Premorbid indicators and risk for schizophrenia: A selective review and update

Keshavan, Matcheri S.; Diwadkar, Vaibhav A.; Montrose, Debra M.; Rajarethinam, Rajaprabhakaran; Sweeney, John A.

doi:10.1016/j.schres.2005.07.004

Cited by 130 publications

(81 citation statements)

References 83 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Studying such a genetic high-risk population of nonpsychotic, young relatives, who are still within age range for developing schizophrenia, is a potentially fruitful research strategy from the standpoint of early identification of schizophrenia Keshavan et al 2005). By contrasting the neurodevelopmental trajectories between young relatives who go on to develop schizophrenia against relatives who remain well, we can better appreciate the early manifestations of schizophrenia which, in turn, could lead to early identification and intervention.…”

Section: Discussionmentioning

confidence: 99%

“…Prevalence of schizophrenia among relatives is higher than the general population (1%), and diminishes with decreased degree of relatedness to the schizophrenia proband -from 48% in monozygotic twins, to 17% dizygotic twins, 13% off springs, 9% full siblings and down to 2% in first cousins. Besides higher rates of schizophrenia, relatives who do not manifest the disorder are more likely to have similar, but less severe, neuroanatomical, electrophysiological, neurocognitive and behavioral deficits seen in schizophrenia probands (Keshavan et al 2005). …”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

MRI brain volume abnormalities in young, nonpsychotic relatives of schizophrenia probands are associated with subsequent prodromal symptoms

2007

Schizophrenia Research

View full text Add to dashboard Cite

Schizophrenia is characterized by subtle but well-replicated total and regional (frontal and temporal) brain tissue volume deficits. Studies of individuals at-risk for developing schizophrenia suggest that the onset of brain volume decrement may closely pre-date overt manifestations of schizophrenia, making brain volume abnormalities potential predictors for early identification. In an ongoing longitudinal morphometric MRI study of young, nonpsychotic first-or second-degree relatives of schizophrenia probands, we compared brain volumes in 46 relatives who are still within age range for developing schizophrenia against comparison groups of 46 schizophrenia patients and 46 healthy volunteers without family history of schizophrenia. Relatives had similar brain volume abnormalities as schizophrenia patients albeit less severe. Relatives had significantly larger whole brain, frontal, temporal and parietal gray matter (GM) volumes than patients. Relatives also had significantly smaller frontal GM volumes than healthy volunteers. Both relatives and patients had significantly larger whole brain WM (specifically parietal WM) volumes compared to healthy volunteers. Abnormally greater WM volumes in relatives and patients are suggestive of genetically-mediated dysmaturation of the age-expected myelination during adolescence through mid adulthood. On prodromal symptoms assessed in relatives one year after MRI brain scans, initial GM deficits as well as larger WM volumes correlated significantly with greater severity of subsequent prodromal symptoms. Together with previous genetic high-risk studies of adolescent or young adult relatives, these findings indicate that premorbid MRI brain abnormalities may be of predictive value for the early identification of schizophrenia.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MRI brain volume abnormalities in young, nonpsychotic relatives of schizophrenia probands are associated with subsequent prodromal symptoms

2007

Schizophrenia Research

View full text Add to dashboard Cite

show abstract

“…Family-based and longitudinal studies implicate developmental perturbations in a range of conditions, including behavior disorders, substance abuse, mood disorders, and psychoses (1)(2)(3). However, virtually all research on developmental neurobiology focuses on schizophrenia, where data implicate a neural circuit connecting the dorsolateral prefrontal cortex, striatum, and hippocampus (4,5). Neurocognitive correlates of schizophrenia, such as deficient working memory, are thought to result from dysfunction in this circuit (6).…”

mentioning

confidence: 99%

Limbic hyperactivation during processing of neutral facial expressions in children with bipolar disorder

