Maturation of Startle Modulation

Ornitz, Edward M.; Guthrie, Donald; Kaplan, Andrea; Lane, Shelly J.; Norman, Robert J.

doi:10.1111/j.1469-8986.1986.tb00681.x

Cited by 96 publications

(77 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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.…”

mentioning

confidence: 99%

See 2 more Smart Citations

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

2004

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Apparatus and Stimulimentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

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

2004

View full text Add to dashboard Cite

show abstract

“…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: 95%

“…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

View full text Add to dashboard Cite

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...

show abstract

Psychotropic drugs in breast milk: No evidence for adverse effects on prepulse modulation of startle reflex or on cognitive level in infants

et al. 1998

View full text Add to dashboard Cite

Reversals in modulation of the startle reflex probably reflect maturational processes in the central nervous system. This study has investigated the longitudinal changes in prepulse modulation of the blink reflex in three groups of individual infants: (a) breast‐fed infants of mentally ill mothers who were prescribed selected psychotropic drugs, (b) bottle‐fed infants of similarly ill and medicated mothers, and (c) breast‐fed infants of healthy control mothers. The acoustic stimulation paradigm and neurophysiological methods were similar to those used in previous studies and, in addition, the infants' development was simultaneously assessed using the Bayley Scales of Infant Development. All the infants were found to be developing normally and across all three groups we observed a clear transition in prepulse modulation of the eye‐blink reflex from small inhibition or facilitation in early infancy (1–4 months) to a robust facilitation in middle infancy (5–8 months). This reversal probably reflects the changing balance of developing neural function in normal infants. There were, therefore, no discernible effects in breast‐fed infants of exposure to small doses of antidepressant or neuroleptic drugs. © 1998 John Wiley & Sons, Inc. Dev Psychobiol 32: 249–256, 1998

show abstract

Maturation of Startle Modulation

Cited by 96 publications

References 33 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

Psychotropic drugs in breast milk: No evidence for adverse effects on prepulse modulation of startle reflex or on cognitive level in infants

Contact Info

Product

Resources

About