Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To further investigate the hypothesis that hyperactivity of the hypothalamic-pituitary-adrenal axis in patients with depression may be mediated by hypersecretion of corticotropin-releasing factor (CRF), the authors measured CRF-like immunoreactivity in CSF samples from 138 neurological control, 54 depressed, and 27 nondepressed (23 schizophrenic and four manic) subjects. The CSF CRF concentration was markedly higher (almost twofold) in depressed patients than in control subjects and nondepressed psychiatric patients. The concentration of CSF CRF was slightly but significantly higher in schizophrenic patients than in control subjects. These findings provide further support for the hypothesis that CRF hypersecretion occurs in major depression.
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PMID:CSF corticotropin-releasing factor-like immunoreactivity in depression and schizophrenia. 349 2

Since its introduction to North America in 1942, the use of epidural catheter analgesia has increased dramatically. Improved equipment, methods and medications have broadened its application to include among others, surgical anesthesia, chronic pain relief and the management of postoperative pain. Numerous techniques for epidural puncture and insertion of the catheter have been described. Although complications have been associated with placement of an epidural catheter, these are rare when performed by an experienced anesthesiologist. Epidural analgesia was first accomplished by blockade with local anesthetics. Bupivacaine has been called the local anesthetic of choice for epidural infusion. Bolus administration of epidural local anesthetics gives effective analgesia; however, its use is limited by brief duration and occasionally severe hypotension. Epidural local anesthetics have been administered by continuous infusion in an attempt to minimize side effects. Nevertheless, hypotension, as well as motor block, numbness, nausea and urinary retention have occurred. Epidural analgesia with local anesthetics is effective in relieving postoperative pain, but its safety and feasibility have been questioned because of the frequent, potentially serious side effects. These problems led to trials of epidural narcotics for postoperative pain management. The exact site of action of epidural narcotic analgesics is debatable; however, the bulk of evidence supports a direct spinal action. Epidural narcotics appear to specifically inhibit nociceptive stimuli. The prolonged and profound analgesia that occurs with epidural narcotics relative to parenteral administration is due to a higher concentration of drug reaching the CSF through the epidural route. Since nervous transmission is not completely blocked this technique cannot provide anesthesia during operation. Morphine has been the most frequently used narcotic for epidural analgesia. Results of several recent, randomized double-blind studies have shown that epidural narcotics give adequate analgesia comparable with that observed with epidural bupivacaine. Epidural morphine provides a greater duration of analgesia and may cause fewer side effects. Improved analgesia has been reported when epidural narcotics are used in combination with local anesthetics. Continuous administration of low dosage epidural narcotics has been shown to have less frequent side effects than bolus administration. Nevertheless, pruritus, urinary retention, hypotension and severe respiratory depression have been reported with both methods.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Epidural catheter analgesia for the management of postoperative pain. 351 98

We used naloxone to investigate the role of central nervous system opiate receptors in the cardiovascular depression of canine hemorrhagic and endotoxic shock. Shock was induced by bleeding dogs into a reservoir to achieve and maintain a mean arterial pressure (MAP) of 45 mmHg for 30 min; at 30 min the reservoir was clamped and the animals were treated with intracerebroventricular (ICV) perfusion of naloxone 0.1 mg/kg (n = 5) or artificial CSF (n = 5) for 30 min. Endotoxemic shock was induced by the iv injection of E. coli endotoxin 1 mg/kg; 15 min later the animals were given naloxone 0.1 mg/kg (n = 5) or artificial CSF (n = 5) ICV for 30 min. ICV naloxone significantly increased MAP, cardiac output (CO), and left ventricular performance (LV dP/dt max) compared to artificial CSF in canine endotoxic shock but not hemorrhagic shock. Naloxone 0.1 mg/kg (n = 5) given into the cisterna magna failed to significantly improve MAP, CO, or LV dP/dt max in dogs subjected to reservoir hemorrhagic shock for 60 min compared to artificial CSF (n = 5). These results are compatible with opiate-receptor-mediated central cardiovascular depression in endotoxic shock and peripheral cardiovascular depression in hemorrhagic shock. Accordingly, the sites of action of naloxone are mainly central in endotoxic shock and peripheral in hemorrhagic shock.
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PMID:Central nervous system is involved in the cardiovascular responses to naloxone in canine endotoxic but not hemorrhagic shock. 359 33

