Sylvian fissure morphology in Prader-Willi syndrome and early-onset morbid obesity

Miller, Jennifer; Couch, Jessica A.; Leonard, Christiana M.; Schwenk, Krista; Towler, Stephen; Shuster, Jonathan J.; Goldstone, Anthony P.; He, Guojun; Driscoll, Daniel J.; Liu, Yijun

doi:10.1097/gim.0b013e31812f720d

Cited by 19 publications

(10 citation statements)

References 38 publications

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“…Larger amount of anomalous fissures in Angelman patients was consistent with severity of impairment in speech development in this syndrome [46]. Although Sylvian fissure's aberrations are present in many conditions connected with speech disturbances only PWS patients presented polymicrogyria of this brain region [45]. Interestingly, PWS patients with mUPD, did not present normal bias toward leftward asymmetry in planar asymmetry, which was present in all other examined groups, such as in PWS due to deletion, healthy siblings control group and patients with early-onset morbid obesity [44].…”

Section: Neuroimaging Studies Of the Brain In Pws And Schizophreniamentioning

confidence: 87%

“…Research on the imprinted-gene effects in brain development allows us to analyze the etiology of psychiatric conditions that involve alterations in early development and functions of the brain and constitutes direct implications for other fields from genetics and epigenetics. Quantitative measurements performed by Miller et al revealed incomplete closure of the insula in patients affected by the syndrome [44,45]. This may lead to the disturbances in pain perception, autonomic control and excessive appetite with food-seeking behaviors present in PWS.…”

Section: Neuroimaging Studies Of the Brain In Pws And Schizophreniamentioning

confidence: 94%

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From Prader–Willi Syndrome to Psychosis: Translating Parent-of-Origin Effects into Schizophrenia Research

et al. 2014

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Prader-Willi syndrome (PWS) is a relatively rare disorder that originates from paternally inherited deletions and maternal disomy (mUPD) within the 15q11-q13 region or alterations in the PWS imprinting center. Evidence is accumulating that mUPD underlies high prevalence of psychosis among PWS patients. Several genes involved in differentiation and survival of neurons as well as neurotransmission known to act in the development of PWS have been also implicated in schizophrenia. In this article, we provide an overview of genetic and epigenetic underpinnings of psychosis in PWS indicating overlapping points in the molecular background of PWS and schizophrenia. Simultaneously, we highlight the need for studies investigating genetic and epigenetic makeup of the 15q11-q13 in schizophrenia indicating promising candidate genes.

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Section: Neuroimaging Studies Of the Brain In Pws And Schizophreniamentioning

confidence: 87%

Section: Neuroimaging Studies Of the Brain In Pws And Schizophreniamentioning

confidence: 94%

From Prader–Willi Syndrome to Psychosis: Translating Parent-of-Origin Effects into Schizophrenia Research

et al. 2014

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“…Sulcal/gyral features appear to have biological and behavioral significance, however. Sulcal/gyral features have been associated with cognitive abilities (Chiarello et al, 2006;Craggs et al, 2006;Clark and Plante, 1998), genetics (Eckert et al, 2006b;Miller et al, 2007) and may reflect patterns of neural connectivity and brain organization (Van Essen 1997;Binder et al, 1996). Measures of sulcal/gyral morphology may provide complementary information to voxel-based measures of brain morphology (Molko et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Manual and automated measures of superior temporal gyrus asymmetry: Concordant structural predictors of verbal ability in children

et al. 2008

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The planum temporale is a region on the posterior surface of the temporal lobe that exhibits robust leftward structural asymmetry, which has been linked to verbal ability in children and adults. Traditionally, structural asymmetry has been quantified with manual assessment of high resolution MRI scans. Such measures require subjective and frequently unreliable determination of highly variable anatomical boundaries. Methodological developments in automated image processing (voxel-based morphometry - VBM) offer the opportunity to obtain objective and reliable measures of structural variation. This study examined the extent to which a VBM measure of gray matter asymmetry in the posterior superior temporal gyrus (pSTG) characterized the same individual variation as a manual measure of planum temporale asymmetry in 99 healthy adults and 39 typically developing children. Planum temporale asymmetry was significantly correlated with pSTG gray matter asymmetry in the samples of adults and children. As a measure of validity we examined the extent to which the VBM measure of pSTG gray matter asymmetry predicted measures of verbal ability that were associated with the manual measure of planum temporale asymmetry in the same children. The two asymmetry measures predicted the same variance in verbal ability. The automated measure of pSTG gray matter asymmetry predicted additional significant variance in verbal ability, however. In addition, a posterior STS region was also identified that significantly predicted verbal ability. These results demonstrate significant advantages of an automated voxel-based measure over a manual measure of planum temporale asymmetry.

