The subtypes of ADHD: ADHD-HI, ADHD-I (ADD), ADHD-C (mixed type) and others.

In ADHD, the subtypes ADHD-HI (predominant hyperactivity), ADHD-C (attention problems and hyperactivity in equal measure) and ADHD-I (predominant inattention) are distinguished. The pure ADHD-HI type is usually diagnosed up to the age of 6, 7 years at the longest, exceptionally up to 14, 15 years. This is probably mainly due to the fact that inattention symptoms can only be reliably diagnosed from this age. ADHD-C could therefore be referred to as ADHD-HI type in later development. In adults with ADHD, attention problems may also remit significantly or disappear, although they remit considerably less frequently than hyperactivity problems: ⇒ ADHD in adults.
The ICD distinguishes between Simple Activity and Attention Disorder (F90.0) and Hyperkinetic Disorder of Social Behavior (F90.1), for which a social behavior disorder is additionally required. The latter is considered (rightly in our opinion) as a comorbidity according to DSM.
The ADHD-HI, ADHD-I, and ADHD-C subtypes have been shown to be valid, whereas the evidence for a subtype of hyperkinetic disorder of social behavior is insufficient¹

SCT is no longer considered a subtype of ADHD. However, because SCT appears to be closely related and highly comorbid to ADHD, we have devoted a separate page to SCT: ⇒ SCT - Sluggish Cognitive Tempo.

In adults, a sex-independent frequency distribution of subtypes was found, from:

• ADHD-C: 56%² to 62%³
• ADHD-I: 31%³ to 37%²
• ADHD-HI: 2%² to 7%³

The question of whether the subtypes differ by different (genetic) causes or neuro(physio)logical processes has been studied many times. The causes and neuro(physio)logical processes are very similar in all subtypes. To date, few truly reliable distinguishing criteria are known. The most relevant difference is the endocrine response to acute stress. Since stress-induced neurotransmitter releases (especially norepinephrine) appear to parallel these subtype-specific cortisol responses to acute stress, this may explain some differences of ADHD-HI/ADHD-C and ADHD-I.

We consider the ADHD subtypes as different (psychological) forms of reaction to one and the same genetic / neurological source of disturbance, where essentially the personality traits are

• Extrovert / introvert
• Neuroticism
  as well as next to it
• The personal way of processing stress (Bis/Bas) as a phenotypic stress response, and
• The learned way of dealing with stress (role model)

determine which subtype an ADHD sufferer develops. These are neurophysiologically reflected in the cortisol stress response. More on this below under 1.2.3.1.

The subtype expression of the affected person is not necessarily stable over the whole life.⁴ We know quite a few affected persons who report a clear change of subtype.

• 1. Subtypes of ADHD according to symptoms
  • 1.1. ADHD-I: predominantly inattentive type
    • 1.1.1. Other names of ADHD-I subtype
    • 1.1.2. Specific symptoms of ADHD-I
    • 1.1.3. Peculiarities of medication
    • 1.1.4. Neurophysiological features of ADHD-I
      • 1.1.4.1. Increased cortisol stress response in ADHD-I
      • 1.1.4.2. Other biomarkers in ADHD-I
    • 1.1.5. EEG image in ADHD-I
    • 1.1.6. Sluggish Cognitive Tempo (SCT) - stand-alone disorder
  • 1.2. ADHD-HI: predominantly hyperactive/impulsive subtype
    • 1.2.1. Additional names
    • 1.2.2. Specific symptoms
    • 1.2.3. Neurophysiological peculiarities in ADHD-HI
      • 1.2.3.1. Flattened cortisol stress response in ADHD-HI
      • 1.2.3.2. Deficient HPA axis disconnection in ADHD-HI
      • 1.2.3.3. Decreased norepinephrine depletion in ADHD-HI?
      • 1.2.3.4. Decreased hippocampal volume in ADHD-HI
      • 1.2.3.5. Indole acetic acid in ADHD-HI
    • 1.2.4. EEG image in ADHD-HI
  • 1.3. ADHD-C - mixed type of ADHD-HI and ADHD-I
    • 1.3.1. ADHD-C with inhibition deficits, without reward deficits
    • 1.3.2. ADHD-C with inhibition deficits and reward deficits
    • 1.3.3. ADHD-C without reward deficits and without inhibition deficits
  • 1.4. Other subtype classifications
    • 1.4.1. ADHD with oppositional behavior disorder (?)
    • 1.4.2. Rage type (?)
    • 1.4.3. Residual type
    • 1.4.4. ADHD adult subtype pair according to Reimherr
      • 1.4.4.1. Inattentive adult subtype
      • 1.4.4.2. Emotionally dysregulated adult subtype
    • 1.4.5. ADHD subtypes according to internalizing / externalizing symptoms
    • 1.4.6. ADHD subtypes by symptom severity
    • 1.4.7. Subtypes according to emotion profiles
• 2. Neurophysiological and endocrine differences of the subtypes
  • 2.1. Dopamine level
    • 2.1.1. Hyperactivity, impulsivity: dopamine deficiency or excess in the striatum
    • 2.1.2. Hyperactivity, impulsivity: dopamine excess in the PFC
  • 2.2. Exaggerated and flattened endocrine stress responses of subtypes
  • 2.3. ADHD subtypes according to EEG
    • 2.3.1. ADHD-HI subtypes according to EEG
      • 2.3.1.1. Theta frontal increased, beta decreased (ADHD-HI with hyperactivity and impulsivity in hypoactive EEG)
      • 2.3.1.2. Beta overactivated (“Overactivated” ADHD-HI)
    • 2.3.2. ADHD-I subtypes in the EEG
      • 2.3.2.1. Delta and theta increased, beta decreased
      • 2.3.2.2. Only alpha activity inflated
      • 2.3.2.3. Theta posterior increased, alpha and beta decreased
      • 2.3.2.4. Only theta frontal midline (FMT) increased
  • 2.4. ADHD subtypes according to QEEG
  • 2.5. Functional differences of nerve conduction pathways in the brain (?)
  • 2.6. Subtypes and serotonin
  • 2.7. Neuro-auditory profiles of subtypes
• 3. ADHD-HI/ADHD-C and ADHD-I as stress phenotypes
• 4. Problem of subdivision into subtypes
• 5. ADHD variants by dopamine level?

