What are the symptoms of Attention Deficit Hyperactivity Disorder (ADHD)?
Most sources agree that an adult ADD/ADHD diagnosis is based on relevant behavioural tendencies as a child (through retrospective questioning). Children or adults can have ADD or ADHD, although the official term used by the American Psychiatric Association diagnostic criteria (DSM) is ADHD.
The DSM-III-R behavioural diagnostic criteria for a child will look for at least eight of the following behaviours occurring over six months with an onset before seven years old:
- Often fidgeting with hands or feet or squirms in seat
- Has difficulty remaining in seat when required to do so
- Is easily distracted by extraneous stimuli
- Has difficulty awaiting turn in games or group situations
- Often blurts out answers to questions before they have been completed
- Has difficulty following through on instructions from others
- Has difficulty sustaining attention in tasks or play activities
- Often shifts from one uncompleted activity to another
- Has difficulty playing quietly
- Often talks excessively
- Often interrupts or intrudes on others
- Often does not seem to listen to what is being said to him or her
- Often loses things necessary for tasks or activities at school or at home
- Often engages in physically dangerous activities without considering possible consequences
(Hallowell and Ratey, 1995, p200)
In diagnosing an adult the criteria is for at least 12 of the following behaviours occurring on a chronic basis, and a childhood history of ADD (Psychiatrists Hallowell and Ratey have compiled this list):
- A sense of underachievement, or not meeting one’s goals (regardless of how much one has actually accomplished)
- Difficulty getting organised
- Chronic procrastination or trouble getting started
- Many projects going simultaneously; trouble with follow through
- A tendency to say what comes to mind without necessarily considering the timing or appropriateness of the remark
- A frequent search for high stimulation
- An intolerance of boredom
- Easy distractability, trouble focusing attention, tendency to tune out or drift away in the middle of a page or conversation, often coupled with an ability to hyperfocus at times
- Often creative, intuitive and highly intelligent
- Trouble in going through established channels, following ‘proper’ procedure
- Impatient; low tolerance of frustration
- Impulsive, either verbally or in action
- A tendency to worry needlessly, endlessly and to scan the horizon looking for something to worry about, alternating with inattention to or disregard for actual dangers
- A sense of insecurity
- Mood swings, mood liability
- Physical or cognitive restlessness
- A tendency toward addictive behaviour
- Chronic problems with self-esteem
- Inaccurate self-observation
- Family history of ADD or manic-depressive illness or depression or substance abuse or other disorders of impulse control or mood
(Hallowell and Ratey, 1995, p201-2)
ADHD and ADD are labels that conveniently group together co-existing behaviours that conventionally and by default are classed as ‘pathological’ and are usually treated by drugs.
What causes ADHD?
The exact cause and origin of ADHD/ADD are unknown, although several theories have been put forward – the newer neurobiological theories distinctly more helpful than the earlier ones of bad parenting and bad behaviour. There is also thought to be a genetic link, although much research into this is still inconclusive.
Researchers (many of which have ADHD/ADD themselves) are keen for research into ADHD/ADD as a syndrome to continue, as well as the removal of the stigma of the pathology, or disorder.
It is generally agreed now that ADHD/ADD has a neurobiological origin, involving the brain and the CNS. The exact mechanism of the ‘disorder’ is still unknown. There is no single gene, neurotransmitter or lesion of the brain that has been found to cause ADHD/ADD. Also, the attentional system, which is involved in consciousness, waking experience, actions and reactions involves nearly all the structures of the brain.
Scientists have not found a way to measure the specific neurotransmitter imbalances that are responsible for ADHD/ADD, however there is enough evidence to say that ADHD/ADD is caused by altered neurochemical systems. Hallowell and Ratey state that ADHD/ADD is most likely “a disregulation along the catecholamine -serotonin axis, a dance where one misstep by one partner creates a misstep by the other” (p. 274).
Experiments with glucose uptake have located differences in the frontal region of the brain – the regulator of behaviour – in adults with ADD. Glucose metabolism and uptake was lower in adults with ADD, with resulting lower energy use in the brain. This was widespread throughout the brain, and most markedly in the prefrontal and premotor regions (Hallowell and Ratey, 1995, p275). This depressed frontal lobe activity is seen as a form of ‘disinhibition’.
An ‘inhibition-disinhibition’ framework is useful for understanding the experience and behaviours of a person with ADHD/ADD. This theory suggests that it is the inability to stop receiving messages that causes the distracted patterns of behaviour in those with ADHD/ADD (Hallowell and Ratey, 1995, p282).
How is ADHD treated conventionally?
The primary symptoms of ADHD/ADD (inattention, distractability, impulsivity, minipanic) are medicated using stimulants or antidepressants, which enhance certain neurotransmitters. The secondary symptoms of ADHD/ADD are treated by a wider range of drugs with a range of actions, depending on the symptom eg: outbursts of rage, impulsivity, OCD.