The authors report the case of a 26 year old non-migrainous man who presented over a 5 week period with a cluster of classical migrainous attacks associated with CSF lymphocytosis. The association of this type of CSF response with attacks of migraine is unusual; in migraine the CSF is normal or may show an isolated increase in protein content (with the exception of the very rare familial hemiplegic migraine). In the reported case, other conditions liable to give rise to migraine and CSF lymphocytosis having been excluded (acute DLE, brucellosis...), this association corresponded to a benign and spontaneously regressive condition, possibly a migraine symptomatic of benign acute lymphocytic meningitis. The authors suggest that a primary meningeal inflammation may have been the cause of the cluster of migraine attacks which in this case were more accompanied perhaps because they induced a wave of depression of cortical activity.
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PMID:[Migraine manifestations and lymphocyte pleocytosis of the cerebrospinal fluid]. 363 29

Fourteen patients with high- (n = 7) and low-dose (n = 7) benzodiazepine (BDZ) dependency presented predominantly with anxious and depressive neurotic symptoms which caused long-term BDZ medication. Their BDZ dependency was characterized by giving preference to the abuse of benzodiazepines with long elimination half-life. Significant enlargement of CSF spaces was only found in high-dose dependent patients. Withdrawal after long-term BDZ medication revealed no differences between high- and low-dose BDZ dependency with respect to onset of withdrawal reaction and the correlation between onset of withdrawal and peak fall of BDZ serum level. The peak of withdrawal was reached 3-4 days later in high-dose BDZ dependent patients compared with those with a low-dose dependency. The peak withdrawal in high-dose dependent patients appeared when the serum BDZ metabolite nordiazepam dropped significantly. No such concomitant appearance of peak withdrawal and drop of serum nordiazepam level could be found in low-dose dependent patients. Specificity and intensity of BDZ withdrawal symptoms were the same for those dependent upon high doses of BDZs and those dependent upon low doses, but a protracted withdrawal was only observed in low-dose BDZ-dependent patients. During the withdrawal period psychopathometric measurements consistently revealed parallel changes in the scores for physical withdrawal symptoms, anxiety and depression. It is not clear whether anxiety and depression are "typical" BDZ withdrawal reactions or represent a "reactivated" state of the psychopathological disturbance which lead to the BDZ dependency. Possible implications for the therapeutical management of BDZ-dependent patients are discussed.
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PMID:Characterization of benzodiazepine withdrawal in high- and low-dose dependent psychiatric inpatients. 367 60

Gamma-aminobutyric acid (GABA) is a putative central neurotransmitter that depresses respiratory neurons and has a metabolism in the brain that is tied to CO2 fixation and H+ metabolism. Therefore, the effect of 3 concentrations of GABA (10, 30, and 50 mM) in different groups of pentobarbital-anesthetized dogs was investigated by ventriculocisternal perfusion for 15 to 45 min. During multiple perfusion sequences, tidal volume (VT) and respiratory frequency were recorded continuously, whereas heart rate (HR), mean systemic arterial pressure (Psa), cardiac output, mean pulmonary arterial pressure, and pulmonary capillary wedge pressure were monitored periodically. Minute ventilation decreased by a reduction in VT. The mean VT (+/- SEM) decreased after 15 min of GABA perfusion from 365.9 +/- 19.5 to 151.0 +/- 15.0 ml with 50 mM GABA in mock CSF, from 272.8 +/- 25.1 to 110.6 +/- 7.4 with 30 mM GABA, and from 223.6 +/- 22.3 to 155.3 +/- 21.8 with 10 mM GABA. A decrease in mean inspiratory flow was associated with the reduction in VT. The decrease in ventilation was associated with respiratory acidosis. At each GABA concentration, mean Psa decreased, whereas HR fell only with 50 mM. Other cardiovascular parameters did not change. Perfusion with mock CSF alone restored cardiorespiratory depression caused by GABA. Mean Psa fell with GABA whether ventilation was kept constant mechanically or not. These results support the hypothesis of a GABA-sensitive mechanism via a population of receptors that affect respiratory and cardiovascular function and are accessible by ventriculocisternal perfusion.
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PMID:Reversible depression of ventilation and cardiovascular function by ventriculocisternal perfusion with gamma-aminobutyric acid in dogs. 371 57

