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Differential diagnostics in ADHD

Differential diagnostics in ADHD

A careful diagnosis of ADHD always requires a differential diagnosis for other disorders that may cause the same or similar symptoms.

1. Differential diagnostics

1.1. Differential diagnosis

Differential diagnosis means making sure that the symptoms are not (also) caused by other causes or disorders and consequently require different treatment.

In the differential diagnosis, it is also important to consider which disorders are typical comorbidities of ADHD. For example, depression can also cause (certain) symptoms of ADHD. Depression is often comorbid with ADHD.
If a disorder is a typical comorbidity of ADHD, and if the burden of the comorbid disorder is not extremely debilitating, an experienced therapist will initially place the treatment focus on the ADHD itself, since successful treatment of the ADHD can often also reduce or completely remit (disappear) the comorbid disorders. Moreover, one in three treatment-resistant depressions is actually the mere consequence of undiagnosed ADHD (overload depression).
Depression, for example, can be treated with various medications. Some antidepressants are also effective (in lower doses) for ADHD. Similarly, stimulants such as methylphenidate or amphetamine drugs are also used against depression. Others (SSRIs) may exacerbate ADHD-I symptomatology in particular. Therefore, before massive treatment of ADHD comorbid depression with conventional antidepressants, the effect of antidepressants effective in ADHD should be considered in a dosage typical for ADHD.
In case of a depression diagnosis, again the typical ADHD symptomatology of dysphoria with inactivity has to be considered, which does not represent depression but is an original ADHD symptom.
Depression and dysphoria in ADHD

1.2. ADHD (ASD, OCD) - homogeneous disorders or purely dimensional grouping?

One study attempted to assign 238 affected individuals who showed different symptoms of ADHD, ASD, and OCD or were healthy controls to homogeneous disorder picture groups based on cortex thickness in 76 cortex regions. This was done using machine learning (weak AI). No homogeneous groups could be formed.1
This suggests that the individual differences between those affected by a disorder are greater than the similarities.

1.3. Comorbidity: the difference from differential diagnosis

While differential diagnosis means to check whether the symptoms that (here:) point to ADHD might not in fact stem from another problem, i.e. that there is no ADHD, comorbidity means that someone who suffers from one disorder (here: ADHD) is at the same time (additionally) affected by another disorder.

Comorbidity to ADHD therefore means that (here:) ADHD is clearly diagnosed and other problems exist in addition to ADHD.
Many disorders have very typical comorbidities - so does ADHD, so it is always necessary to check these once as part of a clean medical history. ADHD - Comorbidity

Most comorbidities typical of ADHD may have gene variants in common with ADHD or the common cause of early childhood stress exposure meeting a gene disposition specific for the respective (co)morbidity.
How ADHD develops: genes + environment

1.4. Prevalence: frequency of mental disorders

33.3% of all Germans and 38.8% of all EU citizens suffer from a mental disorder (within 12 months). Men and women are affected with roughly the same frequency, but with different types of disorders. The age group most frequently affected is 18 to 34 years.2
Of these 33.3%, 1/3 (i.e. a total of 11.1% of all Germans) suffer from more than one disorder. In these cases, there is an open comorbidity of several disorders from different diagnostic groups. The comorbidity with regard to different individual diagnoses from the same group is again significantly higher.
Comorbidities increase with age.2

For comparison of the prevalence values (frequency of occurrence) given below:
ADHD has a prevalence at

  • Children and young people combined 5.29
    according to long-term international meta-analysis of 102 international studies with n = 171,000 subjects3
    • Preschool children: approx. 34
    • Teenagers: approx. 8 %
      • Boys approx. 6 %4
      • Girls approx. 2 %4
        (We suspect that girls are more likely to be unrecognized because of the ADHD-I subtype that is more common among them)
  • Adults
    • Approx. 1 - 4 %4
    • Approx. 3 - 5 %5

Thus, the lifetime prevalence of ADHD would be similar to that of diabetes.6

Friedmann reports that the lifetime prevalence of ADHD in the U.S. increased from 7.8% in 2003 to 11% in 2011.5
This does not result from an increase in ADHD, but that ADHD is now better recognized and more reliably diagnosed.

For further information on the prevalence distribution of ADHD, see:⇒.. Frequency of ADHD (prevalence)

2. Differential diagnosis in ADHD

The following phenomena should be checked in an examination of where ADHD-typical symptoms originate.

2.1. “Healthy” stress response to stressful situation

2.1.1. Acute subjectively threatening stress

An acute and subjectively threatening stress situation can cause the entire ADHD symptomatology in otherwise healthy people.
All ADHD symptoms are stress symptoms. Therefore, all symptoms can be triggered by “normal” severe stress, i.e. by a situationally appropriate but strong perception of stress in healthy people.
With the end of the stressful situation, the symptomatology ends completely in healthy people.
However, if ADHD exists, the stress regulation system is permanently damaged due to genetic causes or a coincidence of a genetic disposition and too long, too intensive (usually early childhood) stress exposure ( Development of ADHD.
ADHD as a chronicized stress regulation disorder.
Therefore, in a differential diagnosis, the first step is to determine whether acute circumstances exist that are so stressful that they can cause the symptoms, for example:

  • Bullying7
    • Depression
    • Fear
    • Shorter sleep
    • Insomnia
    • Worse school grades
    • ADHD symptoms
  • Separation of attachment figures (divorce of parents)
  • Death of close person
  • Loss of the partner
  • Subjectively unsolvable stressful situation (loss of control)
  • Life upheaval (for children: relocation, for adults: insolvency, contentious divorce, etc.)
  • Inappropriate parenting methods (e.g., ignoring child; playing dead until child obeys)
  • Sexual abuse, physical abuse
  • Etc.

ADHD does not exist if the symptoms disappear after the situation is eliminated.

2.1.2. (Unrecognized) giftedness (> 120: 8.98%; > 130: 2.28%)

Prevalence of giftedness: IQ 120 and above: 8.98%, IQ 130 and above: 2.28%

Giftedness is not a disorder. Nevertheless, unrecognized giftedness can give rise to symptoms that are almost identical in nature and composition to ADHD symptoms.

2.1.2.1. Stress reaction unrecognized gifted person as an outsider

Highly gifted people have different interests, think “differently”, have different values and react differently. The lower the social competence with which those affected can bridge their being different, the stranger other children find them. This can trigger negative reactions and even bullying. But even without bullying, the “feeling different” and the “not belonging” (this is not only similar but identical to ADHD sufferers) and the lack of friends can increase to such a massive stress that the ADHD-typical stress symptoms can form.
Affected children are then fidgety, disruptive in class, do the class clown (ADHD-HI-like) or shut down internally, daydreaming away (ADHD-I-like).
However, in addition to the possible stress symptoms of bullied outsiders (which may well include unrecognized gifted individuals because of their otherness), there are a few similarities between ADHD and giftedness that are not stress-induced.

2.1.2.2. Similarities of single typical traits in HB and ADHD

Highly giftedness not only causes faster thinking, but often correlates with typical traits (“character traits”). Many of these traits resemble characteristics that are often observed in ADHD sufferers.
Giftedness and ADHD

We had assumed that the impressive correspondence between the positive characteristics of ADHD described in the ADHD literature and the typical character traits of gifted people described in the gifted literature resulted from the fact that ADHD almost always and giftedness very often correlates with high sensitivity. We assumed that these are character traits that do not result from ADHD or giftedness itself, but that they have their actual root in common high sensitivity.
However, recent data (including from the ADxS.org symptom test, n = 2000, as of July 2020) show no correlation between giftedness and high sensitivity.

Highly gifted as well as ADHD sufferers are attributed from the respective professional literature:

  • Primarily intrinsically motivatable (extrinsically/through external pressure difficult to motivate)
    • Ability to hyperfocus
    • Boredom and concentration problems with uninteresting or monotonous tasks (up to underperforming and excessive error rate)
    • Impatience
    • Tendency to interrupt others
  • Rejection of authority (authority is recognized only qua competence, not qua rank)
  • For some: difficulty in making decisions (too many options and facts to consider); primarily for people who internalize their stress responses, less so for people who externalize stress
  • Smalltalkaversion
  • Diplomacy deficit
  • Crowd aversion
  • High importance of truth, equality, justice
  • Often being perceived by others as weird or strange.

These traits (which do not occur in all HBs, of course, but do occur more frequently in HBs) should therefore be examined closely for their cause during diagnosis.

Unrecognized giftedness is not easy to recognize. Not all gifted people have special abilities. Many gifted people even emphatically reject such a classification for themselves because they do not perceive themselves that way. Here it is important to note the difference between giftedness = disposition and ability = implementation of the giftedness. Many highly gifted people need appropriate support in order to develop their abilities. In addition, not all giftedness lies in school-relevant areas. Mathematical geniuses or the variant of the knowledge-thirsty gifted person are easily recognized as gifted by nature.8910

Highly giftedness is of course not a compelling reason for feeling like an outsider and/or for developing ADHD-like symptoms. Mostly those are affected who cannot compensate their otherness by sufficient social competence.
All the prevalences mentioned are only a rough guide to make the probability of a possible comorbidity visible. And just as naturally, not every child who has ADHD is highly gifted.

2.1.3. Minor aptitude (< 80: 8.98%; < 70: 2.28%)

Underachievement and its consequences for learning performance behavior and reactive behavioral disorders (in case of over / underchallenge) can act like ADHD. ADHD occurs more frequently with underachievement.10
Prevalence of underachievement: IQ 80 and below: 8.98%, IQ 70 and below: 2.28%

In the case of an existing intellectual disability, the DSM-V criteria seem to be only partially suitable for ADHD diagnosis. In particular, the main symptoms of the DSM-V can also result from the giftedness itself. One study was able to correctly diagnose only 46% of ADHD sufferers among underachievers by means of DSM-V. Additional criteria - which the authors do not mention - are said to have increased the diagnostic accuracy of ADHD among the gifted to 82%.11

One study found that the Verbal Fluency Task showed lower phonological and semantic fluency in underachievers than in ADHD sufferers and lower semantic fluency than in dyslexics.12

2.2. Activity level appropriate to age

An activity level that is still age-appropriate, especially in younger children, may show an ADHDS-like symptom pattern.1310

A (very) high activity level in (very) young children may be age-related. This goes back with the development of the brain (which fits the description of ADHD as a developmental delay of the brain, when the activity level is significantly above the usual age-appropriate level). Some children also simply need more time than others at certain stages of development. This is not a disorder, but an individual characteristic that everyone has. Warm attention and patient encouragement, combined with ample opportunity to act out the motor urge to move, are the most sensible ways of reacting here.

