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TIAttention-deficit hyperactivity disorder. AUBiederman J; Faraone SV SOLancet 2005 Jul 16-22;366(9481):237-48. Attention-deficit hyperactivity disorder (ADHD) is a disorder of inattention, impulsivity, and hyperactivity that affects 8-12% of children worldwide. Although the rate of ADHD falls with age, at least half of children with the disorder will have impairing symptoms in adulthood. Twin, adoption, and molecular genetic studies show ADHD to be highly heritable, and other findings have recorded obstetric complications and psychosocial adversity as predisposing risk factors. Converging evidence from animal and human studies implicates the dysregulation of frontal-subcortical-cerebellar catecholaminergic circuits in the pathophysiology of ADHD, and molecular imaging studies suggest that abnormalities of the dopamine transporter lead to impaired neurotransmission. Studies during the past decade have shown the safety and effectiveness of new non-stimulant drugs and long-acting formulations of methylphenidate and amfetamine. Other investigations have also clarified the appropriate role of targeted psychosocial treatments in the context of ongoing pharmacotherapy. ADPediatric Psychopharmacology Unit of the Child Psychiatry Service, Massachusetts General Hospital, and Harvard Medical School, Boston, MA 02114, USA. [email protected] PMID16023516
TIADHD Candidate Gene Study in a Population-Based Birth Cohort: Association with DBH and DRD2. AUNyman ES; Ogdie MN; Loukola A; Varilo T; Taanila A; Hurtig T; Moilanen IK; Loo SK; McGough JJ; Jarvelin MR; Smalley SL; Nelson SF; Peltonen L SOJ Am Acad Child Adolesc Psychiatry. 2007 Dec;46(12):1614-1621. OBJECTIVE:: Attention-deficit/hyperactivity disorder (ADHD) is a common childhood-onset disorder with a significant impact on public health. Although a genetic contribution to risk is evident, predisposing genetic determinants remain largely unknown despite extensive research. So far, the most promising candidate genes have been those involved in dopamine and serotonin pathways. This study tests a series of allelic variants within such candidate genes to determine their potential influence on ADHD susceptibility. METHOD:: We used a population sample ascertained from a birth cohort of a subpopulation of Finland, characterized by founder effect and isolation, thus minimizing genetic heterogeneity. The subjects were systematically ascertained using DSM-IV diagnostic criteria for ADHD from the Northern Finland Birth Cohort 1986 of more than 9,000 individuals, resulting in the study sample of 188 ADHD cases and 166 controls. We genotyped markers in 13 candidate genes, including critical components of dopamine and serotonin pathways. RESULTS:: We report evidence for association of ADHD with allelic variants of the dopamine beta-hydroxylase (DBH) and dopamine receptor D2 (DRD2) genes. CONCLUSIONS:: Our study supports the involvement of the dopamine pathway in the etiology of ADHD; specifically the genes DBH and DRD2 deserve more attention in further studies. ADMs. Nyman, Drs. Loukola, Varilo, and Peltonen are with the National Public Health Institute; Drs. Ogdie, Loo, McGough, Smalley, and Nelson are with the University of California, Los Angeles; Drs. Varilo and Peltonen are with the Broad Institute and the University of Helsinki; Ms. Hurtig, Drs. Taanila, Moilanen, and Jarvelin are with the University of Oulu; and Dr. Jarvelin is with the Imperial College London. PMID18030083
TIBrain imaging of attention deficit/hyperactivity disorder. AUGiedd JN; Blumenthal J; Molloy E; Castellanos FX SOAnn N Y Acad Sci 2001 Jun;931:33-49. Advances in imaging technology allow unprecedented access to the anatomy and physiology of the living, growing human brain. Anatomical imaging studies of individuals with attention deficit/hyperactivity disorder (ADHD) consistently point to involvement of the frontal lobes, basal ganglia, corpus callosum, and cerebellum. Imaging studies of brain physiology also support involvement of right frontal-basal ganglia circuitry with a powerful modulatory influence from the cerebellum. Although not currently of diagnostic utility, further extension and refinement of these findings may offer hope for greater understanding of the core nature of ADHD and possible subtyping to inform treatment interventions. ADChild Psychiatry Branch, National Institute of Mental Health, Building 10, Room 4C110, 10 Center Drive, MSC 1367, Bethesda, MD 20892, USA. [email protected] PMID11462751
