Prestimulation‐Induced Startle Modulation in Attention‐Deficit Hyperactivity Disorder and Nocturnal Enuresis

Ornitz, E M; Hanna, Gregory L.; Traversay, J. De

doi:10.1111/j.1469-8986.1992.tb01717.x

Cited by 126 publications

(89 citation statements)

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“…27 Thus lowered PPI appears to occur among individuals who are subject to unfiltered and irrelevant sensory, cognitive and/or motor perceptions. 19,28 Recently, as compared with 23 sibling controls, PPI among 25 children with 22q11DS was 20% less; secondary analyses suggested that this decrement did not reflect developmental delay. 29 The Attention Network Test (ANT) assesses the efficiency of three relatively segregated brain networks responsible for fundamental aspects of visual attention, including Alerting, Orienting, and Executive functions.…”

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confidence: 88%

“…14,15 Lowered PPI has been shown in children with disorders characterized by a failure of brain inhibitory mechanisms including Tourette's syndrome, 16 posttraumatic stress disorder, 17 fragile X syndrome, 18 and among males with nocturnal enuresis and co-morbid ADHD. 19 Lowered PPI has also been found in adults whose psychiatric syndromes are characterized by poor selective-inhibitory control of attention, including obsessive compulsive disorder, 20,21 panic disorder, 22 social phobia, 23 Asperger's syndrome, 24 Huntington's disease, 25 bipolar mania, 26 and schizophrenia. 27 Thus lowered PPI appears to occur among individuals who are subject to unfiltered and irrelevant sensory, cognitive and/or motor perceptions.…”

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confidence: 99%

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Associations between prepulse inhibition and executive visual attention in children with the 22q11 deletion syndrome

2004

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The 22q11 deletion syndrome (DS) results in the loss of approximately 30 gene copies and is associated with possible physical anomalies, varied learning disabilities, and a specific cluster of neurocognitive deficits, including primary impairment in working memory, executive visual attention, and sensorimotor processing. Retrospective studies have suggested that children with 22q11DS are at 25 times greater risk of developing schizophrenia, thus specification of early brain network vulnerabilities among children with 22q11DS is critical. Previously, we reported that children with 22q11DS as compared with sibling controls had selective deficits in visual executive attention, and subsequently found lowered prepulse inhibition (PPI) in these same children. Visual executive attention and PPI recruit the same brain pathways linking prefrontal cortex to basal ganglia structures. To test the specificity of brain pathway vulnerability among children with 22q11DS, we examined visual executive attention and PPI paradigm data collected during the same test session from 21 children with 22q11DS and 25 sibling controls. We predicted lower %PPI and less efficient executive attention scores, and a significant inverse correlation between measures. %PPI in children with 22q11DS as compared with sibling controls was 20% lower, and visual executive attention efficiency scores 40% worse. As predicted, %PPI was inversely correlated only with executive attention efficiency scores. The implications of these findings with regard to brain pathway vulnerability in children with 22q11DS are considered. These results suggest that children with 22q11DS have early functional abnormality in pathways linking the prefrontal cortex and basal ganglia. Molecular Psychiatry (2005) 10, 553-562.

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confidence: 88%

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confidence: 99%

Associations between prepulse inhibition and executive visual attention in children with the 22q11 deletion syndrome

2004

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“…Compared with matched controls, PPI is deficient in patients with schizophrenia (e.g., Braff et al 1978;Swerdlow et al 2006), Huntington's disease Valls-Sole et al 2004), obsessive-compulsive disorder (OCD) Hoenig et al 2005;Ahmari et al 2012), nocturnal enuresis (Ornitz et al 1992), Asperger's syndrome (McAlonan et al 2002), 22q11 syndrome (Sobin et al 2005), Kleinfelter syndrome (Van Rijn et al 2011), fragile X syndrome (Frankland et al 2004), blepharospasm (Gomez-Wong et al 1998, and Tourette syndrome (Castellanos et al 1996;Swerdlow et al 2001b).…”

Section: The Evolution Of Prepulse Inhibition As a Validated Animal Mmentioning

confidence: 99%

Animal Models of Deficient Sensorimotor Gating in Schizophrenia: Are They Still Relevant?

