Creativity and Brain Networks in ADHD

One characteristic of ADHD that can be annoying and frustrating is “having a head full of thoughts”.

This phenomenological description though, is correlated with clear patterns of neural network activity.

 

It is common for ADHD individuals to have much more co-activation of networks that are usually run in isolation:

The “Default Mode Network” (DMN), is associated with planning or reviewing previous actions. if overactivated it may be associated with rumination or anxiety. The highest DMN activity is found in depression, and the lowest DMN activity so far has been found in senior Tibetan monks, with thousands of hours of meditation experience.

It is usually much less active when an individual is engaged in a task, but one characteristic of ADHD is that it is often not deactivated when one of the Task Positive Networks  (TPN) is active.

Equally there is much co-activation of TPNs in ADHD.

However, recent research shows a clear link between these sort of patterns of multiple network activation and creativity and this now provides a clear neurologically based understanding of just why ADHD is likely to be associated with higher levels of novel idea generation.

http://neurosciencenews.com/creativity-neural-networks-3139

 

The researchers hypothesized that for a creative idea to be produced, the brain must activate a number of different – and perhaps even contradictory – networks. In the first part of the research, respondents were give half a minute to come up with a new, original and unexpected idea for the use of different objects. Answers which were provided infrequently received a high score for originality, while those given frequently received a low score. In the second part, respondents were asked to give, within half a minute, their best characteristic (and accepted) description of the objects. During the tests, all subjects were scanned using an FMRI device to examine their brain activity while providing the answer.

The researchers found increased brain activity in an “associative” region among participants whose originality was high. This region, which includes the anterior medial brain areas, mainly works in the background when a person is not concentrating, similar to daydreaming.

The link to the paper is here:

http://www.ncbi.nlm.nih.gov/pubmed/?term=Generating+original+ideas%3A+The+neural+underpinning+of+originality

 

 Neuroimage 2015 Aug 1;116:232-9. doi: 10.1016/j.neuroimage.2015.05.030. Epub 2015 May 20.

Generating original ideas: The neural underpinning of originality.

Mayseless N, Eran A, Shamay-Tsoory SG

 

 

 

 

 

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Atlas subluxation and accelerated brain ageing

As proposed by the chiropractor Dr Michale Flanagan in his book “The Downside of Upright Posture”:

See:

http://www.upright-health.com/ccsvi.html

It would appear that in the presence of an atlas malalignment, drainage of CSF and venous blood from the brain may be compromised, leading to the accumulation of toxic metabolites like haemosiderin.

Chronic venous ulcers in the ankles of the elderly are another example of this phenomenon.

Until very recently, Dr Flanagan’s suspicion has been unsupported by evidence.

Now we have evidence, and until that is refuted, this hypothesis stands as having both physiological plausibility and scientific evidence:

http://www.ncbi.nlm.nih.gov/pubmed/26344031

 

 

 

 

 

 

 

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ADHD, balance, clumsiness and muscle fatigue

Impairments to executive function are central to the dysfunction in ADHD.

It is understood that clumsiness directly compromises executive function and working memory, but the nature of the definition of ADHD actually obscures the relationship between ADHD and coordination.

Current understandings of the role of subcortical structures in cognitive processes are advanced enough to understand that there is a clear issue in cerebellar and vestibular function in ADHD, and that cerebellar and vestibular dysfunction is also a driver of coordination problems (dyspraxia) and oculomotor problems (associated with effortful reading and, sometimes dyslexia).

There is a huge amount of good material in this study:

he Motor Function Neurological Assessment (MFNU) as an indicator of motor function problems in boys with ADHD  Liv Larsen Stray, Torstein Stray, Synnøve Iversen, Anne Ruud, Bjørn Ellertsen and Finn Egil Tønnessen

Behavioral and Brain Functions20095:22 DOI: 10.1186/1744-9081-5-22

http://behavioralandbrainfunctions.b…9081-5-22#CR41

 

The conclusion of the study is clear cut:

Our hypothesis that there is a discriminative power of the MFNU between boys aged 8–12 years with ADHD (HKD F90.0) and controls without ADHD was strongly supported by the test data across all subtests. Most of the ADHD-subjects achieved a marked to severe ‘Total score’. While there were subjects in the control group who showed problems on some of the subtests, the problems appeared on fewer subtests and with less severity than in children in the ADHD group.