1. Subtypes of ADHD according to symptoms¶

The literature primarily names 3 subtypes of ADHD: The ADHD-I type (1.1.), the ADHD-HI type (see 1.2.) and ADHD-C (see 1.3). While the ADHD-HI subtype is likely to be merely an early form of the mixed type, Sluggish Cognitive Tempo (SCT) is increasingly emerging as an independent disorder. The occasional forms described further are unlikely to represent true subtypes and are mentioned only for the sake of completeness.

Regardless of the typing of ADHD-I, ADHD-HI, and ADHD-C based on observed symptoms, there is a typing based on the different EEG patterns measured ⇒ ADHD subtypes according to EEG. This has not yet gained acceptance, although it may be measurable by objective biomarkers. To date, there is a lack of experience on the different symptomatology of the EEG subtypes and how they respond to specific treatments. An attempt to automatically distinguish the subtypes based on their EEG patterns using AI failed.⁵ It was also only possible to distinguish 84% of ADHD sufferers from non-affected individuals.

1.1. ADHD-I: predominantly inattentive type¶

1.1.1. Other names of ADHD-I subtype¶

• ADHD-I (the term we use today)
• ADS (colloquial, used by us in the past)
• ADD (older international colloquial term)
• ADHD - PI (predominantly inattentive)
• Hypoactive (Prof. Simchen)
• Träumerle (colloquial descriptive)
• Underactivated (distractible due to boredom)

1.1.2. Specific symptoms of ADHD-I¶

ADHD is a symptom cluster. The symptoms do not clearly distinguish the subtypes. In ADHD-I, inattention predominates over hyperactivity, impulsivity and inner restlessness.

• 3 to 6 years⁶

  • Calls are not perceived
    • Therefore does not follow requests
  • Dreamy
  • Stares into space
  • Can hardly deal with anything by himself
    • Daydreaming
    • Thoughts wander
  • Loud group situations are perceived rather unpleasantly
  • Aversion to changes in habitual routines
  • Aversion to fast transitions, must first adjust to new things

• 6 to 10 years:⁷

  • Inattention
    • Can therefore partly not follow lessons
  • Cannot understand some of the material taught
  • Difficulty concentrating
    • On teacher lecture
    • On own work
  • Seems dreamy
  • Lack of active cooperation

• 10 to 20 years:⁷

  • Possibly improvement of attention due to post-development of the brain
  • Attention problems remain at least partially present
    and are still perceived as very burdensome

• Independent of age:

  • The ADHD-I subtype is more introverted (in contrast to the more extroverted ADHD-HI subtype)⁸
  • Internalizing⁹
  • Shy¹⁰
  • Increased susceptibility to internalizing disorders¹¹
    e.g.
    • Anxiety disorders
    • Depression
  • ADHD-I subtype social problems arise from⁸
    • Too shy
    • Passivity
    • Introversion
    • Stillness
  • Disorders primarily in working memory and auditory processing, which places high demands on working memory.¹²
  • More frequent comorbid disorders than ADHD-HI subtype¹³
  • Partial performance disorders more frequent
    • Reading and spelling disability
    • Dyscalculia (arithmetic impairment)
  • Often perform better in spatial reasoning and artistic drawing than in verbal skills.¹⁴
  • Bored rather than distracted.¹⁵
  • Motivation problems rather than inhibition problems.¹⁶
  • Tends to have high self-awareness.¹⁶
  • Lethargic states (to be distinguished from depression)¹⁷
  • A significant subset of ADHD-I are reported to have slowed thinking (Sluggish)¹⁶
    We think the term “slowed thinking” is inaccurate and inappropriate. We see slowed decision making. The ability to think quickly is basically given; we suspect an overabundant blockade of the PFC by noradrenaline and possibly other neurotransmitters via the alpha-1-adrenoceptor. SCT is no longer considered a subtype of ADHD, nor is it considered ADHD-I specific.
  • More frequent allergies due to the excess cortisol reaction. Cortisol promotes the immune defense against external stresses.
  • Hypercortisolism corresponding disorder patterns are¹⁸
    • Depression
    • Anxiety disorder
    • Anorexia
    • Alcoholism
    • Metabolic syndrome
  • Learning Disabilities
    • More frequently than in ADHD-HI⁹
    • A high cortisol response to acute stress, typical of ADHD-I, correlates with poorer memory performance when learning vocabulary after exposure to stress - but only in men. Females might be protected against this by their sex hormones.¹⁹ Cortisol administration also worsened learning performance.
      Cortisol, which is often elevated as a stress response in ADHD-I, blocks retrieval of declarative (explicit) memory via glucocorticoid receptors (GR) in the PFC and hippocampus. Nondeclarative (implicit, intuitive) memory is not affected.²⁰ This could explain the more frequent thinking and memory blocks seen in ADHD-I, and likewise why ADHD-I sufferers often seem to have higher intuition. That the shift in the focus of memory skills leads to a shift in problem-solving patterns would be obvious in any case. Trappmann-Korr calls this “holistic” perception.
      It is likely that not only retrieval (remembering) but also acquisition (learning) and memory consolidation (long-term storage) of information are impaired. Consolidation occurs especially during sleep in the first half of the night, which is characterized by particularly low basal cortisol levels. Consolidation can be prevented by low cortisol administration.²⁰
  • Attention problems
    • Sustained attention (ADHD-HI and ADHD-I subtype)
    • Selective attention (ADHD-I subtype only)²¹

• Negative symptom delineation in ADHD-I:

  • Externalizing behavior disorders and aggressive behavior are atypical in ADHD-I and indicate the ADHD-HI subtype.²².

    • Less frequent symptoms of aggressive or oppositional defiant behavior²³²⁴

  • ADHD-I is therefore less frequently diagnosed because it is less likely to be unpleasantly noticed due to the “comfortable” symptoms of internalized stress management for the environment. In addition, research suffers from the fact that many studies do not differentiate outcomes by subtype and, in particular, do not distinguish ADHD-C from ADHD-I type.

  • Less frequent comorbid oppositional defiant behavior than ADHD-HI subtype.⁸

  • Lower proportion of smokers than ADHD-HI subtype.(The pathways of action of nicotine and methylphenidate are similar)¹⁶

  • Less frequent inflammatory reactions such as neurodermatitis due to the overshooting cortisol response. Cortisol inhibits the inflammatory processes initiated by CRH and instead promotes defense against foreign bodies, which can show up as allergies when overshot

More on the required frequency and intensity of ADHD symptoms at ⇒ Symptoms of ADHD of children by age.

1.1.3. Peculiarities of medication¶

• MPH Responding
  • According to one view, a noticeable proportion of methylphenidate non-responders (MPH does not work). If MPH is effective, low doses are often sufficient.¹⁶
  • According to others, ADHD-HI and ADHD-I do not differ in MPH response rates.²⁵
• A significant proportion of ADHD-I sufferers are more likely to respond to amphetamine medication than to MPH.
• Next to it should be helpful:
  • Nortriptyline
  • Bupropion (if stronger activation is required)

1.1.4. Neurophysiological features of ADHD-I¶

1.1.4.1. Increased cortisol stress response in ADHD-I¶

ADHD-I often appears to be associated with a particularly strong cortisol response to acute stress. ⇒ Changes in cortisol levels in ADHD in: Cortisol and other stress hormones in ADHD