2.3. Primary organic disorders

Sorting by prevalence (frequency of occurrence) in descending order. Prevalence refers to the frequency of the disorder itself, not to the frequency or probability of ADHD in that disorder. Thus, the prevalence of deficiency symptoms is quite high, but the influence of their correction on ADHD symptoms is not resounding

2.3.1. Consequences of sleep disorders (sleep disorders: children 47.1%; adults: 0.6 to 7.8%)

The annual prevalence of sleep disorders in Germany in 2008 was 0.6% (15 to 19 years) to 6.6% (60 years and older) in men and 0.8% (15 to 19 years) to 7.8% (60 years and older) in women.14
Sleep problems in ADHD are extremely common

  • 70 - 80 % of ADHD affected children suffer from sleep problems
  • 20 - 30 % of ADHD affected adults suffer from sleep problems

A Chinese study of 23,791 school children found that 68.7% of children with ADHD had poor sleep quality, compared to 47.1% of children without ADHD.15

See also: ADHD - comorbidity, there on sleep problems

In the case of sleep problems and ADHD, it is difficult to distinguish cause and effect. ADHD very often causes sleep problems and sleep problems often cause ADHD-like symptoms.

In the case of an ADHD diagnosis, comorbid sleep disorders should always be treated with special priority. In addition, medications for sleep problems must be considered for their potential negative impact on ADHD symptoms, just as medications for ADHD must be evaluated to ensure that they do not exacerbate sleep problems. More about the treatment of sleep problems in ADHD: Treatment of sleep problems in ADHD

  • Vigilance disorders in sleep-wake regulation impairments1617
  • Consequences of sleep apnea syndrome10
    Obstructive sleep apnea syndrome (OSAS) is the most common sleep-related breathing disorder. The prevalence is approximately 4% in men and 2% in women.
    Obstructive sleep apnea (OSA) is even more common and reaches strikingly high numbers, especially when subgroups are considered. For example, patients with diabetes mellitus or arterial hypertension have a prevalence of approximately 36%, obese patients have a prevalence of 50%, and patients with refractory arterial hypertension have a prevalence of 83%. Among these, estimates suggest that 80% of male and 90% of female patients with sleep apnea syndrome are undiagnosed and thus untreated.”18
    Breathing pauses in children’s sleep can trigger cognitive distress, causing symptoms that resemble ADHD.19
  • Chronic lack of sleep16
  • Disturbances of the dream sleep phases cause within a few days
    • Increased irritability20
    • Increased impulsivity20
    • Reduced concentration21
    • Reduced attention21
    • Working memory disorders22

Common symptoms of sleep problems and ADHD:23

  • Motor hyperactivity, physical restlessness
  • Concentration problems
  • Attention problems

ADHD symptoms atypical of sleep problems:

  • Inner restlessness (typical in atypical depression, less so in melancholic depression)
  • Impulsivity
  • High fluency of speech (logorrhea, polyphrasia)
  • Thought chasing, thought circling
  • Rapid mood swings
  • Dysphoria with inactivity

Symptoms of sleep problems atypical of ADHD:

  • Drowsiness
  • (Daytime) fatigue

2.3.2. Postconcussion syndrome (consequences of a concussion) (11 to 80 %)

Another name: post-concussion syndrome

Prevalence: probably in 1 / 10 patients with mild traumatic brain injury24
Concussion is the mildest form of traumatic brain injury. In the USA, concussion is assumed to have an incidence of 1.15% (3.8 million / 331 million). This would put the incidence of postconcussion syndrome at approximately 0.115%/year
The prevalence ranges from 11 to 80%.25

In uninjured adolescent athletes, ADHD appears to mimic postcommotion syndrome. ADHD sufferers report more symptoms of postcommotion syndrome than do nonaffected individuals.26 Another study reports prolonged times to recovery from concussion in ADHD.27
One study found no clustering of ADHD in 12-/13-year-old athletes with concussion.28

2.3.3. Deficiency symptoms (5 to 30 %)

2.3.3.1. Vitamin D3 (30 %)

Prevalence D3 deficiency:2930
* 30.2 % inadequately supplied
* 38.4 % Sufficiently supplied
* 31.4 % in need of improvement or oversupplied

  • At the same time, vitamin D3 deficiency seems to be very common in ADHD.31 A D3 administration especially in autumn / winter is recommended.
  • D3 requires fat for absorption, i.e. an intake requires that the preparations contain fat or a simultaneous food intake. A glass of milk should already suffice for this purpose.
2.3.3.2. Vitamin B12 (5 to 30 %)

Prevalence B12 deficiency:3230

  • Young adults 5 to 10
  • Older adults 10 - 30
  • At older ages, concentration and attention problems due to B12 deficiency are virtually phenotypic.
  • B12 can be supplied more safely by means of injections.
  • In the meantime, B12 is also available in tablet form.
  • In contrast, foods with potentially high levels of B12 (spinel algae) are not reliable enough to dose.
2.3.3.3. Zinc (11 %)

Zinc deficiency can exacerbate symptoms of existing ADHD.33

  • Prevalence zinc deficiency:

    • Population-wide
      • Europe: 11 %30
    • Healthy children from 1 to 3 years
      • Western Europe: 31.3 %34
    • in children under five (Disease Control Priorities in Developing Countries 2006).
      • East Asia/Pazifik: 7%
      • Eastern Europe and Central Asia: 10
      • Latin America and Caribbean: 33 %
      • Middle East and North Africa: 46 %
      • Sub-Saharan Africa: 50
      • South Asia: 79 %
  • Zinc deficiency is manifested, among other things, by a deficiency of T and B lymphocytes

  • Zinc deficiency is often accompanied by vitamin A deficiency

  • Zinc is involved in the Ada Repair protein. This repairs (demethylates) methylated phosphate linkers in DNA by transferring the methyl group to the cysteinate S35

  • Vitamin B6

  • Magnesium deficiency

  • Iodine

2.3.4. Migraine (women: 18 %, men 6 %)

Prevalence Women 18 %, Men 6 %
The overall symptom picture is usually quite different from ADHD and is hardly permanent.

2.3.5. Substance abuse (illicit drugs: 10%, nicotine: 16.6 to 25.5%)

Among adults with ADHD, the prevalence of substance abuse is 33.5%.36 The risk for substance abuse among adults with ADHD in the U.S. is increased 1.7 to 7.9-fold.37

The prevalence for substance abuse among German adults in 2019 (12-month prevalence and lifetime prevalence) was:38
Cannabis: 7.1% / 28.3%
Cocaine / crack: 1.1% / 4.1%
Ecstasy: 1.1% / 3.9%
Amphetamines: 1,2 % / 3,8 %
Methamphetamine / crystal meth: 0.2 % / 0.8 %
Smoking (at least 20 cigarettes/day), adults:39

  • Men: 25.5 %
  • Women 16.6 %

Alcohol:40

  • Risky use within 12 months
    • Men 15.6 %
    • Women 12.8 %

Among patients hospitalized for alcohol dependence, one study found an ADHD prevalence of 20.5%.41

If, in addition to ADHD, aggressive and oppositional defiant behavior and low self-esteem are also present, the likelihood of substance abuse is significantly increased, whereas no more frequent substance abuse was found in adolescent ADHD sufferers without these additional symptoms.4243

In our estimation, substance abuse is much more likely to be a consequence of ADHD than a cause of a full ADHD symptom picture. In rarer cases it exists comorbidly. Treatment with stimulants very often eliminates the addictive tendency in ADHD. Modern forms of stimulant drugs are completely unsuitable for abuse as a drug (e.g. Elvanse: lysine-bound prodrug of amphetamine, which is only very slowly converted to the active substance in the intestine).

In the Continuous Performance Test, ADHD sufferers showed more responses to correct timing compared to substance abuse sufferers.44

2.3.6. Addiction / dependence (alcohol: 5%, gambling: 0.31%)

Prevalence: Present in 24.9% of adults with ADHD.13

Alcohol:40

  • Dependency
    • Men 4.8 %
    • Women 2 %
  • Abuse
    • Men 4.6 %
    • Women 1.5 %

In Berlin, 5.0% of the 15-64 year old respondents met the criteria for alcohol dependence according to DSM-IV (men: 6.4%, women: 3.5%).45

In Germany, the prevalence for gambling addiction is 0.31%, and the prevalence for problem gambling is 0.56%.46

In the case of comorbidity of ADHD and addiction, there is an increased probability that ADHD is the causal cause of addiction and not addiction the cause of ADHD. This was shown at least for smoking, cannabis and probably also alcohol.47

With increased gene risk scores for ADHD (polygenic risc scores, PRS), one study also found a 20% increased probability of addiction. There were no differences in the intensity of addiction (use, abuse, dependence) or the type of addictive substances (alcohol, cannabis, other illicit drugs). Conversely, ADHD-PRS explained only 0.2% of the probability of addiction compared to other risk factors.48

One study showed an ADHD prevalence of 16.7% in severely addicted individuals compared to 2.5% in the control group.49
More significantly, 53% of the severely addicted had a socially disordered behavior in childhood or adolescence (up to 15 years) as measured by the SKID-II (control subjects at 2.5%).50 Earlier social behavior disorder (OR = 35.1) compared to childhood hyperkinetic behavior (OR = 5.7) was by far the greater risk factor for severe addiction.51
This suggests to us that addiction plays a role predominantly in ADHD-HI and less in ADHD-I.
Regarding the preference of addictive substances, there is an indication of a more frequent use of cannabis products among people with (former) hyperkinetic behavior. For opiates, cocaine, amphetamines, sedatives and hallucinogens there seems to be no significant difference.52
A co-occurrence of hyperkinetic and socially dysfunctional behavior is associated with an early first use of illicit drugs, but statistically only an earlier and increased use of nicotine could be demonstrated.53
Long-term abuse of dopaminergic drugs (cocaine, amphetamines) leads to long-term downregulation of the dopamine level. Withdrawal symptoms then correspond to ADHD symptomatology. 54 Against this background, the question arises whether ADHD drugs (stimulants), which are known to have no intoxicating effect, might not be helpful in the withdrawal of dopaminergic drugs.
ADHD sufferers with comorbid cocaine addiction showed significant reductions in addictive behaviors when treated with stimulants.55

