxone administration) and isoproterenol (used to elevate cardiac output to 1 l/min higher than the highest value measured after naloxone administration) produced no change in neurologic function. It appears that naloxone can reverse, and morphine exacerbate, focal ischemic neurologic deficits produced in baboons by MCA occlusion. The observed changes in neurologic function are not associated with or mediated by alterations in core temperature or cardiopulmonary functions.

Topics: Animals; Blood Pressure; Body Temperature; Cardiac Output; Cerebrovascular Circulation; Female; Heart; Heart Rate; Hemiplegia; Ischemic Attack, Transient; Male; Morphine; Naloxone; Papio

Topics: Cerebrovascular Disorders; Hemiplegia; Humans; Male; Middle Aged; Naloxone

Two cases of non-familial hemiplegic migraine are described. Naloxone reversed the neurological deficits accompanying attacks, whereas the pain was uninfluenced. The possibility that the opiate-antagonist naloxone facilitates regression of neurological symptoms associated with migraine attacks in general is voiced.

Topics: Adult; Female; Hemiplegia; Humans; Male; Migraine Disorders; Naloxone

Topics: Animals; Brain Ischemia; Cerebrovascular Disorders; Gerbillinae; Hemiplegia; Levorphanol; Male; Morphine; Naloxone; Receptors, Opioid

Stroke induced by a carotid occlusion in gerbils was reversed by intraperitoneal (i.p.) injection of naloxone (1 mg/kg) for up to 30 min. Placebo-treated stroked gerbils died in 48 hr; 40% of gerbils implanted with 10 mg naloxone pellets survived over 2 weeks without neurologic deficit. Intravenous (i.v.) injection of naloxone produced the same transient reversal of hemiplegia in 2 patients with neurologic deficit from cerebral ischemia. These findings suggest the involvement of endorphins and opiate receptors in the pathophysiology of stroke, and suggest the possible clinical use of opiate antagonists in humans in the acute phase of stroke.

Topics: Animals; Brain Ischemia; Gerbillinae; Hemiplegia; Humans; Male; Models, Biological; Naloxone