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PubMed2000

Impulsive aggression in borderline personality disorder.

Impulsive aggressive behaviors that include physical aggression directed towards others, self-mutilation, suicide attempts, domestic violence, substance abuse, and property destruction account for a substantial portion of the morbidity and mortality associated with personality disorders, in particular borderline personality disorder (BPD). Recent genetic, neurobiologic, and diagnostic studies suggest a dimensional approach to BPD symptomatology with impulsive aggression as one of the core dimensions for the disorder. The underlying biologic basis for impulsive aggression is centered on the serotonin hypothesis; that central 5-HT function is inversely related to aggression and suicidality. More recent research refines the theory to include associated brain regions, receptor types and neuromodulators potentially involved in the etiology of aggressivity. Treatment utilizes this information with substantial progress in well-designed placebo-controlled studies of selective serotonin reuptake inhibitors such as fluoxetine, and open-label series of atypical neuroleptics, mood stabilizers, and opioid antagonists

Aggression↗
PubMed2001

End-stage Liver Disease in Children.

The treatment of children with end-stage liver disease involves the coordinated management of nutritional deficiencies, ascites, pruritus, encephalopathy, and portal hypertension. The implementation of management strategies depends upon a parent or guardian to administer the plan in the context of a child at different stages of developmental, physiologic, emotional, and physical maturity. Fat-soluble vitamins (A, D, E, and K) and micronutrient levels should be monitored routinely and supplemented if deficient. In some patients, supplemental nutrition to provide additional energy and protein is needed to ensure optimal growth and development. Ascites often respond to spironolactone and sodium restriction, but may require the addition of a loop diuretic or even abdominal paracentesis. Pruritus significantly impairs the quality of life of patients and is typically treated with ursodeoxycholic acid, rifampin, or an antihistamine. Partial biliary diversion, or liver transplant in some instances, is necessary for patients with self-mutilating pruritus that results from intrahepatic cholestasis. Hepatic encephalopathy is poorly defined in infants and small children. Elevated serum ammonia serves as a surrogate marker for encephalopathy, which is treated with dietary protein restriction and lactulose. The usefulness of medical prophylaxis for esophageal varices has been noted in adults, though such studies have not been performed in children. If variceal bleeding becomes problematic, treatment with endoscopic variceal banding or sclerotherapy is indicated. A surgical shunt to reduce portal pressure is needed in some cases. Orthotopic liver transplant ultimately may be necessary to overcome the unrelenting consequences of end-stage liver disease.

Journal Article↗
PubMed1990

CSF metabolites in borderline personality disorder compared with normal controls.

Cerebrospinal metabolites were measured in 17 patients with borderline personality disorder and 17 normal controls. There were no significant differences between the two groups in levels of 5-hydroxyindoleacetic acid (5-HIAA), homovanillic acid (HVA), or 3-methoxy-4-hydroxyphenylglycol (MHPG). Within the borderline group, lower levels of CSF 5-HIAA were significantly associated with a history of genuine suicide attempts, but were not associated with violence, self-mutilation, or with the presence of major depression. Thus, CSF 5-HIAA levels are not distinctively low in a diagnostic group characterized by impulsivity and suicidal behavior, but within that group may be associated with genuine suicide attempts.

Adult↗
PubMedDate not supplied

Association between borderline personality structure and history of childhood abuse in adult volunteers.

Childhood abuse has been implicated as a leading factor in the development of borderline personality disorder (BPD). Data in this report, drawn from an ongoing study of the therapeutic effect of fluoxetine in BPD patients, were gathered in an attempt to replicate previous findings indicating a history of physical abuse in 71% and sexual abuse in 67% of adult BPD subjects. Thirty-one subjects for a study of the pharmacological treatment of BPD or BPD traits met criteria for the study. Those who had been previously hospitalized for a psychiatric disorder, who had recently been suicidal, or who had recent histories of self-mutilation were excluded. Specific information about childhood abuse was gathered using questions from a previous study of abuse histories in BPD patients. All subjects were then interviewed in greater depth regarding past experiences of abuse as part of the ongoing study of the relationship of childhood attachment experience and adult psychopathology. Six of 31 subjects (19.4%) reported a definite history of childhood physical and/or sexual abuse. Four of these subjects met criteria for full BPD, and two met criteria for BPD traits. Three of 31 subjects reported a history of physical abuse (9.7%); five reported a history of sexual abuse (16.1%). Two of the six who reported abuse reported both physical and sexual abuse. A history of childhood abuse is not necessarily linked to the development of BPD or BPD traits in all individuals. The following hypothesis is suggested: BPD may represent a spectrum of symptomatic severity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Evidence that apomorphine and pergolide induce rotation in rats by different actions on D1 and D2 receptor sites.