TIDevelopmental trajectories of brain volume abnormalities in children and adolescents with attention-deficit/hyperactivity disorder. AUCastellanos FX; Lee PP; Sharp W; Jeffries NO; Greenstein DK; Clasen LS; Blumenthal JD; James RS; Ebens CL; Walter JM; Zijdenbos A; Evans AC; Giedd JN; Rapoport JL SOJAMA 2002 Oct 9;288(14):1740-8. CONTEXT: Various anatomic brain abnormalities have been reported for attention-deficit/hyperactivity disorder (ADHD), with varying methods, small samples, cross-sectional designs, and without accounting for stimulant drug exposure. OBJECTIVE: To compare regional brain volumes at initial scan and their change over time in medicated and previously unmedicated male and female patients with ADHD and healthy controls. DESIGN, SETTING, AND PARTICIPANTS: Case-control study conducted from 1991-2001 at the National Institute of Mental Health, Bethesda, Md, of 152 children and adolescents with ADHD (age range, 5-18 years) and 139 age- and sex-matched controls (age range, 4.5-19 years) recruited from the local community, who contributed 544 anatomic magnetic resonance images. MAIN OUTCOME MEASURES: Using completely automated methods, initial volumes and prospective age-related changes of total cerebrum, cerebellum, gray and white matter for the 4 major lobes, and caudate nucleus of the brain were compared in patients and controls. RESULTS: On initial scan, patients with ADHD had significantly smaller brain volumes in all regions, even after adjustment for significant covariates. This global difference was reflected in smaller total cerebral volumes (-3.2%, adjusted F(1,280) = 8.30, P =.004) and in significantly smaller cerebellar volumes (-3.5%, adjusted F(1,280) = 12.29, P =.001). Compared with controls, previously unmedicated children with ADHD demonstrated significantly smaller total cerebral volumes (overall F(2,288) = 6.65; all pairwise comparisons Bonferroni corrected, -5.8%; P =.002) and cerebellar volumes (-6.2%, F( 2,288) = 8.97, P<.001). Unmedicated children with ADHD also exhibited strikingly smaller total white matter volumes (F(2,288) = 11.65) compared with controls (-10.7%, P<.001) and with medicated children with ADHD (-8.9%, P<.001). Volumetric abnormalities persisted with age in total and regional cerebral measures (P =.002) and in the cerebellum (P =.003). Caudate nucleus volumes were initially abnormal for patients with ADHD (P =.05), but diagnostic differences disappeared as caudate volumes decreased for patients and controls during adolescence. Results were comparable for male and female patients on all measures. Frontal and temporal gray matter, caudate, and cerebellar volumes correlated significantly with parent- and clinician-rated severity measures within the ADHD sample (Pearson coefficients between -0.16 and -0.26; all P values were <.05). CONCLUSIONS: Developmental trajectories for all structures, except caudate, remain roughly parallel for patients and controls during childhood and adolescence, suggesting that genetic and/or early environmental influences on brain development in ADHD are fixed, nonprogressive, and unrelated to stimulant treatment. ADChild Psychiatry Branch, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, USA. [email protected] PMID12365958
TICortical abnormalities in children and adolescents with attention-deficit hyperactivity disorder. AUSowell ER; Thompson PM; Welcome SE; Henkenius AL; Toga AW; Peterson BS SOLancet 2003 Nov 22;362(9397):1699-707. BACKGROUND: Results of structural brain imaging studies of patients with attention-deficit hyperactivity disorder have shown subtle reductions in total brain volume and in volumes of the right frontal lobe and caudate nucleus. Although various conventional volumetric and voxel-based methods of image analysis have been used in these studies, regional brain size and grey-matter abnormalities have not yet been mapped over the entire cortical surface in patients with this disorder. We aimed to map these features in patients with attention-deficit hyperactivity disorder. METHODS: We used high-resolution MRI and surface-based, computational image analytic techniques to map regional brain size and grey-matter abnormalities at the cortical surface in a group of 27 children and adolescents with attention-deficit hyperactivity disorder and 46 controls, who were group-matched by age and sex. FINDINGS: Abnormal morphology was noted in the frontal cortices of patients with attention-deficit hyperactivity disorder, with reduced regional brain size localised mainly to inferior portions of dorsal prefrontal cortices bilaterally. Brain size was also reduced in anterior temporal cortices bilaterally. Prominent increases