Common symptoms of addiction / substance abuse and ADHD:23

  • Impulsivity
  • (inner) restlessness, motor hyperactivity
  • Concentration problems
  • High fluency of speech (logorrhea, polyphrasia)

ADHD symptoms atypical of addiction/substance abuse:

  • Thought chasing, thought circling
  • Attention problems
  • Dysphoria with inactivity
  • Mood swings

Symptoms of addiction/substance abuse that are atypical of ADHD:

  • Substance Abuse
    • Excessive consumption of a substance, even if serious consequences are present
  • Addiction / Dependence
    • Excessive consumption to the point of dependence on the drug
    • Very difficult to stop

2.3.7. Thyroid problems (cumulative 7% to 14% in women, 2.75% to 3.5% in men)

See also the guideline of the Arbeitsgemeinschaft ADHS der Kinder- und Jugendärzte e.V., status 2014.10

2.3.7.1. Hyperthyroidism (women 1 - 2 %, men 0.25 - 0.5 %)

Prevalence: 1-2% in women, 0.25-0.5% in men565716

ADHD-like symptoms may include:58

  • Nervousness
  • Aggression
  • Irritability
  • Increased feeling of anxiety up to fearfulness
  • (extreme) jumpiness
  • Difficulty to relax
  • Sleep disorders

Other symptoms not typical of ADHD may include:58

    • Sweating
      • Palpitations
      • Atrial fibrillation
      • (strong) trembling
      • Diarrhea
      • Strong weight loss
      • Fatigue
      • Weakness
      • Additional occurring psychosis
2.3.7.2. Hypothyroidism / underactive thyroid gland (from 60 years approx. 2 %)

From the age of 60, about 2% of the population is affected by hypothyroidism.16

ADHD-like symptoms may result from hypothyroidism59
Hypothyroidism becomes more common with age (usually a consequence of Hashimoto’s autoimmune thyroiditis).

Hypothyroidism often develops slowly, which is why symptoms are difficult to detect.

2.3.7.3. Hashimoto’s thyroiditis (women 4.5 - 9.5 %, men 0.5 - 1 %)

Hashimoto’s (Struma lymphomatosa Hashimoto) is an autoimmune disorder that causes hypothyroidism59
The prevalence of Hashimoto’s in Germany is about 5 to 10 %. Prevalence and incidence increase with age. Women in the 3rd-5th decade of life are affected about 10 to 20 times more often than men.60

ADHD-like symptoms may include:58

    • depressive moods
      • Apathy
      • Rapid exhaustion
      • Concentration disorders.

Other symptoms not typical of ADHD may include:58

    • Fatigue
      • In extreme cases: delusions / suicidal thoughts
      • Weight gain
      • Slowed heartbeat
      • Slowed reflexes
      • Decreased libido.

It is reported that adrenal insufficiency (an attenuated production of cortisol by the adrenal gland) often leads to thyroid insufficiency. Treatment of the thyroid with thyroxine then increases the cortisol demand on the adrenal gland. However, if the adrenal gland is already so weakened that the increased cortisol production completely overwhelms it, a collapse of the adrenal gland can be the result, which further reduces cortisol production, which is why the adrenal gland should be considered and treated before thyroxine treatment.61

An attenuated cortisol stress response is often present in ADHD-HI. *⇒ Cortisol and other stress hormones in ADHD *This could be a sign of mild adrenal insufficiency. However, this is often likely to result from pituitary weakness due to CRH receptor downregulation. To distinguish this from adrenal insufficiency, see Hypocortisolism (adrenocortical insufficiency) In this article.
However, adrenal collapse due to thyroxine therapy is not reported as typical in ADHD.

2.3.8. Restless legs syndrome (children 2 %, adults 5 to 10 %)

Prevalence:62

  • Children 2 %
  • Adults 5 - 10

Restless Legs correlates with ADHD symptoms.1617
Intense sugar consumption - especially in people who do not tolerate sugar well - can cause twitching in the limbs (especially the legs), which can act similarly to a mild form of restless legs and can be a hindrance to falling asleep.

2.3.9. Prenatal harm from alcohol (0.8% to 8.2%)

Other names: Fetal Alcohol Syndrome, Embryofetal Alcohol Syndrome, alcohol effects, FAE, FAS, alcohol embryopathy
Prevalence: 0.8 to 8.2% of all births, with approximately 10% of all cases developing full symptomatology.63

Around 15 to 30% of all mothers continue to drink alcohol during pregnancy.63 The risk to unborn children is considerable.
This problem is also considered to be a possible cause of ADHD.64 The risk of ADHD among FAE/FAS sufferers is said to be increased 10-fold.65 One study found 70% of adopted children with Fetal Alcohol Spectrum Disorder to have ADHD later in life.66

Differential diagnosis of FAS and ADHD

Symptoms of FAS alone (according to Wikipedia; black and lean), also in ADHD (bold/red):

  • Physical area
    • Growth disorders, short stature, underweight
    • Comparatively small head circumference (microcephaly), underdevelopment of the brain (microencephaly)
    • In profile, flat-looking midface with flat upper jaw region, receding chin (micrognathia) and a short, flat nose (snub nose) with nostrils initially pointing forward (plug nose)
    • Narrow (upper) lip red (missing cupido bow) and little modulated, flat or missing middle groove (philtrum) between nose and upper lip
    • Small teeth, increased tooth spacing
    • Specially shaped and low set ears
    • Comparatively small eyes with narrow, partly drooping eyelids (ptosis)
    • Sickle-shaped skin fold at the inner corners of the eyes (epicanthus medialis)
    • Anti-mongoloid (downward-outward, lateral-caudal sloping) eyelid axes
    • Hemangioma (blood sponge)
    • Coccyx dimple
    • Muscle weakness (muscle hypotonia), underdevelopment of the musculature
    • Weakness of connective tissue, lack of subcutaneous fat tissue
    • Special hand furrows, flat hand line relief
    • Cleft palate can be caused by alcohol consumption during pregnancy
  • Organic area, physical malformations
    • Speech disorders
      *(ADHD itself shows no or only weak speech disorders, but frequent comorbidity partial performance disorders; speech disorders are rare and rather atypical in ADHD)
    • Hearing Impairments
    • Sleep disorders
    • Eating and swallowing disorders, often absent or excessive sense of hunger
      *(in ADHD, loss of appetite is more likely to be a consequence of medication; obesity, however, is a more frequent comorbidity of ADHD)
    • Ocular malformations, multiple clefts, myopia, hyperopia, astigmatism, strabismus
    • Heart defects, often septal defects
    • Cleft palate
    • Alcohol cardiomyopathy (alcohol-induced heart muscle damage)
    • Deformities in the urogenital region
      • Kidney malformations
      • Developmental disorder of the urethra (hypospadias)
      • Undescended testicle (cryptorchidism)
      • Enlargement of the clitoris (clitoral hypertrophy)
    • Inguinal hernia
    • Dislocation of the hip (hip luxation)
    • Spinal curvature (scoliosis)
    • Abnormalities of the ribs and vertebrae (e.g. block vertebrae)
    • Funnel chest, keel chest
    • Underdevelopment of the finger end links with nail hypoplasia
    • Shortening and bending of the little finger, partly permanent curvature
    • Adhesion of ulna and radius
  • Neurological-cognitive area
    • General developmental retardation up to independence
    • Lack of concentration, learning disability, cognitive disability
    • Difficulty in understanding abstract things and logical relationships
    • Problems with capturing terms like soon, before, after, soon, the day after tomorrow.
    • Problems in the mathematical area, e.g. estimating numbers, understanding the time and dealing with money values*
      *(In the case of ADHD, dyscalculia may be a comorbid partial performance disorder)
    • Seizures, epilepsy
    • Emotional instability, fluctuations of balance, moods and emotional expressions
    • Frequent long-lasting temper outbursts
    • Hyperactivity
    • Hyperexcitability (hyperexcitability of the central nervous system)*
      *(In ADHD: High sensitivity)
    • Hypersensitivity or hyposensitivity to often even mild pain, temperature, touch stimuli, etc.*
      *(ADHD: High Sensitivity)
    • Under- or Overreactions to tactile stimuli*
      *(ADHD: High Sensitivity)
    • Trustfulness (e.g. going along with strangers)
    • Increased willingness to take risks, recklessness, thus increased accident proneness
    • Aggressiveness* and destructiveness
      *(ADHD itself not, but common comorbidity)
    • Above-average reaction times (ADHD not, rather above-average changing reaction times)
    • Inattention, easy distractibility up to sensory overload by various environmental stimuli (lights, colors, sounds, movements, people, etc.)
  • Behavioral problems
    • Motor coordination difficulties due to developmental delays in fine and gross motor skills and poor eye-hand coordination (“clumsiness”)
    • Problem solving difficulties* (same approaches over and over again without variables)
      *(in ADHD rather disorganization due to frequent forgetting of details, but also impaired learning)
    • Self-stimulating, sometimes self-injurious behavior
    • Impatience and spontaneity on the one hand, difficulty in making decisions on the other hand
    • Dissocial and oppositional behavior* *(Not in ADHD itself, but more often comorbid oppositional deficit behavior, dissocial behavior also not a comorbidity)
    • Failure to recognize consequences
    • Difficulty fitting into and feeling comfortable in social settings appropriately*
      *(In ADHD-HI because of inner tension and urge to move, in ADHD-HI and ADHD-I because of overstimulation leading to symptoms of exhaustion and overload; often also social phobia, in ADHD-I because of tendencies to withdraw and dream away)
    • Ignorance of verbal instructions, uncooperative and oppositional behavior when limits are set verbally (failure to take “no” for an answer)
      *(In ADHD rather overhearing, forgetting, or going over it in enthusiasm. No systematic ignoring as in FAE).
    • Insensitivity or lack of understanding of nonverbal signals through gestures, facial expressions and body language of other people
    • Meaningful understanding of instructions, but inability to execute appropriately*
      *(nevertheless different in ADHD, rather organizational inability due to planning, scatterbrainedness, forgetfulness than comprehensive inability)
    • Often anxious-worried and chronically frustrated attitude
    • Low frustration tolerance
    • Quick fatigability

2.3.10. Seizure disorders (epilepsy: 0.5 to 1 %)

The prevalence of epilepsy is 0.5% to 1%.67

Source10

  • Pyknolepsy16
  • Seizure disorder with absences or complex partial seizures1617
  • Epilepsy-related seizure forms (absences)68

2.3.11. Hydrocephalus (hydrocephalus) (0.4 - 0.8 %; over 65 years 3 %)

Prevalence: 0.4 - 0.8%, > 65 years: approx. 3%69

Children with hydrocephalus are at nearly three times the risk for ADHD.70
In old age, hydrocephalus often occurs comorbid with Alzheimer’s disease and vascular dementia.