We found that motor problems are present in a higher percentage in the ADHD group than the around 50% reported in previous studies

When the ‘moderate problems’ and ‘severe’ scores (score 1 and 2) were combined, the ADHD group presented problems within a range of 80% (‘Catch ball’ and ‘Walking’) to 96% (‘Dynamic balance, 1 leg’ and ‘Diadochokinesis, left’). The control group typically presented few, if any severe problems.

The paper also provides clear links to studies supporting balance dysfunction in ADHD

Also noteworthy: Methylphenidate improves co-ordination while it is in our system, and this effect persists even after years of use.


Now- for limitations-
The underlying issues with balance are mentioned here- but the paper does not go far enough in tying the balance and co-ordination together here.
In our work we have almost invariably observed that children with ADHD display a high muscle tone in the gross movement muscles, especially the m. Sacrospinalis, m. Latissimus dorsi and in m. Psoas major

That chronic muscle tension really destabilises both gross motor and fine motor control– and it often leaves one feeling tired, disrupts sleep and leaves one feeling too dull and stiff to get up in the morning.

The real cause of that tension in the “gross movement muscles” described above is that lack of balance causes our system to tighten up- so we do not fall over.

In addition, the muscle tension patterns are usually asymmetrical and the resultant mild functional kyphoscoliosis causes considerable additional loading, fatigue and discomfort for many patients.

The term”sacrospinalis” as used in this paper is outdated, and the general term conceals some functionally important detail. “Semispinalis” refers to a group of muscles called the “erector spinae” – and it actually consists of 3 groups of muscle.

Each group has a lumbar, a thoracic and a cervical part

Spinalis:

Longissimus:

Iliocostalis :

A commonly seen posture in Adult ADHD patients involves chronic unilateral contraction of Iliocostalis.

This gives rise to a posture in which the shoulder is pulled backwards and down on the tense side, while the sacrum is pulled up, tilting the pelvis to create an apparent leg shortening on the tense side (Leg length alignment asymmetry).

As I have now examined hundreds of adult ADHD patients I can report that this postural deformity is very common in ADHD and it is always associated with asymmetrical upper cervical muscular tension/ tenderness/ fatigue. I would suggest that addressing this tension pattern and the associated functional thoracic kyphoscoliosis is an important part of any rehabilitation program for ADHD that is addressing postural correction, as without it there will be a continuing source of upper neck muscle tension and continuing asymmetric distortion of afferent somatosensory input from the neck to the brain. (see below for details).

The role of disturbed input sensory information from tight upper neck muscles (especially the asymmetrically tight neck muscles associated with malalignment between the joints between the skull and the first three vertebrae in the neck) is not acknowledged in this paper however it is addressed here:

J Phys Ther Sci. 2015 Jan;27(1):259-63. doi: 10.1589/jpts.27.259. Epub 2015 Jan 9.

Determine the effect of neck muscle fatigue on dynamic visual acuity in healthy young adults.

Al Saif AA1, Al Senany S2.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4305577/

Highlights:

Postural and visual stability are dependent upon efficient and accurate central processing of visual, vestibular, and somatosensory afferent input1). This afferent input under- goes multimodal sensory integration in several areas of the brain and brainstem in order to provide efferent output to maintain postural equilibrium and oculomotor control. In- accurate sensory information from dysfunctional sensory end organs leads to a sensory mismatch, causing postural and/or visual instability.

For example, altered somatosensory input, particularly from the upper cervical spine structures, can disturb the vestibular system,

Moreover, evidence suggests that upper cervical muscle fatigue may be an important contributing factor to altered postural stability in people with neck pain because neck muscle fatigue has been shown to modify the discharge of sensory receptors in neck muscles and affect proprioception

These findings suggest that normal eye movement is partially dependent upon accurate sensory input from the cervical spine13). There is also evidence to suggest that the cervical spine influences eye movements via the vestibular system14). Stimulation of the deep cervical spine mechanoreceptors has a measurable impact on the vestibulo-ocular reflex (VOR)

The results of this study suggest that there is a measurable interaction between neck proprioception and the VOR in subjects with normal vestibular function. Also, abnormal neck muscle proprioceptive signals may give rise to asymmetric functioning of the VOR and contribute to postural and visual instability.