Apomorphine and the ergot derivative pergolide induced dose-dependent contralateral rotation in rats with unilateral 6-hydroxydopamine denervation of the ascending dopamine pathways. This was interpreted as an action on supersensitive receptors. However, large differences were found when comparing apomorphine and pergolide dose-response curves as well as the patterns of rotational behaviour the compounds elicited. Pergolide had a steep dose-response curve, while apomorphine had a flatter curve reaching a plateau at the dose of 1 mg/kg s.c. In doses higher than 1 mg/kg, apomorphine induced self-mutilation, while this was infrequent after pergolide. Apomorphine induced a two-peak pattern of rotation that never occurred when the same rats were tested with the ergot derivative. Both drugs induced dose-dependent ipsilateral rotation in animals with unilateral striatal kainic acid lesions but at doses 100 times higher. This effect was interpreted as an action on normosensitive receptors situated on the intact side. The differences between apomorphine and pergolide may be explained in terms of actions on different dopamine receptors, since the agonists were differently inhibited by neuroleptics acting on D1- or D2-type receptors. The D1/D2 antagonist cis-flupenthixol blocked both apomorphine and pergolide with similar potency, while sulpiride, a substituted benzamide devoid of any effect on D1 receptors, was a poor inhibitor of the apomorphine response. In contrast, sulpiride blocked pergolide rotation at doses 1000 times lower than those needed to block apomorphine rotation. Our results suggest the existence of functionally distinct sites related to the D1/D2 receptor classification.

Animals↗
PubMed1988

The deafferentation syndrome in the rat: effects of intraventricular apomorphine.

A deafferentation syndrome, produced in rats by dorsal root ganglionectomies, is expressed as scratching of partially deafferented limb areas and/or biting of anesthetic limb areas. This self-mutilation may be objective evidence of dysesthesias, thus serving as an experimental model to study chronic dysesthesias and/or pain from deafferentation in man. This study included behavioral observations of the syndrome and the effects of intraventricular apomorphine, a dopamine agonist, on its expression. Thirty-eight female Sprague-Dawley rats underwent unilateral C5-T2 dorsal root ganglionectomies followed immediately by stereotactically guided cannulation of the right lateral ventricle in 20 of the rats. For 2 weeks continuously via an osmotic minipump, 10 rats received apomorphine (5 micrograms/h) and 10 others received L-ascorbate (the vehicle). Rats with ganglionectomies only, as well as those receiving L-ascorbate, demonstrated early onset, more severe and later onset, less severe biting groups (P less than 0.05 Mann-Whitney U). Animals receiving apomorphine exhibited low autotomy scores irrespective of time of bite onset. Among the control groups, but not the experimental animals, the earlier the onset of biting, the more severe was the autotomy. The rats receiving vehicle via the minipump had earlier bite onsets than the rats in the ganglionectomy only group. This may indicate that the presence of the minipump is a stress which can accelerate the onset of biting. Intraventricular apomorphine can affect the deafferentation syndrome in the rat; it seems to decrease the level of autotomy and disrupt the relationship of bite onset with degree of biting.

Afferent Pathways↗
PubMed1992

Dental and oral findings in patients with familial dysautonomia.

Familial dysautonomia is an inherited autosomal recessive disease found almost exclusively in Ashkenazi Jews. It is characterized by selective damage to the sensory, motor, and autonomic peripheral nervous system. The main clinical features include decreased pain sensation, impaired temperature and blood pressure regulation, lack of tearing, absent tendon reflexes, and fungiform papillae on the tongue. The purpose of this study was to explore in depth and to verify the oral and dental status in familial dysautonomia. Twenty-two patients and 44 match-paired healthy persons of Ashkenazi descent were examined. Patients and parents had only little concern for their oral condition. Caries prevalence was lower than normal and plaque accumulation increased in all patients. Dental trauma was found in 59% of the patients, and 32% showed orodental self-mutilation. Dental age was within normal range, and dental arch measurements implied proportionally small jaws and little crowding. The low caries rate may be related to the known "hypersalivation" in familial dysautonomia and/or a possible change in the salivary composition and content, caused by chronic autonomic denervation.