2.3.12. Prolactinomas (0.02 - 0.05 %)

Prevalence: 30 to 50 / 100000 (0.02 to 0.05 %)

Prolactinomas are prolactin-secreting (benign) tumors
ADHD- Neurotransmitters - Messenger substances

2.3.13. Phenylketunorie (PKU) (0.0125 %)

Other names; Følling’s disease, Fölling’s disease, phenylpyruvic acid oligophrenia, oligophrenia phenylpyruvica
Prevaöenz; 1 / 8.000 (0,0125 %)

Phenylketonuria sufferers often show symptoms of ADHD, although the subtypes with hyperactivity seem to predominate.71727374

Phenylketonuria (PKU) is a recessive disorder of phenylalanine metabolism due to mutations of the phenylalanine hydroxylase gene). PKU results in a significant excess of phenylalanine (hyperphenylalaninemia). Since phenylalanine and tyrosine pass through the blood-brain barrier through the same transporters, and these transporters have a higher affinity for phenylalanine, when there is excess phenylalanine in the blood, too little tyrosine enters the brain. Tyrosine is a precursor for dopamine, which further gives rise to norepinephrine and epinephrine. Therefore, an excess of phenylalanine in the blood leads to a lack of dopamine, norepinephrine, and epinephrine in the brain.75 In addition, phenylalanine excess causes changes in cerebral myelin and protein synthesis, as well as reduced levels of serotonin in the brain.76 ADHD and phenylketonuria thus have the common feature of a dopamine deficiency.7377

2.3.14. Consequences of severe brain infections (cumulative 0.05% to 0.16%)

Sources687817

2.3.14.1. Encephalitis (cumulative 0.03%)

Prevalence:79
Autoimmune encephalitis 13.7/100,000 (0.0137%)
infectious encephalitides 11.6/100,000 (0.0116%)
viral encephalitis 8.3/100,000 (0.0083%)

Brain infection with inflammatory change due to invading microorganisms.
Encephalitis destroys the cells in the substantia nigra that make dopamine.
Those affected by the encephalitis epidemic of 1914 to 1917 showed typical symptoms of ADHD as it progressed. Children developed hyperactive motor skills, adults Parkinson’s symptoms.
The symptoms are consequences of dopamine deficiency, as it is characteristic for ADHD. These symptoms could be reproduced in animal experiments as a consequence of disturbed dopamine production.80

See also Viral infections as a cause of ADHD in the article Age-independent physical stress as ADHD environmental cause in the chapter Development.

2.3.14.2. Perinatal hypoxemia (0.001 to 0.009%)

Prevalence: 1 to 9 / 100,000 (0.001 to 0.009%)((Hypoxic-ischemic encephalopathy (HIE), Orpha.net))

Oxygen deprivation during birth is a major cause of early childhood brain damage (FKHS).
Led to the death of dopamine-producing cells in the substantia nigra in animal experiments, resulting in a decrease in dopamine levels of up to 70%.81
Hypoxemia is associated with adenosine excess. Adenosine inhibits dopamine

2.3.14.3. Bacterial infections (cumulative 0.01% in women, 0.12% in men)
  • Meningitis: meningitis
    • Prevalence: 0.5 / 100,000 (0.0005 %)82
  • Brain abscesses: 0.3-1.3 /100,000 per year (0.0003% to 0.0013%)
    • Local infection of the brain tissue. Starts as focal encephalitis (cerebral phlegmon, “cerebritis”). As it progresses, slowly develops into a collection of pus with a connective tissue capsule
  • Syphilis (prevalence 11.5/100,000 (0.115%) in men, 0.9/100,000 (0.009%) in women)

2.3.15. Neurofibromatosis type 1 (0.029%)

Other names: Von Recklinghausen disease, Recklinghausen’s disease, neurofibromatosis Recklinghausen, peripheral neurofibromatosis
Prevalence of about 1:3500 (0.029%) one of the most common hereditary neurological diseases. Neurofibromatosis type 1 shows malformations of the skin and the central nervous system. Neurofibromatoses are nerve tumors

Among 128 neurofibromatosis type 1 -affected individuals (53.1% girls), 28.9% (37/128) were found to have ADHD, including 20 ADHD-C, 15 ADHD-I, and 2 ADHD-HI
Other comorbidities of neurofibromatosis type 1 were macrocephaly (head circumference more than 2 SDs above age average, 37.5%), headache (18.6%), cognitive impairment (7.8%), motor deficits (6.2%), and epilepsy (4.68%). MRI revealed T2-weighted hyperintensities in the basal ganglia and/or cerebellum (70.5%), optic nerve gliomas (25.8%), plexiform neurofibromas (9.3%), Chiari malformation type 1 (6.7%), arachnoid cysts (5%), central nervous system gliomas (3.1%).83

Diagnostic criteria - at least 2 of the following symptoms:84

  • Six or more café-au-lait spots (CAL) > 5 mm in diameter prepubertally and > 15 mm postpubertally.
  • Freckling in axilla or inguinal region.
  • Two or more neurofibromas of any type or a plexiform neurofibroma (PNF)
  • Glioma of the visual pathway
  • Two or more iris nodules identified by slit lamp examination, or two or more choroidal abnormalities (CAs) detected as irregular bright nodules by optical coherence tomography (OCT) or near infrared imaging (NIR imaging).
  • Specific bony lesions such as wedge bone dysplasia, anterolateral bowing of the tibia, or pseudarthrosis of the long tubular bones.
  • A heterozygous pathogenic (= disease-causing) NF1 variant with an allele frequency of 50% in normal tissues such as leukocytes.

2.3.16. Velocardiofacial syndrome (22q11DS) (0.01 to 0.05%)

Other names: CATCH 22, Cayler cardiofacial syndrome, Di George syndrome, DiGeorge sequence, microdeletion 22q11.2, monosomy 22q11, Sedlackova syndrome, Sphrintzen syndrome, syndrome of conotruncal anomaly with facial dysmorphia, Takao syndrome

22q11.2 deletion syndrome (DS)85

The prevalence of velocardiofacial syndrome is 1 - 5 / 10,000 (0.01 to 0.05 %)86

2.3.17. Cortisol disorders (cumulative 0.0042 to 0.0048%)

2.3.17.1. Hypocortisolism (adrenocortical insufficiency) (0.004%)

Sources:8788

Addison’s disease: prevalence: 4/100,000 (0.004%).
Weaker forms are significantly more common.

Since basal cortisol levels are slightly reduced in ADHD (in ADHD-HI as in ADHD-I), ADHD could be called very mild adrenal insufficiency (adrenal weakness).

2.3.17.2. Hypercortisolism (Cushing’s syndrome) (0.0002 to 0.0008%)

Prevalence: 8/1,000,000 in men (0.0008%), 2/1,000,000 in women (0.0002%)89

  • ACTH-dependent form (80 % of cases)
    • Micro- or macroadenoma of the anterior pituitary gland produces ACTH (= Cushing’s disease)
    • (mostly malignant) tumors outside the pituitary gland (often bronchial carcinomas) as cause for ectopic ACTH production
  • ACTH-independent form (20 % of cases)
    Overproduction of glucocorticoids (cortisol) and mineralocorticoids by adrenal cortex
    • Adrenocortical adenoma (pure cortisol overproduction)
    • Adrenocortical carcinoma (increased production of cortisol and androgens)
    • Nodular hyperplasia of the adrenal cortex

2.3.18. Moyamoya (0.0001% to 0.0009%)

Moyamoya is particularly common in Japan.
Prevalence
Worldwide: 1 / 1,000,000 to 9 / 1,000,000 (0.0001 % to 0.0009 %)90
Japan: 1 / 30,000 to 1 / 9,500 (0.0033% to 0.0105%)
Incidence Japan: 1 / 280,000 to 1 / 89,000

Moyamoya is a narrowing or occlusion of cerebral arteries leading to relative anemia (stroke and transient ischemic attack) in the brain. Many small compensatory vessels form as bypasses.
Moyamoya may present with symptoms confusable to ADHD.91

2.3.19. Hamartoma of the hypothalamus (0.0005%)

Prevalence: 1 / 200,000 (0.0005 %)92

A hamartoma is a tumor-like, benign tissue change due to defectively differentiated or scattered germinal tissue. A hypothalamic hamartoma can produce a variety of hormones and cause premature puberty, obesity, and epilepsy in addition to ADHD symptoms, conduct disorder, oppositional defiant behavior, antisocial behavior, tantrums, intellectual regression, and cognitive impairment. 60% of those affected by a hypothalamic hamartoma develop externalizing disorders (especially in boys and in epilepsy), and 30% develop internalizing disorders.9394 MPH can significantly improve ADHD triggered by a hypothalamic hamartoma, as can treatment with a gonadotropin-releasing hormone (GnRH) analog.95 In severe cases, stereotactic laser surgery could be helpful.96