Our findings are consistent with previous studies, which reported, that reduced proprioceptive acuity contributes to sensory mismatches and possibly an asymmetry of the VOR. This phenomenon is probably due to disturbances in the neural connections between the three sensory systems (somatosenory, vestibular, and vision) that can lead to mismatched sensory input, causing conflicts among all inputs from the different sensory systems).

So if we put this all together we now understand thatmwe can look at ADHD as a series of causal loops in which there is a feedback loop with muscle tension and poor posture being generated as a response to poor balance (The drivers here would be an increase in muscle tone in response to percieved instability, and a secondary postural deformity driven by the stress response (via the rubrospinal tracts).

The muscle tension will drive restlessness and will alternate with periods of loss of tone due to simple fatigue due to overtensioning of the muscles.

That muscle tension then impairs co- ordination (hence executive function and working memory) directly as the demand placed on the cerebellum to continually recalculate the force required for any movement to correct for shifts in muscle tone.

The muscle tension also generates distorted body position information as the posture adopted (head forwards) fatigues the suboccipital muscles and the sternocleidomastoids.

Then the brain has to cope with a sensory mismatch, leading to problems in spatial perception (losing things, getting lost, being unable to locate the sources of sounds).

The stress response worsens matters by dropping thresholds of sensory awareness and leading to sensory overload.

Finally, the impact of all this confusing information input into the CNS is a dysregulation of the autonomic system as an increasingly confused and fatigued brain continually readjust energy distribution settings (blood flow etc) to appropriately manage the currently perceived situation.

This data on altered proprioception and neck muscle fatigue also provides a clear explanation for the persistence of pain and dysfunction following upper neck injuries such as whiplash, or upper cervical birth trauma:
Following injury, the protective muscle spasm is accompanied by a loss of awareness of position and stability that actually perpetuates the problem.
In understanding this we are now able to understand quite precisely the key neuromuscular mechanisms for the association between birth trauma to the upper neck and dyspraxia, dysgnosia and ADHD as proposed by Biedermann in “Manual Therapy in Children”:
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Safety of long term stimulants in ADHD

While there has been concern about the safety of stimulant medication both for treatment of ADHD and for other indications, current evidence suggests that these concerns may not only be overstated, they may be totally wrong, and , in many situations, long term cause of stimulants may be so beneficial that to deny access to the may be irresponsible.

This document is meant for both patients and clinicians.

For patients the bits you need to read are in bold:

Long-term amphetamine exposure in some animal species is known to produce abnormal dopamine system development or nerve damage,[12][13] but, in humans with ADHD, pharmaceutical amphetamines appear to improve brain development and nerve growth.

Carvalho M, Carmo H, Costa VM, Capela JP, Pontes H, Remião F, Carvalho F, Bastos Mde L (August 2012). “Toxicity of amphetamines: an update”. Arch. Toxicol. 86 (8): 1167–1231. doi:10.1007/s00204-012-0815-5 (https://dx.doi.org /10.1007%2Fs00204-012-0815-5). PMID 22392347 (https://www.ncbi.nlm.nih.gov/pubmed/22392347).

Berman S, O’Neill J, Fears S, Bartzokis G, London ED (October 2008). “Abuse of amphetamines and structural abnormalities in the brain” (https://www.ncbi.nlm.nih.gov/pmc/articles /PMC2769923). Ann. N. Y. Acad. Sci. 1141: 195–220. doi:10.1196/annals.1441.031 (https://dx.doi.org/10.1196%2Fannals.1441.031). PMC 2769923 (https://www.ncbi.nlm.nih.gov /pmc/articles/PMC2769923). PMID 18991959 (https://www.ncbi.nlm.nih.gov/pubmed/18991959).

Hart H, Radua J, Nakao T, Mataix-Cols D, Rubia K (February 2013). “Meta-analysis of functional magnetic resonance imaging studies of inhibition and attention in attention-deficit/hyperactivity disorder: exploring task-specific, stimulant medication, and age effects”. JAMA Psychiatry 70 (2): 185–198. doi:10.1001/jamapsychiatry.2013.277 (https://dx.doi.org /10.1001%2Fjamapsychiatry.2013.277).

