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Clonidine (2-(2,6-dichlorophenylamino)-2-imidazoline hydrochloride, St155, Catapres), after administration of a single large dose, was found to induce automutilation in mice housed individually in the absence of objects to bite. This abnormal behavior was not significantly altered with chronic administration of the drug, and showed no behavior induced by the same drug in mice caged in groups.
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A case is described of a young man who produced surgical emphysema of his left forearm using a 2-ml syringe with a modified needle. It is believed that this is the second reported example of this type of artefact. Other cases may occur with the present high incidence of drug abuse and increasing general access to syringes.
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This paper describes an automutilation syndrome (OAS) in three species of captive octopuses, Octopus dolfleini, O. bimaculoides, and O. maya, characterized by external arm and mantle lesions. Three clinical patterns in nine animals had similar and characteristic gross and histopathologic features. Axial nerve or brachial artery lesions were observed in six of the nine cases and vascular lesions were seen in two of eight cases with mantle ulcerations. A relationship between automutilation in the octopus and dysesthesias due to neural or vascular pathology is proposed.
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A successful extraoral chin-stabilized lip injury guard is described that protects the lower lips of patients in vegetative coma from self-inflicted injury. The guard does not interfere with routine daily mouth care and will not compromise the patient's airway if it were dislodged.
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Clonidine-induced automutilation in mice was investigated as a putative experimental model for human self-injurious behaviour. Clonidine (20, 50 and 100 mg/kg, ip) produced dose-related self-biting, causing severe automutilation in mice which had been isolated and food-deprived for 24 h. This clonidine-induced behaviour was significantly attenuated by pharmacological treatments which selectively augment central serotonergic or reduce central dopaminergic activity. Conversely, the clonidine effect was potentiated by pharmacological agents which selectively reduce or enhance central serotonergic and dopaminergic activity, respectively. Drug-induced alterations in central noradrenergic or cholinergic activity had no significant effect on the self-mutilatory behaviour induced by clonidine. The automutilation induced by clonidine in mice appears to be a good experimental model for human self-injurious behaviour, since the latter has been postulated to result from serotonin deficiency and/or facilitation of central dopaminergic activity.
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In rats, bilateral injection of muscimol (30-60 ng/site) into the medial substantia nigra zona reticulata exerted an antinociceptive effect in the hotplate and tail-flick tests. Injections of muscimol into the substantia nigra also induced intense stereotyped behavior and self-injurious behavior (SIB). Tail-flick and hindpaw-lick responses were inhibited between 30 and 120 min after muscimol, but recovered by 240 min. The antinociceptive responses were not due to motor impairment or ataxia induced by muscimol because a variety of highly-coordinated stereotyped behavioral responses, including rearing, sniffing, head bobbing and licking occurred concurrently. Injection of muscimol into the deep mesencephalic nucleus (DpMcN) also inhibited the tail-flick and hindpaw-lick responses and caused stereotyped behavior but did not induce self-injurious behavior. Injections of muscimol into the substantia nigra, angled (45 degrees) to avoid passing through the deep mesencephalic nucleus, still exerted antinociceptive activity and caused self-injurious behavior. Bilateral microinjections of baclofen (300 ng), 4,5,6,7-tetrahydroisoxazols (5,40c)pyridin-3-ol (THIP; 300 ng), sodium valproate + D,L-diaminobutyric acid (1 microgram), substance P (2.5 micrograms) or D-Pro2-D-Trp7.9-substance P (2.5 micrograms), all suppressed hindpaw-lick responses, although only THIP reduced tail-flick responses. None of these treatments evoked self-injurious behavior. Naloxone (10 mg/kg), picrotoxin (5 mg/kg) or atropine (10 mg/kg) injection of muscimol into the substantia nigra (60 ng) or a single pretreatment with p-chlorophenylalanine diethyl ester (PCPA; 500 mg/kg; 48 hr prior to muscimol) failed to suppress the hindpaw-lick response or self-injurious behavior. These results suggest that the injection of muscimol into the substantia nigra evokes a centrally-mediated antinociception which alone is not sufficient to induce self-injurious behavior. Both antinociception and self-injurious behavior after injection of muscimol into the substantia nigra appear unrelated to cholinergic, serotoninergic, or naloxone-sensitive nociceptive systems; however, the role of activation of gamma-aminobutyric acid (GABA) receptors in these actions of muscimol also remains to be clarified.
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