The role of frontal lobe dysfunction in childhood hyperkinesis

Mattes, Jeffrey A.

doi:10.1016/0010-440x(80)90017-6

Cited by 196 publications

(83 citation statements)

References 46 publications

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“…This study also found that the ADHD group showed regional hypoactivity of attention and motor control areas including the daMCC, superior prefrontal cortex, and premotor cortex. Most ADHD imaging studies have sought to identify localized brain dysfunction, and the prefrontal cortex was one of the first areas to be studied, because of similarities between patients with ADHD and those with frontal lobe injuries (Barkley, 1997;Barkley et al, 1992;Mattes, 1980). Structural imaging studies on ADHD have identified both significantly smaller global cerebral volumes of B3 to 4% in ADHD, as well as specifically smaller prefrontal volumes in ADHD (Seidman et al, 2004b;Valera et al, 2007).…”

Section: Cfp Attention Networkmentioning

confidence: 99%

Attention-Deficit/Hyperactivity Disorder and Attention Networks

Bush

2009

Neuropsychopharmacol

298

251

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Research attempting to elucidate the neuropathophysiology of attention-deficit/hyperactivity disorder (ADHD) has not only shed light on the disorder itself, it has simultaneously provided new insights into the mechanisms of normal cognition and attention. This review will highlight and integrate this bidirectional flow of information. Following a brief overview of ADHD clinical phenomenology, ADHD studies will be placed into a wider historical perspective by providing illustrative examples of how major models of attention have influenced the development of neurocircuitry models of ADHD. The review will then identify major components of neural systems potentially relevant to ADHD, including attention networks, reward/feedbackbased processing systems, as well as a 'default mode' resting state network. Further, it will suggest ways in which these systems may interact and be influenced by neuromodulatory factors. Recent ADHD imaging data will be selectively provided to both illustrate the field's current level of knowledge and to show how such data can inform our understanding of normal brain functions. The review will conclude by suggesting possible avenues for future research.

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Section: Cfp Attention Networkmentioning

confidence: 99%

Attention-Deficit/Hyperactivity Disorder and Attention Networks

Bush

2009

Neuropsychopharmacol

298

251

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“…There is a striking similarity in symptoms between patients with lesions in the prefrontal cortex (PFC) and individuals with ADHD (Benton 1991;Heilman et al 1991;Levin 1938;Mattes 1980), which suggests an important role of the PFC in ADHD. Three studies using magnetic resonance imaging (MRI) found a decreased volume of the right PFC in children with ADHD, while no such result was found regarding the left PFC (Castellanos et al 1996b;Filipek et al 1997;Hynd et al 1990).…”

Section: Functional and Structural Abnormalitiesmentioning

confidence: 99%

“…In addition, patients with frontal brain lesions show some behavioural similarities with ADHD patients (Benton 1991;Heilman et al 1991;Levin 1938;Mattes 1980) and ADHD has been shown to be highly heritable (Bobb et al 2005;Fisher et al 2002;Teicher et al 2000). These findings suggest that ADHD is based on some specific neurobiological dysfunctions.…”

Section: Introductionmentioning

confidence: 99%

Animal models of attention deficit/hyperactivity disorder (ADHD): a critical review

Sontag

Tucha

Walitza

et al. 2010

ADHD Atten Def Hyp Disord

103

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Attention deficit/hyperactivity disorder (ADHD) involves clinically heterogeneous problems including attention deficits, behavioural hyperactivity and impulsivity. Several animal models of ADHD have been proposed, ranging from models with neurotoxic lesions to genetically manipulated animals. An ADHD model is supposed to show phenomenological similarities with the disorder, i.e. it should mimic the three core symptoms (face validity). A model should also conform to an established or hypothesized pathophysiological basis of the disorder (construct validity).Finally, an animal model should be able to predict previously unknown aspects of the neurobiology of ADHD or to provide potential new treatments (predictive validity). The currently proposed models are heterogeneous with regard to their pathophysiological alterations and their ability to mimic behavioural symptoms and to predict response to medication. This might reflect the heterogeneous nature of ADHD. Since the knowledge about the biology of ADHD from human studies is limited, one cannot at present decide which model best represents ADHD or certain ADHD subtypes. Animal models with good face and predictive validity may be useful for investigations of the underlying biological substrates of ADHD. At present, the models in use should be described as animal models of ADHD-like symptoms rather than models of ADHD.

