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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Cervical Malalignment and the “Reality Hologram”

Most of us navigate our way through the world believing that what we see really is “out there” and exists exactly as we perceive it.

This is far from the truth, and, in fact we have no way of knowing, for instance whether even something as basic as our perception of the colour red is in any way comparable to someone else’s perception of the same red object.

We take this for granted, but the distinction between what is perceived and what exists becomes more obvious when we consider various insects who can see colours that are beyond the range of our visual apparatus.

In fact, regardless of whatever reality exists “out there” outside of our heads– we actually know nothing of it.

All that any of us consciously knows is knows is the sum total of all the sensory data presented to our our conscious minds by our sensory apparatus, and integrated and structured into a meaningful whole by our brains. To complicate matters even further there is a process by which the overwhelming majority of sensory data are excluded from conscious awareness by a highly refined subcortical gating process, which occurs especially in the thalami. This process of selection of sensory data relevant to consciousness is termed “sensory integration”.

The neurology of hologrammatic model of consciousness is well understood in neuroscience and is the main subject of the book “Self Comes To Mind” by the neurologist Antonio Damasio. As a curious aside, the same model is clearly referenced in one of the core texts of Mahayana Buddhism- The Heart Sutra.

In this “Self Comes To Mind” Damasio outlines the fact that one of the most important aspects of brain function is the mapping and cross referencing of all the various sorts of sensory data that our brain perceives.

One of the key anatomical structures responsible for the collating and cross referencing of this sensory input is a pair of brainstem nuclei called the superior colliculi.

Ref “Self Comes to Mind” Antonio Damasio

p67: “The superior collicilus is an important provider of those visual maps, and even has the ability to relate those visual maps to auditory and body-based maps”.

Page 83 “The superior colliculus has 7 layers. Layers I -III are the “superficial” layers, while layers IV through VII are called “deep”. All the connections coming into and going out of the superficial layers have to do with vision, and layer II, the main superficial layer, recieves signals from the retina and from the primary visual cortex. These superficial layers assemble a retinotopic map of the contralateral visual field.

The deep layers of the superior colliculus contain, in addition to a map of the visual world, topographical maps of auditory and somatic information, the latter hailing from the spinal cord as well as the hypothalamus. The three varieties of maps- visual, auditory and somatic are in spatial register. This means that they are stacked in such a precise way that the information available for one map for, say vision, corresponds to another map related to hearing or body state. There is no other place in the brain where information available from vision, hearing and multiple aspects of body states is so literally superimposed, offering a prospect of efficient integration. The integration is made all the more significant by the fact that its results can gain access to the motor system (via nearby structures in the periaqueductal gray as well as via the cerebral cortex).

Damasio then goes on to discuss the action that occurs when a lizard flicks out its tongue and catches a passing fly- and the fact that most of the critical relaying and cross referencing of information (including information about the lizard’s hydration and energy status) occurs in the superior colliculus.

Now this model works well if there is a stable one to one relationship between the information entering the brain and the actual source of the information.

The presence of an upper cervical malalignment introduces two difficult elements-

As an example let us assume a minor forwards rotation of the right atlas articular process on the right occipital condyle.

This introduces false information into the brain (effectively informing the affected individual that the right side of his body is pointing to the right and not straight forwards).

This can be demonstrated reasonably straightforwardly by performing a Fukuda test: Instead of being able to march up and down on the spot with eyes shut the individual will drift forwards and to the right. Equally, the affected individual will tend to drift to the right when walking or swimming and sit in the right hand side of the lane when driving. They will also tend to erroneously throw to the right of their target if they can be encouraged to try (many people with this injury will be sufficiently ashamed of their poor co-ordination to refuse even trying to throw a ball).

Now ordinarily our brains can adapt to a distortion in the input information and reconstruct an effective hologram– providing that that distortion remains stable.

A good example of this adaptability of brain function can be seen in this video at about 4 minutes:

http://www.youtube.com/watch?v=yxa85kUxBDQ

(Being Human: Perception and the Brain)

However- in the case of the man throwing the ball at the screen, he has the advantage of being given an acute distortion of his perception (in terms of the prism lenses he was asked to wear and then remove) and he had the added advantage of being told what had been done to him. Given the advantage of being told he actually started correcting his function quite rapidly. It is notable that towards the end of the experiment the prism glasses are removed and the subject has to re-adapt his motor behaviour to cancel out the correction that his brain had started to factor in.

However- the unfortunate individual with an upper cervical malalignment must battle with an unidentified mismatch between body position and proprioceptive input- and associated muscle spasm as the body braces to protect the spinal cord.