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“…These shifts in gut hormones may possibly correspond to the change between the poor feeding and FTT stage and the hyperphagia and obesity stage of PWS [Eiholzer et al, 2003; Butler et al, 2004; Goldstone, 2004; Bittel et al, 2005; Haqq et al, 2008; Bizzarri et al, 2010]. Individuals with PWS have also been shown to have structural brain abnormalities which may contribute to appetite aberrations [Miller et al, 2007a; Iughetti et al, 2008]. Functional MRI studies indicate that these individuals have an increased reward value to food and have increased activation of the limbic and paralimbic areas of the brain that drive eating behaviors, even post-meal, indicating that brain abnormalities likely also play a role in the appetite in this syndrome [Shapira et al, 2005; Holsen et al, 2006, 2009; Miller et al, 2007b; Dimitropoulos and Schultz, 2008; Hinton et al, 2010].…”

Section: Introductionmentioning

confidence: 99%

Nutritional phases in Prader–Willi syndrome

Miller

Lynn

Driscoll

et al. 2011

American J of Med Genetics Pt A

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364

373

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Prader–Willi syndrome (PWS) is a complex neurobehavioral condition which has been classically described as having two nutritional stages: poor feeding, frequently with failure to thrive (FTT) in infancy (Stage 1), followed by hyperphagia leading to obesity in later childhood (Stage 2). We have longitudinally followed the feeding behaviors of individuals with PWS and found a much more gradual and complex progression of the nutritional phases than the traditional two stages described in the literature. Therefore, this study characterizes the growth, metabolic, and laboratory changes associated with the various nutritional phases of PWS in a large cohort of subjects. We have identified a total of seven different nutritional phases, with five main phases and sub-phases in phases 1 and 2. Phase 0 occurs in utero, with decreased fetal movements and growth restriction compared to unaffected siblings. In phase 1 the infant is hypotonic and not obese, with sub-phase 1a characterized by difficulty feeding with or without FTT (ages birth—15 months; median age at completion: 9 months). This phase is followed by sub-phase 1b when the infant grows steadily along a growth curve and weight is increasing at a normal rate (median age of onset: 9 months; age quartiles 5–15 months). Phase 2 is associated with weight gain—in sub-phase 2a the weight increases without a significant change in appetite or caloric intake (median age of onset 2.08 years; age quartiles 20–31 months;), while in sub-phase 2b the weight gain is associated with a concomitant increased interest in food (median age of onset: 4.5 years; quartiles 3–5.25 years). Phase 3 is characterized by hyperphagia, typically accompanied by food-seeking and lack of satiety (median age of onset: 8 years; quartiles 5–13 years). Some adults progress to phase 4 which is when an individual who was previously in phase 3 no longer has an insatiable appetite and is able to feel full. Therefore, the progression of the nutritional phases in PWS is much more complex than previously recognized. Awareness of the various phases will aid researchers in unraveling the pathophysiology of each phase and provide a foundation for developing rational therapies. Counseling parents of newly diagnosed infants with PWS as to what to expect with regard to these nutritional phases may help prevent or slow the early-onset of obesity in this syndrome.

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Sylvian fissure morphology in Prader-Willi syndrome and early-onset morbid obesity

Cited by 19 publications

References 38 publications

From Prader–Willi Syndrome to Psychosis: Translating Parent-of-Origin Effects into Schizophrenia Research

From Prader–Willi Syndrome to Psychosis: Translating Parent-of-Origin Effects into Schizophrenia Research

Manual and automated measures of superior temporal gyrus asymmetry: Concordant structural predictors of verbal ability in children

Nutritional phases in Prader–Willi syndrome

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