Maturation of Prestimulation‐Induced Startle Modulation in Girls

Ornitz, Edward M.; Guthrie, Donald; Sadeghpour, Mojdeh; Sugiyama, Toshiro

doi:10.1111/j.1469-8986.1991.tb03381.x

Cited by 67 publications

(62 citation statements)

References 37 publications

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“…This is especially true in children. 14,15 (The paradigm used in this study included a 100 ms short-lead interval duration.) In fact, the neural pathways that influence latency have proven to be somewhat elusive and the brain mechanisms that participate in the response latency effect have been investigated far less frequently than those associated with startle modulation.…”

Section: Discussionmentioning

confidence: 99%

“…The presentation of cartoons during PPI has been shown to reduce movement and engage children's interest. 14,15 The experimenter sat behind the participant positioned to monitor both the participant and the apparatus throughout the session.…”

Section: Apparatus and Stimulimentioning

confidence: 99%

“…13 PPI in children has been shown to approach adult levels (50-75%) by approximately age 8, and by this time gender differences observed in adults are also apparent, with PPI values in males 25-30% higher than those in females. 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.…”

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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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Section: Discussionmentioning

confidence: 99%

Section: Apparatus and Stimulimentioning

confidence: 99%

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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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“…Prepulse inhibition in children has been shown to approach adult levels (50%-75%) by approximately age 8, and by this time the gender differences observed in adults are also apparent, with prepulse inhibition values in males 25%-30% higher than those in females (20,21).…”

Section: Nih-pa Author Manuscriptmentioning

confidence: 97%

“…Latency of response peak and onset are also modulated by lead stimuli. However, while inhibition occurs reliably among adults at short-lead interval durations ranging from 30 to 500 msec (19), latency effects appear far more sensitive to shortlead interval durations (i.e., 120 versus 250 msec), especially in children (20,21). The neural pathways that influence latency are elusive, however, and response inhibition (prepulse inhibition) has become better defined.…”

Section: Nih-pa Author Manuscriptmentioning

confidence: 99%

Lower Prepulse Inhibition in Children With the 22q11 Deletion Syndrome

Sobin¹,

Kiley-Brabeck²,

Karayiorgou³

2005

AJP

100

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Objective-The 22q11 deletion syndrome is associated with a range of possible physical anomalies, probable ongoing learning disabilities, and a specific constellation of neuropsychological deficits, including impairments in selective and executive visual attention, working memory, and sensorimotor functioning. It has been estimated that 25% of the children with 22q11 deletion syndrome go on to develop schizophrenia in late adolescence or adulthood. This is of urgent concern. Specification of early brain network vulnerabilities may provide a basis for early intervention while indicating critical links between genes and severe psychiatric illness. Neuropsychological studies of children with 22q11 deletion syndrome have implicated an array of potentially aberrant brain pathways. This study was conducted to determine whether preattentive processing ("sensorimotor gating") deficits are present in this population.Method-The authors administered a test of prepulse inhibition to 25 children with 22q11 deletion syndrome and their 23 sibling comparison subjects, ages 6-13. It was predicted that the children with 22q11 deletion syndrome would have lower prepulse inhibition than the comparison subjects.Results-Prepulse inhibition in the children with 22q11 deletion syndrome (26.06%) was significantly less than that of the sibling comparison subjects (46.41%). Secondary analyses suggested that this decrement did not reflect developmental delay, and lower prepulse inhibition was associated with particular subsyndromal symptoms in some children.Conclusions-Sensorimotor gating is lower in children with 22q11 deletion syndrome. These findings may indicate specific brain circuits that are anomalous in 22q11 deletion syndrome.The 22q11 deletion syndrome results from a meiotic deletion of genetic material at the q11.2 site on chromosome 22. It occurs in 1 of every 6,000 births (1) and in over 90% of the cases is de novo (2). Associated congenital anomalies occur in some but not all children and may include heart defects, immunologic deficits, craniofacial dysmorphologies, velopharyngeal defects such as overt or submucous cleft palate, or inflammation-related pain syndromes (3). Before the identification of a single underlying deletion, the different clinical labels described a child's primary physical anomaly and included "conotruncal anomaly face syndrome" (heart defect with facial dysmorphologies), "velocardiofacial syndrome" (velopharyngeal, heart, and facial anomalies), and "DiGeorge syndrome" (immunologic insufficiency).Broadly speaking, the academic and neuropsychological profile of children with 22q11 deletion syndrome is more consistent than their physical phenotype. Gross motor, fine motor, and expressive language delays have been identified in the early years (4) and are followed by learning disabilities and academic failures, attention impairment, and behavioral anomalies in an estimated 90%-100% of the school-age children with this syndrome (5,6 NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manu...

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Assessing the Validity of an Animal Model of Deficient Sensorimotor Gating in Schizophrenic Patients

Swerdlow¹

1994

Arch Gen Psychiatry

677

380

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Psychiatric researchers need specific animal models to better understand the neurobiology of schizophrenia. Prepulse inhibition (PPI), the reduction in startle produced by a prepulse stimulus, is diminished in schizophrenic patients. Theoretically, deficient PPI in schizophrenic patients reflects a loss of sensorimotor gating that may lead to sensory flooding and cognitive fragmentation. In rats, PPI is disrupted by systemic administration of dopamine agonists or by manipulations of neural circuitry linking the limbic cortex, striatum, pallidum, and pontine reticular formation. This loss of PPI in rats may be a useful model for studying the neurobiology of impaired sensorimotor gating in schizophrenic patients. We assessed the face, predictive, and construct validity of this animal model. Face validity was supported: stimulus manipulations produced parallel changes in PPI in humans and rats, and the dopamine agonist apomorphine disrupted PPI in rats, mimicking PPI deficits in schizophrenics. Predictive validity was supported: the ability of antipsychotics to restore PPI in apomorphine-treated rats correlated with clinical antipsychotic potency (rs = .991) and D2-receptor affinity (rs = .893). Antipsychotics that restore PPI in apomorphine-treated rats include "typical" antipsychotics and the "atypical" antipsychotic clozapine. Construct validity was supported: PPI was disrupted in rats when dopamine was infused into the nucleus accumbens; this effect was blocked by haloperidol. The loss of PPI in dopamine-activated rats may be a valid animal model of sensorimotor gating deficits in schizophrenic patients. This model may help us understand the neurobiology of cognitive deficits in schizophrenic patients.

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Maturation of Prestimulation‐Induced Startle Modulation in Girls

Cited by 67 publications

References 37 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

Lower Prepulse Inhibition in Children With the 22q11 Deletion Syndrome

Assessing the Validity of an Animal Model of Deficient Sensorimotor Gating in Schizophrenic Patients

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