Neurocognitive Impairments in Nonpsychotic Parents of Children With Schizophrenia and Attention-Deficit/Hyperactivity Disorder

Asarnow, Robert F.; Nuechterlein, Keith H.; Subotnik, Kenneth L.; Fogelson, David L.; Torquato, Richard D.; Payne, Diana L.; Asamen, Joy; Mintz, Jim; Guthrie, Donald

doi:10.1001/archpsyc.59.11.1053

Cited by 75 publications

(49 citation statements)

References 52 publications

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“…The data suggest that neuromotor, language and verbal memory dysfunctions [20][21][22] as well as some subtle selfperceived cognitive-affective discomforts are increased in SSchP. This finding further confirms previous reports [8,9] on BS in unaffected first-degree relatives of schizophrenics (which differed from controls in the same, but a less marked way as schizophrenics did [8,9]), allowing the sketching out of BSABS subsyndrome patterns across the samples.…”

Section: Discussionsupporting

confidence: 89%

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Subjective Experience of Schizotropic Vulnerability in Siblings of Schizophrenics

Maggini¹,

Raballo

2004

Psychopathology

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Abnormal neuropsychological and cognitive functions in nonpsychotic relatives of schizophrenics are currently the subject of intense interest, mainly because of attention being focused again on the theoretical construct of schizotaxia. Contextually, in recent years the issues of subjective experiences have once again become central and respectable topics in psychopathological research. Among self-experiential disturbances, basic symptoms (BS), stemming from Jaspersian phenomenological psychopathology, are considered the first, protopathic, subjective reverberation of the neurobiological deficit of schizophrenia. Thus BS are expected to be detectable in nonpsychotic relatives of schizophrenia patients. The aim of the present study was to compare the degrees of such anomalous subjective experiences, assessed in siblings of schizophrenic patients, schizophrenia spectrum patients (schizotypals and schizophrenics) and nonclinical controls. Different profiles of BS were obtained in the samples. An increasing gradient of BS ranging from nonclinical to clinical samples, with unaffected siblings in the intermediate position, occurred for some of the BS clusters (i.e. ‘thought, language, perception and motor disturbances’ and ‘impaired bodily sensations’). Other BS clusters (i.e. ‘disorders of emotion and affect’ and ‘increased emotional reactivity’) turned out to be typical of the clinical subgroups, whereas an enhanced tolerance to normal stress significantly distinguished the sibling specimen from the other ones. The heterogeneity of these patterns suggests that BS constellations may be underpinned by different psychopathological processes and that cognitive and bodily BS may be clinical target phenotypes for schizotropic liability screening.

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Section: Discussionsupporting

confidence: 89%

“…Thus, BS are likely to identify subtle expressions of genetic liability to schizophrenia (as well as the neuromotor and neurocognitive abnormalities that aggregate in the nonpsychotic first-degree relatives [10,11,[20][21][22]) subjectively perceived as unelaborated, yet discomforting, interferences in daily experience [24][25][26].…”

Section: Introductionmentioning

confidence: 99%

Subjective Experience of Schizotropic Vulnerability in Siblings of Schizophrenics

Maggini¹,

Raballo

2004

Psychopathology

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“…Cognitive impairments seem to be genetically linked to schizophrenia since non-psychotic parents of childhood-onset schizophrenic patients performed worse in neurocognitive tasks than parents of ADHD children (Asarnow et al, 2002) and relatives of schizophrenic patients revealed a higher percentage of ADHD symptoms (31%; especially higher scores on magical ideation, perceptual aberration and more neurological impairments) than relatives of healthy controls (Keshavan et al, 2003).…”

Section: Comorbid Associations Of Schizophrenia and Adhd?mentioning

confidence: 99%

Dopaminergic dysbalance in distinct basal ganglia neurocircuits: Implications for the pathophysiology of parkinson’s disease, schizophrenia and attention deficit hyperactivity disorder