1.1.4.2. Other biomarkers in ADHD-I¶

Underactivation of the PFC in ADHD-I is explained by correlating stress responses of cortisol, norepinephrine, and dopamine in the brain. See more at ⇒ Neurotransmitters in stress
* A large increase in norepinephrine / dopamine shuts down the PFC. This deactivation of the PFC occurs through alpha 1-adrenoceptors, which have lower norepinephrine and cortisol affinity than alpha 2-adrenoceptors and are therefore only addressed at very high norepinephrine and cortisol levels.^2627282930
Thus, a particularly large increase in DA and NE during severe stress could lead to (frequent) underactivation of the PFC, as is typical in ADHD-I.
This background could explain Raynaud’s and hypertension problems in some ADHD-I sufferers, which are also mediated by alpha-1-adrenoceptors.
The question is whether alpha-1-adrenoceptor antagonists, which have been used successfully against Raynaud’s disease and hypertension, might not also be helpful against the PFC blockades in ADHD-I.
To date, only alpha-2-adrenoceptor agonists have been used and are likely to be considered third-line agents. Guanfacine addresses alpha-2-A and alpha-2-D, while yohimbine addresses alpha-2-B adrenoceptors. Agonization of the more affine alpha-2 receptors is contrary in effect to antagonization of alpha-1 receptors. As with the cortisol receptors, the lower affinity receptor is responsible for shutting down the system and is only addressed at very high levels of neurotransmitter. If the more affine receptors are too strong, the less affine shut-off receptors are not activated.
Guanfacine and yohimbine occupy the more affine alpha-2 receptors, leaving more neurotransmitter for the less affine alpha-1 receptors, which are thus more easily addressed.

CRH also affects the PFC and, at high levels of CRH, can impair it.
Increased cortisol responses to a stressor correlate with increased variance in response time.³¹ Increased variance in response times could be explained by an impairment in the performance of the PFC, as is particularly pronounced in the ADHD-I subtype. This impairment could be explained by norepinephrine responses to acute stress that are also elevated, analogous to the cortisol response. Some diagnosticians pay particular attention to this variance in response times in an ADHD-I diagnosis.
Cortisol leads to a decrease in cortisol and norepinephrine
This negative feedback is the result of cortisol (it shuts down the HPA axis again) and is independent of the synchronicity of the release of cortisol and norepinephrine on stress
The dopamine D4 receptor (DRD4) has a special role in PFC, which is why Diamond³² assumes that disruption of the DRD4 7R gene is associated with ADHD-I. We do not believe this to be true.
Noble found that the A1, B2, and intron 6 1 gene polymorphisms of DRD2, as well as the DRD4 7R polymorphism, were associated with an elevated Novelty Seeking (Sensation seeking) Score. However, none of these polymorphisms correlated with a high Harm Avoidance Score (BIS), which is typical for ADHD-I.³³
High Novelty Seeking / Sensation Seeking rates are associated with high aversion to boredom and correlate with impulse control disorders.³⁴ Boredom is a cause of inattention in ADHD-I, whereas impulse control problems are atypical for ADHD-I and more typical for ADHD-HI.

In ADHD-I, there is often said to be a deficiency of serotonin.³⁵

ADHD-I may have lower orexin A levels than the ADHD-HI subtype and than nonaffected individuals.³⁶ For more on orexin, see ⇒ Orexin/Hypocretin In the section ⇒ Hormones in ADHD in the section ⇒ Neurological aspects.

1.1.5. EEG image in ADHD-I¶

See below under “Subtypes in ADHD according to EEG”.

1.1.6. Sluggish Cognitive Tempo (SCT) - stand-alone disorder¶

SCT is now considered a separate disorder independent of ADHD, although SCT and ADHD are very often comorbid. However, there are SCT sufferers without ADHD.
More about SCT at ⇒ SCT - Sluggish Cognitive Tempo.

1.2. ADHD-HI: predominantly hyperactive/impulsive subtype¶

1.2.1. Additional names¶

• ADHD-HI (used by us)
• ADHD (colloquially inaccurate collective term for all subtypes; we therefore use ADHD as a collective term)
• ADHD (English; used internationally, but there also a collective term for all subtypes)
• ADHD-PH (predominantly hyperactive/impulsive)
• ADHD-H/I (hyperactive/impulsive)
• Fidget (colloquially descriptive)