2.3.20. Allergies (with motor restlessness)

Source16

2.3.21. Visual, hearing disorders

Sources1016

2.3.22. Lesions of the left cerebral hemisphere

  • Attention selection impairs97
    • E.g. in situations that require quick decisions between relevant and irrelevant stimuli
    • Frequently increased number of errors in choice-response tasks or extended response times

Lesions of the OFC have been known since the case of Phineas Gage (Harlow 1848) and are associated with specific symptoms:98

  • often dramatic changes in personality
  • impulsive
    • often reckless, risky behavior
    • often conflicts with the law
    • disinhibited in terms of instinctive behaviors
    • Problems with drive control
  • irritable
  • argumentative
  • Tendency to crude humor
  • Disregard for social and moral principles
  • severe attention deficit
    • strong distractibility by external or internal stimuli

The OFC normally has inhibitory functions. These take place via efferents to:98

  • Hypothalamus
  • Basal Ganglia
  • other neocortical areas, including in the PFC

2.3.23. Organic brain damage

Source16

2.3.24. Status epilepticus during sleep (ESES)

Other names: Bioelectric status epilepticus during sleep, CSWS, CSWS syndrome, ESES syndrome, Epileptic encephalopathy with continuous spike-wave discharges in slow-wave sleep
Prevalence: unknown. Orphan disorder (rare).99

Epilepsy with continuous spike-wave discharges during sleep (CSWS) is a rare epileptic encephalopathy in children. It is characterized by seizures, electroencephalographic patterns of status epilepticus during sleep (ESES), and cognitive developmental regression.100

ESES is associated with ADHD-like symptoms. In one study, treatment with ACTH reduced ADHD symptoms by an average of 67%.101 Another study by the same authors found similar improvements with ACTH in ADHD and in stuttering.102

2.3.25. Traumatic or space-occupying cerebral disorders/other psychoorganic syndromes with cerebral damage and/or psycho-mental retardation

Source10

2.4. Drug side effects

Significant effects usually only with continuous therapy.

Examples:

  • Anticonvulsants
    e.g.
  • Beta-mimetics10
  • Drug-induced Hypovitaminosis of the B vitamins
    Vitamin B-12 deficiency causes ADHD-like symptoms
  • Neuroleptics16104105
  • Benzodiazepines16104105
    Benzodiazepines reduce the activity of the locus coeruleus and thus reduce the transport of norepinephrine to other parts of the brain.106 The disturbance of the norepinephrine production of the locus coeruleus is at the same time ADHD-typical.
  • Antihistamines16104105
  • Antiepileptic drugs104105
  • Isoniazid16105
  • Bronchiospasmolytics104105
  • Isoniazid104105
  • Selective serotonin reuptake inhibitors (SSRIs)
    SSRIs (namely citalopram and escitalopram) are suspected to increase the action of dopamine reuptake transporters.107. Overactive dopamine reuptake transporters are a possible cause to induce the dopamine deficiency that triggers ADHD symptoms (especially in the striatum) by reuptaking presynaptically released dopamine even before it has had a chance to provide its communication effect at the postsynapse. ADHD - neurotransmitters - messenger substances

2.5. Mental and psychiatric disorders

2.5.1. Anxiety disorders (annual prevalence: 22.9% (women), 9.7% (men))

Prevalence: 22.9% of all women, 9.7% of all men within one year.210
Prevalence in girls under 18 years: 7.85%.108
Anxiety disorders co-morbidly exist in 25% of ADHD sufferers,109 16.7% of ADHD affected children and 27.2% of ADHD affected adults.13 Other sources cite 15% to 35%110 and 35.6% among adults in England in 2007.111

Performance anxiety is particularly common.112

Common symptoms of anxiety disorders and ADHD:23

  • Inner restlessness
  • Concentration problems
  • Attention reduced
  • Mood swings
  • Sleep problems

ADHD symptoms atypical of anxiety disorders:

  • High fluency of speech (logorrhea, polyphrasia)
  • Thought chasing, thought circling
  • Impulsivity (atypical for ADHD-I)

Symptoms of anxiety disorders atypical of ADHD:

  • Fatigue
  • Muscle tension

Anxiety in ADHD may partially reduce impulsivity and response inhibition deficits, exacerbate working memory deficits, and appears to be qualitatively different from pure anxiety. Comorbid anxiety in ADHD appears to have divergent expressions:110113

  • Seem increased
    • Negative affect
    • Mood disorders
    • Disruptive social behavior
    • Attention problems
    • School phobia
  • Seem reduced
    • Anxious / phobic behavior
    • Social competence
2.5.1.1. Panic disorder (3.2 to 3.6%)

Prevalence panic disorder: 3.2% to 3.6%114

2.5.1.2. Generalized anxiety disorder (1.9 to 31.1%)

Prevalence of generalized anxiety disorder: 1.9% to 31.1%114

2.5.2. Excretory disorders (enuresis, defecation) (children: 18.5%)

18.5% of children with ADHD are affected.13

2.5.3. Affective disorders (10 to 17 %)

Prevalence:
Lifetime: 10 % to 17115
under 18 years: Girls 2.54%, boys 1.10%.116

Affective disorders are described in 27.9% of ADHD affected children and in 57.9% of ADHD affected adults13. Further, a prevalence of 37.1% for mood instability and 29.9% for depression in adults in England in 2007 is reported.117

2.5.3.1. Depression (10% (men) 20% (women))

12% to 50% of children with ADHD also have depression, which is 5 times more common than children without ADHD.110 A study of young adult depression sufferers reported a lifetime ADHD prevalence of 25.9%,118 which is also about five times.
The lifetime prevalence of major depression is 15%119; women are affected twice as often as men, i.e., women 20%, men 10%.

In children with ADHD, emotional dysregulation occurs before comorbid depression.120121 This is not surprising, since emotional dysregulation is an original ADHD symptom, whereas depression can occur as a comorbid disorder. Nevertheless, the degree of emotional dysregulation in children with ADHD seems to moderate the likelihood of later depression.122

Depression must be distinguished from mere dysphoria with inactivity, which is a typical symptom of ADHD and does not represent depression. Treatment with antidepressants would be incorrect here.
See Depression and dysphoria in ADHD In this chapter.

Common symptoms of depression and ADHD:23

  • Inner restlessness (typical in atypical depression, less so in melancholic depression)
  • Concentration problems
  • Attention problems123
  • Memory problems123
  • Sleep problems
  • Daytime sleepiness (typical in atypical depression, atypical in melancholic depression, possible in ADHD)
  • Negative self-image112

ADHD symptoms atypical of depression:

  • Rapid mood swings
  • Dysphoria only during inactivity
  • High fluency of speech (logorrhea, polyphrasia)
  • Thought chasing, thought circling
  • Impulsivity (atypical of ADHD-I, atypical of melancholic depression)

Symptoms of depression atypical of ADHD:

  • Permanent depressive mood (even with things that are actually interesting)
  • Low mood in the morning (melancholic depression)
  • Low mood in the evening (atypical depression)
  • Weight loss (in ADHD at best as side effect of stimulants)
  • Decreased interest in activities (in ADHD more likely withdrawal due to increased sensitivity or social phobia)
  • Suicidal thoughts

In ADHD sufferers, depression typically occurs years after the onset of ADHD symptoms.124 In this case, the underlying ADHD, which is often the cause of the depression, must be treated in addition to the existing depression. Otherwise, the depression would only be treated as a secondary symptom of ADHD.125124113
About 34% of all treatment-resistant depression is due to previously undiagnosed ADHD.

2.5.3.2. Bipolar disorder (annual prevalence: 3.1% (women), 2.8% (men))

Prevalence: 3.1% of all women, 2.8% of all men within one year2

Bipolar disorder is characterized in particular by alternation between depressive and manic symptoms. The changes can occur at different speeds. A change to a full-blown manic episode does not always occur.

ADHD is more common than average in people with bipolar, but the comorbidity with ADHD is probably weaker than in relation to other mental disorders.110

In a reaction test study, both ADHD and bipolar sufferers showed significantly increased variability of infrequent slow responses than controls, whereas bipolar sufferers showed significantly increased speed and variability of typical responses in the flanker task compared to ADHD sufferers and controls.126

2.5.3.2.1. Depressive episode of bipolar disorder

The common and different symptoms of depressive episode of bipolar disorder and ADHD correspond to those of depression and ADHD.

See above under Depression as well as Depression and Dysphoria in ADHD In the section⇒ In-depth presentation of individual ADHD symptoms in the chapterSymptoms.

2.5.3.2.2. Manic episode of bipolar disorder

Common symptoms of manic episode of bipolar disorder and ADHD:

  • Concentration problems23
  • Attention problems12323
  • Memory problems12323
  • Sleep problems23
  • Daytime sleepiness (typical in atypical depression, atypical in melancholic depression, possible in ADHD)23
  • Rapid mood swings127 23
  • Thought chasing, thought circling127 23
  • Impulsivity (atypical for ADHD-I)12723
  • Problems to relax (ADHD-HI, Bipolar in manic phase)127
  • Regulation of one’s own arousal.Inner restlessness, restlessness127

ADHD symptoms atypical of manic episodes:

  • Dysphoria only during inactivity

Symptoms of Bipolar that are atypical of ADHD:

  • Alternation between depressive and manic phases

In ADHD, mood swings tend to be triggered (reactive) and pass quickly with distraction, whereas bipolar manic episodes tend to be more continuous and prolonged.128

2.5.3.3. Cyclothymia (13 %)

Cyclothymia (cyclothymia) is a rapid change of moods without reaching the intensity of symptoms of Bipolar Disorder. Cyclothymia has a prevalence of 13% in the general population.

Zyclothymia has been found in 75% of all bipolar sufferers and is significantly increased in ADHD and depression.129

2.5.4. Circumscribed developmental disorders (partial performance disorders) according to ICD-10 (approx. 10 to 15 % (?))

Partial performance disorder is reported to be a common comorbidity (especially in ADHD-I subtype without hyperactivity).
Dyspraxia, on the other hand, is a purely motor development disorder that is more commonly confused with ADHD-HI (without inattention).

