User:James 173/Draft page only - Scientific research into ADHD
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Scientific research into attention deficit hyperactivity disorder (ADHD) has taken place for over a hundred years. The weight of scientific evidence is considered by scientists and many other ADHD organisations to show overwhelmingly[citation needed] that ADHD is a condition with demonstrable roots in genetics and neurological functioning, and strong conceptual links between the biological findings and classical impairment symptoms.
ADHD is highly prevalent (est. 2-5%) and not known to be specific to any culture, suggesting origins as an adaptive behavior in human history. In a large proportion of ADHD cases the condition is shown to be largely inherited or predisposed genetically, that it is a complex heterogenous (multi-factor) condition,[citation needed] and is linked both to genetic mutations affecting brain functions impaired by ADHD and (via brain scans) to a number of neurotransmitter abnormalities. Neurological areas affected are those which other research had also shown as responsible for functions impaired in ADHD. Other research has studied ADHD and diet, ADHD and the autonomic system (in particular the vagus nerve which is implicated in emotional regulation and allostasis[citation needed]), and many other areas of interest in ADHD. In society, ADHD was studied and gained prominence as a paediatric (childhood) condition in education; only later did further studies lead to acceptance as lifelong and often disabling into adulthood.
For these reasons, findings cover a broad area. Genetically some 80%[citation needed] of ADHD - and common ADHD symptoms such as circadian rhythm disorders (sleep cycle dysfunction) - are likely to be explained genetically or have proven genetic links.[citation needed] Neurologically ADHD is linked to disregulation of major neurotransmitters such as dopamine, glutamate, norepinephrine, and others known to play important roles in learning, memory, self-motivation, and self-regulation.[citation needed] In cardiology and the autonomic nervous system ADHD has some level of established association with vagal tone and disregulation. Functionally ADHD correlates in standard tests with well defined areas of functional impairment and test responsiveness.[citation needed] Social research shows ADHD has a high correlation with certain negative social outcomes related to employment, relationships, and (in some cases) criminality resulting from exceedingly poor emotional regulation and impulsivity.[citation needed]
Treatments and responses to ADHD have also received much scientific scrutiny, in part due to earlier disputes as to the nature of ADHD, fears of inappropriate or over-prescribing, and long term prescribing, and a search for alternate effective approaches. Stimulant and non-stimulant approaches, and medications targeting different neurological systems, have been investigated, along with repurposed medications such as hypotensives used in other conditions. Diet has been studied, in particular nutritional supplements that may compensate for known ADHD neurocorrelates or their precursors. Therapeutic treatments such as cognitive behavioral therapy (CBT), and coping mechanisms such as ADHD-specific planning and task structuring, have been researched to symptomatically address social outcomes of ADHD and redress the deficits of regulation.
Theories of ADHD propose to explain the underlying etiology of ADHD, which has at times been seen as a sign of minimal brain damage or a social construct. Such theories still exist but are considered disproven.[citation needed] The model known as low arousal theory, along with developmental theories which consider ADHD as a condition of impaired neurological (self-) regulation and consequent inadequacy of executive functioning, have received positive reception in scientific literature and are widely seen as theoretically satisfactory, and as the current mainstream theories.[citation needed]
ADHD expression and associated conditions[edit]
ADHD expression and symptoms[edit]
Comorbidities, associated/non-core conditions, and confounds[edit]
Expression at varying life stages (inc. excitotoxicity coverage)[edit]
See below, touch on here
Biological findings[edit]
Genetic[edit]
Neurological[edit]
Autonomic nervous system and vagal tone[edit]
Environmental and neonatal[edit]
Psychological and in vivo findings[edit]
Standard tests[edit]
Ability to self manage ("genuine impairment vs. willpower" studies)[edit]
Social studies findings (sociology)[edit]
In children and education[edit]
Adult ADHD[edit]
Consequences (inc. coverage of criminality research in some cases)[edit]
Risks and life progress (inc. excitotoxicity coverage)[edit]
Researched treatments & management[edit]
(See "management")
Medication findings[edit]
Stimulants[edit]
Rationale for stimulant use in ADHD[edit]
It is not always intuitive why a stimulant would be used to treat sufferers who are already hyperactive, as it seems paradoxical. Current evidence suggests that ADHD itself is a paradoxical condition. In other words the hyperactivity and impulsivity are themselves symptoms of lowered regulatory brain functions such as the dopamine, norepinephrine, serotonin and glutamate processes that are the brain's major drivers of internal self-inhibition, self-control, learning, reward, and motivation. ADHD affects the brain by reducing the functioning of these critical systems to an underperforming level; hyperactivity, distractability, impulsivity, and the other failings of regulation seen in ADHD occur by result. Methylphenidate and other stimulants can improve the levels of relevant neurotransmitters in the brain, allowing better self-regulation and increased control of executive functions within the brain, hence improved mental focus and self-control,[1] and in this way help to compensate for the defective processes.