Spencer TJ, Brown A, Seidman LJ, Valera EM, Makris N, Lomedico A, Faraone SV, Biederman J (September 2013). “Effect of psychostimulants on brain structure and function in ADHD: a qualitative literature review of magnetic resonance imaging-based neuroimaging studies” (https://www.ncbi.nlm.nih.gov/pmc/articles /PMC3801446). J. Clin. Psychiatry 74 (9): 902–917. doi:10.4088/JCP.12r08287 (https://dx.doi.org /10.4088%2FJCP.12r08287). PMC 3801446 (https://www.ncbi.nlm.nih.gov/pmc/articles /PMC3801446). PMID 24107764 (https://www.ncbi.nlm.nih.gov/pubmed/24107764).

Frodl T, Skokauskas N (February 2012). “Meta- analysis of structural MRI studies in children and adults with attention deficit hyperactivity disorder indicates treatment effects.”. Acta psychiatrica Scand. 125 (2): 114–126. doi:10.1111/j.1600-0447.2011.01786.x (https://dx.doi.org /10.1111%2Fj.1600-0447.2011.01786.x). PMID 22118249 (https://www.ncbi.nlm.nih.gov /pubmed/22118249).

When used at low (therapeutic) doses, amphetamine produces unambiguous improvements in cognition, including working memory, episodic memory, and inhibitory control, in normal healthy adults.

Spencer RC, Devilbiss DM, Berridge CW (June 2015). “The Cognition-Enhancing Effects of Psychostimulants Involve Direct Action in the Prefrontal Cortex”. Biol. Psychiatry 77 (11): 940–950. doi:10.1016/j.biopsych.2014.09.013 (https://dx.doi.org /10.1016%2Fj.biopsych.2014.09.013).

PMID 25499957 (https://www.ncbi.nlm.nih.gov /pubmed/25499957).

Ilieva IP, Hook CJ, Farah MJ (January 2015). “Prescription Stimulants’ Effects on Healthy Inhibitory Control, Working Memory, and Episodic Memory: A Meta-analysis”. J. Cogn. Neurosci.:

While Addiction is a serious risk with heavy recreational amphetamine use but is unlikely to arise from typical medical use at therapeutic doses.[80][81][41]

Westfall DP, Westfall TC (2010). “Miscellaneous Sympathomimetic Agonists” (http://www.accessmedicine.com /content.aspx?aID=16661601). In Brunton LL, Chabner BA, Knollmann BC. Goodman & Gilman’s Pharmacological Basis of Therapeutics (12th ed.). New York, USA: McGraw-Hill. ISBN 9780071624428.

Kollins SH (May 2008). “A qualitative review of issues arising in the use of psycho-stimulant medications in patients with ADHD and co-morbid substance use disorders”. Curr. Med. Res. Opin. 24 (5): 1345–1357. doi:10.1185/030079908X280707 (https://dx.doi.org /10.1185%2F030079908X280707). PMID 18384709 (https://www.ncbi.nlm.nih.gov/pubmed/18384709). “When oral formulations of psychostimulants are used at recommended doses and frequencies, they are unlikely to yield effects consistent with abuse potential in patients with ADHD.”

Stolerman IP (2010). Stolerman IP, ed. Encyclopedia of Psychopharmacology. Berlin, Germany; London, England: Springer. p. 78. ISBN 9783540686989.

While there had been concern about long term use of stimulants being a risk for Parkinson’s disease ( through excitotoxic nerve damage), it would now appear that the reverse is true:

http://www.ncbi.nlm.nih.gov/pubmed/23160937 CNS Drugs. 2013 Jan;27(1):1-14. doi: 10.1007/s40263-012-0017-y.Methylphenidate: a treatment for Parkinson’s Disease?Devos D1, Moreau C, Delval A, Dujardin K, Defebvre L, Bordet R.

Relationships and performance:

Children with ADHD who use stimulant medications generally have better relationships with peers and family members,[22][33] generally perform better in school, are less distractible and impulsive, and have longer attention spans.[22][33]

Millichap JG (2010). “Chapter 3: Medications for ADHD”. In Millichap JG. Attention Deficit Hyperactivity Disorder Handbook: A Physician’s Guide to ADHD (2nd ed.). New York: Springer. pp. 111–113. ISBN 9781441913968.

