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Evidence for A selective developmental neurocognitive deficit in pediatric OCD
Abstracts
ubnonnalities in orbital prefrontal cortex and ils ventral striatal largl:!t fields are involved in cuusing obsessivl:! and compulsive symptoms. In llnimal models amI studies of patients wilh le.!
88. EVIDENCE FOR A SELECTIVE DEVELOPMENTAL NEUROCOGNITIVE DEFICIT IN PEDIATRIC OeD D. Rosenberg, D. Averbach. K. O'Hearn. E. Dick, B. Birmaher, & J. Sweeney University of Pittsburgh MediCA' Cenler, 3811 O'H:lra Street, Pittsburgh, PA 15213 Disturbances in orbital prefromal cortex and its ventral striatal target fields have been idenlified in neuroimaging sludies of obse~sive compulsive disorder (OeD). In anim:ll models and studies of pUlients with lesions to this br:lin circuitry, II selective disturbance in the ability to suppress responses to irrelevant slimuli has been demonstrated. Such a deficit in rcspon~e suppression might underlie the apparent inhibitory deficit suggested by the ~ymptomuloJogy of OCD. To dale, lillie direct evidence of such II deficlt hilS been rcpOrtCl1. Further. tllthougn OeD commonly emerges during childhood or adolescence, few studies have examined psychotropic·naive pedialric patients nem lhe onset of illness to study the role of atypicD.1 developmental processes. Oculomotor tests were udministcrcd to 18 medication·naive, non-depressed OeD patients 8.8-16.9 yenrs of :lge, and 18 clIse-matched healthy comparison subjects, to assess three welt delineated aspects of prefrontal cortical function: the ability 10 suppress responses. to volitionally ex.ecute delayed responses. lind to Ilnticipnte predictable evenls. A significantly higher percel1lage of respllnse suppression fallures was observed in OCD patients, particulnrly ill younger patients, compared to their cll!ie-matehed eonlrols. No significant differences between OeD patients llnd controls were observed on other prefrontal cortical functions. Severity of OeD symptoms was
DlOL PSYCIIIA1'RY 1996;39:500-666
525
relaled to response suppression deficits. An npparcnl delay in acquisition nbitity of approximntcly fOUf years was observed in OCD subjcl:ts. A basic disturbance of neurobchilvioral inhibition in OCD was detected whieh may underlie the repetitive symptomalic behavior that characterb:es the illness. Behavioral response inhibilion abnonnalities in OeD may be related to fllilures ill developmenlal maturotion of f.-onto-slrialnl circuitry, panicularly orbital prcfrontal·\,entral striatal circuits.
89. ISOLATION-REARED MACAQUES ARE HYPOSENSITIVE TO STIMULI IN A TWOHOrrLE CHOICE PARADIGM LA. Paul 1.2, lA. Englishl. 2 , K. Ndebele M. Wellons I.:.!, & A. Halaris l
,
,2,
ILab. Neurobehavioral Phannllcol. & Immunol.. Div. Neurobiol. Behav. Res,; 2 Dept. Psychiatry. Univ. Miss. Merl. elf., Jtlckson. MS 39216 Diminished plensure in nctivities (nnhedonia) is a central symptom of major depression. Willner et al (1991) reponed a rodenl model of anhedonin after chronic mild stress (eMS) ex.posure defined as rcduced preference for sweetened WOlter (V5. unsweetened) in a 2-bottlc choice procedure, This WOlS reversed by chronic antidepressants.lsolation.reared rhesus mac:lques also have behavioral abnonmtlitics that can be reversed by antidepressants. We hypothesized that, like CMS rats. their preference for sweetened wall:!r would be reduced in a 2·bollle choice procedure (wllter+sucrose at 7 concentrations vs waler). We also measured intake of biller solutions (quinine+wlller at 4 concentrations YS wlller), to test for D. !nore general diminished responsivencss to stimuli.lsolation·reared mtlenqucs (3 female, I male) nnd controls (5 f
ubnonnalities in orbital prefrontal cortex and ils ventral striatal largl:!t fields are involved in cuusing obsessivl:! and compulsive symptoms. In llnimal models amI studies of patients wilh le.!
