Cardiac arrest in a young woman treated with amitriptyline combined with levopromazine.
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The neuroleptic malignant syndrome (NMS) is an idiosyncratic reaction to neuroleptic drugs, made up of hyperthermia, muscular rigidity, disturbance of level of consciousness and autonomic dysfunction. It is potentially lethal and should be kept in mind whilst using anti-psychotic drugs; as most patients treated by them require further anti-psychotic treatment, the clinician faces the problem of treating those patients after a NMS episode, yet reports in the literature have generally neglected the problem of late management. A patient suffering from a psychosis and NMS is presented, and a rationale for management offered.
The occurrence of neuroleptic malignant syndrome (NMS) was studied prospectively in two series of consecutive psychiatric in-patients (n = 223). The first group (n = 120) suffered from schizophrenia and was treated only with haloperidol. The second group (n = 103) was treated with diverse neuroleptics. All patients were on a single antipsychotic agent with no anticholinergic drug as prophylaxis. The incidence of full NMS per admission and first neuroleptic exposure was 5/223 (2.2%). Patients with bipolar affective disorder and those treated with injections were significantly over-represented in the NMS group.
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Repeated administration of a large dose of methamphetamine (MA) (25 mg/kg, i.p. twice daily for 4 days) to mice enhanced locomotor activity and decreased stereotyped behavior following a subsequent injection of MA. Simultaneous determinations of catecholamines revealed a depletion of brain dopamine. The moderate doses of haloperidol significantly enhanced MA-induced locomotor activity in mice. A significant enhancement of MA-induced locomotor activity was observed in the rats pretreated with 6-hydroxydopamine into the striatum, and this effect correlated negatively with the striatal dopamine level. These results suggest that hypofunction of striatal dopaminergic neuron systems induced by repeated administration of MA may be one of possible mechanisms of the enhancement of MA-induced locomotor activity due to the decrease of stereotyped behavior.
Trials of different drug combinations for use in rabbits, guinea-pigs, rats, hamsters and mice are described in detail and experience over a 5-year period evaluated. Combinations of fentanyl citrate, fluanisone and diazepam provided exceptionally good anaesthesia in each species and were considered superior to other injectable agents.
The results of a preliminary evaluation of etorphine/methotrimeprazine ('Small Animal Immobilon') and midazolam in rats and mice are reported, and this regimen is compared to fentanyl/fluanisone/midazolam in mice. In rats, a surgical plane of anaesthesia with good muscle relaxation was produced, but blood gas analysis showed the presence of severe hypoxia, hypercapnia and acidosis. In mice etorphine/methotrimeprazine/midazolam and fentanyl/fluanisone/midazolam produced adequate anaesthesia, but blood gas analysis showed severe respiratory depression with both regimens. Since etorphine/methotrimeprazine/midazolam produced severe respiratory depression in rats and mice it is suggested that this regimen is used with caution. Administration of supplemental oxygen would seem advisable when using either etorphine/methotrimeprazine/midazolam or fentanyl/fluanisone/midazolam in rats and mice.
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The glucose tolerance curve in alcoholics in delirium tremens was similar to that seen in hepatogenic diabetes. The secretion of immunoreactive insulin and somatotropin after glucose was similar in patients with delirium tremens and alcoholic hallucinosis.
A psychosis in a 5 years old girl is reported. By the 2nd month of her illness there was clear mental regression, with disorders of contact, motricity, speech, instinctive behavior and pragmatism. Neurologic and electroencephalographic abnormalities, together with the psychiatric symptoms, lead to the diagnostic of organic psychosis. High doses of neuroleptics were used and there was progressive remission of the symptoms, beginning at the 3rd month of disease. The etiologic diagnosis (being more probable a demyelinizing encephalitis) and the therapeutic effect of the neuroleptics are discussed.
To date, no universally applicable recommendations are available for the treatment of patients with postherpetic neuralgia. A mixture of clinical anecdotes, experimental findings and observations from clinical trials form the basis of the medical arsenal for this condition. Tricyclic antidepressants are commonly used, and clinical experience and several investigations have documented their effectiveness. Today, single entity antidepressants, which can be combined with neuroleptics to increase analgesia, are generally recommended for the treatment of postherpetic neuralgia. Some authors also recommend the additional administration of an opioid if analgesia is inadequate. Just over a decade ago, opioids were considered ineffective for the treatment of neuropathic pain; however, more recent investigations relating to the use of opioids, primarily in the treatment of nontumour-related chronic pain, have led to a revision of their use in neuropathic pain. Nevertheless, the use of opioid therapy for neurogenic pain remains controversial. Tramadol is a synthetic, centrally acting analgesic with both opioid and nonopioid analgesic activity. The nonopioid component is related to the inhibition of noradrenaline (norepinephrine) reuptake and stimulation of serotonin (5-hydroxytryptamine; 5-HT) release at the spinal level. In this regard, there are parallels with antidepressants, which are believed to potentiate the effect of biogenic amines in endogenous pain-relieving systems. There is evidence that, in tramadol, both mechanisms act synergistically with respect to analgesia. The aim of this pilot study was to investigate, for the first time, the analgesic efficacy and tolerability of tramadol, compared with the antidepressant clomipramine, in the treatment of postherpetic neuralgia. If necessary, clomipramine was used in combination with the neuroleptic levomepromazine. The study allowed individualised dosages at predetermined intervals up to a maximum daily dose of tramadol 600mg and clomipramine 100mg, or clomipramine 100mg with or without levomepromazine 100mg. 21 (60%) of 35 randomised patients (> or = 65 years) received the study medication over the 6-week period [tramadol n = 10; clomipramine with or without levomepromazine) n = 11]. After 3 weeks' treatment the dosage in both groups remained almost constant for the rest of the 6-week treatment phase (mean daily dose: tramadol 250 to 290mg; clomipramine 59.1 to 63.6mg). Only 3 patients required the combination of clomipramine and levomepromazine. At the outset, both groups recorded an average pain level of 'moderate' to 'very severe'. In correlation with increasing the study medication, this had decreased to 'slight' by the end of the treatment, when 9 of 10 patients in the tramadol group and of 6 of 11 patients in the clomipramine group retrospectively rated their analgesia as excellent, good or satisfactory. The psychological/physical condition of the patients did not change significantly during tramadol treatment. Sensitivity and depression parameters decreased in the clomipramine group. The incidence of adverse events for all patients was similar in both groups (tramadol 76.5%; clomipramine with or without levomepromazine 83.3%). In conclusion, tramadol would appear to be an interesting therapeutic alternative for pain relief in postherpetic neuralgia, particularly in patients who are not depressed. In clinical practice, tramadol and clomipramine can best be used differentially. For example, tramadol could be the drug of first choice in patients with obvious cardiovascular disease (not an uncommon problem in the > or = 65 year age group) in whom antidepressants are contraindicated, and similarly in patients in whom an antidepressant effect is not required. (ABSTRACT TRUNCATED)
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