Rich

Vinton

Roberson‐Nay

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

279

303

View full text Add to dashboard Cite

Reflecting a paradigm shift in clinical neuroscience, many chronic psychiatric illnesses are now hypothesized to result from perturbed neural development. However, most work in this area focuses on schizophrenia. Here, we extend this paradigm to pediatric bipolar disorder (BD), thus demonstrating traction in the developmental psychobiology perspective. To study amygdala dysfunction, we examined neural mechanisms mediating face processing in 22 youths (mean age 14.21 ؎ 3.11 yr) with BD and 21 controls of comparable age, gender, and IQ. Event-related functional MRI compared neural activation when attention was directed to emotional aspects of faces (hostility, subjects' fearfulness) vs. nonemotional aspects (nose width). Compared with controls, patients perceived greater hostility in neutral faces and reported more fear when viewing them. Also, compared with controls, patients had greater activation in the left amygdala, accumbens, putamen, and ventral prefrontal cortex when rating face hostility, and greater activation in the left amygdala and bilateral accumbens when rating their fear of the face. There were no between-group behavioral or neural differences in the nonemotional conditions. Results implicate deficient emotion-attention interactions in the pathophysiology of BD in youth and suggest that developmental psychobiology approaches to chronic mental illness have broad applicability.amygdala ͉ faces ͉ functional MRI R ecently, psychology and psychiatry have witnessed a major paradigm shift: virtually all chronic adult mental illnesses are now thought to result from long-term perturbations in neural development. Two lines of research support this perspective: family-based͞longitudinal studies and neurobiological studies. Family-based and longitudinal studies implicate developmental perturbations in a range of conditions, including behavior disorders, substance abuse, mood disorders, and psychoses (1-3). However, virtually all research on developmental neurobiology focuses on schizophrenia, where data implicate a neural circuit connecting the dorsolateral prefrontal cortex, striatum, and hippocampus (4, 5). Neurocognitive correlates of schizophrenia, such as deficient working memory, are thought to result from dysfunction in this circuit (6). An important next step is the extension of the developmental neurobiological approach to other mental illnesses and other neural systems associated with information processing and emotion regulation.For several reasons, bipolar disorder (BD) is an ideal illness in which to expand the emerging developmental paradigm by conducting neurobiologically oriented developmental research. BD causes marked disruption in social, academic, and family function. Major questions persist concerning the boundaries of the condition in children; neurobiological data might ultimately resolve them. Most importantly, research in adult patients and animals implicates a circuit encompassing the amygdala, striatum, and ventral prefrontal cortex (VPFC) in the pathophysiology of BD (7). This circu...

show abstract

“…En pacientes esquizofrénicos y familiares de primer grado 35 , así como en el trastorno esquizoafectivo, también se han descrito alteraciones de la latencia y la precisión de los MSs dirigidos a un estímulo (prosacádicos) y de los movimientos de persecución, con retraso en el inicio y lentificación e intrusiones sacádicas en el curso de los mismos 36 . Las alteraciones oculomotoras se consideran un marcador biológico de esquizofrenia aplicable a la detección precoz de personas con riesgo de desarrollar la enfermedad 37 .…”

Section: Trastornos Oculomotores En Patología Psiquiátricaunclassified

Physiopathology and recording techniques of the ocular movements

Gila

Villanueva

Cabeza

2010

An Sist Sanit Navar

View full text Add to dashboard Cite

RESUMENEn el control de la motilidad ocular intervienen varios sistemas funcionales. Los reflejos vestíbulo-oculares y optocinéticos son respuestas automáticas para compensar los movimientos de la cabeza y del entorno visual y poder estabilizar la imagen retiniana sobre un determinado punto de fijación. Los movimientos sacádicos son rápidos desplazamientos de la fijación de un punto a otro del campo visual. Los movimientos de persecución lenta consisten en el seguimiento de estí-mulos móviles con la mirada. Finalmente, existen movimientos involuntarios de muy escasa amplitud que se producen durante el mantenimiento de la fijación. Cada modalidad funcional de movimiento depende de circuitos neuronales específicos que trabajan coordinadamente para codificar la contracción de los músculos oculomotores correspondiente a la posición adecuada en cada momento. Estos sistemas neuronales pueden verse alterados por múltiples procesos neurológicos de diferente naturaleza y localización dando lugar a una variada gama de trastornos oculomotores. Se revisan los aspectos más destacados de la fisiopatología y de los sistemas de registro de los movimientos oculares.Palabras clave. Movimientos oculares. Sacadas. Seguimiento ocular. Espiga presacádica. Supresión sacádica. ABSTRACTA number of functional systems are involved in the control of eye movements. The vestibulo-ocular and optokinetic reflexes are automatic responses that compensate for the movements of the head and those of the visual environment in order to stabilize the retinal image on a given fixation point. The saccadic movements are quick displacements of fixation from one to another point in the visual field. The smooth pursuit movements consist in the gaze following a moving target. Finally, there are some involuntary movements of very small amplitude during fixation maintenance. Each functional modality of movement depends on specific neuronal circuits that work in a coordinated manner for encoding the contraction of the oculomotor muscles to reach an adequate position at every moment. These neuronal systems can be altered by many neurological processes of different kinds and localizations, causing a broad variety of oculomotor disturbances. The most salient aspects of the physiopathology and the recording systems of eye movements are reviewed.

show abstract

Premorbid indicators and risk for schizophrenia: A selective review and update

Cited by 130 publications

References 83 publications

MRI brain volume abnormalities in young, nonpsychotic relatives of schizophrenia probands are associated with subsequent prodromal symptoms

MRI brain volume abnormalities in young, nonpsychotic relatives of schizophrenia probands are associated with subsequent prodromal symptoms

Limbic hyperactivation during processing of neutral facial expressions in children with bipolar disorder

Physiopathology and recording techniques of the ocular movements

Contact Info

Product

Resources

About