This situation is bad enough if that individual acquires an atlas malalignment in later life, but should the injury occur at birth or in infancy the malalignment can impact upon the whole of neuromotor and perceptual development, resulting in the syndromes that the orthopedic surgeon Heiner Biedermannn calls KISS ( Kinematic Instability with Suboccipital Strain) in infants and KIDD (Kiss induced Dyspraxia and Dysgnosia) in schoolage children. KIDD is clinically indistinguishable from ADHD.

(Ref “Manual Therapy in Children” Ed Heiner Biedermann).

Individuals with an acquired rotatory malalignment of the upper cervical spine have their situation complicated by spasm and guarding of the upper cervical joints, resulting in a fixed hyperextension of the C0-1 joint, a tendency to a sitting posture with thoracic kyphosis and forward head posture

(the orthopedic and autonomic consequences of which will be discussed in another post). However, of direct relevance to the theme of this article, the persistent forward head posture vastly reduces mobility of the facet joints in the upper cervical spine. Proprioceptive input from these facet joints and related musculature is one of the major sources of the stimulus that drives the operation of consciousness. In particular the resting tension of the suboccipital musculature is especially important. Suboccipital spasm causes an inhibitory post synaptic output from the cerebellum- which is forwarded back to these muscles and forward to the contralateral frontal lobe. Thus individuals with a right atlanto-occipital malalignment will suffer chronic suppression of left frontal lobe activity and be more prone to being right hemisphere dominant in their function. In itself this is one of the major drivers of the dysregulated impulsive emotionality of the ADHD individual.

Again as an aside from the main theme, the relative immobility of the upper cervical facet joints leads (via reduced proprioceptive input) to a decrease in endorphin production, upregulating the individual’s sensitivity to pain.

So it can be seen that upper cervical malalignments can directly lead to a series of serious consequences impacting upon perception, attention and motor output.

Firstly there is a subtle balance impairment. This balance impairment (in conjunction with motor impairment) can be seen in the subtle clumsiness of most ADHD individuals (who are very prone to bumping into solid objects like doorways and the corner of tables), though some individuals manage to master particular tasks, and can make very fine, though injury prone, athletes. Often though these individuals will retain subtle clumsiness inother domains of function. The balance impairment will also often show up in a fear of heights and in falling dreams. It can be demonstrated by testing for Romberg’s sign, and by assessing heel toe gait with eyes open and closed. (The worse gait with eyes closed clearly illustrates an underfunctioning vestibulocerebellar system and over reliance on vision to navigate through the world). These problems represent a direct and severe drain on working memory- an acknowledged problem in ADHD.

Secondly, there are perceptual issues as well- such as difficulty with 3 dimensional orientation, and confusion between left and right. Dyslexia may well be an expression of this problem. Individuals with significant malalignment issues also have great difficulty in mirroring activity when being taught new movements. This can be seen very well in activities that require high attention to detail- such as Tai Chi. I would argue that the great capacity of us ADHD individuals to lose things is, in part related to these perceptual issues, as is our notably higher risk of car accidents.

I would argue that in the presence of upper cervical instability the individual is presented with an ever changing variability in the correspondence of body position, proprioceptive information reaching the brain stem, balance information from the vestibular apparatus and visual input. The problem is made more complex by the tendency of affected individuals to hold the head tilted, further increasing the complexity of processing required to maintain the coherent “reality hologram” required to act asa template for motor output.

In this context the issues of sensory integration seen in ADHD (and in other psych disorders) become more comprehensible. It is arguable that much of the intolerance of many ADHD individuals for noisy or chatoic environments or for certain tactile, taste or odour stimuli simply reflects the functioning of a system struggling to integrate mismatched sensory information.

At this point it may be worth reporting my personal experience with my unstable upper cervical spine. When the spine is out of alignment for any period of time, I will develop a cluster of predictable symptoms- a predictable pattern of right sided muscular spasm and body pain, dysarthria, difficulty in challenging motor tasks such as reverse parking my car, and blurred vision in the right eye. I also will rapidly develop sensory integration issues- such as intolerance of noisy environments or tight fitting clothing.The blurred vision is particularly interesting, as with ongoing meditation practice I have developed the capacity to see directly that what I am seeing is a distortion of visual input- such that upright objects in my right visual field appear distorted – with their upper parts pushed to the right. This distortion is reversible in real time if I loosen, unlock and straighten my upper cervical spine, which I can now usually manage without the assistance of a manual therapist, thanks to my Qi Gong / Tai Chi training.

[The issue of reporting personal experience in a blog that aims to focus on scientifically verifiable data is a thorny one- but I hope that the readers will forgive me putting this observation “out there” in the hope that someone can point me in the direction of some already completed scientific research data on this subject. However, the intermittent dysarthria has been verified by my own physician].

