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Results for “Respiratory Paralysis”

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At least 19 recordsLinked to original sources
PubMed1988

GABA involvement in naloxone induced reversal of respiratory paralysis produced by thiopental.

No agent is yet available to reverse respiratory paralysis produced by CNS depressants, such as general anesthetics. In this study naloxone reversed respiratory paralysis induced by thiopental in rats. 25 mg/kg, i.v. thiopental produced anesthesia without altering respiratory rate, increased GABA, decreased glutamate, and had no effect on aspartate or glycine levels compared to controls in rat cortex and brain stem. Pretreatment of rats with thiosemicarbazide for 30 minutes abolished the anesthetic action as well as the respiratory depressant action of thiopental. 50 mg/kg, i.v. thiopental produced respiratory arrest with further increase in GABA and decrease in glutamate again in cortex and brain stem without affecting any of the amino acids studied in four regions of rat brain. Naloxone (2.5 mg/kg, i.v.) reversed respiratory paralysis, glutamate and GABA levels to control values in brain stem and cortex with no changes in caudate or cerebellum. These data suggest naloxone reverses respiratory paralysis produced by thiopental and involves GABA in its action.

Animals↗
PubMed1986

Respiratory paralysis secondary to epidural anesthesia in a dog.

Transient respiratory paralysis developed in a 12-year-old spayed female Cocker Spaniel that received an anesthetic epidurally for excisional biopsy of perianal masses. Paralysis developed almost immediately after injection of 2.5 ml of 2% lidocaine (1 ml/4.9 kg), and was managed by mechanical ventilation and appropriate fluid therapy IV until spontaneous respiration returned. The respiratory paralysis was attributed to the excessive cranial extent of the anesthetic block.

Anesthesia, Epidural↗
PubMed2006

Predicting the recovery of ventilatory activity in central respiratory paralysis.

OBJECTIVE: To assess the value of the diaphragmatic response to transcranial magnetic stimulation (TMS) in predicting the recovery of ventilatory activity after CNS lesions responsible for central respiratory paralysis. METHODS: The authors studied 11 long-term ventilator-dependent patients with central respiratory paralysis (description group: spinal trauma 10, medullary ischemia 1) and 16 patients with central respiratory paralysis for less than 10 weeks (prognostic group, evaluated after a 1-year follow-up: spinal trauma 8, medullary ischemia 4, radiation myelitis 1, subdural hematoma 1, complication of neurosurgery 2). RESULTS: In the description group, all the patients had a bilaterally abolished diaphragm response. In the prognostic group, six patients were fully ventilator dependent because of a complete absence of ventilatory activity at follow-up time. They lacked any diaphragm response. The 10 other patients had recovered ventilatory activity and full (n = 9) or partial (n = 1) ventilatory autonomy. In nine cases, diaphragm response was present at least on one side, with a normal latency (right: 15.6 +/- 1.5 milliseconds; left: 16.2 +/- 2.2 milliseconds). The test had 100% specificity (95% CI 52 to 100) and 90% sensitivity (95% CI 54 to 99) to predict the recovery of ventilatory activity. CONCLUSION: Electrophysiologic studies of the diaphragm in response to transcranial magnetic stimulation may help predict the recovery of central respiratory paralysis within 1 year.

Adolescent↗
PubMed1994

Evidence for involvement of amino acid neurotransmitters in anesthesia and naloxone induced reversal of respiratory paralysis.

General anesthetics render a person unconscious and may produce respiratory paralysis at therapeutic doses. No pharmacological agent is available to restore respiration and the mechanism/s of anesthesia or apnea is not clearly understood. In this report, we present evidence to show that naloxone reversed respiratory failure induced by thiopental, ketamine, halothane but not that induced by phenobarbital. Furthermore, 25 mg/kg, i.v. thiopental, 140 mg/kg, i.v. ketamine, and 3% halothane produced anesthesia without significantly altering respiratory rate, increased GABA and decreased glutamate (except ketamine and phenobarbital) levels in rat brain stem and cortex, but not in caudate and cerebellum. Aspartate, glycine and alanine levels were not affected in four brain regions studied. Pretreatment with TSC for 30 minutes did not change GABA or glutamate contents, but abolished the anesthetic as well as the respiratory depressant actions of the anesthetics. Increasing the doses of anesthetics produced respiratory failure with further rise in GABA and fall in glutamate in brain stem and cortex. Naloxone reversed respiratory paralysis and restored GABA close to control values in rat brain stem and cortex with no changes in caudate or cerebellum. Data presented here suggest that GABA may be necessary to produce loss of consciousness and naloxone reverses anesthetic induced respiratory failure.

Anesthesia↗
PubMed1989

Respiratory paralysis as a presenting symptom in Japanese encephalitis--a case report.

In the literature there are rare reports on Japanese encephalitis (JE) mimicking poliomyelitis or presenting as respiratory paralysis. A case of JE presenting as respiratory paralysis is described. The 22-year-old male was well until five days earlier, when he experienced the acute onset of headache and fever. Four days after onset he developed dysphagia and respiratory difficulty, and a tracheotomy was performed. The following day he lapsed into semicoma and the respiration had to be maintained by an artificial ventilator. He regained consciousness by the 10th day after onset. He became able to comprehend questions and express himself by gestures. But the respiration was still paralytic, and assisted ventilation via a tracheotomy had to be continued. The case was clinically diagnosed as encephalitis. Bulbar poliomyelitis was initially considered due to the clinical features of aseptic meningitis, respiratory paralysis, pharyngeal paralysis with pooling secretions in the pharynx, tachycardia and elevated blood pressure. But poliovirus culture obtained from stool and appropriate serological studies were negative. The diagnosis of encephalitis due to JE virus was confirmed by hemagglutination inhibition test (acute phase HI titer 1:320; convalescent phase HI titer 1.1280).

Adult↗
PubMed1988

The treatment of acute polyradiculoneuritis with respiratory paralysis.

This paper reports 504 cases admitted with acute polyradiculoneuritis (AP) to Beijing Children's Hospital from 1975 through 1984. 343 of the 504 cases (68.1%) with AP had respiratory paralysis and in 198/504 (39.3%), tracheotomy was performed. In this study, none of the patients received steroids. We attempted to assess the grades of respiratory paralysis and established the criteria for tracheotomy. We also must perform the following procedures: 1) Artificial ventilation must be used correctly, 2) The secretion should be aspirated regularly in order to maintain a clear airway, 3) Sterilization must be strictly conducted to prevent cross infection. As a result, of 504 cases with AP 9 died, the mortality rate being 1.79%. The study suggests tracheotomy should be performed early and it is one of the most important procedures in the treatment of AP with respiratory paralysis.

Acute Disease↗