Search

Obsessive compulsive disorder (OCD) is a debilitating condition, the etiology of which is poorly understood, in part because it often remains undiagnosed/untreated for a decade or more. Characterizing the etiology of compulsive disorders in animal models may facilitate earlier diagnosis and intervention. Doberman pinschers have a high prevalence of an analogous behavioral disorder termed canine compulsive disorder (CCD), which in many cases responds to treatments used for OCD. Thus, studies of CCD may help elucidate the etiology of compulsive disorders. We compared brain structure in Dobermans with CCD (N=8) and unaffected controls (N=8) to determine whether CCD is associated with structural abnormalities comparable to those reported in humans with OCD. We obtained 3 Tesla magnetic resonance structural and diffusion images from anesthetized Dobermans and subjected images to segmentation, voxel based morphometry, and diffusion tensor analyses. CCD dogs exhibited higher total brain and gray matter volumes and lower dorsal anterior cingulate cortex and right anterior insula gray matter densities. CCD dogs also had higher fractional anisotropy in the splenium of the corpus callosum, the degree of which correlated with the severity of the behavioral phenotype. Together, these findings suggest that CCD is associated with structural abnormalities paralleling those identified in humans with OCD. Accordingly, the CCD model, which has a number of advantages over other animal models of OCD, may assist in establishing the neuroanatomical basis for and etiology of compulsive disorders, which could lead to earlier diagnosis of and new treatments for humans and animals with these disorders., (Copyright © 2013 Elsevier Inc. All rights reserved.)

A Bernese mountain dog was diagnosed with complex partial seizures that were supported by electroencephalographic findings. Clinical signs of the problem included "star gazing," fly snapping, licking, vacuous chewing, and ongoing anxiety. Treatment with Huperzine A, a compound isolated from Chinese club moss with NMDA receptor blocking activity, anticholinesterase activity, and anticonvulsant properties, produced useful suppression of the abnormal behavior for more than months. A relapse occurred when the dog was treated with tramadol for joint pain and the improvement that had been made was not recaptured with Huperzine A. At this stage, phenobarbital therapy was instituted and the dog improved greatly. The role of Huperzine A in controlling seizures is discussed.

Dogs naturally suffer the same complex diseases as humans, including mental illness. The dog is uniquely suited as a model organism to explore the genetics of neuropsychiatric disorders. Historical breed demographics have enriched purebred populations for founder effect mutations with tractable architectures, making genotypic analyses advantageous. Over a pet's lifetime, owners observe the animal's stress tolerance, arousal, and anxiety, and can inform on rich behavioral profiles for phenotypic analyses. Here we leverage these strengths in a search for inherited fac-tors that exacerbate canine compulsive disorder (CCD), the dog counterpart to human obsesssive compulsive disorder (OCD). Our rationale is that identifying pathways that predispose to disease severity will expand therapeutic options, and ultimately bring relief to those patients suffering the most. We have performed a GWAS of purebred Doberman pinschers that compares severely affected cases to moderately affected cases (24:70). This GWAS identified two statistically sig-nificant risk loci, on CFA34 and CFA11, and a third with suggestive evidence on CFA16. The locus on CFA34 includes a cluster of 5-HT3 receptor genes (HTR3C, HTR3D, and HTR3E) that implicate a serotonergic pathway that is routinely targeted by anti-OCD medications. The locus on CFA11 is syntenic with human CTXN3-SLC12A2 (5q35.1), an inherited risk factor for schiz-ophrenia. The third locus harbors teneurin-3 (TENM3), a modulator of the hypothalamic-pituitary-adrenal (HPA) axis, with effects on stress tolerance and stress-related behavior. We dis-cuss candidate genes and putative functional variants in light of pharmacological responsiveness, psychiatric comorbidity, and the potential for gene-by-environment interactions in the genetic etiology of OCD and CCD. [ABSTRACT FROM AUTHOR]

Abstract: Medication plays an important role in the treatment of canine compulsive disorders (CCD). Not all cases can be managed with the current medications, and new pharmacological options are needed. This case series assesses the efficacy of the NMDA receptor blocker memantine as a possible new treatment option for CCD. Thirteen dogs with different manifestations of CCD were enrolled in the study, and data from 11 dogs were available for analysis. A behavioral and clinical history was obtained for each dog. Further medical tests were performed if deemed necessary. The main presenting complaints in the included cases were light/shadow chasing, spinning/circling, and tail chasing. All dogs were either treated with memantine alone or memantine was added to ongoing fluoxetine treatment. All owners of dogs included in the study were provided with a specific behavior modification plan in addition to the pharmacological treatment. Memantine was administered orally twice a day at a starting dose of 0.3-0.5 mg/kg. The dose was increased over time if necessary, and side effects permitting, to a dose not higher than 1 mg/kg. The owners were asked to use a clinical global impression scale (CGI) on a daily basis to assess the severity of their dog''s compulsive behaviors. This score was obtained daily for up to 4 consecutive weeks, and average weekly scores were calculated. Seven (64%) of the dogs included in the study showed a reduction in the severity of CCD, with CGI scores reduced by the second week of treatment. Only 1 out of 11 dogs showed a side effect (increased frequency of urination) that was potentially related to the medication. The results suggest that memantine may be an effective, well-tolerated option for the treatment of CCD either as a sole treatment or as an add-on to fluoxetine. Further studies are needed to investigate the efficacy of memantine in the treatment of CCD. [Copyright &y& Elsevier]

Objective—To evaluate blanket and flank sucking and any association with pica in Doberman Pinschers. Design—Survey and case-control study. Animals—153 Doberman Pinschers (77 dogs with blanket or flank sucking and 76 unaffected dogs). Procedures—Owners of Doberman Pinschers with blanket sucking, flank sucking, or both were surveyed regarding the age of onset, triggers, frequency, duration, interruptability, and associated medical and behavioral consequences. A putative association of blanket sucking and flank sucking with pica was examined by comparison of affected dogs with unaffected dogs. Results—Apart from the difference in the object of oral activity between blanket and flank suckers, age of onset was the only variable that differed between dogs with the 2 conditions. Dogs with blanket or flank sucking had a higher prevalence of pica than the unaffected population. Conclusions and Clinical Relevance--Blanket and flank sucking are apparently related conditions that can occur with sufficient intensity to cause medical sequelae. These nonnutritive suckling behaviors share similarities with other canine compulsive disorders and are associated with pica. Veterinarians should advise owners that flank and blanket sucking are abnormal, potentially harmful behaviors in dogs. Treatment should be considered for severely affected dogs or when flank or blanket sucking is associated with medical problems. [ABSTRACT FROM AUTHOR]

Objective: To determine the effect of intravenous acepromazine on the electroencephalogram (EEG) of normal Beagle dogs. Sample Population: Twelve healthy beagle dogs Procedures: Dogs were sedated and the EEG recorded for 20 minutes. Acepromazine was then injected intravenously in either low or high dose with the order chosen randomly and EEG recording continued for 30 minutes. Each dog received low and high dose in the study and at least a week was allowed to elapse between doses. Five dogs for the placebo group were chosen at random from the pool of dogs and received saline instead of acepromazine, with the same EEG recordings made. Results: Multiple ANOVA and independent t-tests were used to analyze data in commercially available statistical software. EEG activity was not altered significantly by either low or high dose acepromazine administered intravenously. Conclusions and Clinical Relevance: EEG activity is not altered significantly in normal dogs by the low or high dose of acepromazine used in this study. [ABSTRACT FROM AUTHOR]