1.2.2. Specific symptoms¶

• Clear expression of
  • Hyperactivity
  • Impulsivity
• No inattention
  • If inattention occurs in addition to hyperactivity / impulsivity: ADHD-C, see below
• Social problems very common
  arise because ADHD-HI subtype
  • Puts others before the head
  • Takes things away from them
  • Can not wait for his turn
  • Appears too direct and decisive
  • Behaves in a disruptive manner and
  • Acts without considering the feelings of others³⁷
• Rather extroverted (in contrast to the more introverted ADHD-I subtype)⁹⁸
• Frequent conduct disorder and (comorbid) aggressive behavior³⁸.
• More often existing comorbidity to oppositional defiant behavior¹⁶
• Disorders primarily in behavioral inhibition¹⁶ and executive functions³⁹
• Is distractible rather than bored¹⁶
• Has an inhibition problem rather than a motivation problem.¹⁶
• Tendency to low self-awareness¹⁶
• Good response to methylphenidate.
  The nonresponder rate (MPH does not work) is reported to be 10%.⁴⁰
• The striatum is primarily affected. The fact that DAT1 plays an important role in the striatum and MPH primarily targets the DAT explains the good effect of MPH in ADHD-HI.¹⁶
• Higher proportion of smokers than in ADHD-I subtype. (Nicotine, like methylphenidate, acts as a stimulant)¹⁶
• Hyperactive/impulsive type often only precursor in childhood/adolescence for later ADHD-C⁴¹⁴²
• Boys are 5 times more likely to be affected than girls⁴³.
• More frequent inflammatory responses than ADHD-I subtype due to flattened cortisol response to stress. Cortisol inhibits the inflammatory immune response mediated by CRH.
• Hypocortisolism corresponding disorder patterns are¹⁸
  • Atypical depression
  • Inflammation problems⁴⁴
    • E.g. irritable bowel syndrome
    • E.g. neurodermatitis
  • Fatigue
    Cortisol inhibits proinflammatory effect of CRH
    promotes cytokines such as interleukin 1 and 6; thereby (as with fever) “sickness behavior”:
    • Fatigue
    • Lack of initiative
    • Fatigue
    • E.g. Chronic Fatigue Syndrome
    • E.g. burnout
  • Pain sensitivity
    Cortisol inhibits prostaglandin synthesis (= disinhibition of prostaglandins)
    Prostaglandins modulate pain perception
    thereby systemic lowering of the pain threshold (pain symptoms “migrate”)
    Hypocortisolism may promote inflammatory processes in the spinal cord (chronicized pain)
    • E.g. fibromyalgia⁴⁵
    • E.g. Chronic lower abdominal pain
  • Stress intolerance
    Cortisol inhibits locus coeruleus, thereby decreasing norepinephrine release in CNS
    Low cortisol response results in impaired norepinephrine inhibition = elimination of important stress brake
    Hypocortisolism thereby causes stress intolerance, irritability, sensitivity to sensory stimuli (noise, etc.)
    Hypocortisolism could promote emergence of intrusions as observed in PTSD⁴⁶

Negative symptom delineation in ADHD-HI:

• If inattention and hyperactivity (the latter also as inner drive) exist, the so-called ADHD-C is present.
  Inattention can usually only be detected between the ages of 6 and 15. ADHD-HI (with hyperactivity without attention problems) can therefore be considered an early form of the later mixed type.⁴¹⁴⁷
  The question of whether ADHD exists entirely without inattention has not been conclusively answered. We tend to assume this, although this is likely to be a rather rare manifestation.
  The higher the aptitude, the better the coping mechanisms. The older the affected individuals are, the more remitted individual symptoms may be, which is why a lack of (well-concealed) inattention in test settings does occur. Similarly, a high intrinsic interest of affected individuals in the tests leads to an equalization of test performance compared to nonaffected individuals. This is plausible when the stress benefit and thus the mechanisms of the stress symptom inattention are considered.
• In ADHD-HI, allergies appear to occur less frequently than in the ADHD-I subtype because of the more frequently flattened cortisol response to stress. Cortisol increases the immune response to external stresses such as allergens.

1.2.3. Neurophysiological peculiarities in ADHD-HI¶

In ADHD-HI (with hyperactivity/impulsivity) and likewise in correlated aggression, the release of catecholamines and cortisol in response to acute stressors is often decreased or absent compared with nonaffected individuals, whereas the cortisol stress response is typically increased in ADHD-I affected individuals compared with nonaffected individuals.

1.2.3.1. Flattened cortisol stress response in ADHD-HI¶

ADHD-HI is often associated with a flattened cortisol response to acute stress. ⇒ Cortisol in ADHD

1.2.3.2. Deficient HPA axis disconnection in ADHD-HI¶

Since cortisol not only mediates stress symptoms, but at the same time shuts down the HPA axis, a reduced cortisol stress response results in a lack of braking of the HPA stress system.
⇒ The HPA axis/stress regulation axis And ⇒ The autonomic nervous system.

1.2.3.3. Decreased norepinephrine depletion in ADHD-HI?¶

Cortisol further causes a breakdown of norepinephrine.
A too low cortisol response to acute stress and a consequently too low norepinephrine depletion could possibly explain a permanent overactivation of the PFC in ADHD-HI/ADHD-C.
A slightly increased (dopamine and) norepinephrine level in the PFC increases its activation and causes improved cognitive performance.^4849505152 Only a strong increase in norepinephrine / dopamine shuts down the PFC.^2627282930

