beta-endorphin and Cerebral-Infarction

Experimental studies in animal models suggest that the endorphin system may be implicated in the pathogenetic mechanism of cerebral ischemic lesions. Naloxone has been shown to possess a beneficial effect on the neurologic deficit associated with cerebral ischemia in animal experiments, probably because of its endorphin antagonist properties. By contrast, the results of clinical trials are contradictory. Moreover, the true significance of high plasma levels of beta-endorphin in patients with acute focal cerebral infarct (AFCI) has not yet been elucidated. We have evaluated 23 patients with established AFCI, in whom plasma levels of beta-endorphin and corticotropin (ACTH) were simultaneously measured during the first 48 hours after the onset of the disease. The results were compared with those from a control group. In a subgroup of 9 cases new measurements were made after 7 days. In the patients with AFCI, significantly lower levels of beta-endorphin and ACTH than in the control group were found. One week later, a moderate nonsignificant increase in the plasma level of beta-endorphin was found. The localization and estimated size of the infarct area were not relevant. Probably, the plasma levels of beta-endorphin will need to be considered before naloxone therapy is indicated, and only if it is confirmed that the plasma levels of beta-endorphin reflect changes at the cerebral level, as the pathophysiological role of these opioids in AFCI has not yet been established.

Topics: Acute Disease; Adrenocorticotropic Hormone; Adult; Aged; Aged, 80 and over; beta-Endorphin; Cerebral Infarction; Female; Humans; Male; Middle Aged

To investigate the role of endogenous opioid peptides in the pathophysiology of cerebral ischaemia, the CSF levels of immunoreactive beta-endorphin and leu-enkephalin in 16 patients with cerebral infarction were measured. Both the CSF beta-endorphin and leu-enkephalin levels in the acute stage of cerebral infarction were significantly higher than the values in the chronic stage. The CSF concentrations of the two peptides revealed a positive correlation in the acute but not the chronic stage. The increased endogenous opioid peptides in the CSF in the acute stage may modify the evolution of cerebral infarction.

Topics: Acute Disease; Aged; beta-Endorphin; Cerebral Infarction; Chronic Disease; Endorphins; Enkephalin, Leucine; Humans; Middle Aged; Radioimmunoassay

Seven cases of chronic pain were treated by intrathecal administration of 30 micrograms of beta-endorphin and dynorphin-(1-13). Compared with saline, both peptides were able to suppress pain for periods up to 4.5 and 7 hours on the average, respectively. No significant side reactions were noticed during the entire investigation.

Topics: Adult; Aged; beta-Endorphin; Cerebral Infarction; Dynorphins; Endorphins; Female; Herpes Zoster; Humans; Injections, Spinal; Male; Middle Aged; Neoplasms; Pain, Intractable; Peptide Fragments; Wounds, Gunshot

Endorphins have been implicated in the pathophysiology of both spinal cord injury and cerebral ischemia. This review examines the nature of the experimental evidence to support this hypothesis. Present studies suggest that naloxone administration improves neurological function and outcome in the setting of the spinal cord trauma by centrally inhibiting an opiate receptor-mediated diminution of spinal cord flow. In the setting of spinal shock, naloxone administration is associated with improvement in vital sign and cardiovascular parameters as measured by mean arterial pressure, cardiac output, body temperature, and ventilation. Experiments using a variety of animal stroke models similarly support the notion that naloxone improves neurological function in the setting of cerebral ischemia by a stereospecific opiate receptor-mediated effect, but this improvement does not seem to be accompanied by augmentation of blood flow to affected areas of the brain or by any improvement in vital signs or cardiovascular parameters as seen in spinal cord trauma. A variety of mechanisms are discussed to explain these observations. The therapeutic implications of administering opiate agonists and antagonists in the setting of neurological deficits are outlined for the neurosurgeon.

Topics: Animals; beta-Endorphin; Brain Ischemia; Cats; Cerebral Infarction; Cerebrovascular Circulation; Endorphins; Evoked Potentials, Somatosensory; Hemodynamics; Naloxone; Rats; Receptors, Opioid; Respiration; Spinal Cord; Spinal Cord Injuries

beta-Endorphin was measured in cerebrospinal fluid (CSF) and plasma in patients with cerebral infarction at acute (4 to 48 hours) and chronic (1 month) stages. Only CSF samples obtained in the acute stage showed beta-endorphin values that were statistically higher than those measured in a control population. This finding suggests that infarction at its acute stage gives rise to an increased release of beta-endorphin. Such a mechanism is consistent with the possibility that the reported therapeutic effect of naloxone in cerebral ischemic lesions may result in part from the antagonism of the centrally released endorphin, beta-endorphin.

Topics: Adult; Aged; beta-Endorphin; Cerebral Infarction; Endorphins; Humans; Middle Aged; Naloxone