2.5.4.1. Dyspraxia (5 to 6 %)

Prevalence 5 to 6130131

Dyspraxia is also called the “clumsy child syndrome” or “clumsy child syndrome”.
Dyspraxia is a developmental disorder that lasts throughout life.
Dyspraxia is very often comorbid with ADHD or ASD.
Children with dyspraxia show no abnormalities in intelligence.

There are different forms of dyspraxia.

2.5.4.1.1. Motor dyspraxia / circumscribed developmental disorder of motor functions (UEMF)

Problems with:

  • Motor slowdown
  • Balance problems
    • Impaired gait
    • Difficulty getting dressed while standing
  • Clumsiness in complex movements requiring balance and dexterity132
    • Catch ball
    • Bounce
    • Jump
    • Climbing
    • Bike
    • Swimming
    • Couple dance
  • Impaired automation of fine motor and gross motor activities
    • Impaired handwriting
      • Difficulty in guiding the pen with the correct pressure
      • Problems to keep boundaries of the sheet.
      • Writing on the computer goes much better
    • Problems tying shoelaces or bows
    • Problems closing buttons
    • Difficulty eating with knife and fork
    • Problems to cut out a figure cleanly
    • Frequent dropping of things
    • Problems with careful handling of glasses or dishes
    • Difficulty pouring into glasses
    • Problems with crafting or wrapping gifts
  • Difficulty in acquiring new motor skills
  • Impaired eye-hand coordination
  • Frequent confusion of right and left
  • Problems with the order of the clothes when dressing
  • Rapid fatigue during physical activity
    • Sports
    • Hiking
    • Physical play
  • Easy distractibility during tasks
    • Too much information on one sheet confuse
    • Improved task performance with larger line spacing, larger font size

No problems with:

  • Hyperactivity.
2.5.4.1.2. Ideomotor dyspraxia

Problems with:133

  • Execution of the own plan of action
  • Complete actions
  • Writing difficulties
  • Action difficulties
  • Execution of understood instructions impaired
  • Order is easily confused
  • Impairment of imaginative or creative play

No problems with:

  • Describe sequences of movements
  • Recognize mistakes of others
  • Read
  • Talk
2.5.4.1.3. Ideatory dyspraxia

Difficulty planning and describing motor actions, but they do not have motor limitations.133

Problems with:

  • Form series (associated with weakness of memory)
  • Describe sequences of actions
  • Read words
  • Work fast
  • Keep order

No problems with:

  • Imitate individual movement sequences
  • Write words
2.5.4.1.4. Verbal dyspraxia

Approximately 30% of children with dyspraxia also have a verbal developmental delay = verbal dyspraxia.134

Verbal dyspraxia is a disorder of speech motor planning. The speech organs are not affected (tongue, vocal cords).

  • Problems of planning the speech movements
  • Difficulty pronouncing the right words at the right time in the right order.
  • Frequent coughing or swallowing when ingesting food
    • Sequence of sucking, swallowing and breathing difficult
    • High saliva production when changing food from porridge to solid meals
  • Language development significantly delayed
    • Significantly later start to speak
    • Initially only a few “babbling” sounds
    • Later often vowel language without consonants (“Oaaaa”, “Eeea”).
  • Often problems with gross motor skills at the same time (see motor dyspraxia)
    • Stumble
    • Bump into each other, many bruises
    • Learning Difficulties
      • Read
      • Spell

The risk factors for the development of dyspraxia are still unclear. As with ADHD, environmental influences during pregnancy and birth seem to increase the risk.

2.5.4.2. Developmental coordination disorders

The extent to which the concept of Developmental Coordination Disorders differs from that of Circumscribed Developmental Disorders of Motor Function and Developmental Coordination Disorder (DCD) is unclear.

There are said to be different subtypes with six main symptom groups:

  1. general instability / slight tremor
  2. decreased muscle tone
  3. increased muscle tone
  4. Inability to perform a uniform movement or to combine individual movement elements into an overall movement
  5. Inability to form written symbols
  6. Difficulties in visual perception associated with the development of the eye muscles

Affected individuals with Developmental Coordination Disorders are said to have 50% ADHD as well.

The risk of ADHD is also increased in children 4 to 5 years of age with Developmental coordination disorder. However, the DSM-5 scale seems to apply less frequently here.135

2.5.4.3. Partial performance disorders

The comorbidity of ADHD and learning disorders is reported between 10% and 90%.110
Learning disorders are said to correlate with ADHD-I more often than with ADHD-HI.136 In ADHD sufferers, writing disorders are said to be twice as common as reading, math, or spelling disorders.137

2.5.4.2.1. Reading and spelling disorder (dyslexia) (5 %)

Present in 17.6% of children with ADHD.13
Dyslexia is reported to be more common in ADHD-I than in ADHD-HI.138

2.5.4.2.2. Dyscalculia (5 %)

Dyscalculia is reported to be more common in ADHD-I than in ADHD-HI.138

2.5.5. Post-traumatic stress disorder (PTSD, PTSD) (5% (men), 10% (women))

Prevalence: 10% of all adult women and 5% of all adult men experience post-traumatic stress disorder.1617
60% of all men and 50% of all women have at least one potentially traumatizing experience in their lives.139
Of these, suffer from PTSD:

  • Rape victims: 49 %140
  • Severe beating or physical assault: 31.9%140
  • Victims of crime: 25%140
  • Sexual assault without rape: 23.7%140
  • Serious accident (car or train): 16,8 %140
  • Shooting or stabbing: 15.4%140
  • Sudden death of a close or loved one: 14.3%140
  • Childhood life-threatening illness: 10.9%140
  • Victims of potentially traumatic experiences without crime: 9.4%140
  • Witnesses to a murder or violent assault: 7.3%140
  • Natural disaster: 3.9140

Sleep problems are common in ADHD as well as in PTSD. In PTSD, these often develop in the first 2 weeks after the traumatizing event and are often characterized by persistent nightmares,141 which is also not typical for ADHD. In ADHD, on the other hand, sleep disturbances usually persist throughout life.

2.5.6. Tic disorders, Tourette syndrome (1 to 15 %)

Source10

Prevalence: 1% in primary school age (varying severity), 15% in elementary school age (incl. mild and transient forms).142
Tic disorders are present in 9.5% of ADHD affected children.13
31%143 to 55%144 of children with tic disorders also exhibit ADHD.

2.5.7. Internet addiction (3.9% (2019) to 7.8% (2020))

Prevalence: among students in Germany 3.9% (2019) to 7.8% (2020, corona lockdown year) 145
Internet addiction was distinguished by one study into two subtypes: one subtype that correlated with impulsivity and ADHD-HI and another subtype that correlated with compulsivity.146

2.5.8. Social behavior disorder (1.5 to 5%)

Other names: Conduct Disorder
Source10

Prevalence: in primary school age about 1.5%, in adolescents about 5%.147
Oppositional defiant disorder is reported to be present in 46.9% of ADHD affected children, social behavior disorders in another 18.5%.13
Comorbidity between ADHD-HI and social behavior disorder is reported to be 15% to 85% of cases, depending on study design and direction of association, 4.7 times more common overall than in unaffected individuals.148
Oppositional defiant behavior and other social disorders are considered by some experts as a subtype of ADHD (rage type). We rather suspect it to be a disorder of its own, which has a high comorbidity to ADHD.

Differentiation from ADHD: Aggression in (purely) ADHD sufferers is reactive, defensive motive, no intention to harm.97149 Aggression in ADHD sufferers often arises from a misjudgement of situations, after which they defend themselves (supposedly rightly). ADHD sufferers thus show reactive rather than proactive aggressiveness.150

2.5.9. Emotionally unstable personality / borderline (1 - 4 % (women), 1 % (men))

Prevalence Borderline: 1% - 3%151 to 5%152153 Prevalence increases to 11% in psychiatric patients and up to 50% in inpatients.154

75% of borderline victims are women.

In Borderline, in addition to a symptom similarity to ADHD, a comorbid occurrence of ADHD is often noted.155156 One study addresses the question whether one of the disorders (ADHD or Borderline) can change over time to one of the other disorders. Seemingly, ADHD is more likely to be considered an antecedent disorder and Borderline a subsequent disorder in adulthood. A major environmental difference reported in Borderline was the increased number of traumatic childhood experiences.157 This, as well as the different genetic disposition described below, argue against a regular developmental sequence between the two disorders. Nevertheless, we know individual cases in which we consider a development of ADHD to a later Borderline or a later occurrence of Borderline to be a plausible explanation of the symptom picture.

Since Borderline is associated with a genetic disposition on the MAO-A gene, which is at the same time associated with aggression and behavioral disorders, Borderline is likely to co-occur primarily with ADHD-HI and rarely with ADHD-I.
ADHD resembles a personality disorder in its course (early onset, persistent behavior patterns, and possible persistence into adulthood).158
There are voices that consider ADHD-HI (with hyperactivity) and Borderline as a continuum varied by symptom intensity. Hallowell reports an ADHD-HI type with borderline overtones.159 We also see a striking relationship to the point of strong confusability in layman’s terms, but assume that the aggressiveness added in Borderline is mediated by genes not typical of ADHD. As the correlated gene variants indicate, ADHD is characterized by a deficit of dopamine and norepinephrine in the dlPFC and striatum, whereas Borderline tends to have normal levels of dopamine in the PFC and an excess of dopamine in the striatum (see below).

Borderline and ADHD have very similar symptoms, which are easily confused, and a high comorbidity. About 50% of borderline sufferers also suffer from ADHD.
The “inner pressure” described in borderline (which can lead to self-injurious behavior) is also known in ADHD.

Differentiation of the symptomatology of ADHD and Borderline:160

The previous assumption that ADHD and Borderline differ by the time of onset (ADHD earlier, Borderline later) has since been questioned.156

Common symptoms of borderline and ADHD:

  • Impulsivity23161 162 163
    • Much stronger in ADHD-HI than in borderline
    • High impulsivity in borderline is thought to indicate ADHD-HI comorbidity.
    • Different view: high aggressive impulsivity an endophenotype of BPD.164 We think this is more likely because DAT 9R, the gene suspected for aggressive-impulsive behavior in borderline, is not associated with ADHD. (see below).
    • One study found increased self-reported impulsivity in ADHD and borderline, but increased action impulsivity only in ADHD165
    • Addiction problems161
  • Affective lability (ADHD-HI) / affective instability (borderline)161
    • In ADHD-HI sufferers (with hyperactivity) and borderline sufferers, behavioral and affect regulation are similarly disturbed.