1.2.3.4. Decreased hippocampal volume in ADHD-HI¶

A fairly large study reported decreased hippocampal volume in ADHD-HI as opposed to ADHD-I and nonaffected individuals.
* ADHD-HI: reduction in hippocampal areas⁵³
* CA1
* CA4
* Molecular layer
* Granule cell band of the dentate gyrus
* Presubiculum
* Subiculum
* Hippocampal tail
* Other hippocampal regions were not reduced in size
* ADHD-I: no reliable differences in hippocampal volume to controls⁵³
* Finally, reduced hippocampal areas correlated with higher behavioral ADHD indices. For example, a smaller subiculum correlated with a higher overall ADHD-HI index and higher hyperactivity/impulsivity and lower IQ.⁵³

1.2.3.5. Indole acetic acid in ADHD-HI¶

In ADHD-HI sufferers with comorbid depressive symptoms, one study found significantly higher morning than evening levels of indole acetic acid. MPH reduced this by 50%. MPH simultaneously reduced morning levels of indolepropionic acid and returned the diurnal profile to that of healthy control subjects.⁵⁴

• SHR exhibit behavioral subgroups corresponding to ADHD-HI and ADHD-I
  • One study found SHR (Spontaneous(ly) hypertensive rat) subgroups that differed significantly with respect to impulsivity. Impulsive SHR, compared with non-impulsive SHR and WKY (as controls; no behavioral subgroups were found in the latter), showed⁵⁵
    • Reduced noradrenaline levels
      • In the cingulate cortex
      • In the medial-frontal cortex
    • Reduced serotonin turnover
      • In the medial-frontal cortex
    • Reduced density of CB1 cannabinoid receptors
      • In PFC
      • Acute administration of a cannabinoid agonist reduced impulsivity in impulsive SHR, with no change in WKY

1.2.4. EEG image in ADHD-HI¶

See below under subtypes in ADHD by EEG.

1.3. ADHD-C - mixed type of ADHD-HI and ADHD-I¶

• Clear expression in all three core symptom areas:
  • Hyperactivity (in children; in adults; inner restlessness)
  • Impulsivity
  • Inattention
    • Problems with sustained attention (ADHD-C and ADHD-I)
    • Fewer problems with selective attention (ADHD-I subtype only)²¹
• Corresponds largely to hyperkinetic disorder according to ICD-10.2.3.1. subgroups of ADHD-C

A larger study of adolescents found three subgroups of ADHD-C in which the specific symptomatology was simultaneously evident in brain structure changes measurable by fMRI in brain systems known to be involved in these cognitive functions.⁵⁶

A small study replicated previous research that frontal delta and theta power are higher in ADHD-C than in ADHD-I and TD groups.⁵⁷

1.3.1. ADHD-C with inhibition deficits, without reward deficits¶

Inhibitory deficits means deficits in executive functions and inhibitory cognitive functions.

Subfunction within

• Different frontal lobes
• Parietal lobe
• Subcortical
• Cerebellar regions

in the inhibition of motor responses

and

Anomalies

• Of the posterior default mode
• In the ventral striatum

during error handling.

Executive function deficits also show up in other studies^58596061

Subfunction in

• Frontalgyrus
  • Pre-supplementary motor area (pre-SMA)
  • Middle frontal gyrus
  • Precentral frontal gyrus
• Insula
• Caudates
• Thalamus

Hyperfunction in the

• Inferior frontal gyrus
• Postcentral gyrus
• Precuneus

1.3.2. ADHD-C with inhibition deficits and reward deficits¶

Overactivation in

• Mostly non-overlapping cortical and subcortical regions

during error processing as well as

• Overactivated amygdala regions and
• Overactivated ventral striatal regions,

when they made an effort to receive rewards.

1.3.3. ADHD-C without reward deficits and without inhibition deficits¶

This was the most frequent subgroup. According to the absence of the mentioned particular symptoms, no neurological abnormalities were found

1.4. Other subtype classifications¶

We do not consider the “subtypes” mentioned below, which have been mentioned sporadically in the literature, to be true subtypes of ADHD.

1.4.1. ADHD with oppositional behavior disorder (?)¶

Oppositional behavior disorder, in our opinion, is a comorbidity that occurs primarily in ADHD-HI type and is not a subtype of ADHD-HI.
Significantly, even among those who hypothesize subtypes of ADHD with oppositional behavior disorder, it is described only in association with the ADHD-C and ADHD-HI types, but not with the (stress phenotypically introverted) ADHD-I type.

1.4.2. Rage type (?)¶

The Rage type is rarely described as a separate type. It is probably meant to denote ADHD-HI with aggressive comorbidity.

Similarly, a subtype with increased emotional irritability/irritability is suggested.⁶²

1.4.3. Residual type¶

The residual type is occasionally referred to as a partially regressed ADHD that is no longer fully developed but is still present.
This is not a subtype of ADHD, but may explain why there are sometimes ADHD sufferers who lack individual leading symptoms (e.g., with a largely full symptom picture without attention problems).