  1. Huang YS, Tsai MH (July 2011). “Long-term outcomes with medications for attention-deficit hyperactivity disorder: current status of knowledge”. CNS Drugs 25 (7): 539–554. doi:10.2165/11589380-000000000-00000 (https://dx.doi.org

Methylphenidate has the potential to induce euphoria due to its pharmacodynamic effect (i.e., dopamine reuptake inhibition) in the brain’s reward system.[80] At therapeutic doses, ADHD stimulants do not sufficiently activate the reward system, or the reward pathway in particular, to induce persistent ΔFosB gene expression in the D1-type medium spiny neurons of the nucleus accumbens;[77][80][87] consequently, when used medically and as directed, methylphenidate use has no capacity to cause an addiction.[77][80][87]

77. Malenka RC, Nestler EJ, Hyman SE (2009). “Chapter 15: Reinforcement and Addictive Disorders”. In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. p. 368. ISBN 9780071481274. “Cocaine, [amphetamine], and methamphetamine are the major psychostimulants of abuse. The related drug methylphenidate is also abused, although it is far less potent. These drugs elicit similar initial subjective effects ; differences generally reflect the route of administration and other pharmacokinetic factors. Such agents also have important therapeutic uses; cocaine, for example, is used as a local anesthetic (Chapter 2), and amphetamines and methylphenidate are used in low doses to treat attention deficit hyperactivity disorder and in higher doses to treat narcolepsy (Chapter 12). Despite their clinical uses, these drugs are strongly reinforcing, and their long-term use at high doses is linked with potential addiction, especially when they are rapidly administered or when high-potency forms are given.”

Kim Y, Teylan MA, Baron M, Sands A, Nairn AC, Greengard P (2009). “Methylphenidate-induced dendritic spine formation and DeltaFosB expression in nucleus accumbens” (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2650365). Proc. Natl. Acad. Sci. U.S.A. 106 (8): 2915–20. doi:10.1073/pnas.0813179106 (https://dx.doi.org/10.1073%2Fpnas.0813179106). PMC 2650365 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2650365). PMID 19202072 (https://www.ncbi.nlm.nih.gov/pubmed/19202072). “Despite decades of clinical use of methylphenidate for ADHD, concerns have been raised that long-term treatment of children with this medication may result in subsequent drug abuse and addiction. However, meta analysis of available data suggests that treatment of ADHD with stimulant drugs may have a significant protective effect, reducing the risk for addictive substance use (36, 37). Studies with juvenile rats have also indicated that repeated exposure to methylphenidate does not necessarily lead to enhanced drug-seeking behavior in adulthood (38). However, the recent increase of methylphenidate use as a cognitive enhancer by the general public has again raised concerns because of its potential for abuse and addiction (3, 6–10). Thus, although oral administration of clinical doses of methylphenidate is not associated with euphoria or with abuse problems, nontherapeutic use of high doses or i.v. administration may lead to addiction (39, 40).”

Nestler EJ (December 2013). “Cellular basis of memory for addiction” (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3898681). Dialogues Clin. Neurosci. 15 (4): 431–443. PMC 3898681 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3898681). PMID 24459410 (https://www.ncbi.nlm.nih.gov/pubmed/24459410). “DESPITE THE IMPORTANCE OF NUMEROUS PSYCHOSOCIAL FACTORS, AT ITS CORE, DRUG ADDICTION INVOLVES A BIOLOGICAL PROCESS: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. … A large body of literature has demonstrated that such ΔFosB induction in D1-type NAc neurons increases an animal’s sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement … Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.41. … Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict.4″

2013 Jan;27(1):1-14. doi: 10.1007/s40263-012-0017-y.

Legal status:methylphenidate:

Legal status

Clearly given the benefits above and the lack of addictive potential at therapeutic doses this restricted use of psychostulants is not based on any sound evidence at all– is just nutty. These medications should be able to be prescribed by and any doctor competent to handle them. A permit should be required to prevent doctor shopping and to ensure that the supervising doctor is overseeing the whole tratment. ( IE ensuring that all is being done to minimise the symptoms and consequences of ADHD in all pateints being treated).

Internationally, methylphenidate is a Schedule II drug under the Convention on Psychotropic Substances.[131]

In the United States, methylphenidate is classified as a Schedule II controlled substance, the designation used for substances that have a recognized medical value but present a high potential for abuse. In the United Kingdom, methylphenidate is a controlled ‘Class B’ substance. Possession without prescription carries with a sentence up to 5 years and/or an unlimited fine, and supplying it is 14 years and/or an unlimited fine.[132] In Canada, methylphenidate is listed in Schedule III of the Controlled Drugs and Substances Act (along with LSD, psychedelic mushrooms, and mescaline, among others), and is illegal to possess without a prescription, pursuant to Part G (section G.01.002) of the Food and Drug Regulations under the Food and Drugs Act. In New Zealand, methylphenidate is a ‘class B2 controlled substance’. Unlawful possession is punishable by six-month prison sentence and distribution of it is punishable by a 14-year sentence.