in grey matter were recorded in large portions of the posterior temporal and inferior parietal cortices bilaterally. INTERPRETATION: The frontal, temporal, and parietal regions are heteromodal association cortices that constitute a distributed neural system, which subserves attention and behavioural inhibition. We have identified region-specific anatomical abnormalities in cortical components of attentional systems, which may help better account for the symptoms of attention-deficit hyperactivity disorder. ADUniversity of California at Los Angeles, Laboratory of Neuro Imaging, Department of Neurology, 710 Westwood Plaza, Room 4-238, Los Angeles, CA 90095-1769, USA. [email protected] PMID14643117
TIDorsolateral prefrontal and anterior cingulate cortex volumetric abnormalities in adults with attention-deficit/hyperactivity disorder identified by magnetic resonance imaging. AUSeidman LJ; Valera EM; Makris N; Monuteaux MC; Boriel DL; Kelkar K; Kennedy DN; Caviness VS; Bush G; Aleardi M; Faraone SV; Biederman J SOBiol Psychiatry. 2006 Nov 15;60(10):1071-80. Epub 2006 Jul 28. OBJECTIVES: Gray and white matter volume deficits have been reported in a number of studies of children with attention-deficit/hyperactivity disorder (ADHD); however, there is a paucity of structural magnetic resonance imaging (MRI) studies of adults with ADHD. This structural MRI study used an a priori region of interest approach. METHODS: Twenty-four adults with DSM-IV ADHD and 18 healthy controls comparable on age, socioeconomic status, sex, handedness, education, IQ, and achievement test performance had an MRI on a 1.5T Siemens scanner. Cortical and sub-cortical gray and white matter were segmented. Image parcellation divided the neocortex into 48 gyral-based units per hemisphere. Based on a priori hypotheses we focused on prefrontal, anterior cingulate cortex (ACC) and overall gray matter volumes. General linear analyses of the volumes of brain regions, adjusting for age, sex, and total cerebral volumes, were used to compare groups. RESULTS: Relative to controls, ADHD adults had significantly smaller overall cortical gray matter, prefrontal and ACC volumes. CONCLUSIONS: Adults with ADHD have volume differences in brain regions in areas involved in attention and executive control. These data, largely consistent with studies of children, support the idea that adults with ADHD have a valid disorder with persistent biological features. ADHarvard Medical School, Department of Psychiatry, Center for Morphometric Analysis, Massachusetts General Hospital, Fruit Street, Boston, MA 02114, USA. [email protected] PMID16876137
TICortical thinning of the attention and executive function networks in adults with attention-deficit/hyperactivity disorder. AUMakris N; Biederman J; Valera EM; Bush G; Kaiser J; Kennedy DN; Caviness VS; Faraone SV; Seidman LJ SOCereb Cortex. 2007 Jun;17(6):1364-75. Epub 2006 Aug 18. Attention-deficit/hyperactivity disorder (ADHD) has been associated with structural alterations in brain networks influencing cognitive and motor behaviors. Volumetric studies in children identify abnormalities in cortical, striatal, callosal, and cerebellar regions. In a prior volumetric study, we found that ADHD adults had significantly smaller overall cortical gray matter, prefrontal, and anterior cingulate volumes than matched controls. Thickness and surface area are additional indicators of integrity of cytoarchitecture in the cortex. To expand upon our earlier results and further refine the regions of structural abnormality, we carried out a structural magnetic resonance imaging study of cortical thickness in the same sample of adults with ADHD (n = 24) and controls (n = 18), hypothesizing that the cortical networks underlying attention and executive function (EF) would be most affected. Compared with healthy adults, adults with ADHD showed selective thinning of cerebral cortex in the networks that subserve attention and EF. In the present study, we found significant cortical thinning in ADHD in a distinct cortical network supporting attention especially in the right hemisphere involving the inferior parietal lobule, the dorsolateral prefrontal, and the anterior cingulate cortices. This is the first documentation that ADHD in adults is associated with thinner cortex in the cortical networks that modulate attention and EF. ADDepartments of Neurology and Radiology Services, Center for Morphometric Analysis, Health Sciences & Technology Athinoula A. Martinos Center, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02129, USA. [email protected] PMID16920883