88. EVIDENCE FOR A SELECTIVE DEVELOPMENTAL NEUROCOGNITIVE DEFICIT IN PEDIATRIC OeD D. Rosenberg, D. Averbach. K. O'Hearn. E. Dick, B. Birmaher, & J. Sweeney University of Pittsburgh MediCA' Cenler, 3811 O'H:lra Street, Pittsburgh, PA 15213 Disturbances in orbital prefromal cortex and its ventral striatal target fields have been idenlified in neuroimaging sludies of obse~sive compulsive disorder (OeD). In anim:ll models and studies of pUlients with lesions to this br:lin circuitry, II selective disturbance in the ability to suppress responses to irrelevant slimuli has been demonstrated. Such a deficit in rcspon~e suppression might underlie the apparent inhibitory deficit suggested by the ~ymptomuloJogy of OCD. To dale, lillie direct evidence of such II deficlt hilS been rcpOrtCl1. Further. tllthougn OeD commonly emerges during childhood or adolescence, few studies have examined psychotropic·naive pedialric patients nem lhe onset of illness to study the role of atypicD.1 developmental processes. Oculomotor tests were udministcrcd to 18 medication·naive, non-depressed OeD patients 8.8-16.9 yenrs of :lge, and 18 clIse-matched healthy comparison subjects, to assess three welt delineated aspects of prefrontal cortical function: the ability 10 suppress responses. to volitionally ex.ecute delayed responses. lind to Ilnticipnte predictable evenls. A significantly higher percel1lage of respllnse suppression fallures was observed in OCD patients, particulnrly ill younger patients, compared to their cll!ie-matehed eonlrols. No significant differences between OeD patients llnd controls were observed on other prefrontal cortical functions. Severity of OeD symptoms was
DlOL PSYCIIIA1'RY 1996;39:500-666
525
relaled to response suppression deficits. An npparcnl delay in acquisition nbitity of approximntcly fOUf years was observed in OCD subjcl:ts. A basic disturbance of neurobchilvioral inhibition in OCD was detected whieh may underlie the repetitive symptomalic behavior that characterb:es the illness. Behavioral response inhibilion abnonnalities in OeD may be related to fllilures ill developmenlal maturotion of f.-onto-slrialnl circuitry, panicularly orbital prcfrontal·\,entral striatal circuits.
89. ISOLATION-REARED MACAQUES ARE HYPOSENSITIVE TO STIMULI IN A TWOHOrrLE CHOICE PARADIGM LA. Paul 1.2, lA. Englishl. 2 , K. Ndebele M. Wellons I.:.!, & A. Halaris l
,
,2,
ILab. Neurobehavioral Phannllcol. & Immunol.. Div. Neurobiol. Behav. Res,; 2 Dept. Psychiatry. Univ. Miss. Merl. elf., Jtlckson. MS 39216 Diminished plensure in nctivities (nnhedonia) is a central symptom of major depression. Willner et al (1991) reponed a rodenl model of anhedonin after chronic mild stress (eMS) ex.posure defined as rcduced preference for sweetened WOlter (V5. unsweetened) in a 2-bottlc choice procedure, This WOlS reversed by chronic antidepressants.lsolation.reared rhesus mac:lques also have behavioral abnonmtlitics that can be reversed by antidepressants. We hypothesized that, like CMS rats. their preference for sweetened wall:!r would be reduced in a 2·bollle choice procedure (wllter+sucrose at 7 concentrations vs waler). We also measured intake of biller solutions (quinine+wlller at 4 concentrations YS wlller), to test for D. !nore general diminished responsivencss to stimuli.lsolation·reared mtlenqucs (3 female, I male) nnd controls (5 f