The improvement in perceptuo-motor function following adjustment to the upper cervical spine is clearly demonstrated in Heiner Biedermann’s book Manual Therapy in Children on page 170, which illustrates improvement in drawing ability in a 6 year old child over a 5 week period following a single adjustment to the upper cervical spine.

I note also recent work in which the issue of unstable gaze in ADHD (usually improved by stimulants) is discussed and proposed as a part of a diagnostic work up for ADHD.

ref: ADHD subjects fail to suppress eye blinks and microsaccades while anticipating visual stimuli but recover with medication

Moshe Fried a, Eteri Tsitsiashvili a, Yoram S. Bonneh b, Anna Sterkin a, Tamara Wygnanski-Jaffe c,d, Tamir Epstein e, Uri Polat a,

Vision Research

Volume 101, August 2014, Pages 62–72

This phenomenon would certainly be at least partially explicable in the light of the issue of mismatching information being fed into the superior colliculi- which play a major role in regulating eye movement.

A further clinical observation relevant to the improvement in function on stimulants may be the simple one that individuals on stimulants and quietly engaged in an interesting task tend to hold a more upright posture- and so would tend to have unstable joints settle into place and reduce the mismatch of information entering the brainstem. Again, this is speculative, but it may well provide a further mechanism for the function of these medications.

Finally, I would note that where present, such cervical malalignments would also provide a very clar cut explanation for the dyspraxia/ Developmental Coordination Delay seen in about ½ of all ADHD individuals, and the lesser degrees of problems with co-ordination seen ain many others.

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Is ADHD being over medicalised and is that process driven by drug companies?


This one is just too pathetic:

http://www.ibtimes.com/higher-rates-…groups-1727751

Recent growth of reported ADHD diagnoses and prescriptions, especially in adults, isnt simply due to an increasse in the number of people who have the condition, writes Brandeis University social science Professor Peter Conrad in a recent paper published in “Social Science and Medicine”

One major flaw in Prof Brandeeis argument is that the science points to a large pool of undiagnosed ADHD in middle aged adults:
http://www.plosone.org/article/info%…l.pone.0031500

According to this study, the rate of diagnosable ADHD in the sample population of middle aged Australian adults was 6.2%. (My estimate as an ADHD aware clinician who has ADHD himself is that that would be in the right ball park at least).

I doubt that the rate of diagnosed ADHD in this population is more than 0.5%– it was about 0.2% a few years ago according to a survey done by the NSW health department.

So it is clear that in the middle aged population there is a great deal of undiagnosed ADHD. In this setting it is difficult to see whether there is any real increase at all in the last few years.

Actually I think there is- as the distribution of ADHD within the USA is not even- it clusters especially in very poor states with high rates of intrafamily trauma and also in Eastern seaboard states where kids live a more controlled and regulated life. It is lowest in more rural midwest states where children lead more active lives in more intact and healthy rural communities. Given Dr John Ratey’s observations about the overlap of the neurology of attention and movement it is clear that healthy outdoor play is essential to normal brain development- and that todays latchkey kids who spend more time on line and less time playing in the street may well be at risk of abnormal brain development.

Speaking as a clinician who was diagnosed at age 46, I see many cases of ADHD. After my diagnosis I realised to my alarm that I had, unknowingly been seeing ADHD adults for years- they were coming in with alcohol abuse, with habitual overeating, with chronic pain syndromes, with metabolic syndrome with marital and child rearing difficulties and with refractory anxiety and depression.

ADHD causes serious difficulties for those of us who have it, until we master it. Stimulant medication is only a part of the treatment regimen but it is a vital part for many of us. (My own personal treatment regimen is firmly anchored in mindfulness and I now practice largely in mindfulness and have a qualification as a meditation teacher. I could not have got there without access to dexamphetamine).

If it is true that the drug companies are playing a role in increasing ADHD awareness, I can only congratulate them, as my profession (especially in Australia) has abdicated its responsibility to the community in its regressive and incompetent attitude to the diagnosis and management of ADHD.

While my ADHD was diagnosed at age 46, I had had a strong clinical suspicion that I had ADHD based on my reading. However I was scared to seek diagnosis. I was afraid of being labelled eccentric or taking supposedly “dangerous medications”.

In the end I had to fire 2 psychiatrists before finding an individual competent to diagnose me, and that process took 2 years. By the time that process was done the damage to my marriage caused by my ADHD behaviours was irreparable.

People like Prof Conrad who focus on abstruse speculations about issues such as medicalisation cause real harms by scaring individuals away from seeking appropriate investigation and treatment and should be recognised for the menace that they are.

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