Neurological soft signs discriminating mood disorders from first episode schizophrenia

Boks, Marco P.; Liddle, Peter F.; Burgerhof, Johannes G. M.; Knegtering, Rikus; Bosch, RJ van den

doi:10.1111/j.1600-0447.2004.00298.x

Cited by 73 publications

(57 citation statements)

References 45 publications

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“…A balance between glutamate and dopamine activity is thus important for undisturbed information processing -hypoglutamatergic and also hyperdopaminergic activity result in reduced activation of the striatum and may induce psychotic symptoms. Boks et al (2004) investigated neurological soft signs in 191 first episode schizophrenic patients, comparing them with mood disorders and healthy controls. Coordination deficits -probably reflecting fronto-cerebellar malfunctions -increased reflexes, dyskinesia and surprisingly also catatonia were not significantly increased compared to mood disorders.…”

Section: Abnormalities Of Neuronal Circuits In Schizophreniamentioning

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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Section: Abnormalities Of Neuronal Circuits In Schizophreniamentioning

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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“…Neurological soft signs have been observed in patients with disorders other than schizophrenia (Bombin et al, 2005). However, individuals with schizophrenia exhibit more neurological soft signs than patients with substance abuse (Kinney, Yurgelun-Todd, & Woods, 1999;Mohr et al, 1996), bipolar disorder (Kinney et al, 1999), obsessive compulsive disorder (Bolton et al, 1998), nonschizophrenic psychosis , and mood disorders (Krebs, Gut-Fayand, Bourdel, & Olie, 2000;Boks, Liddle, Burgerhof, Knegtering, & van den Bosch 2004). Although neurological soft signs are not unique to schizophrenia, examining these characteristics across the schizotypy continuum may further enhance our ability to identify individuals at risk for schizophrenia and related disorders.…”

Section: Neurological Soft Signs and Schizophreniamentioning

confidence: 99%

Neurological Soft Signs in Psychometrically Identified Schizotypy

Kaczorowski

Barrantes‐Vidal

Kwapil

2010

Schizophrenia Research

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Patients with schizophrenia often exhibit structural brain abnormalities, as well as neurological soft signs, consistent with its conceptualization as a neurodevelopmental disorder. Neurological soft signs are mild, presumably nonlocalizing, neurological impairments that are inferred from performance deficits in domains such as sensory integration, motor coordination, and motor sequencing. The vulnerability for schizophrenia is presumed to be expressed across a broad continuum of impairment referred to as schizotypy. It is hypothesized that nondisordered people along the schizotypy continuum should exhibit elevated rates of neurological soft signs. The present study examined the relation of psychometrically identified positive and negative schizotypy with neurological soft signs using the Neurological Evaluation Scale (NES) in a nonclinically ascertained sample of young adults (n = 177). As hypothesized, negative, but not positive, schizotypy was related to increased neurological soft signs in tasks that assessed fine and gross motor coordination, motor sequencing, eye movement abnormalities, and memory recall. However, positive schizotypy was associated with increased neurological soft signs in tasks related to sensory integration dysfunction. In general, the positive x negative schizotypy interaction term was unrelated to individual neurological soft sign tasks. The findings support: a) the theory that the vulnerability for schizophrenia is expressed across a broad continuum of subclinical and clinical impairment referred to as schizotypy; b) the multidimensional structure of schizotypy; and c) the notion that schizotypy is an appropriate construct for understanding the etiology and development of schizophrenia-spectrum disorders. NEUROLOGICAL SOFT SIGNS IN PSYCHOMETRICALLY IDENTIFIEDSCHIZOTYPY by

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“…Indeed, employing a meta-analysis examining neurocognitive deficits, Heinrichs and Zakzanis (118) observed that motor abnormalities exhibited the second highest effect size. Importantly, it appears that first episode, drug naïve patients exhibit motor control abnormalities in excess of healthy controls (123) and there is little relationship between the level/duration of antipsychotic treatment and motor abnormalities (26, although see 124), highlighting that these signs are most probably not a consequence of anti-psychotic medication.…”

Section: Schizophreniamentioning

confidence: 99%

The cerebellum and motor dysfunction in neuropsychiatric disorders

Gowen

Miall

2007

MCER

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The cerebellum is densely interconnected with sensory-motor areas of the cerebral cortex, and in man, the great expansion of the association areas of cerebral cortex is also paralleled by an expansion of the lateral cerebellar hemispheres. It is therefore likely that these circuits contribute to non-motor cognitive functions, but this is still a controversial issue. One approach is to examine evidence from neuropsychiatric disorders of cerebellar involvement. In this review, we narrow this search to test whether there is evidence of motor dysfunction associated with neuropsychiatric disorders consistent with disruption of cerebellar motor function. While we do find such evidence, especially in autism, schizophrenia and dyslexia, we caution that the restricted set of motor symptoms does not suggest global cerebellar dysfunction. Moreover, these symptoms may also reflect involvement of other, extra-cerebellar circuits and detailed examination of specific sub groups of individuals within each disorder may help to relate such motor symptoms to cerebellar morphology.

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Neurological soft signs discriminating mood disorders from first episode schizophrenia

Abstract: NSS are the result of circuitry dysfunctions rather than overall dysfunction and a particular set of NSS shows specificity for schizophrenia.

Cited by 73 publications

References 45 publications

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

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

Neurological Soft Signs in Psychometrically Identified Schizotypy

The cerebellum and motor dysfunction in neuropsychiatric disorders

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