Swerdlow

Light

2015

Translational Neuropsychopharmacology

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Animal models of impaired sensorimotor gating, as assessed by prepulse inhibition (PPI) of startle, have demonstrated clear validity at face, predictive, and construct levels for schizophrenia (SZ) therapeutics, neurophysiological endophenotypes, and potential causative insults for this group of disorders. However, with the growing recognition of the heterogeneity of the schizophrenias, and the less sanguine view of the clinical value of antipsychotic (AP) medications, our field must look beyond "validity," to assess the actual utility of these models. At a substantial cost in terms of research support and intellectual capital, what has come from these models, that we can say has actually helped schizophrenia patients? Such introspection is timely, as we are reassessing not only our view of the genetic and pathophysiological diversity of these disorders, but also the predominant strategies for SZ therapeutics; indeed, our field is gaining awareness that we must move away from a "find what's broke and fix it" approach, toward identifying spared neural and cognitive function in SZ patients, and matching these residual neural assets with learning-based therapies. Perhaps, construct-valid models that identify evidence of "spared function" in neural substrates might reveal opportunities for future therapeutics and allow us to study these substrates at a mechanistic level to maximize opportunities for neuroplasticity. Such an effort will require a retooling of our models, and more importantly, a re-evaluation of their utility. For animal models to remain relevant in the search for schizophrenia therapeutics, they will need to focus less on what is valid and focus more on what is useful.

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“…A number of psychiatric illnesses with manifested dysfunction in attentional mechanisms are hypothesized to involve pathology of the NE system (AstonJones et al, 1999). PPI deficits can be seen in many of these conditions including attention-deficit-hyperactivity disorder (ADHD), schizophrenia, and post-traumatic stress disorder (PTSD); interestingly, with ADHD, this PPI disruption is seen only with attended-to prepulses Castellanos et al, 1996;Grillon et al, 1996;Hawk et al, 2003;Ornitz et al, 1992). Thus, clarifying the nature of PPI modulation by NE may further our understanding of how this system regulates functions that are relevant to the information processing-related deficits observed in these illnesses.…”

Section: Introductionmentioning

confidence: 99%

Disruption of Prepulse Inhibition after Stimulation of Central but not Peripheral α-1 Adrenergic Receptors

Alsene

Carasso²,

Connors

et al. 2006

Neuropsychopharmacol

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Prepulse inhibition (PPI) refers to the attenuation of startle when a weak prestimulus precedes the startling stimulus. PPI is deficient in several psychiatric illnesses involving poor sensorimotor gating. Previous studies indicate that a1 adrenergic receptors regulate PPI, yet the extent to which these effects are mediated by central vs peripheral receptors is unclear. The present studies compared the effects of intracerebroventricular (ICV) vs intraperitoneal (IP) delivery of several a1 receptor agonists on PPI. Male Sprague-Dawley rats received either cirazoline (0, 10, 25, 50 mg/5 ml), methoxamine (0, 30, 100 mg/5 ml), or phenylephrine (0, 3, 10, 30 mg/5 ml) ICV immediately before testing. Separate groups received either cirazoline (0, 0.25, 0.50, 0.75 mg/kg), methoxamine (0, 2, 5, 10 mg/kg), or phenylephrine (0, 0.1, 2.0 mg/kg) IP 5 min before testing. PPI, baseline startle responses, and piloerection, an index of autonomic arousal, were measured. Cirazoline disrupted PPI; effective ICV doses were approximately six times lower than effective IP doses. Methoxamine disrupted PPI after ICV infusion but failed to affect PPI with IP doses that were up to 30-fold higher than the effective ICV dose. Phenylephrine disrupted PPI with ICV administration, but did not alter PPI after IP injection of even a 20-fold higher dose. None of the ICV treatments altered baseline startle magnitude, but phenylephrine and methoxamine lowered startle after administration of high systemic doses. Piloerection was induced by cirazoline via either route of administration, and by IP methoxamine and phenylephrine, but not by ICV infusion of methoxamine or phenylephrine. These findings indicate that a1 receptor-mediated PPI disruption occurs exclusively through stimulation of central receptors and is dissociable from alterations in baseline startle or autonomic effects.

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Prestimulation‐Induced Startle Modulation in Attention‐Deficit Hyperactivity Disorder and Nocturnal Enuresis

Cited by 126 publications

References 66 publications

Associations between prepulse inhibition and executive visual attention in children with the 22q11 deletion syndrome

Associations between prepulse inhibition and executive visual attention in children with the 22q11 deletion syndrome

Animal Models of Deficient Sensorimotor Gating in Schizophrenia: Are They Still Relevant?

Disruption of Prepulse Inhibition after Stimulation of Central but not Peripheral α-1 Adrenergic Receptors

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