Both concentrations of total 3-methoxy-4-hydroxyphenylglycol (MHPG) and 3,4-dihydroxyphenylglycol (DHPG) in the human urine, plasma and CSF were determined with a high-pressure liquid chromatography with electrochemical detection in order to clarify the dynamic change in these noradrenaline metabolites. Three different biological fluids were collected simultaneously from 16 orthopedic patients who were regarded clinically as substitutes for normal subjects. In the urine, the MHPG concentrations were 1.67 +/- 0.65 micrograms/mg creatinine (mean +/- S.D.) and DHPG 0.39 microgram/mg creatinine +/- 0.21. The plasma levels were 21.16 ng/ml +/- 9.58 for MHPG, and 19.58 ng/ml +/- 8.13 for DHPG. The CSF levels of MHPG and DHPG were 24.08 ng/ml +/- 8.10 and 34.76 ng/ml +/- 11.46, respectively. The CSF levels of these metabolites were correlated significantly with those in the plasma (r = 0.852, p less than 0.001 for MHPG; r = 0.799, p less than 0.001 for DHPG), while no significant correlations were found between the urinary levels and either the plasma or CSF levels of these metabolites. In the urine, the MHPG levels were proportional to the DHPG levels, while the former were inversely proportional to the latter in the plasma or CSF. Neither the MHPG nor DHPG levels in the urine from depressed patients revealed to have any significant correlation with their clinical assessments using the Hamilton Rating Scale Score (HRS). The patients were treated with an antidepressant active selectively on the noradrenergic system, and no significant changes in urinary excretion of these metabolites were observed before and after the drug treatment. These findings suggest that in the case of psychiatric disorders such as depression, these compound levels in the plasma or CSF would provide more important information than those in the urine.
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PMID:Studies on 3-methoxy-4-hydroxyphenylglycol (MHPG) and 3,4-dihydroxyphenylglycol (DHPG) levels in human urine, plasma and cerebrospinal fluids, and their significance in studies of depression. 377 51

In order to evaluate long-term intrathecal morphine therapy for cancer pain, whatever its location, 121 patients (80% were ambulatory patients) treated between April 1979 and April 1985 at the Cancer Institute of Montpellier (Centre Paul-Lamarque) were assessed. Morphine was stored in a presternal insulin syringe, protected by a sterile and waterproof dressing. A bolus administration of morphine via a subcutaneous lombo-epigastric subarachnoid catheter was scheduled every 12 h. This "closed" device was opened for refilling in an operating room only. The mean follow-up was 68 days (maximum: 13 months). More than 15,000 intrathecal injections were made. The mean daily amount of morphine required was 2.3 mg (extremes: 0.75 and 21 mg). All patients developed tolerance, requiring an adjustment of morphine dosages every 30 to 45 days. With the isobaric morphine solution, good or very good analgesia was achieved in 82% of patients, even in those suffering from thoracic or otolaryngologic pain. Mechanical complications (catheter coming out of the subarachnoid space in 7.67% of cases, leakage of CSF along the catheter in 9.16% of cases) were related to the exteriorization of the proximal catheter tip. With the exception of errors in manipulation, neither infection nor clinical respiratory depression were noticed. Nausea and vomiting were frequent but resolved spontaneously within a few days. Urine retention (33%) occurred mainly in men over 65 years, after pelvic surgery or radiotherapy. Because of the absence of a defined zone of analgesia, the small volumes required and the "ready for use" preparation, intrathecal isobaric morphine therapy will lead to easy self-administration via an implanted pump in the future.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Long-term intrathecal isobaric morphine therapy]. 377 64

A case of delayed respiratory depression following an intrathecal injection of hyperbaric morphine hydrochloride is reported. This injection was made during a lumbar myelography in a 60 year old patient suffering from metastatic epiduritis unrelieved by oral or parenteral drugs. The differences in densities between the CSF, hyperbaric opiate solution and contrast medium explain the migration of the morphine hydrochloride from the lumbar thecal space to the basal cisternae, giving a fall in the responsiveness to CO2 of the brain stem respiratory centres. Parenteral naloxone did not reverse this ventilatory depression. Only the myosis and the analgesia disappeared. After 16 h of various attempts of reversal by parenteral injections, an intrathecal injection of naloxone was tried. This small dose (0.1 mg), given intrathecally, resulted in a prompt return to normal of respiratory function.
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PMID:[Respiratory depression after intrathecal injection of morphine: value of in situ naloxone]. 384 Sep 64

The few studies reported to date suggest that CSF cortisol is increased in depression and mania compared to normal subjects but that this increase is not specific to these disorders, since increased levels occur in other psychiatric and neurologic disorders. The CSF elevation is probably secondary to cortisol changes in the blood, but CSF levels appear to be more stable. The diurnal change in CSF may also be greater than that in blood. The significant correlation between CSF and blood levels observed in monkeys has not been found in humans. Future studies must control for time of day, as well as diagnostic factors, and ideally should include other measures of cortisol function, such as urinary excretion or the DST. Regulation of CSF cortisol is not well understood, and its relationship to other brain chemistries is unclear.
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PMID:CSF cortisol in affective illness. 384 51


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