In other words, ADHD does not press the car's 'accelerator', even though that is how it may appear; rather it causes a non-obvious fault in the car's 'brakes' so they do not reliably work at the 'driver's' command. Stimulants improve the 'brakes' so they respond more correctly to the driver.
Studies showing biological and functional impacts of ADHD on the brain, and of stimulants on ADHD brain activity, are described below. The theory itself is known as low arousal theory.
This explains why someone hyperactive due to ADHD is calmed by stimulants, while someone not suffering from ADHD who takes these medications will become temporarily overexcited or hyperactive.[citation needed] In ADHD the brain has abnormally low levels of certain neurotransmitters so at a physical level, the brain cannot properly co-ordinate self-regulation over focus, hyperactivity and other impulses. Improved levels allows more usual self control to resume. A non-ADHD brain does not benefit this way, but simply experiences increased activity or hyperactivity.
Stimulants improve this control by reducing ("inhibiting") the activity of receptors within pre-synaptic neurons which are responsible for relevant neurotransmitter removal (known as "transport" and "reuptake") within the brain.[1] Drugs that work this way are therefore classed as reuptake inhibitors. They act as a stimulant in the sense that by reducing reuptake, they stimulate extracellular concentrations of these neurotransmitters and related brain activity to increase to a more functional level so that self-regulation becomes more effective, and ADHD's disregulation symptoms are reduced.[2]
Common stimulants[edit]
Methylphenidate (MPH; Ritalin, Concerta, Metadate, or Methylin) - Norepinephrine-dopamine reuptake inhibitor
Modafinil, Adrafinil, and Armodafinil
Nutritional findings[edit]
Behavioral and management findings[edit]
Management of other associated symtoms and conditions[edit]
Complex cases[edit]
Speculative and currently examined[edit]
Aspects of ADHD noted in scientific findings as worth future review.
Biological[edit]
Management[edit]
Associated matters[edit]
Theories[edit]
Background
In these theories, genetic, neurotransmitter and other causes lead to the developing brain being unable to develop appropriately the functions required for self-regulation, focus, and self-direction, leading to the classic symptoms of ADHD.
Evidence for this includes evidence of these neurological dysfunctions, as well as evidence that pharmaceutical enhancement of the neurotransmitters involved in regulation alleviates the symptoms of ADHD.
Low arousal and executive functioning[edit]
Other[edit]
Anecdotal findings covered in reputable non-science sources[edit]
A number of findings have not been the subject of research but are widely reported in ADHD-related contexts, guidance, books, and the like.
(for completeness)
References[edit]
- ^ a b Tomasi D, Volkow ND; et al. (14 February 2011). "Methylphenidate enhances brain activation and deactivation responses to visual attention and working memory tasks in healthy controls". Neuroimage. 54 (4): 3101–3110. doi:10.1016/j.neuroimage.2010.10.060. PMC 3020254. PMID 21029780.
{{cite journal}}: Explicit use of et al. in:|author=(help) - ^ Stephen M. Stahl (2 March 2009). Antidepressants. Cambridge University Press. p. 73. ISBN 978-0-521-75852-9. Retrieved 10 May 2012.