Pathophysiology of NSS in ADHD

Pasini, Augusto; D’Agati, Elisa

doi:10.1080/15622970902789148

Cited by 32 publications

(36 citation statements)

References 63 publications

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“…It is clear that there is an alteration in the neural networks and a possible central role of dopamine for sensory problems that cannot be linked to specific cerebral lesions in children with ADHD 14. One of the prominent neuroanatomical markers for children and adolescents with ADHD is widespread cortical thickness reductions 15.…”

Section: Introductionmentioning

confidence: 99%

Sensory Processing Problems in Children with ADHD, a Systematic Review

Ghanizadeh

2011

Psychiatry Investig

215

131

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One of the most common psychiatric disorders in children is attention deficit hyperactivity disorder (ADHD). Its course and outcome are heterogeneous. Sensory processing problems impact the nature of response to daily events. ADHD and sensory problems may occur together and interact. No published review article about sensory processing problems in children with ADHD were found. A systematic search, conducted on Pub-Med (up to January 2010), and Google Scholar, yielded 255 abstracts on sensory processing problems in children including 11 studies about sensory problems in children with ADHD. Sensory processing problems in children with ADHD is not a well studied area. Sensory processing problems in children with ADHD are more common than in typically developing children. Findings do not support that ADHD subtypes are distinct disorders with regard to sensory processing problems. However, co-morbidity with oppositional defiant disorder and anxiety are predictors of more severe sensory processing problems in children with ADHD.

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Section: Introductionmentioning

confidence: 99%

Sensory Processing Problems in Children with ADHD, a Systematic Review

Ghanizadeh

2011

Psychiatry Investig

215

131

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“…However, marked improvement or complete resolution of NSS following treatment with MPH was described (Lerer and Lerer, 1976). More research is needed to assess the sensory and motor soft signs associated with ADHD and to integrate clinical evidence with neuroimaging findings, neuropsychological dysfunction and pharmacological effects of the drugs commonly used to treat the disorder (Pasini and D'Agati, 2009). …”

Section: Role Of Methylphenidate On Synaptic Plasticity and Myelinationmentioning

confidence: 99%

“…In addition to the main symptoms of inattention, impulsiveness and hyperactivity, neurological soft signs (NSS) are often associated with ADHD (Pasini and D'Agati, 2009). NSS are discrete motor and sensory disorders that cannot be linked to specific cerebral lesions (Shafer et al, 1983).…”

Section: Introductionmentioning

confidence: 99%

Overflow movements and white matter abnormalities in ADHD

D’Agati

Casarelli

Pitzianti

et al. 2010

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Multiple motor abnormalities have been identified in some children with Attention Deficit/Hyperactivity Disorder (ADHD). These include persistence of overflow movements, impaired timing of motor responses and deficits in fine motor abilities. Motor overflow is defined as co-movement of body parts not specifically needed to efficiently complete a task. The presence of age-inappropriate overflow may reflect immaturity of the cortical systems involved in automatic motor inhibition. Theories on overflow movements consistently implicate impairments in white matter (WM) tracts, including the corpus callosum. WM connections might be altered selectively in brain networks and thus influence motor behaviours. We reviewed the scientific contributions on overflow movements and WM abnormalities in ADHD. They suggest that WM abnormalities in motor/premotor circuits, which are important for motor response inhibition, might be responsible for overflow movements in patients with ADHD.

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“…Converging evidence indicates that the pathophysiology of ADHD has multiple origins [26][27][28][29][30][31][32] ; for instance, norepinephrine (NE) has long been implicated [33,34] . In this paper, we review research progress in the relevant fi elds, focusing on the potential relationship between prefrontal α 2A -adrenoceptors and ADHD in nonhuman primates [35][36][37][38][39] .…”

Section: Introductionmentioning

confidence: 99%

Prefrontal cortical α2A-adrenoceptors and a possible primate model of attention deficit and hyperactivity disorder

Sun

Luo

et al. 2015

Neurosci. Bull.

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Attention deficit and hyperactivity disorder (ADHD), a prevalent syndrome in children worldwide, is characterized by impulsivity, inappropriate inattention, and/or hyperactivity. It seriously afflicts cognitive development in childhood, and may lead to chronic under-achievement, academic failure, problematic peer relationships, and low self-esteem. There are at least three challenges for the treatment of ADHD. First, the neurobiological bases of its symptoms are still not clear. Second, the commonly prescribed medications, most showing short-term therapeutic efficacy but with a high risk of serious side-effects, are mainly based on a dopamine mechanism. Third, more novel and effi cient animal models, especially in nonhuman primates, are required to accelerate the development of new medications. In this article, we review research progress in the related fi elds, focusing on our previous studies showing that blockade of prefrontal cortical α 2A -adrenoceptors in monkeys produces almost all the typical behavioral symptoms of ADHD.Keywords: prefrontal cortex; α 2A -adrenoceptors; cognitive functions; attention defi cit and hyperactivity disorder; animal models ·Review· IntroductionAttention deficit and hyperactivity disorder (ADHD) is one of the most prevalent childhood neurodevelopmental conditions, affecting 3-5% of grade-school children worldwide [1] . It is characterized by i nappropriate levels of inattention, i mpulsivity, and/or hyperactivity [2][3][4] . These symptoms develop in childhood, and can persist into adolescence and adulthood [5] . ADHD seriously affects cognitive development [6][7][8] , and, without appropriate treatment, has consequences for the risk of anxiety, substance abuse, and depression in adulthood [ 2, 5, 9] .T he neurobiological bases o f ADHD symptoms are still not clear [10] . Clarifying them can help better understand the biological vulnerabilities that may underlie ADHD in a specifi c patient and how to modulate the responses to treatment, thereby contributing to better and more effective therapy.It has been suggested that the symptoms involve a dopaminergic mechanism in the prefrontal cortex (PFC) and striatum [11, 12] . Experimentally decreased dopamine (DA) release in the PFC results in ADHD-like symptoms [13, 14] .To date, DA dysregulation is thought to be central to the neurobiology of ADHD, and its pharmacological treatment, such as m ethylphenidate (MPH, i.e. Ritalin) [15][16][17] , levels the DA c oncentration in the synapse and extrasynaptic space in the PFC as a blocker of the DA transporter. MPH ameliorates inappropriate inattention [18][19][20] , decreases impulsivity [21] , and enhances inhibitory control [22] . However, as MPH is a prescription psychostimulant, there are strong concerns over drug dependence, paranoia, schizophrenia, and behavioral sensitization that might be caused by longterm therapy, similar to other stimulants [23][24][25].Converging evidence indicates that the pathophysiology of ADHD has multiple origins [26][27][28][29][30][31][32] ; for i...

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Pathophysiology of NSS in ADHD

Cited by 32 publications

References 63 publications

Sensory Processing Problems in Children with ADHD, a Systematic Review

Sensory Processing Problems in Children with ADHD, a Systematic Review

Overflow movements and white matter abnormalities in ADHD

Prefrontal cortical α2A-adrenoceptors and a possible primate model of attention deficit and hyperactivity disorder

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