A.U. Luescher, DVM, PhD, DACVB
Department of Veterinary Clinical Science, Purdue University, West Lafayette, IN, USA
Introduction
It has long been recognized that otherwise healthy animals, when kept in captivity, may develop strange behaviors. These behaviors appear abnormal because they are performed out of context, are often exaggerated, directed towards unnatural stimuli or objects, and are often performed repetitively in a constant manner. Well-known examples include pacing in polar bears27,35 and other carnivores, tongue playing in giraffes and okapis, feather plucking in parrots, repetitive regurgitation and reingestion in primates,1 and weaving in elephants.31 Compulsive behavior is very common in domestic livestock. In these species such behavior, particularly when stereotypic, has always been considered to be confinement-induced conflict behavior, and has been linked to specific husbandry practices.37 Compulsive behavior is also common in pets.21 Stereotyped compulsive behavior is one of the most studied abnormal behaviors in domestic animals,18 and much interest has been devoted to the topic in laboratory animals as well.3 Although early progress has been made to validate the diagnosis of compulsive disorder,10 further work is needed. The following working definition of compulsive disorder (CD) has been proposed: “Behaviors that are usually brought on by conflict, but that are subsequently shown outside of the original context. The behaviors might share a similar pathophysiology (e.g., changes in serotonin, dopamine and beta-endorphin systems). Compulsive behaviors seem abnormal because they are displayed out of context and are often repetitive, exaggerated or sustained.”11
Causes of Compulsive Disorder
Compulsive behaviors are considered to be an expression of stress, frustration, and/or conflict.37 Various forms of conflict behavior are caused by frustration or conflict and have been studied in a variety of species.13 Prolonged and/or repetitive frustration and conflict may result in the conflict behaviors becoming generalized to other contexts (i.e., they emancipate from their original cause).24,26 They are also believed to evolve gradually from more variable behavior to short sequences of a few simple behavioral elements.4 Furthermore, it appears that the level of arousal necessary to trigger the performance of these behaviors diminishes as the behavior develops into a compulsive disorder.11
While the above outlined development of compulsive behavior may be typical for locomotory behavior, case histories of affected dogs indicate that self-directed oral behavior is displayed from the start in various contexts and does not increase in frequency. Also, these behaviors are typically shown in situations with little outside stimulation but presumably a high level of internal arousal. There is some evidence that locomotory and oral compulsive behaviors differ neurophysiologically as well.2
From clinical cases in dogs, it is obvious there may be genetic factors controlling the development of CD: some breeds may be particularly susceptible to developing a CD and others may develop a particular compulsive behavior if the environment is conducive to the development of CD. A genetic predisposition for certain compulsive behaviors has also been demonstrated in lines of Thoroughbred horses,33 and breed has been shown to affect the likelihood of various compulsive behaviors being performed by horses.22
Any stressor, be it social, climatic, nutritional, or disease related, is likely to contribute to the performance of compulsive behavior. These factors may either be causal, or they may simply increase arousal levels and thus the likelihood that an already established compulsive behavior is performed (i.e., act as modulating factors).25
Pathophysiology of Compulsive Disorder
The pathophysiology of CD is not well understood. Most evidence stems from drug effects on the performance of compulsive behavior. Large doses of dopaminergic drugs such as amphetamine and apomorphine are effective in inducing stereotyped behavior in animals3 or exaggerating spontaneous compulsive behavior,2 while the dopamine antagonist haloperidol results in suppression of spontaneously occurring stereotyped behavior.16
Beta-endorphins have been implicated in stereotypy performance because beta-endorphin receptor blockers can be effective in reducing stereotypies.5,6 However, the concept that performance of stereotypies is rewarded by endorphin release is no longer supported: cribbing in horses did not result in an increase in blood endorphin levels, and their pain sensitivity was actually increased during cribbing compared to when they were not cribbing.19 Furthermore it has been suggested that beta-endorphins may play a significant role only early on in the development of stereotyped behavior.16
Because of similarities of animal CD and human obsessive-compulsive disorder, drugs inhibiting serotonin reuptake have been used to treat dogs with CD.9 The effectiveness of such drugs implies that serotonin is involved in animal CD. Direct evidence of serotonin involvement has also been presented.32 However, the role of serotonin in CD is not well understood.15
Treatment
Treatment consists of environmental modification and, where necessary, pharmacologic intervention. In the following, treatment is listed in order of implementation.
