naloxone has been researched along with Central-Nervous-System-Diseases* in 8 studies
2 review(s) available for naloxone and Central-Nervous-System-Diseases
Article | Year |
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The use of antidotes in the management of central nervous system depression.
Topics: Antidotes; Benzodiazepines; Central Nervous System Depressants; Central Nervous System Diseases; Emergency Medicine; Ethanol; Flumazenil; Humans; Naloxone; Narcotic Antagonists; Narcotics | 1997 |
Neuropeptides and central nervous system injury. Clinical implications.
It has been proposed that endogenous opioids play a pathophysiologic role in the secondary injury that follows spinal trauma, brain trauma, and cerebral ischemia. Opiate antagonists, at high doses, have been found to improve outcome in various experimental models of central nervous system injury. Thyrotropin-releasing hormone, which appears to act in part as a functional antagonist of opioid systems, has proved effective in the treatment of experimental spinal cord and brain trauma. The literature relating to these developments is reviewed, with emphasis on the potential clinical application of these classes of substances. Topics: Animals; Cats; Central Nervous System Diseases; Dynorphins; Humans; Ischemic Attack, Transient; Naloxone; Narcotic Antagonists; Narcotics; Rabbits; Spinal Cord Injuries; Thyrotropin-Releasing Hormone | 1986 |
6 other study(ies) available for naloxone and Central-Nervous-System-Diseases
Article | Year |
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Adult clonidine overdose: prolonged bradycardia and central nervous system depression, but not severe toxicity.
There are limited reports of adult clonidine overdose. We aimed to describe the clinical effects and treatment of clonidine overdose in adults.. This was a retrospective review of a prospective cohort of poisoned patients who took clonidine overdoses (>200 μg). Demographic information, clinical effects, treatment, complications (central nervous system and cardiovascular effects) and length of stay (LOS) were extracted from a clinical database or medical records.. From 133 admissions for clonidine poisoning (1988-2015), no medical record was available in 14 and 11 took staggered ingestions. Of 108 acute clonidine overdoses (median age 27 years; 14-65 years; 68 females), 40 were clonidine alone ingestions and 68 were clonidine with co-ingestants. Median dose taken was 2100 μg (interquartile range [IQR]: 400-15,000 μg). Median LOS was 21h (IQR: 14-35 h) and there were no deaths. Glasgow coma score [GCS] <15 occurred in 73/108 (68%), and more patients taking co-ingestants (8/68; 12%) had coma (GCS <9) compared to clonidine alone (2/40; 5%). Miosis occurred in 31/108 (29%) cases. Median minimum HR was 48 bpm (IQR: 40-57 bpm), similar between clonidine alone and co-ingestant overdoses. There was a significant association between dose and minimum HR for clonidine alone overdoses (p = 0.02). 82/108 (76%) had bradycardia, median onset 2.5 h post-ingestion (IQR: 1.7-5.5 h) and median duration 20 h (2.5-83 h), similar for clonidine alone and co-ingestant overdoses. There were no arrhythmias. Three patients ingesting 8000-12,000 μg developed early hypertension. Median minimum systolic BP was 96 mmHg (IQR: 90-105 mmHg) and hypotension occurred in 26/108 (24%). 12/108 patients were intubated, but only 2 were clonidine alone cases. Treatments included activated charcoal (24), atropine (8) and naloxone (23). The median total naloxone dose was 2 mg (IQR: 1.2-2.4 mg), but only one patient given naloxone was documented to respond with partial improvement in GCS.. Clonidine causes persistent but not life-threatening clinical effects. Most patients develop mild central nervous system depression and bradycardia. Naloxone was not associated with improved outcomes. Topics: Adolescent; Adult; Aged; Antidotes; Antihypertensive Agents; Atropine; Bradycardia; Central Nervous System Diseases; Clonidine; Drug Overdose; Female; Glasgow Coma Scale; Humans; Length of Stay; Male; Middle Aged; Naloxone; Retrospective Studies; Young Adult | 2017 |
A novel use of naloxone as a treatment for eucalyptus oil induced central nervous system depression.
Topics: Aged; Central Nervous System Diseases; Eucalyptus; Female; Humans; Injections, Intravenous; Naloxone; Plant Oils; Treatment Outcome | 2011 |
Central anticholinergic syndrome strikes again.
Topics: Adjuvants, Anesthesia; Adult; Anesthesia, General; Anesthetics, Intravenous; Central Nervous System Diseases; Cholinesterase Inhibitors; Electrocardiography; Female; Glucose; Glycopyrrolate; Heart Block; Heart Rate; Humans; Midazolam; Middle Aged; Naloxone; Narcotic Antagonists; Physostigmine; Propofol; Respiration, Artificial; Syndrome | 2006 |
Sick sisters.
Topics: Analgesics, Opioid; Central Nervous System Diseases; Child; Child, Preschool; Diagnosis, Differential; Female; Humans; Miosis; Morphine; Naloxone; Oxycodone; Poisoning; Respiratory Insufficiency; Siblings; Treatment Outcome | 2005 |
Central nervous system manifestations of an ibuprofen overdose reversed by naloxone.
Ibuprofen overdose is usually characterized by GI upset, dizziness, and mild sedation. On rare occasions, severe complications such as respiratory failure, metabolic acidosis, renal failure, coma, and death have been reported in both adults and children. Presently, treatment of acute ibuprofen intoxication with complications requires supportive therapy until the symptoms resolve over 24 to 48 hours. We report the case of an 11-month-old female infant with a depressed level of consciousness after ingestion of ibuprofen whose mental status markedly improved with administration of naloxone. Topics: Acidosis; Anti-Inflammatory Agents, Non-Steroidal; Antidotes; Central Nervous System; Central Nervous System Diseases; Drug Overdose; Female; Humans; Ibuprofen; Infant; Naloxone | 2000 |
Analgesic effect of intrathecal ketamine in rats.
The analgesic effect of ketamine hydrochloride 200, 400, 800 and 1600 micrograms kg-1, administered intrathecally in rats, was evaluated using the tail-flick test. A short-lived analgesic effect was demonstrated with the larger doses and this could be abolished by pretreatment with naloxone hydrochloride 200 micrograms kg-1. Intrathecal morphine 100 micrograms kg-1 produced a more profound analgesic effect than intrathecal ketamine 1600 micrograms kg-1. There were three deaths shortly after intrathecal injection of ketamine. Histopathological examination of the spinal cords and nerve roots of these rats revealed the presence of vacuoles in the cells of the posterior root ganglion. Other rats sacrificed for histopathological examination showed no changes attributed to the injectate. Topics: Analgesia; Animals; Central Nervous System Diseases; Female; Ganglia, Spinal; Injections, Spinal; Ketamine; Male; Morphine; Naloxone; Rats; Rats, Inbred Strains | 1983 |