Adolescent↗
PubMed1981

Development of physical dependence on t-butanol in rats: an examination using schedule-induced drinking.

Rats were exposed to various concentrations of t-butanol as their only available fluid in either the home cage or a schedule-induced drinking situation previously shown to induce overdrinking of ethanol. When animals consumed at least 3 g/kg/day of t-butanol for 90 days, independent of conditions, withdrawal symptoms were observed. This daily intake occurred only when the concentration of t-butanol was 3% (v/v) or greater. The schedule-induction procedure did not induce t-butanol overdrinking at any concentration tested as it does with ethanol, but its use did result in increased probability of the occurrence of withdrawal symptoms over the home cage condition. In no cases was the severity of withdrawal from t-butanol as great as previously reported for ethanol. When the concentration of t-butanol was increased to 3.5% (v/v), severe toxic reactions were found, that included anorexia, self-mutilation, and deaths from no specific determinable causes.

Animals↗
PubMed1989

Serotonergic innervation of the rat caudate following a neonatal 6-hydroxydopamine lesion: an anatomical, biochemical and pharmacological study.

6-Hydroxydopamine (6-OHDA) treatment of neonatal rats resulted in a dose-related loss of striatal dopamine (DA). These reductions corresponded closely with the loss of tyrosine hydroxylase-containing terminals at this brain site. Striatal serotonin (5-HT) concentration increased only after DA was maximally depleted by the highest dose of 6-OHDA. Quantitative immunohistochemistry revealed that the increased 5-HT content after neonatal 6-OHDA lesioning was due to a proliferation of 5-HT nerve terminals. The density of immunoreactive 5-HT-containing terminals appeared to increase more than did the 5-HT content. The present study examined whether 5-HT hyperinnervation was playing a role in behavioral responses induced by D1-DA agonists and antagonists in neonatally lesioned rats, because reports have suggested that these drugs may interact with 5-HT receptors. However, SCH-23390, the D1-DA antagonist (0.3 mg/kg), did not alter behavioral responses to 5-HTP and SKF-38393 (3 mg/kg), a D1-DA agonist did not produce any signs of activating 5-HT receptors in 5,7-DHT-lesioned rats. These data indicate that these compounds affecting D1-DA receptors do not have a significant effect on 5-HT function at doses which have maximal effects on D1-DA receptor function. Pretreatment with the 5-HT antagonist methysergide did not produce a change in apomorphine-induced locomotion and did not antagonize the self-mutilation or the other behaviors produced by L-DOPA or SKF-38393 in neonatally lesioned rats, suggesting that 5-HT hyperinnervation is not responsible for these drug-induced changes in neonatal 6-OHDA-lesioned rats.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1994

Intrathecal excitatory amino acid (EAA) agonists increase tail flick latencies (TFLs) of spinal rats.

The facilitation of spinal nociceptive reflexes that occurs after spinal transection reveals the existence of descending, supraspinally mediated inhibition. Substantial evidence indicates that the excitatory amino acids (EAAs) are involved in these spinal circuits. Therefore, it was hypothesized that reflex facilitation in the spinal animal might be due to the removal of inhibitory input normally exerted on the spinal action of EAAs. If so, the facilitatory decrease in reflex latency, observed in the spinal preparation, might be potentiated by intrathecal (IT) administration of EAA agonists. This was tested by comparing the effect of IT injections of N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) on the thermally elicited tail flick (TF) response of Intact and acute spinal rats. In intact rats, a low (0.25 nM) dose of NMDA produced a hyperalgesic decrease in latency, relative to saline, whereas higher doses produced an overall increase in latency. A large dose (0.5 microM) produced overt signs of toxicity (crippling, self-mutilation, and loss of the reflex). Only the highest (1.0 nM) dose of AMPA affected the response, resulting in a significant increase. After spinal transection, the hyperalgesic reaction to 0.25 nM of NMDA was absent, and latencies were significantly increased by 1.0 nM. The toxic reaction to 0.5 microM appeared to be potentiated. Tail flick responses to AMPA were also significantly increased in spinal rats. Contrary to the prediction, reflex latencies were significantly increased by these drugs after spinal transection. It was suggested that, although the spinal action of EAAs appears to be supraspinally modulated, this influence may be facilitatory rather than inhibitory.