TILongitudinal mapping of cortical thickness and clinical outcome in children and adolescents with attention-deficit/hyperactivity disorder. AUShaw P; Lerch J; Greenstein D; Sharp W; Clasen L; Evans A; Giedd J; Castellanos FX; Rapoport J SOArch Gen Psychiatry. 2006 May;63(5):540-9. CONTEXT: Data from a previous prospective study of lobar volumes in children with attention-deficit/hyperactivity disorder (ADHD) are reexamined using a measure of cortical thickness. OBJECTIVE: To determine whether regional differences in cortical thickness or cortical changes across time characterize ADHD and predict or reflect its clinical outcome. DESIGN, SETTING, AND PARTICIPANTS: Longitudinal study of 163 children with ADHD (mean age at entry, 8.9 years) and 166 controls recruited mainly from a local community in Maryland. Participants were assessed with magnetic resonance imaging. Ninety-seven patients with ADHD (60%) had 2 or more images and baseline and follow-up clinical evaluations (mean follow-up, 5.7 years). MAIN OUTCOME MEASURES: Cortical thickness across the cerebrum. Patients with ADHD were divided into better and worse outcome groups on the basis of a mean split in scores on the Children's Global Assessment Scale and persistence/remission of DSM-IV-defined ADHD. RESULTS: Children with ADHD had global thinning of the cortex (mean reduction, -0.09 mm; P=.02), most prominently in the medial and superior prefrontal and precentral regions. Children with worse clinical outcome had a thinner left medial prefrontal cortex at baseline than the better outcome group (-0.38 mm; P=.003) and controls (-0.25 mm; P=.002). Cortical thickness developmental trajectories did not differ significantly between the ADHD and control groups throughout except in the right parietal cortex, where trajectories converged. This normalization of cortical thickness occurred only in the better outcome group. CONCLUSIONS: Children with ADHD show relative cortical thinning in regions important for attentional control. Children with a worse outcome have "fixed" thinning of the left medial prefrontal cortex, which may compromise the anterior attentional network and encumber clinical improvement. Right parietal cortex thickness normalization in patients with a better outcome may represent compensatory cortical change. ADChild Psychiatry Branch, National Institute of Mental Health, Bethesda, MD 20892-1500, USA. [email protected] PMID16651511
TIThe neural correlates of attention deficit hyperactivity disorder: an ALE meta-analysis. AUDickstein SG; Bannon K; Castellanos FX; Milham MP SOJ Child Psychol Psychiatry. 2006 Oct;47(10):1051-62. BACKGROUND: Attention deficit/hyperactivity disorder (ADHD) is one of the most prevalent and commonly studied forms of psychopathology in children and adolescents. Causal models of ADHD have long implicated dysfunction in fronto-striatal and frontal-parietal networks supporting executive function, a hypothesis that can now be examined systematically using functional neuroimaging. The present work provides an objective, unbiased statistically-based meta-analysis of published functional neuroimaging studies of ADHD. METHODS: A recently developed voxel-wise quantitative meta-analytic technique known as activation likelihood estimation (ALE) was applied to 16 neuroimaging studies examining and contrasting patterns of neural activity in patients with ADHD and healthy controls. Voxel-wise results are reported using a statistical threshold of p < .05, corrected. Given the large number of studies examining response inhibition, additional meta-analyses focusing specifically on group differences in the neural correlates of inhibition were included. RESULTS: Across studies, significant patterns of frontal hypoactivity were detected in patients with ADHD, affecting anterior cingulate, dorsolateral prefrontal, and inferior prefrontal cortices, as well as related regions including basal ganglia, thalamus, and portions of parietal cortex. When focusing on studies of response inhibition alone, a more limited set of group differences were observed, including inferior prefrontal cortex, medial wall regions, and the precentral gyrus. In contrast, analyses focusing on studies of constructs other than response inhibition revealed a more extensive pattern of hypofunction in patients with ADHD than those of response inhibition. CONCLUSIONS: To date, the most consistent findings in the neuroimaging literature of ADHD are deficits in neural activity within fronto-striatal and fronto-parietal circuits. The distributed nature of these results fails to support models emphasizing dysfunction in any one frontal sub-region. While our findings are suggestive of the primacy of deficits in frontal-based neural circuitry underlying ADHD, we discuss potential biases in the literature that need to be addressed before such a conclusion can be fully embraced. ADNYU Child Study Center, New York, NY 10016, USA. PMID17073984