1.4.4. ADHD adult subtype pair according to Reimherr¶

Reimherr et al, in 8 replication studies of 1,490 ADHD-affected adults, found two clusters, the inattentive adult subtype and the emotionally dysregulated adult subtype.⁶³. The finding is consistent with an earlier study by the authors.⁶⁴
Both subtypes benefited equally from MPH treatment.

1.4.4.1. Inattentive adult subtype¶

• Inattentive
• Emotionally dysregulated

1.4.4.2. Emotionally dysregulated adult subtype¶

Emotional dysregulation manifests itself in the following ways, among others

• Anger
• Affective instability
• Emotional overreactivity

1.4.5. ADHD subtypes according to internalizing / externalizing symptoms¶

Katsuki et al describe four ADHD subtypes using a cluster analysis of emotion and behavioral symptoms in children 4-15 years of age with ADHD:⁶⁵

• “Strongly internalizing/externalizing.”
  • Overlap of internalizing and externalizing symptoms
    • Possibly moderated by emotional dysregulation and associated neurophysiological correlates
  • High rate of comorbid autism spectrum disorders
  • Increased autistic features
• “Inattention and Internalization.”
  • High rate of predominant inattention (ADHD-I)
• “Aggression and Externalization
  • High rate of comorbid oppositional defiant behavior
  • High rate of comorbid behavioral disorder
• “Minor psychopathology”
  • Low values on all syndrome scales

1.4.6. ADHD subtypes by symptom severity¶

Volk et al defined seven subtypes.⁶⁶⁶⁷ They are presented according to frequency (% in parentheses). In addition, the frequency of the comorbidities depression, ODD (Oppositional Defiant Disorder) and CD (Conduct Disorder) within the respective group is given.

• “mild ADHD symptoms” (53.4%)
• “slight inattention” (12.3%)
  thereof
  • Comorbid depression 9.3 %
  • Comorbid ODD 7.7 %
  • Comorbid CD 6.2 %
• “severe inattention” (12.1%)
  • Comorbid depression 6.6
  • Comorbid ODD 24.5 %
  • Comorbid CD 10.2 %
• “mild combined symptoms” (6.6%)
  • Comorbid depression 10.7
  • Comorbid ODD 30.2 %
  • Comorbid CD 13.6 %
• “severe combined symptoms” (6.1%)
  • Comorbid depression 8.3
  • Comorbid ODD 56.6
  • Comorbid CD 12.5 %
• “talkative impulsive” (6, 5 %)
  • Comorbid depression 1.9
  • Comorbid ODD 24 %
  • Comorbid CD 4.9 %
• “Hyperactive” (3%)
  • Comorbid depression 4.4
  • Comorbid ODD 16.7
  • Comorbid CD 2.2 %

1.4.7. Subtypes according to emotion profiles¶

One study divided ADHD into three subtypes based on character traits and emotion profiles:⁶²

• Mild ADHD subtype
  • Normal emotional functioning was found in this group of ADHD sufferers.
• Distressed ADHD subtype
  • This subytp was characterized by a particularly high level of distress.
• Irritable ADHD subtype
  • This subtype showed high negative affect and had the highest external validity.
  • Increased susceptibility to anger
  • The subtype was moderately stable over time and improved prospective prediction of clinical outcomes beyond standard baseline indicators.
  • De subtype was not reducible to ADHD-HI + oppositional defiant disorder (ODD), ADHD-HI + disruptive mood dysregulation disorder, or other patterns of comorbidity.

2. Neurophysiological and endocrine differences of the subtypes¶

Hyperactivity is neurologically anchored in the striatum; inattention is neurologically anchored primarily in the PFC.⁶⁸

A further distinction may need to be made between inattention from boredom due to an underactivated PFC (in ADHD-I) and distractibility due to overactivation of the PFC (in ADHD-HI).

2.1. Dopamine level¶

This section deals with the question whether different subtypes (according to symptom expression) correlate with certain dopamine (effect) levels. The question whether dopamine deficiency and dopamine excess are possibly different disorders or at least distinguishable variants of ADHD is addressed at the end of this chapter.

2.1.1. Hyperactivity, impulsivity: dopamine deficiency or excess in the striatum¶

Hyperactivity and impulsivity, as exhibited by the ADHD-HI subtype (without inattention) or ADHD-C (with inattention), are caused (with respect to ADHD) primarily by deviations of dopamine levels from optimal dopamine levels in the right hemispheric striatum (involving the frontostriatal loop consisting of the PFC, caudate nucleus, and globus pallidus, but not the putamen).⁶⁸⁶⁹⁷⁰

According to the prevailing opinion in the literature, ADHD is caused by a dopamine deficiency. However, it is known from animal models (e.g., the DAT-KO mouse) that an excess of dopamine in the striatum can also trigger hyperactivity. See ⇒ For more information ADHD in animal models in the chapter ⇒ Neurological aspects. As long as ADHD is not defined (and diagnosed) neurobiologically as a dopamine deficit in the striatum (and/or PFC) but is diagnosed on the basis of symptoms alone, both variants must be considered. Excess as well as deficiency of neurotransmitters cause almost the same symptoms according to the inverted-U-model, because the functionality of signal transmission is only given at optimal neurotransmitter levels. However, the evidence for a deficiency of phasic dopamine in the striatum in ADHD is by far in the majority.