Animals↗
PubMed1988

Unilateral dorsal rhizotomy decreases monoamine levels in the rat spinal cord.

In the rat, unilateral dorsal cervicothoracic rhizotomy (C5-T2) resulted in autotomy of the ipsilateral limb. The onset of self-mutilation was variable and attained the maximum degree 8-9 weeks after the dorsal root section. Fifteen and 60 days after the lesion the monoamines dopamine (DA), noradrenaline (NA) and serotonin (5-HT) as well as the 5-HT metabolite 5-hydroxyindoleacetic acid (5-HIAA) were measured by high performance liquid chromatography at different levels of the spinal cord. The lesion induced a significant decrease in the spinal levels of DA and NA, both ipsilateral and contralateral to the lesion, not only in the deafferented region but also from T3 downwards. The changes in DA levels were more marked and of earlier onset than those of NA. The decrease in 5-HT and its metabolite 5-HIAA was only observed in the more caudal regions of the non-deafferented ipsilateral cord. The more conspicuous lessening in spinal monoamine levels coincided approximately with the maximum intensity of autotomy. The present results suggest that dorsal rhizotomy induces distant changes in the brainstem nuclei where descending aminergic pathways originate.

Animals↗
PubMed1990

Chronic administration of amphetamine increases glutamic acid decarboxylase activity in the rat substantia nigra.

The glutamate decarboxylase activity in the rat cerebellum, frontal cerebral cortex, hypothalamus, substantia nigra and nucleus caudatus, was measured after either acute or chronic administration of (+)-amphetamine (1.35 and 5.4 mg/kg, i.p.). It was found that following 45 days of treatment the highest dose of the drug induced a selective increase of glutamate decarboxylase activity in the substantia nigra. Also in addition to the known changes in body weight, behavior and food-intake, some of the rats (5 out of 80 rats) treated with the highest dose of (+)-amphetamine developed a self-mutilating behavior. These results suggest that after the repeated administration of a high dose of (+)-amphetamine the activity of the striatonigral GABAergic pathway is increased and supports the idea that gamma-aminobutyric acid output neurons might convey dopamine-related functions.

Amphetamines↗
PubMed1991

Intrathecal administration of clonidine suppresses autotomy, a behavioral sign of chronic pain in rats after sciatic nerve section.

The effect of chronic intrathecal (i.t.) administration of the alpha 2 adrenoceptor agonist clonidine on self-mutilation behavior (autotomy) after unilateral transection of the sciatic nerve was studied in rats. Rats injected with 10 micrograms clonidine twice daily for 21 days, starting 1 h before nerve section, autotomized significantly less than saline controls. However, in the few rats which received clonidine and autotomized, clonidine did not delay the onset of autotomy compared to saline controls. Termination of clonidine injection after 21 days resulted in increased autotomy within 1-4 days. No sedation or motor impairment was found after this dose of i.t. clonidine. It is suggested that clonidine may be useful in treating neuropathic pain in humans.

Animals↗
PubMed1980

Autotomy following nerve injury: genetic factors in the development of chronic pain.

Several weeks following transection and ligation of the hind limb nerves in rats, the animals often attack their anaesthetic foot ("autotomy"). This behaviour is thought to reflect a sensory pathology analogous to anaesthesia dolorosa. We report here that the extent of autotomy varies greatly in genetically different populations of rats. Rats of one population, LC2, showed high autotomy levels; rats of another, LC1, showed very low autotomy levels. The main genetic difference between these two populations is the presence of inbred Lewis rat stock in the LC1 population. Pure Lewis strain rats proved to have very low autotomy levels. Thus, constitutional differences between different rat populations effect the extent of autotomy. These data may bear on the fact that after seemingly identical nerve injuries, some humans develop chronic pain syndromes and others do not. Our rat strains may provide a model for investigating the physiological basis of constitutional susceptibility to chronic pain.

Age Factors↗
PubMed1989

Autotomy behavior in rats following peripheral deafferentation is suppressed by daily injections of amitriptyline, diazepam and saline.