In Australia, methylphenidate is a ‘Schedule 8’ controlled substance. Such drugs must be kept in a lockable safe before being handed out and possession without prescription carries hefty fines and even imprisonment. In Sweden, methylphenidate is a List II controlled substance with recognized medical value. Possession without a prescription is punishable by up to three years in prison.[133]

In France, methylphenidate is covered by the “narcotics” schedule, prescription and distribution conditions are restricted with hospital-only prescription for the initial treatment and yearly consultations.[134]

Finally, ADHD is a highly prevalent and highly impairing condition.

Conservative estimates in Australia are about the 4% mark in adults.

A recent paper has shown the incidence in middle aged adults is about 6%

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0031500A Population-Based Study of Attention Deficit/Hyperactivity Disorder Symptoms and Associated Impairment in Middle-Aged Adults

A review of the data presented from Prof Alistair Vance of the Royal Children’s Hospital yielded the following figures:

Out of every 100 children with ADHD, about 66 will still be diagnosable as ADHD , about 5 will have full resolution of their ADHD and the remaining 29 or so will have symptoms but fall below diagnostic thresholds.

My experience in ADHD suggests that many of that group will fall back into diagnosable ADHD if hit by a crisis.

My overall observations as a GP (about 20 years in the same practice watching many of my middle aged and elderly patients slip into dementia), suggest to me that the ADHD pattern may be a precursor to neurodegenerative disorders – such as Alzheimer’s and Caparisons. In this setting symptoms like restless legs may be a prodrome of conditions such as Parkinson’s disease.

Given my current awareness of the field of evidence based neuroscience (formerly called functional neurology) and a field that specialises in neurological rehabilitation, there is every reason to believe that this would be a predicted outcome of lifelong ADHD. Given my personal experience of rehabilitation provided by practitioners of functional neurology it is clear that this downhill slide can not only be halted, it can be reversed.

The information on which this summary was based can be found on line by looking at the Wikipedia articles on Dextroamphetamine and Methylphenidate as downloaded Monday 24 May 2015. I do not regard Wikipedia as a routinely reliable source, however this material is properly referenced, so it is worth considering.

 

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Underdiagnosis of ADHD related to chronic underresourcing of medicine in Australia

An interesting article from the Australian Medical Association: https://ama.com.au/ausmed/adhd-under-recognised-not-over-diagnosed-expert Here is  a short excerpt Dr Coghill said the symptoms of ADHD needed to be present, persistent, to have started early in life and to have caused significant impairment. It means that accurate diagnosis is not simply a matter of ticking off a list of observed behaviours, but of gathering and assessing information about the patient’s life. “We are very clear in these guidelines that you need to collect not only information about symptoms, but also a child’s development; how they are managing broader areas of life,” he said. It means that it is “probably not possible” to make a diagnosis of ADHD in one visit to the doctor, and each consultation was likely to be time consuming. Dr Coghill acknowledged this as a constraint in the Australian system of primary care, where low fees put the pressure on doctors to churn through patients as quickly as possible. So we can see that the Australian medical system is actually quite unable to come to terms with one of the commonest generators of illness in Western society. It is clear that ADHD is very financially disabling- so it seems that the Australian medical system, supposedly equitable, systematically discriminates against a group prone to higher incidence of most common Western illnesses by failing to provide the resources to get to the bottom of their problems.  This is an interesting state of affairs when we are prepared to spend vast amounts of money on dubious new chemotherapeutic products that, at best, extend life of cancer sufferers by a few months. So it seems that under resourcing is thed river for under diagnosis.

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Scientific evidence for the power of positive thinking

This page will be regularly updated as more information is gathered.

Is there scientific proof we can heal ourselves? Dr Lissa Rankin MD

http://noetic.org/research/project/online-spontaneous-remission-bibliography-project/

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Neuroplastic Change induced by Meditation

Finally there is an increasing body of research to support the proposition that meditation practice produces not only desirable behavioural change.

It is reasonable for the public to be skeptical of new therapies and to want some supporting evidence.

This page will gather links to some of the more accessible and succinct summaries of current published research available on the internet:

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