TIAttention-deficit/hyperactivity disorder (ADHD) as a noradrenergic disorder. AUBiederman J; Spencer T SOBiol Psychiatry 1999 Nov 1;46(9):1234-42. This review revisits the thesis that a dysregulation of the central noradrenergic networks may underlie the pathophysiology of ADHD. We review the pertinent neurobiological and pharmacological literature on ADHD. The noradrenergic system has been intimately associated with the modulation of higher cortical functions including attention, alertness, vigilance and executive function. Noradrenergic activation is known to profoundly affect the performance of attention, especially the maintenance of arousal, a cognitive function known to be deficient in ADHD. Data from family, adoption, twin, and segregation analysis strongly support a genetic hypothesis for this disorder. Although molecular genetic studies of ADHD are relatively new and far from definitive, several replicated reports have found associations between ADHD with DAT and D4 receptor genes. Brain imaging studies fit well with the idea that dysfunction in fronto-subcortical pathways occurs in ADHD with its underlying dysregulation of noradrenergic function. A wealth of pharmacological data (within and without the stimulant literature) provides strong evidence for selective clinical activity in ADHD for drugs with noradrenergic and dopaminergic pharmacological profiles. Available research provides compelling theoretic, basic biologic and clinical support for the notion that ADHD is a brain disorder of likely genetic etiology with etiologic and pathophysiologic heterogeneity. Neurobiological and pharmacological data provide compelling support for a noradrenergic hypothesis of ADHD and suggest that drugs with noradrenergic activity may play an important role in the therapeutics of this disorder. ADPediatric Psychopharmacology Unit, Massachusetts General Hospital, Boston 02114, USA. PMID10560028
for you to admit there is no diagnostic test for ADHD and other such so called illnesses
and that it is purely observational and subjective and your claim was false and deceptive
What about autism and vaccines. I got young boys, they are fine, but how many more shots do I let them get.
Maybe not the place but judging by the posts it looks like an answer may be here.
SUMMARY AND CONCLUSIONS Based upon the above discussion, several conclusions can be drawn:
- The prevalence of autism and ASD appears to have increased over the last several decades. Much of this trend is accounted for by changes in case definition and increased awareness of autism [24]. Whether or not the actual incidence of autism has increased is unclear.
- Multiple large, well-designed epidemiologic studies [2-5,27,56,58,65] and systematic reviews [28,35,64] have found insufficient evidence to support an association between the MMR vaccine and autism. In its latest review, the Immunization Safety Review Committee of the IOM concludes that the evidence favors rejection of a causal relationship between MMR vaccine and autism [35].
- Similarly, well-designed epidemiologic studies have failed to find an association between vaccines and multiple sclerosis or type 1 diabetes mellitus.
Though neither specific childhood vaccines nor vaccine components, such as thimerosal, have been proven by scientific study to have a causal relationship with the development of autism, there is evidence that other factors, including genetics, are important in the development of autism
- The administration of childhood vaccines has led to a decline in the incidence of childhood diseases that can have severe sequelae. Withholding vaccines from a child because of a hypothetical risk places the child at risk for actual infection that may have actual sequelae.
What about autism and vaccines. I got young boys, they are fine, but how many more shots do I let them get.
Maybe not the place but judging by the posts it looks like an answer may be here.
What about autism and vaccines. I got young boys, they are fine, but how many more shots do I let them get.
Maybe not the place but judging by the posts it looks like an answer may be here.
eots - I have been ignoring you on this issue because trying to convince you of anything other than what you think is true is like trying to get a dead man to walk.
but...