1. If possible, the cause of the problem should be identified and addressed. The environment should be changed to accommodate the most important species-typical behaviors. Environmental enrichment is not useful unless it specifically targets the behavior that is frustrated, and/or the behaviors most commonly performed by the species in question.
2. Stressors may be additive, and once a compulsive behavior is established, environmental stress may serve to perpetuate it. This includes situations where important releasing stimuli for species typical behavior are lacking, and situations in which an aversive stimulus such as inappropriate climatic conditions, an aggressive group member, or proximity of visitors cannot be avoided. It is therefore indicated to try to reduce environmental stress as much as possible.
3. In most cases, particularly in those that have been going on for a long time, drug therapy may prove necessary. Beta-endorphin antagonists such as naloxone, nalmefene and naltrexone have been suggested to be used for treatment. Beta-endorphin antagonists have high first-pass metabolism and a short half-life, and most are only effective as injectables. Only naltrexone is available as an oral formulation, because in humans its first metabolite, 6β-naltrexol, is an active beta-endorphin antagonist. However, this metabolite is not formed in some species such as dogs,8 and clinical suppression of compulsive behavior in dogs is short-lasting.7 In spite of a report supporting its effectiveness at 2.2 mg/kg PO SID–BID in dogs,36 its use for the treatment of CD, at least in dogs, must be questioned.
Haloperidol has been used experimentally to reduce compulsive behavior in many species. It proved effective in suppressing stereotyped jumping in bank voles.16 Haloperidol decanoate was used to reduce bar biting in sows at 250 mg IM per sow.34 Haloperidol suppressed tongue playing in cattle.30 A dose for haloperidol has not been established for companion animals. Landsberg et al.17 list 1–4 mg per dog PO BID. This author has used it only in a few cases of dogs with compulsive disorder at 1–2 mg per dog, invariably without success. The use of haloperidol for treating feather picking in birds was reported.20 In one case two African grey parrots were treated successfully with haloperidol at 0.4 mg/kg/day for 7 months.14
As is the case with human obsessive-compulsive disorder, pharmacologic intervention is most likely achieved with serotonin reuptake inhibitors. A clinical trial involving 51 dogs with a variety of compulsive behaviors has been performed for the tricyclic antidepressant, clomipramine.12 Some success was reported for treatment of feather picking in psittacine birds with clomipramine at 1 mg/kg PO SID or divided BID.28 Clinical trials on cases of canine acral lick dermatitis have been performed for clomipramine, fluoxetine and sertraline.29 Paroxetine has also been used clinically, but its effect has not been evaluated. Fluoxetine has been used successfully to suppress pacing in a polar bear at the Calgary Zoo.27 Fluoxetine was given at 0.62 mg/kg SID for 77 days, then the dose was increased to 1 mg/kg SID. In companion animals we usually give a drug for 3 weeks after it appears to have an effect, then wean off gradually over 3 weeks to avoid a rebound effect.
4. Instead of modulating the brain serotonin system by inhibiting the reuptake and metabolism of serotonin in the presynaptic neuron, a tryptophan supplement can be fed. Tryptophan is a precursor of serotonin. Some success in the treatment of compulsive behavior in horses has been reported at a dose of 2 g/horse BID, or approximately 5 mg/kg BID.23
5. In persistent cases a program of counterconditioning (more correctly termed response substitution) might be considered. If this option is chosen, treatment has to be implemented with great consistency in order to be effective. It is very important that the animal be distracted every time it is about to perform the compulsive behavior, and an alternative behavior be solicited.
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