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PubMed1990

Naltrexone attenuates self-injurious behavior in mentally retarded subjects.

The effect of naltrexone on the frequency of self-injurious behavior (SIB) was investigated in 6 male subjects with profound mental retardation. Following a double-blind placebo-controlled crossover design, naltrexone was administered in a dose of 50 mg once daily for 3 consecutive weeks. In 2 of 5 subjects, a significant decrease of SIB frequency could be demonstrated, and in 1, a tendency to a reduction was found. No effect on duration of restrain time was found in 3 subjects. These data suggest that disturbances of the endogenous opioid systems may be involved in the pathophysiology of SIB of certain patients.

Administration, Oral↗
PubMed1986

Involvement of the midbrain reticular formation in self-injurious behavior, stereotyped behavior, and analgesia induced by intranigral microinjection of muscimol.

Bilateral microinjection of muscimol (60 ng), a gamma-aminobutyric acid (GABA) agonist, into the central region of the substantia nigra (pars reticulata) produced self-injurious behavior (SIB), stereotyped behavior and analgesic-like effects in rats. Bilateral electrolytic lesions of the midbrain reticular formation ventrolateral to the periaqueductal gray matter completely blocked the SIB but had little effect on stereotyped behavior produced by intranigral muscimol. Lesions of the midbrain reticular formation reduced the antinociceptive effect of intranigral muscimol on the tail-flick but not on the hot-plate test. Bilateral microinjection of muscimol (10-100 ng) into the midbrain reticular formation produced intense stereotyped behavior and had an analgesic-like effect on the hot-plate test but not on the tail-flick test. Stereotyped behavior appeared to interfere with the paw-lick response on the hot-plate test. These data suggest that the antinociceptive effect of intranigral muscimol on the tail-flick test is mediated by fibers that project to or pass through the midbrain reticular formation and that analgesia may play an important role in muscimol-induced SIB. The midbrain reticular formation does not appear to be involved in the stereotyped behavior produced by intranigral muscimol.

Animals↗
PubMed1989

D1 dopamine receptor-mediated substance P depletion in the striatonigral neurons of rats subjected to neonatal dopaminergic denervation: implications for self-injurious behavior.

The present study examined the influences of dopamine (DA) receptor stimulation on enkephalin (Met5-enkephalin; ME) and tachykinin (substance P; SP) systems of basal ganglia of Sprague-Dawley rats, lesioned as neonates with 6-hydroxydopamine (6-OHDA). It has been proposed that the neonatal 6-OHDA-lesioned rat could serve as a model for the DA deficiency and self-injurious behavior (SIB) observed in the childhood neurological disorder. Lesch-Nyhan syndrome. In agreement with earlier work, the present study found that the neonatal 6-OHDA treatment at 3 days of age, reduced DA and caused an increase in ME and a decrease in SP content in the striatum and substantia nigra, when tested as adults. Administration of the DA precursor, L-dihydroxyphenylalanine (L-DOPA), to lesioned animals, induced SIB; increased DA and DOPAC levels; produced a greater decrease (-64%) in SP levels in the striatum and substantia nigra than was observed with lesion alone (-28%). The L-DOPA-induced decrease in SP levels and the SIB observed in the lesioned animals were blocked by pretreatment with the D1 receptor antagonist, SCH-23390. Moreover, administration of the D1 receptor agonist, SKF-38393, but not the D2 agonist, LY-171555, to lesioned animals mimicked the L-DOPA responses in all respects, except that the agonists did not alter DA or DOPAC levels. None of the DA agonists or antagonists treatments affected lesion-induced increase in ME levels in the striatum. These results indicate for the first time, that SIB precipitated by DA agonists in neonatal dopaminergic denervated animals, is associated with a marked and selective decrease in SP in the striatonigral SP neurons. This process has two components: (a) a retarded development of the SP system due to neonatal dopaminergic denervation: and (b) a depletion of the remaining SP, presumably by enhanced release due to D1 DA receptor-mediated activation of striatonigral SP neurons.

Animals↗
PubMed1989

Postcordotomy spontaneous dysesthesias in macaques: recurrence after spinal cord transection.