but...I will try to cloud the issue by posting lengthy pseudo science..that ultimately..call all of
this as theory..and confirm eots is correct..there is no definitive diagnostic test for ADHD
TIAttention-deficit hyperactivity disorder. AUBiederman J; Faraone SV SOLancet 2005 Jul 16-22;366(9481):237-48. Attention-deficit hyperactivity disorder (ADHD) is a disorder of inattention, impulsivity, and hyperactivity that affects 8-12% of children worldwide. Although the rate of ADHD falls with age, at least half of children with the disorder will have impairing symptoms in adulthood. Twin, adoption, and molecular genetic studies show ADHD to be highly heritable, and other findings have recorded obstetric complications and psychosocial adversity as predisposing risk factors. Converging evidence from animal and human studies implicates the dysregulation of frontal-subcortical-cerebellar catecholaminergic circuits in the pathophysiology of ADHD, and molecular imaging studies suggest that abnormalities of the dopamine transporter lead to impaired neurotransmission. Studies during the past decade have shown the safety and effectiveness of new non-stimulant drugs and long-acting formulations of methylphenidate and amfetamine. Other investigations have also clarified the appropriate role of targeted psychosocial treatments in the context of ongoing pharmacotherapy. ADPediatric Psychopharmacology Unit of the Child Psychiatry Service, Massachusetts General Hospital, and Harvard Medical School, Boston, MA 02114, USA. [email protected] PMID16023516TIADHD Candidate Gene Study in a Population-Based Birth Cohort: Association with DBH and DRD2. AUNyman ES; Ogdie MN; Loukola A; Varilo T; Taanila A; Hurtig T; Moilanen IK; Loo SK; McGough JJ; Jarvelin MR; Smalley SL; Nelson SF; Peltonen L SOJ Am Acad Child Adolesc Psychiatry. 2007 Dec;46(12):1614-1621. OBJECTIVE:: Attention-deficit/hyperactivity disorder (ADHD) is a common childhood-onset disorder with a significant impact on public health. Although a genetic contribution to risk is evident, predisposing genetic determinants remain largely unknown despite extensive research. So far, the most promising candidate genes have been those involved in dopamine and serotonin pathways. This study tests a series of allelic variants within such candidate genes to determine their potential influence on ADHD susceptibility. METHOD:: We used a population sample ascertained from a birth cohort of a subpopulation of Finland, characterized by founder effect and isolation, thus minimizing genetic heterogeneity. The subjects were systematically ascertained using DSM-IV diagnostic criteria for ADHD from the Northern Finland Birth Cohort 1986 of more than 9,000 individuals, resulting in the study sample of 188 ADHD cases and 166 controls. We genotyped markers in 13 candidate genes, including critical components of dopamine and serotonin pathways. RESULTS:: We report evidence for association of ADHD with allelic variants of the dopamine beta-hydroxylase (DBH) and dopamine receptor D2 (DRD2) genes. CONCLUSIONS:: Our study supports the involvement of the dopamine pathway in the etiology of ADHD; specifically the genes DBH and DRD2 deserve more attention in further studies. ADMs. Nyman, Drs. Loukola, Varilo, and Peltonen are with the National Public Health Institute; Drs. Ogdie, Loo, McGough, Smalley, and Nelson are with the University of California, Los Angeles; Drs. Varilo and Peltonen are with the Broad Institute and the University of Helsinki; Ms. Hurtig, Drs. Taanila, Moilanen, and Jarvelin are with the University of Oulu; and Dr. Jarvelin is with the Imperial College London. PMID18030083
TIThe neural correlates of attention deficit hyperactivity disorder: an ALE meta-analysis. AUDickstein SG; Bannon K; Castellanos FX; Milham MP SOJ Child Psychol Psychiatry. 2006 Oct;47(10):1051-62. BACKGROUND: Attention deficit/hyperactivity disorder (ADHD) is one of the most prevalent and commonly studied forms of psychopathology in children and adolescents. Causal models of ADHD have long implicated dysfunction in fronto-striatal and frontal-parietal networks supporting executive function, a hypothesis that can now be examined systematically using functional neuroimaging. The present work provides an objective, unbiased statistically-based meta-analysis of published functional neuroimaging studies of ADHD. METHODS: A recently developed voxel-wise quantitative meta-analytic technique known as activation likelihood estimation (ALE) was applied to 16 neuroimaging studies examining and contrasting patterns of neural activity in patients with ADHD and healthy controls. Voxel-wise results are reported using a statistical threshold of p < .05, corrected. Given the large number of studies examining response inhibition, additional meta-analyses focusing specifically on group differences in the neural correlates of inhibition were included. RESULTS: Across studies, significant patterns of frontal hypoactivity were detected in patients with ADHD, affecting anterior cingulate, dorsolateral prefrontal, and inferior prefrontal cortices, as well as related regions including basal ganglia, thalamus, and portions of parietal cortex
