Specific neurobiological mechanisms underlie motor clumsiness
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The retrieved literature notes that motor difficulties or neurological signs of clumsiness occur in conditions like ADHD, Asperger syndrome, and schizophrenia, but indicates that specific neurobiological mechanisms explaining these symptoms remain insufficiently understood.
Attention Deficit Hyperactivity Disorder (ADHD) is the most common neurobehavioural disorder of childhood. Motor performance appears to be impaired for an important sub-set of this population.This structured review draws attention to the neurological mechanisms that could potentially explain these difficulties.In August 2010, Medline, PsychINFO and Embase databases were searched with keywords related to ADHD, neuroimaging modalities and motor performance.Four studies were retrieved that examined both motor performance and possible neural substrates. Each study explored different hypotheses and no common conclusion is emerging. The cortical activation dysregulation hypothesis, the cerebellar dysfunction hypothesis and the delayed white matter maturation hypothesis were proposed, applying combinations of motor observations and neuroimaging findings.Published literature to date is insufficient to confirm specific hypotheses. Additional studies coupling discrete motor evaluations to neuroimaging techniques are needed in children with ADHD to better understand the neurobiological mechanisms of their motor difficulties.
Asperger syndrome in 23 Swedish children.
Twenty-three Swedish children aged five to 18 years who fulfilled specific criteria for Asperger syndrome were examined and compared with an age- and IQ-matched group with infantile autism. The boy:girl ratio was 10:1. Less than 10 per cent were mentally retarded and 17 per cent were of above-average intelligence. Apart from motor clumsiness (very common in the Asperger group) and reduced optimality in the prenatal and perinatal periods (more common in the autistic group), there was very little in the clinical or neurobiological backgrounds to suggest a clear distinction between Asperger syndrome and infantile autism.
Published in Developmental medicine and child neurology (1989)
Rajna Knez,1– 3 Dejan Stevanovic,1 Elisabeth Fernell,1 Christopher Gillberg1 1Gillberg Neuropsychiatry Centre, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; 2Department of Pediatrics, Skaraborg Hospital, Skövde, Sweden; 3School of Health Sciences, University of Skövde, Skövde, SwedenCorrespondence: Rajna Knez, Gillberg Neuropsychiatry Centre, Institute of Neuroscience and Physiology, Sahlgrenska Academy, University of Gothenburg, Kungsgatan 12, vån 2, Göteborg, 41119, Sweden, Email rajna.knez@gu.seAbstract: Early Symptomatic Syndromes Eliciting Neurodevelopmental Clinical Examinations (ESSENCE) is an umbrella term covering a wide range of neurodevelopmental difficulties and disorders. Thus, ESSENCE includes attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), and other neurodevelopmental disorders (NDDs) and difficulties, with a variety of symptoms in cognitive, motor, sensory, social, arousal, regulatory, emotional, and behavioral developmental domains, frequently co-occurring and likely having partly common neurobiological substrates. The ESSENCE concept is a clinical paradigm that promotes organizing NDDs in everyday clinical practice according to their coexistence, symptom dimensions overlapping, and treatment possibilities. Despite increased knowledge regarding NDDs, the neurobiological mechanisms that underlie them and other ESSENCE-related problems, are not well understood. With
therapy is of particular help. Neurological soft signs of clumsiness and loss of fine motor movement are often found in schizophrenia, which may resolve
Schizophrenia is a mental disorder characterized variously by hallucinations (typically, hearing voices), delusions, disorganized thinking or behavior, and flat or inappropriate affect. Symptoms develop gradually and typically begin during young adulthood. There is no objective diagnostic test; diagnosis is based on observed behavior, a psychiatric history that includes the person's reported exper
An estimated 70% of those with schizophrenia have cognitive deficits, and these are most pronounced in early-onset and late-onset illness. These are often evident long before the onset of illness in the prodromal stage, and may be present in childhood or early adolescence. They are core features but not considered core symptoms,…
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A 2015 Cochrane review found unclear evidence of benefit from brain stimulation techniques to treat the positive symptoms of schizophrenia, in particular auditory verbal hallucinations (AVHs). Most studies focus on transcranial direct-current stimulation (tDCM), and repetitive transcranial magnetic stimulation (rTMS). Techniques based on focused ultrasound for deep brain stimulation could provide insight for the treatment of AVHs.