Riederer²,

2006

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The basal ganglia form a forebrain system that collects signals from a large part of the neocortex, redistributes these cortical inputs both with respect to one another and with respect to inputs from the limbic system, and then focuses the inputs of this redistributed, integrated signals into particular regions of the frontal lobes and brainstem involved in aspects of motor planning and motor memory. Movement disorders associated with basal ganglia dysfunction comprise a spectrum of abnormalities that range from the hypokinetic disorder (from which Parkinson's disease, PD, is the best-known-example) at one extreme to the hyperkinetic disorder (exemplified by Huntington's disease and hemiballism) at the other. In addition to disorders of movement, major mental disorders including schizophrenic-like states and attention deficit hyperactivity disorder (ADHD) have been linked to abnormalities in the basal ganglia and their allied nuclei. In this paper we discuss recent evidence indicating that a dopamine-induced dysbalance of basal ganglia neurocircuitries may be an important pathophysiological component in PD, schizophrenia and ADHD. According to our model, the deprivation of dopaminergic nigro-striatal input, as in PD, reduces the positive feedback via the direct system, and increases the negative feedback via the indirect system. The critical consequences are an overactivity of the basal ganglia output sites with the resulting inhibition of thalamo-cortical drive. In schizophrenia the serious cognitive deficits might be partly a result of a hyperactivity of the inhibitory dopamine D(2) transmission system. Through this dysinhibition, the thalamus exhibits hyperactivity that overstimulates the cortex resulting in dysfunctions of perception, attention, stimulus distinction, information processing and affective regulation (inducing hallucinations and delusions) and motor disabilities. Recent studies have strongly suggested that a disturbance of the dopaminergic system is also involved in the pathophysiology of ADHD. The most convincing evidence comes from the demonstration of the efficacy of psychostimulants such as the dopamine transporter (DAT) blocker methylphenidate in the symptomatic treatment of ADHD. Genetic studies have shown an association between ADHD and genes involved in dopaminergic neurotransmission (for example the dopamine receptor genes DRD4 and DRD5, and the DAT gene DAT1). DAT knockout mice display a phenotype with increased locomotor activity, which is normalized by psychostimulant treatment. Finally, imaging studies demonstrated an increased density of DAT in the striatum of ADHD patients. Which system is disturbed and whether this system is hyper- or hypoactive is not unambiguously known yet.

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“…Of note, some studies have suggested a link between childhood-onset ADHD and schizophrenia but the nature of this remains unclear (Asarnow et al, 2002;Subotnik et al, 2005). That said, adults with ADHD show a range of psychosocial deficits, which partially overlap with deficits seen in schizophrenia.…”

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confidence: 99%

Decrements in Sustained Attention Across Trials in a Continuous Performance Test

Lysaker

Tsai

Henninger

et al. 2010

Journal of Nervous &Amp; Mental Disease

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Deficits in attention are a stable feature of schizophrenia and likely to interfere with social function. In this study, we explored whether 2 types of attentional dysfunction, increasingly variable and declining reaction times over the course of a continuous performance task, were linked to psychosocial deficits. Participants were 102 adults with schizophrenia spectrum disorders in ongoing outpatient treatment. Concurrent assessments included the Conners' Continuous Performance Test II, the Inventory of Interpersonal Problems, and the Ways of Coping Questionnaire. Analysis of covariance controlling for global performance on the Continuous Performance test suggested that participants with a pattern of increasingly variable performance on the task (n = 14) reported being more domineering and taken advantage of socially, than those whose performance was less variable (n = 88). No differences were found between groups for assessments of coping or between participants who showed a declining vs non-declining reaction time.

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Neurocognitive Impairments in Nonpsychotic Parents of Children With Schizophrenia and Attention-Deficit/Hyperactivity Disorder

Cited by 75 publications

References 52 publications

Subjective Experience of Schizotropic Vulnerability in Siblings of Schizophrenics

Subjective Experience of Schizotropic Vulnerability in Siblings of Schizophrenics

Dopaminergic dysbalance in distinct basal ganglia neurocircuits: Implications for the pathophysiology of parkinson’s disease, schizophrenia and attention deficit hyperactivity disorder

Decrements in Sustained Attention Across Trials in a Continuous Performance Test

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