    • Rapid mood swings23

    • Emotional dysregulation is even more pronounced in borderline than in ADHD. ADHD sufferers have a better use of adaptive cognitive emotional strategies than borderline sufferers.166 All emotions are perceived significantly more intensely (and with more distressing intensity) than in non-affected individuals.153

    • In Borderline, behavioral dysregulation also does not occur in neutral life circumstances, but only in stressful moments.162

  • Attention Deficit Disorder
    • In ADHD often with too little arousal (lack of activation / stimulation)161
    • In BPS more often during a rise in tension as a dissociative phenomenon158
  • Dissatisfaction
  • Dysphoria with inactivity
  • Boredom (ADHD-HI) / Dysphoria, Boredom, Emptiness (Borderline)
  • Self-esteem issues / grievability / rejection sensitivity161
  • Excitability, outbursts of anger
  • Stress intolerance
    • Stressors lead to significantly higher stress levels in borderline, which decline much more slowly than in non-affected individuals.153
  • Conflictual relationships (ADHD-HI) / instability in relationships (borderline)161
  • Social weakness, impaired social behavior
  • Sleep problems common
    • Borderline often shows a prolonged REM phase and nightmares (on average every 2nd night).141 Nightmares are atypical for ADHD.
    • Difficulty falling asleep, shortened sleep duration, low sleep efficiency with subjectively less restful sleep are common in Borderline,141 as well as ADHD.
    • Difficulty falling asleep in borderline is said to improve well with clonidine.141 Probably guanfacine could also be helpful.
  • Inner restlessness, restlessness23
    • Required voltage reduction
      • In ADHD-HI (more often men): sports, sex161
      • In BPD (more often women): Dissociation, freezing, self-harm,161 sex

ADHD symptoms atypical of Borderline:

  • Concentration problems23
  • Attention problems23
  • Cognitive impairments165
  • Hyperactivity
  • Dysphoria with inactivity
  • High fluency of speech (logorrhea, polyphrasia)23
  • Thought chasing, thought circling23
  • Executive function disorders
    • Disorganized
  • One study found increased self-reported impulsivity in ADHD and borderline, but increased action impulsivity only in ADHD165
  • Reaction time slowing,167 although other studies have also found shortened reaction times in ADHD

Symptoms of borderline that are atypical of ADHD:

  • Self-harming / self-injurious behavior
    Impulsive behavior in response to intense negative feelings (“negative urgency”)165 is one of the most distinctive symptoms that characterizes Borderline.168
    • E.g. scratching (nevertheless not every self-injurious behavior is borderline)
      • Self-injury reduces subjective stress levels and objective amygdala activity, which are very high after a stress test, in borderline sufferers (by increasing connectivity in frontal-limbic brain regions that dampen amygdala activity), whereas it further increases (lower) stress levels and objective amygdala activity in unaffected individuals.153
  • Think black and white
    • Shades of gray, a both/and, mediating positions are difficult to perceive and hard to bear.
    • In discussions, sufferers tend to take extreme positions. For interlocutors, this can feel like the person is sliding off a bar of soap - either left or right, but unable to take a middle both/and or mediating position.
  • Identity Disorders
  • Dissociation
  • Abandonment fears23
    • Feel lonely, even when among people153. We suspect that this is much more pronounced in Borderline than in ADHD.
  • Unstable relationships, unstable self-image23
  • Suicidal thoughts23
  • Paranoid symptoms23
  • Strong sense of guilt and shame

In comorbid ADHD + Borderline in particular are said to be more pronounced:156

  • Impulsivity (as in ADHD alone)
  • Symptoms of regulation of traits and emotions (than in Borderline alone)

In children and adolescents, certain character traits increase the risk of borderline personality disorder later in life:154

  • Affective instability
  • Negative affectivity
  • Negative emotionality
  • Inappropriate anger
  • Poor emotional control
  • Impulsivity
  • Aggression

Borderline sufferers differ from sufferers of other personality disorders primarily by a pronounced histrionic as well as by more frequent narcissistic, bipolar / cyclothyme or aggressive expression. There is greater lability in relation to anger and anxiety, as well as greater oscillation of occurrence between depression and anxiety. The level of intensity of emotion perception is surprisingly not higher. In contrast, obsessive-compulsive, schizoid, and anxious-avoidant expressions are less frequent. These results are independent of gender.169

Dopaminergic substances (stimulants) can provoke impulsive and aggressive behavior in borderline.164 This indicates an excess of dopamine in borderline, which is different from the dopamine deficit in ADHD.
This is consistent with research findings that Borderline correlates with DAT1 gene variants 9/9 and 9/10, which cause lower DAT expression in the striatum, so higher dopamine levels in the striatum should be expected due to lower dopamine degradation by DAT.170

The 9-repeat variant of the DAT1 gene causes an excess of dopamine in the synaptic cleft, because the dopamine transporters then insufficiently reuptake the dopamine presynaptically. DAT 9R is associated with affective disorders and borderline.171
Borderline correlates more often with170

  • DAT1 9/9 (OR = 2.67)
  • DAT1 9/10 (OR = 3.67)
  • HTR1A G/G (OR = 2.03)

The risk for borderline increases for carriers of the gene variant combinations170

  • DAT1 9/10 and HTR1A G, G (OR = 6.64)
  • DAT1 9/9 and C/G (OR = 5.42).

ADHD is not associated with DAT1 9R, but with DAT1 10/10, which causes increased DAT expression in the striatum, which is associated with increased dopamine clearance and therefore decreased dopamine levels in the striatum. This now explains why stimulants that increase dopamine and norepinephrine levels in the PFC and striatum work well in ADHD, whereas they can be counterproductive in borderline.

5 HTTPLR and 5-HT2c are two other canditate data genes in Borderline.172

Borderline sufferers may have more regional μ-opioid receptors in some brain regions and fewer regional μ-opioid receptors in other brain regions. Emotional dysregulation (sadness) is thought to correlate with deviation in μ-opioid receptors compared with unaffected individuals.173

Antipsychotics produce significant but small improvement in cognitive perceptual symptoms, mood lability, and global functioning in BPD. The effect is more pronounced with respect to anger/rage. They have no significant effect on behavioral impulsivity, depression, and anxiety.174

2.5.10. Obsessive-compulsive disorder (1 to 3 %)

Source10

Prevalence: lifetime prevalence of 1 to 3%,175176 according to other sources 4.2% of all women, 3.5% of all men within one year.2
Girls under 18 years: Prevalence 0.96%, boys 0.63%.116

Olfactory disorders (disorders of the sense of smell) are common in ASD and obsessive-compulsive disorder, but not in ADHD.177

2.5.11. Antisocial personality disorder (0.2 - 3%)

Source178

  • High impulsivity
  • Strong Novelty Seeking / Sensation Seeking
  • Self-centeredness / egocentricity
  • Lack of empathy towards others
    • Not being able to feel how others feel

Subgroups of antisocial personality disorder:

  • Impulsive type
    • Frequent comorbidity to ADHD-HI / ADHD-C
    • Emotionally highly sensitive / hyperreactive
    • Increased excitability
    • High impulsivity
    • Reactive aggression - as an immediate reaction to triggers
    • Low stress tolerance
  • Psychopathic type
    • Rare comorbidity to ADHD-HI / ADHD-C
    • Emotionally insensitive / hyporeactive
    • Active aggression - purposeful, instrumental violence
    • No increased arousal when frustrated
    • No reduced stress tolerance

Differentiation from ADHD: Aggression in (purely) ADHD sufferers is reactive, defensive motive, no intention to harm 97 149 Aggression in ADHD sufferers often arises from a misjudgement of situations, after which they (supposedly rightly) defend themselves. We see in this a connection to Rejection Sensitivity as an overshooting sensitivity to supposed or actual rejection / offendability. ADHD sufferers thus show a reactive and not a proactive aggressiveness.150

Common symptoms of antisocial personality disorder and ADHD:23

  • Impulsivity (atypical for ADHD-I)
  • Rapid mood swings

ADHD symptoms atypical of antisocial personality disorder:

  • Inner restlessness (typical in atypical depression, less so in melancholic depression)
  • Concentration problems
  • Attention problems
  • Dysphoria with inactivity
  • High fluency of speech (logorrhea, polyphrasia)
  • Thought chasing, thought circling

Symptoms of antisocial personality disorder atypical of ADHD:

  • Criminal behavior
  • Deception of others
  • Disregard for self and others
  • Lack of remorse

2.5.12. Narcissism (0.5 to 2.5%)

Prevalence 0.5% to 2.5%.

Narcissism and ADHD share some possible symptoms. Similar are:

2.5.13. Schizophrenic disorder (1%)

Lifetime prevalence is approximately 1%.57
Girls under 18 years: Prevalence 0.76%, boys 0.48%.116

Schizophrenia usually develops after adolescence. However, it is usually preceded by childhood precursors that do not resemble schizophrenia itself but appear to genetically indicate schizophrenia.179

The negative symptoms of schizophrenia are based on dopamine deficiency. They are similar to ADHD symptoms.
The positive symptoms, on the other hand, are based on an excess of dopamine (dopamine hypothesis).