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“…However, in humans, an overresponse to stress can be maladaptive, resulting in the expression or exacerbation of many neuropsychiatric disorders, including a number of features that indicate abnormal functioning of the PFC (Mattes, 1980;Weinberger et al, 1986;Deutch, 1993;Fibiger, 1995). The influence of dopaminergic neurons in the PFC on the PFC functions in neuropsychiatric disorders remains obscure, but some observations support the idea that these neurons play a role in the pathogenesis of certain neuropsychiatric disorders.…”

Section: Clinical Relevancementioning

confidence: 99%

“…All these disorders involve a working memory deficit caused by prefrontal cortical (PFC) dysfunction (Mattes, 1980;Weinberger et al, 1986;Deutch, 1993;Fibiger, 1995). Several antidepressants increase dopamine (DA) levels in the PFC (Tanda et al, 1994), and raising the DA level in patients with Parkinson's disease with L-3,4-dihydroxyphenylalanine improves their working memory deficit (Lange et al, 1992).…”

mentioning

confidence: 99%

Chronic Stress Induces Impairment of Spatial Working Memory Because of Prefrontal Dopaminergic Dysfunction

et al. 2000

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Although the mechanism responsible for cognitive deficits in stress-related neuropsychiatric disorders has been obscure, prefrontal cortical (PFC) dopaminergic dysfunction is thought to be involved. In animals, the mesoprefrontal dopaminergic system is particularly vulnerable to stress, and chronic stress induces working memory impairment. However, the relation between the working memory impairment and altered dopaminergic activity in chronically stressed rats is unclear. Furthermore, the change of dopaminergic activity in the PFC induced by stress is thought to express as a stress response, not as a disorder of organic function. We have previously reported that chronic stress administered by water immersion and restraint for 4 weeks induces a organic disorder such as hippocampal neuronal degeneration. We therefore examined whether chronically stressed (4 weeks) and recovered (10 d) rats show a working memory impairment caused by reduced dopamine (DA) transmission in the PFC, as suspected in the neuropsychiatric disorders. The stress impaired the spatial working memory evaluated by T-maze task and induced a marked reduction of DA transmission concomitant with an increase in DA D1 receptor density in the PFC. This memory impairment was sufficiently ameliorated by intra-PFC infusion of 10 ng SKF 81297, a D1 receptor-specific agonist. Pretreatment with intraperitoneal injection of 20 g/kg SCH 23390, a D1 receptor antagonist, reversed the SKF 81297 response. These results indicate that chronic stress induces working memory impairment through a D1 receptor-mediated hypodopaminergic mechanism in the PFC. These findings provide important information for understanding of the mechanisms underlying PFC dysfunction in stress-related neuropsychiatric disorders.Key words: chronic stress; working memory; prefrontal cortex; dopaminergic neuron; D1 receptor; cognitive deficit Exposure to stress is known to precipitate or exacerbate many neuropsychiatric disorders such as depression, Parkinson's disease, schizophrenia, and others (Schwab and Zieper, 1965;Mazure, 1995). All these disorders involve a working memory deficit caused by prefrontal cortical (PFC) dysfunction (Mattes, 1980;Weinberger et al., 1986;Deutch, 1993;Fibiger, 1995). Several antidepressants increase dopamine (DA) levels in the PFC (Tanda et al., 1994), and raising the DA level in patients with Parkinson's disease with L-3,4-dihydroxyphenylalanine improves their working memory deficit (Lange et al., 1992). These findings suggest that a reduced dopaminergic transmission in the PFC is responsible for the working memory deficits in the neuropsychiatric disorders.In animals, reduced PFC dopaminergic function or blockade of DA receptor in the PFC of monkeys and rats impairs working memory function (Brozoski et al., 1979;Simon et al., 1980;Bubser and Schmidt, 1990), which supports the observations in the neuropsychiatric disorders. In addition, an exposure to acute stress in monkeys or rats has been reported to produce working memory impairment, which can be blocked by...

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The role of frontal lobe dysfunction in childhood hyperkinesis

Cited by 196 publications

References 46 publications

Attention-Deficit/Hyperactivity Disorder and Attention Networks

Attention-Deficit/Hyperactivity Disorder and Attention Networks

Animal models of attention deficit/hyperactivity disorder (ADHD): a critical review

Chronic Stress Induces Impairment of Spatial Working Memory Because of Prefrontal Dopaminergic Dysfunction

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