Monkeys chronically attack the hypoalgesic hindlimb after thoracic contralateral anterolateral cordotomy or hemisection. This compulsive behavior could be induced by innocuous stimulation in the hypoalgesic region, and it also appeared to occur spontaneously. The postcordotomy spontaneous compulsive self-directed behavior was studied in 4 macaques after subsequent upper lumbar crush spinal transection. Despite the paraplegia and bilateral analgesia/anesthesia, this spontaneous abnormal behavior continued to be directed to the same hindlimb as before transection, but not to the opposite hindlimb. Hence, it is concluded that the recurring syndrome originated from the initial contralateral cordotomy. The rationale for the presumption of postcordotomy spontaneous dysesthesias is presented, and the experimental results are offered in refutation of alternative interpretive hypotheses. In conjunction with previous findings, these results lead to the argument that postcordotomy dysesthesias are caused by a neuropathological compensatory response to partial deafferentation of brain somatosensory neurons.

Afferent Pathways↗
PubMed1993

Spinal dynorphin immunoreactivity increases bilaterally in a neuropathic pain model.

Increased spinal levels of dynorphin, an endogenous opioid kappa agonist, are seen in models of both chronic and acute hyperalgesia. This study determined the extent and localization of spinal immunoreactive dynorphin following sciatic cryoneurolysis (SCN), a neuropathic pain model produced by a peripheral nerve freeze lesion. SCN results in behaviors associated with neuropathic pain such as autotomy (the gnawing and scratching of the affected limb), touch-evoked and mechanical allodynia, and spontaneous nociceptive behavior. Following SCN, 4 rats that displayed autotomy and 3 rats that did not were randomly chosen for immunohistochemical staining of dynorphin-like immunoreactivity (DLIR). The area of DLIR above a standardized threshold level was quantified in both dorsal horns of each spinal cord section using a computer-assisted image analyzer to express DLIR in pixels. DLIR was observed both ipsilateral and contralateral to the injured peripheral nerve. In addition, the area of DLIR was significantly greater (P = 0.05) in rats that showed autotomy behavior (mean = 52.6 x 10(3) +/- 25.6) compared to rats with no autotomy (mean = 13.8 x 10(3) +/- 4.78). In sharp contrast to the ipsilateral dynorphin increases observed in other neuropathic pain models, we observe a bilateral increase at 21 days following SCN.

Animals↗
PubMed1995

Cerebrospinal alterations of immunoreactive dynorphin A after unilateral dorsal rhizotomy in the rat.

Possible alterations of immunoreactive dynorphin A (ir-dyn A) were investigated at different levels of the spinal cord and in discrete brain regions of male rats 10, 30 and 60 days after unilateral dorsal rhizotomy, i.e., during the development of deafferentation pain and autotomy behavior that follows afferent nerve interruption. Dorsal rhizotomy caused an increase of spinal ir-dyn A at 10 days in the cervical segment; subsequent assays showed a progressive increase in other spinal regions too. At the last observation, 60 days after rhizotomy, neuropeptide levels were still significantly higher than in sham-lesioned animals in the cervical, thoracic and lumbosacral spinal cord. The spinal ir-dyn A changes were both ipsi- and contralateral to the lesion. No alterations were found in the brainstem and midbrain and a not significant decrease was observed in the hypothalamus. In the striatum and cortex, however, there was a bilateral significant increase 30 days after surgery and a constant and significant elevation was detected in the hippocampus at all three intervals. These data cast additional light on the neurochemical changes caused by the interruption of afferent nerves, followed by development of the deafferentation pain syndrome in laboratory animals and human beings. They also support the concept of central neuroplasticity in pathological pain and indicate that the opioid neuropeptide dynorphin is involved.

Analysis of Variance↗
PubMed1989

Acrobatic ears: a cause of petrified auricles.

Calcified ear cartilages are rarely encountered and only 12 histologically proven cases have been documented. The case presented is of ossified auricles in a teenager and has many interesting features. Acrobatic manipulation of the auricles as a cause of the lesion was one of the distinguishing features.

Adolescent↗
PubMedDate not supplied

Continuous observation for psychiatric inpatients: a critical evaluation.

Continuous observation is a procedure used in most psychiatric inpatient units to manage acute and escalating risk in patients. Yet, it is virtually unstudied and unreported. The present study, conducted in a psychiatric teaching hospital, compared 102 inpatients who required continuous observation with 102 control subjects. Continuous observation was provided by nursing staff, and was used for 13% of inpatients. The most common reasons for continuous observation were risk of self-harm, overstimulation by the environment, and violence. Five clinical factors that predicted the use of continuous observation as well as another set of factors that correlated with a history of violence were found. Almost two thirds of patients required brief episodes lasting less than 72 hours (mean, 28 hours). These appeared to be effective and practical. However, when continuous observation exceeded 72 hours, it often became problematic and ineffective. We recommend that after 72 hours of continuous observation, patients' clinical management should be reviewed by the treatment team and changed.

Arousal↗