Medications for ADHD/ADD interact with the catecholamine system (epinephrine (adrenaline), norepinephrine (noradrenaline) and dopamine) to correct the dysregulated attentional processes and stop the ‘rush of experience’.
Both stimulants and anti-depressants increase the levels of neurotransmitters they affect allowing more of them to be available for use by the brain – specifically enhancing the functioning and use of neurotransmitters in the frontal region, smoothing out and regulating attentional functioning.
The exact location of the drugs mechanism in the brain is unknown, because of the lack of precise knowledge about the genesis of ADHD/ADD. One theory is that the drugs work on an impaired action of norepinephrine in the limbic system – in between the lower brain and the cortex.
The effects of the drugs are felt in the cortex and stimulants have an immediate effect, indicating that they work directly at the synapse, improving cell-to-cell communication. Other drugs for different neurobiological disorders work more slowly, on building receptor receptivity, for example.
Conventional approaches often combine medication with psychological therapies such as CBT and psychotherapy.
How can craniosacral principles be applied to the treatment of ADHD?
According to one source, there are several conditions that may “accompany, resemble or mask ADD” (Hallowell and Ratey, 1995, p203). These include:
- Anxiety disorder
- Bipoloar disorder or mania
- Disorders of impulse control
- Fatigue, chronic
- History of fetal alcohol syndrome
- Hyperthyroidism or hypothyroidism
- Lead poisoning
- Learning disabilities
- Personality disorders
- Substance abuse
- Tourette’s syndrome
With this range of conditions, while it is a given in conventional medicine that each of these separate conditions would receive separate treatment methods, or drugs, the fact that they may also resemble or mask ADD supports the idea of wholeness that is central to craniosacral therapy. Underneath the symptom(s) is the wholeness of the system itself, and the same basic structures and mechanisms that can be resourced and supported through craniosacral therapy.
In relation to ADHD/ADD it is also interesting to note that there is not one single structure in the brain that governs attentional systems and behaviour, and that the exact mechanism of the problem is unknown. Where conventional medicine works on the basis of narrowing down the focus of treatment, to the catecholamine-serotonin axis, for example, craniosacral therapy looks to work with the system as a whole, including all the structures that may or may not be involved in causing the symptoms of ADHD.
Ideas that there may be a genetic cause to ADHD/ADD are pre-empted by epigenetics and gene expression, which is an underlying theme in craniosacral approaches (Kennedy, 2011)
Addressing pre- and perinatal issues can also help to shift from identifying with symptoms to working with the whole picture.
Maternal stress and smoking has been linked to ADHD symptoms (Rodriguez and Bohlin, 2005). This raises the question of how the nervous system of the developing baby is affected and primed by stress in the womb. A baby can become ‘programmed’ to deal with a stressful environment, with a tendency towards sympathetic nervous system activation. Similar research has shown that stress during pregnancy can affect neurobehavioural development (Van de Bergh et al, 2005).
Birth trauma often causes sympathetic nervous system activation and dissociative patterns, which Sills believes are linked to attention deficit problems (Sills, 2004, p. 257, 260, 320, 371).
Structural compressions and torsions can affect areas of the brain that cause symptoms of ADHD/ADD (Dalton, 2011). Dalton also suggests that restricted drainage of blood and cerebrospinal fluid from the brain (cranial venous sinuses), which can often happen as a result of structural birth trauma, is also a common indicator when there are symptoms of ADHD/ADD present. Issues with the occipito-atlantal joint as a result of birth trauma are also thought to be a common indicator (Upledger, 1999).
Generally, using craniosacral principles and treating the whole person would include: orienting to the RTM, cranial bones, cranial venous sinuses, brain, spine and spinal cord, and assessing for and treating hypo- or hyper arousal states. Changes through craniosacral therapy would free up pressure on and disregulation of the CNS, which could bring about a relief of symptoms.
Driven to Distraction: Recognizing and coping with Attention Deficit Disorder. E. Hallowell and J. Ratey (1995)
Craniosacral Biodynamics, Volume Two. F. Sills (2004)
Is ADHD really a Genetic Disorder? G. Kennedy (2011)
Are maternal smoking and stress during pregnancy related to ADHD symptoms in children? A. Rodriguez and G. Bohlin (2005)
Antenatal maternal anxiety and stress and the neurobehavioural development of the fetus and child: links and possible mechanisms. A review. B. R. Van den Bergh, E.J. Mulder, M. Mennes and V. Glover (2005)
ADD, ADHD, Hyperactivity. J. Dalton (2011)
Symptoms and Conditions. J. Upledger (2008)
ADD Holistic Discussion Group. J. Upledger (1999)