The study of potential biomarkers that would help in diagnosis and treatment of schizophrenia is an active area of research as of 2020. Possible biomarkers include markers of inflammation, neuroimaging, brain-derived neurotrophic factor (BDNF), and speech analysis. Some markers such as C-reactive protein are useful in detecting levels of inflammation implicated in some psychiatric disorders but they are not disorder-specific. Other inflammatory cytokines are found to be elevated in first episode psychosis and acute relapse that are normalized after treatment with antipsychotics, and these may be considered as state markers. Deficits in sleep spindles in schizophre
Cognitive impairments do not usually respond to antipsychotics, and there are a number of interventions that are used to try to improve them; cognitive remediation therapy is of particular help. Neurological soft signs of clumsiness and loss of fine motor movement are often found in schizophrenia, which may resolve with effective treatment of FEP. === Onset === Onset typically occurs between the late teens and early 30s, with the peak incidence occurring in males in the early to mid-twenties, and in females in the late twenties. Onset before the age of 17 is known as early-onset, and before the age of 13, as can sometimes occur, is known as childhood schizophrenia or very early-onset.
These genes code for stress response proteins needed in the control of the HPA axis, and their interaction can affect this axis. Response to stress can cause lasting changes in the function of the HPA axis possibly disrupting the negative feedback mechanism, homeostasis, and the regulation of emotion leading to altered behaviors. The question of how schizophrenia could be primarily genetically influenced, given that people with schizophrenia have lower fertility rates, is a paradox. It is expected that genetic variants that increase the risk of schizophrenia would be selected against, due to their negative effects on reproductive fitness.
Viral infections of the brain during childhood are also linked to a risk of schizophrenia during adulthood. Cat exposure is also associated with an increased
The ICD criteria are typically used in European countries; the DSM criteria are used predominantly in the United States and Canada, and are prevailing in research studies. In practice, agreement between the two systems is high. The current proposal for the ICD-11 criteria for schizophrenia recommends adding self-disorder as a symptom. A major unresolved difference between the two diagnostic systems is that of the requirement in DSM of an impaired functional outcome. WHO for ICD argues that not all people with schizophrenia have functional deficits and so these are not specific for the diagnosis.
It may be necessary to rule out a delirium, which can be distinguished by visual hallucinations, acute onset and fluctuating level of consciousness, and indicates an underlying medical illness. Investigations are not generally repeated for relapse unless there is a specific medical indication or possible adverse effects from antipsychotic medication. In children hallucinations must be separated from typical childhood fantasies. It is difficult to distinguish childhood schizophrenia from autism. == Prevention == Prevention of schizophrenia is difficult as there are no reliable markers for the later development of the disorder.
The study of potential biomarkers that would help in diagnosis and treatment of schizophrenia is an active area of research as of 2020. Possible biomarkers include markers of inflammation, neuroimaging, brain-derived neurotrophic factor (BDNF), and speech analysis. Some markers such as C-reactive protein are useful in detecting levels of inflammation implicated in some psychiatric disorders but they are not disorder-specific. Other inflammatory cytokines are found to be elevated in first episode psychosis and acute relapse that are normalized after treatment with antipsychotics, and these may be considered as state markers.
Deficits in sleep spindles in schizophrenia may serve as a marker of an impaired thalamocortical circuit, and a mechanism for memory impairment. MicroRNAs are highly influential in early neuronal development, and their disruption is implicated in several CNS disorders; circulating microRNAs (cimiRNAs) are found in body fluids such as blood and cerebrospinal fluid, and changes in their levels are seen to relate to changes in microRNA levels in specific regions of brain tissue. These studies suggest that cimiRNAs have the potential to be early and accurate biomarkers in a number of disorders including schizophrenia.
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