Amitriptyline, a tricyclic antidepressant (TCA), was effective in suppressing self-mutilation of a peripherally deafferented hind paw in rats ('autotomy'). This effect was not due to the drug's sedative effect, since locomotor activity was not lower in treated than untreated rats. Daily injections of normal saline also suppressed autotomy, but for a shorter period of time than amitriptyline. This effect was not apparent in diazepam-treated rats, suggesting that the saline injection delayed autotomy as a result of stress-induced anti-nociception. Since amitriptyline is effective in humans in alleviating certain chronic pain disorders, these results further corroborate the suggestion that autotomy is a model of chronic pain, sensitive to centrally acting analgesics and to some forms of stress.

Amitriptyline↗
PubMed1991

Suppression of neuropathic pain behavior in rats by a non-psychotropic synthetic cannabinoid with NMDA receptor-blocking properties.

HU211 is a novel synthetic derivative of tetrahydro-cannabinol (THC), the active marijuana ingredient. The stereochemistry of HU211 is enantiomeric to that of THC. In contrast to THC, HU211 is not psychotropic. This agent exhibits other types of biological activities; it is a non-competitive NMDA receptor blocker and has antinociceptive activity when injected with cupric chloride. This study examined its effects in autotomy, a behavioral model of neuropathic pain. Autotomy, a behavior of self-mutilation of denervated areas, was induced in Sabra rats by cutting the sciatic and saphenous nerves. We found that injections of HU211 (2.5 mg/kg) with cupric chloride (0.8 mg/kg) every 2nd day markedly suppressed autotomy during the injection period by delaying its average onset day and reducing the incidence of severe autotomy. Moreover, suppression of autotomy was retained in the postinjection period (for at least 30 days) but only when the drug was injected intraperitoneally. Lesser effects were achieved by subcutaneous injections. Cupric chloride or HU211 alone were ineffective. The general behavior and open field motor activity indicated that the effects of HU211 with Cu++ on autotomy were not due to sedation or ataxia but presumably due to antinociception mediated by NMDA receptor blockade.

Animals↗
PubMed1991

Studies in autotomy: its pathophysiology and usefulness as a model of chronic pain.

An interesting behavioral syndrome results in animals from the same or similar types of lesions that lead to deafferentation pain in humans; many neurectomized animals begin to scratch, bite, or self-mutilate their denervated limb, a phenomenon termed autotomy. The proposition that this behavior in animals is a response to the chronic pain of peripheral nerve injury has met with considerable controversy. If this issue were resolved, then a better understanding of the neurophysiology of autotomy might help elucidate the mechanisms of the human conditions. To determine the association between deafferentation and the autotomy behavior, we developed a pharmacologically induced functional deafferentation preparation using chronic perineural lidocaine infusion of the sciatic nerve. This 'chronic lidocaine' model's behavior was compared with that of the neurectomy model. While autotomy was noted in 80% of the latter group, no animal undergoing a chronic perineural infusion of lidocaine autotomized. We thus conclude that autotomy is not a response to non-painful sensory deafferentation, but rather that this behavior is a response to pain. We also studied the development of autotomy in a variety of other focal denervation preparations. On the basis of these data, we conclude that autotomy is not due to loss of sensory input on a functional basis nor to an action potential-mediated process. Rather, nerve damage which coincidentally involves sensory loss is necessary and sufficient for the development of this behavior. We suggest that interruption of a humoral feedback process homeostatically operating within the first order sensory neuron with its effect exerted post-synaptically leads to autotomy. The evidence supports the existence of a loss of a transportable, humoral autotomy inhibitory factor.

Afferent Pathways↗
PubMedDate not supplied

Clinical correlations in partial hypoxanthine guanine phosphoribosyltransferase deficiency.

Erythrocyte assays for hypoxanthine guanine phosphoribosyltransferase (HGPRT) activity performed on two male half-siblings with hyperuricemia, produced results consistent with classic Lesch-Nyhan syndrome. Due to the absence of neurologic abnormalities, cognitive deficits, or self-mutilation, HGPRT activity was measured by intact fibroblast assay which revealed partial enzyme deficiency. The presence of an unstable mutant enzyme may have led to the discrepancy between the erythrocyte and fibroblast studies. This discrepancy emphasizes the difficulty in assaying this enzyme solely utilizing red blood cell studies to determine a patient's course. In order to provide an accurate prognosis and relevant genetic counseling, measurement of this enzyme utilizing intact fibroblasts is critical after establishing a diagnosis of HGPRT deficiency in a hyperuricemic male lacking typical clinical manifestations of Lesch-Nyhan syndrome, but having enzyme activity of erythrocytes consistent with the diagnosis.

Child, Preschool↗