Schizophrenia is also thought to be caused by a combination of genetic factors and environmental influences. Environmental influences for schizophrenia have been identified as emotional trauma, social stress or hallucinogenic drugs.
Genes + early childhood stress as a cause of other mental disorders

COMT rs4680, which is implicated in schizophrenia (as one of 50 or more candidate genes), enhances the degradation of dopamine and norepinephrine by forming a more active and thermally stable COMT enzyme.180 This causes higher schizotypal symptoms.
This can be reconciled with the recent dopamine hypothesis, according to which the positive symptoms of schizophrenia are not caused by a generally increased level of dopamine in the frontal cortex (and in the nucleus accumbens, a part of the striatum), but by an increased activity (firing rate) of the mesolimbic system, which in turn is caused or influenced by a lack of dopamine in the ventral tegmentum.180

Schizophrenia and attention:

  • Sensitivity to sensory stimulation increased97
  • High sensitivity causes sensory overload97
  • Attentional selection for individual events disturbed97
  • Concentration/maintenance of concentration on relevant aspects of a task disturbed.97

Symptoms of schizophrenia atypical of ADHD:

  • Drawings are non-spatial, no three-dimensional representation
  • Irony / sarcasm are not understood
  • Olfactory disturbances.177

2.5.14. Psychoses (1 %)

2.5.15. Autism spectrum disorder (ASD) (0.9%)

Sources8910

Prevalence ASA: approx. 0.9%181
About 42%182 to 50%183 of all ASD sufferers also suffer from ADHD.
It is likely that ADHD and autism have common neurological/genetic roots.184

  • Profound developmental disorder
    Prevalence: approx. 0.6 %181
  • Autism56
    Prevalence: approx. 0.3 %181
  • Asperger’s
    Prevalence: approx. 0.084 %181
  • Disintegrative disorder56
    Prevalence: 0.008% (One affected person in 12500 people)181
  • Rett syndrome56
    Prevalence: 0.006% (One affected person in 10000 to 17000 people)185181
    Concerns only girls
    Rett syndrome symptoms:185
    • Stereotypies of the hands (washing movements)
    • Partial autistic behavior
    • Dementia
    • Reduced head growth
    • Epileptic seizures (later stage)
    • Spasticity (later stage)
    • Apraxias
    • Muscle atrophy
    • Movement disorders in the area of the thorax
    • Social behavior and play development strongly inhibited
    • Social interest continues

Differential diagnosis to ADHD:

Children with ASD had 15 or more of the 30 symptoms (mean: 22 = 73%) of the Checklist for Autism Spectrum Disorder symptoms, whereas children with ADHD had an average of 4 symptoms (13.3%), none of which had 15 or more. ADHD symptoms, on the other hand, were common among children with ASD.186
ADHD-affected children showed elevated scores on the Social Responsiveness Scale (SRS), but these did not approach the scores of ASD-affected children.187

In favor of ASS:188

  • Inattention more likely due to too much detail orientation in ASD (vs. overlooking details in ADHD)
  • Concentration breaks down when routines are disrupted in ASD (vs. lack of routines and jumping quickly between different things in ADHD)
  • The unexpected is seen as an unpleasant irritation and disruption of one’s own structure (rather than as a welcome change in ADHD)
  • Routines due to own need for structure (vs. tedious getting used to routines in order not to lose structure too much in ADHD)
  • High difficulty in social situations due to inner uncertainty about how to behave properly (vs. ticking off due to careless behaviors in ADHD)
  • Difficulty grasping social rules of play (vs. difficulty adhering to well-grasped social rules of play in ADHD)
  • High attention to detail blows up time frames for activities (vs. project cancellations due to change of interest in ADHD)
  • Needs order for own inner structure, tends to find things in disorder (compared to not being able to keep order due to other priorities in ADHD)
  • Deviation from the plan leads to irritation (versus frequent deviations from the plan due to own spontaneity and impulsiveness)
  • Reduced flexibility (compared to rather slightly impaired flexibility in ADHD)
  • Concentration can be maintained on prolonged and repetitive tasks (vs. difficulty maintaining concentration on monotonous boring tasks in ADHD)
  • Motor restlessness tends to occur in agitated situations to relieve (versus motor restlessness in calm situations to stimulate in ADHD)
  • Motor restlessness more from aversion to something = running away (versus from interest in something = running towards in ADHD)
  • Loose conversations or small talk unpopular, as own thought structures are thwarted; sometimes compensation by strict conversation (not present in ADHD)
  • Lack of feeling for situation and mood (present in ADHD)
  • Interrupting others rarely (like ADHD-I, different from ADHD-HI / ADHD-C)
  • Having to wait in a rather dark, completely non-stimulating room is a rather pleasant idea (very unpleasant in ADHD-HI / ADHD-C; both possible in ADHD-I)

In ASD, the intracortical pathway (facilitation) seems unimpaired, whereas in ASD with comorbid ADHD, the intracortical pathway seems impaired. This could represent a biomarker to distinguish ASD from ADHD.189

Neurophysiologically, pathing is the promotion of a reflex or nerve cell activity by lowering the stimulus threshold for the transmission of the action potential of a nerve cell. Pathing occurs mainly with repeated excitation of the same nerve pathways or by the summation of subthreshold stimuli.190

ASD as well as ADHD showed slower orienting responses to relatively unexpected spatial target stimuli compared with controls, which was associated with higher amplitudes of pupil dilation in ASD. ADHD showed shorter cue-evoked pupil dilation latencies than ASA and controls.191

Several studies addressed differences between ASD and ADHD:

  • Lower verbal comprehension in ASD than in ADHD192
  • Lower vocabulary in ASD192
  • Lower comprehension in ASD192
  • Worse image concepts in ASD192
  • Worse image completion with ASS192
  • Slower processing speed with ASD192
  • Lower social judgment in ASD192
  • Poorer response to name call at 24 months of age in ASD193
  • Higher shifting with ASS194
  • Poorer emotional self-regulation in ASD194
  • ASD, like dyslexia, shows deficits in global motion processing, unlike ADHD. ASD and dyslexia show significantly lower flicker fusion frequency than healthy controls or ADHD subjects.195

ADHD compared to ASD:

  • Poorer working memory typical for ADHD, less so for ASD192194
  • Planning and organization problems (largely determined by working memory) typical for ADHD, less so for ASD194
  • Inhibition problems typical for ADHD, less so for ASD194
  • Fewer points in the Digit Span for ADHD than for ASD192
  • Worse graphomotor processing in ADHD192

ADHD like ASD show structural abnormalities in the PFC, cerebellum, and basal ganglia. Affected individuals with comorbid ASD and ADHD showed no significant differences in the volumes of the PFC, cerebellum, or basal ganglia. However, they had significantly lower volumes of the left postcentral gyrus, but only children, not adolescents.196

ASD is characterized by high aggression and risk-taking behavior. In addition, ASD is disproportionately involved in child abuse.197 Aggression and high-risk behavior are also hallmarks of the ADHD-HI subtype.

One review article found blood norepinephrine levels approximately doubled in ADHD and approximately halved in ASA, compared to unaffected individuals. In contrast, serotonin blood levels were increased fourfold in ASA and decreased more than fourfold in ADHD.198

2.5.16. Fragile X syndrome (0.22% (males) to 0.66% (females))

Prevalence: 1/150 (0.66%) women, 1/456 (0.22%) men in the U.S199
Source1016

2.5.17. Pervasive developmental disorders (PDD) (0.06%)

Prevalence: 60/100,000 (0.06%)

PDD is characterized by severe deficits in social behavior and communication, and repetitive and stereotyped interests and behaviors. There are often comorbidities to decreased intelligence, ADHD, aggression, and obsessive-compulsive disorders.200

2.5.18. Wilson Disease (0.0033%)

Wilson Disease (prevalence: 1 in 30,000 people, 0.0033%) is associated with excessive copper levels
Affected individuals with Wilson Disease show symptoms that are confusable with ADHD.201
Wilson Disease is associated with an ATP7B gene defect and shows an excess of copper.
Although dopamine-β-hydroxylase, which converts dopamine to norepinephrine, is dependent on copper for this, it does not appear to be involved in Wilson’s disease.

2.5.19. Monoamine neurotransmitter disorders

Monoamine neurotransmitter disorders are genetic defects in transporters or deficiencies in precursors, cofactors, or degradation enzymes of monoamines (e.g., dopamine).202

Symptoms of severe dopamine deficiency may include:203

Symptoms of severe serotonin deficiency may include:203

  • Temperature problems
  • Sweating
  • Dystonia

To detect deficiencies of precursors and specific metabolic defects, the measurement of pterins (especially biopterin and neopterin) in urine is helpful:

*GTP cyclohydrolase 1 deficiency (GCH 1)

2.5.19.1. Genetically determined BH4 disorders (approx. 0.0002 %)

Genetic disorders of tetrahydrobiopterin synthesis (BH4, an important enzyme for dopamine synthesis) such as

  • autosomal recessive (AR) guanosine triphosphate cyclohydrolase deficiency (GTPCH deficiency)
    • Prevalence less than 1 / 1,000,000 (less than 0.0001%)204
    • 46 % of all BH4 disorders
  • 6-pyruvoyl tetrahydropterin synthase (PTPS) deficiency
    • Prevalence: 1 / 500,000 to 1/ 1,000,000 (0.0001 % to 0.0002 %) 205
    • 54 % of all BH4 disorders

appear to co-occur with ADHD and other mental disorders such as anxiety, depression, aggression, or oppositional defiant behavior.206

See also Tyrosine hydroxylase In the article Dopamine formation.

2.5.19.2. Missing or strongly reduced DAT

There are (rarely) people without or with very much reduced DAT. However, these show other symptoms that are not ADHD-typical (e.g. early childhood Parkinson’s dystonia) and are therefore rarely misdiagnosed with ADHD and rather with cerebral palsy. Many affected individuals die as teenagers.207 Excess extracellular dopamine leads to decreased production of dopamine (and thus decreased storage of dopamine in vesicles) and downregulation or desensitization of dopamine receptors through activation of presynaptic D2 autoreceptors, resulting in phasic dopamine deficiency and dopamine action deficiency.202

2.5.20. Predominantly environment-related behavioral problems

Predominantly milieu-related behavioral problems means, for example, lack of attention and stimulation, physical and/or mental abuse, media abuse, intra-family conflicts and sibling conflicts10
According to our understanding, this description corresponds to the environmental causes of most mental disorders such as ADHD, depression, anxiety disorders, borderline, etc., all of which can arise when environmental causes, usually stressful experiences in the first 6 years of life, permanently manifest an existing genetic disposition by means of epigenetic change. Predominantly environment-related behavioral disorders are therefore unsuitable to define a separate disorder.
How ADHD develops: genes or genes + environment
Genes + early childhood stress as a cause of other mental disorders

2.5.21. Separation problems with severe family conflicts

Source68


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