. When focusing on studies of response inhibition alone, a more limited set of group differences were observed, including inferior prefrontal cortex, medial wall regions, and the precentral gyrus. In contrast, analyses focusing on studies of constructs other than response inhibition revealed a more extensive pattern of hypofunction in patients with ADHD than those of response inhibition. CONCLUSIONS: To date, the most consistent findings in the neuroimaging literature of ADHD are deficits in neural activity within fronto-striatal and fronto-parietal circuits. The distributed nature of these results fails to support models emphasizing dysfunction in any one frontal sub-region. While our findings are suggestive of biases in the literature that need to be addressed before such a conclusion can be fully embraced. ADNYU Child Study Center, New York, NY 10016, USA. PMID17073984Tthe primacy of deficits in frontal-based neural circuitry underlying ADHD, we discuss potential IAttention-deficit/hyperactivity disorder (ADHD) as a noradrenergic disorder. AUBiederman J; Spencer T SOBiol Psychiatry 1999 Nov 1;46(9):1234-42. This review revisits the thesis that a dysregulation of the central noradrenergic networks may underlie the pathophysiology of ADHD. We review the pertinent neurobiological and pharmacological literature on ADHD. The noradrenergic system has been intimately associated with the modulation of higher cortical functions including attention, alertness, vigilance and executive function. Noradrenergic activation is known to profoundly affect the performance of attention, especially the maintenance of arousal, a cognitive function known to be deficient in ADHD. Data from family, adoption, twin, and segregation analysis strongly support a genetic hypothesis for this disorder. Although molecular genetic studies of ADHD are relatively new and far from definitive, several replicated reports have found associations between ADHD with DAT and D4 receptor genes. Brain imaging studies fit well with the idea that dysfunction in fronto-subcortical pathways occurs in ADHD with its underlying dysregulation of noradrenergic function. A wealth of pharmacological data (within and without the stimulant literature) provides strong evidence for selective clinical activity in ADHD for drugs with noradrenergic and dopaminergic pharmacological profiles. Available research provides compelling theoretic, basic biologic and clinical support for the notion that ADHD is a brain disorder of likely genetic etiology with etiologic and pathophysiologic heterogeneity. Neurobiological and pharmacological data provide compelling support for a noradrenergic hypothesis of ADHD and suggest that drugs with noradrenergic activity may play an important role in the therapeutics of this disorder. ADPediatric Psychopharmacology Unit, Massachusetts General Hospital, Boston 02114, USA. PMID10560028
for you to admit there is no diagnostic test for ADHD and other such so called illnesses
and that it is purely observational and subjective and your claim was false and deceptive
BULLSHIT! I love how you can believe 9/11 truther theories and deny the holocaust, but medical diagnosis of learning diabilities, well that is too far out there!
i HAVE NEVER DENIED THE HOLOCAUST...but as a zionist you will take any critsim of Isrel and deceptivly try to distort it
Go work with a child who is ADHD and not on his/her meds and then you will have all the proof you need! God don't you ever get sick of believing in crazy conspiracy theories?
I know your conspiracy theory here: The pharmaceutical companies and the child
psychologist field cooked up learning disabilities so the psychologist would have a surplus of willing and able bodies that seek their services and the pharmaceutical companies would have a cash crop they could sell to children! <== that theory sounds like BS to me!
there is not one sentence in all xotoxi posted that supports his lie that there one defintive diagnostic test for ADHD...NOT ONE........because there isnt..
there is not one sentence in all xotoxi posted that supports his lie that there one defintive diagnostic test for ADHD...NOT ONE........because there isnt..
EOTS: Post a link to a quote of mine where I claim that "there is one definitive diagnostic test for ADHD".
You can't...because there isn't...
Quote: Originally Posted by xotoxi
And for each "chemical imbalance" there are chemicals that can and have been measured...but in a day to day clinical setting, these lab test would be too costly or invasive to perform, but instead have been correlated with clinical findings.
Quote: Originally Posted by xotoxi
And for each "chemical imbalance" there are chemicals that can and have been measured...but in a day to day clinical setting, these lab test would be too costly or invasive to perform, but instead have been correlated with clinical findings.
deception
I'm not talking about the psychological aspects of hitting your thumb.
I'm just talking about the acute pain that you experience. That is a chemical imbalance. But we don't measure any blood tests to prove it.
There are lots of disorders that we measure blood work to diagnose. There are also lots of disorders that we assess clinical findings to diagnose. High cholesterol is an example of the former and high blood pressure is an example of the latter.
And for each "chemical imbalance" there are chemicals that can and have been measured...but in a day to day clinical setting, these lab test would be too costly or invasive to perform, but instead have been correlated with clinical findings.
However, I don't really need to spend any more time explaining anything to you, because you are eots. Any discussion with you is a certified waste of time.
no I accept your admission no such test exsist....and it is not because it is to costly or invasive but simply because no such test exist
thank you for cofirming this....FACT