Because dopamine degradation in the striatum occurs primarily via DAT, whereas dopamine degradation in the PFC occurs primarily via NET and COMT rather than DAT, the DAT-10R gene variant correlated strongly with hyperactivity and impulsivity, but not with inattention.⁷¹⁶⁸

2.1.2. Hyperactivity, impulsivity: dopamine excess in the PFC¶

Insofar as the predominant view in the literature is that there is dopamine deficiency in the striatum in hyperactivity and impulsivity (in ADHD-HI and ADHD-C),⁷² the dopamine seesaw between the striatum and the PFC subsequently leads to increased dopamine levels in the PFC in hyperactivity and impulsivity (in ADHD-HI and ADHD-C). See ⇒ for more details The dopamine seesaw between PFC and subcortical regions (including striatum) In the article ⇒ Dopamine in the chapter ⇒ Neurological aspects

In healthy individuals, a high level of dopamine in the PFC appears to lead to a low level of dopamine in the striatum and vice versa.
A fully utilized PFC (high dopamine level) simply does not seem to need any stimuli from the reinforcement/motivation center and therefore signals to it: “closed due to overcrowding - give it a rest”. The striatum then sulks silently (underactivated = low dopamine). This is a normal, healthy control loop.
Prolonged tonic dopamine deficiency in the striatum leads to upregulation of D2 autoreceptors (due to very prolonged dopamine excess in the PFC), which in turn leads to upregulation of dopamine transporters in the striatum. See ⇒ Up- and downregulation of the dopamine transporter In the article ⇒ Dopamine in the chapter ⇒ Neurological aspects. This could explain DAT overactivity, which would help explain or enhance the tonic dopamine deficiency in the striatum hypothesized in ADHD. .

Since hyperactivity can be mediated by a deficiency of phasic dopamine in the striatum, it would be understandable from this why this only occurs in ADHD-HI and ADHD-C, which are said to have a permanent overactivation of the PFC. The ADHD-I-typical underactivation of the PFC should rather cause a dopamine excess in the striatum due to the associated dopamine deficiency in the PFC. Studies show a dopamine deficiency in the striatum in ADHD, but do not differentiate between subtypes.⁷²

2.2. Exaggerated and flattened endocrine stress responses of subtypes¶

In ADHD-I, the endocrine stress responses appear to be much stronger than in ADHD-HI and ADHD-C.
An endocrine stress response is the amount of hormone (and neurotransmitter) release in response to an acute stressor.
The ADHD-I subtype often shows a hypercortisol stress response, whereas the ADHD-HI and ADHD-C often correlate with a flattened cortisol stress response. Thus, the ADHD-I subtype is typically a case of hypercortisolism, whereas ADHD-HI- and ADHD-C are more a case of hypocortisolism.
⇒ Changes in cortisol levels in ADHD in: Cortisol and other stress hormones in ADHD

Because hypocortisolism may represent a long-term sequential response to hypercortisolism when downregulation (⇒ upregulation) occurs because of persistently elevated cortisol levels Downregulation/Upregulation; ⇒ Altered hormone and neurotransmitter levels according to stress phase in the article ⇒ The stress systems of humans - basics of stress In the chapter ⇒ Stress) of the glucocorticoid (cortisol) receptor systems occurs, it could be concluded that the ADHD-I type represents a precursor and the ADHD-HI and ADHD-C a subsequent stage of ADHD. However, this is contradicted by the fact that the type of cortisol response to acute stress tends to represent a stress phenotype that is already found in healthy individuals. In disorders with externalizing symptoms - aggression, ODD, CD, etc. - the cortisol responses to acute stress are regularly flattened, in disorders with internalizing symptoms - depression, anxiety, etc. - the cortisol responses are regularly elevated.

Increases in cortisol are associated with stress-induced release of norepinephrine and α1-adrenergic receptor activation.⁸³⁸⁴ Parallel to the neurotransmitter-norepinephrine and cortisol correlation issue discussed here, there is a correlation between cortisol and dopamine release.⁸⁵ Cortisol levels correlate positively with AMPH-induced dopamine release in the left ventral striatum and dorsal putamen.

We assume that the cortisol, epinephrine, norepinephrine and dopamine responses in the brain to acute stress correlate, so that a high cortisol response to acute stress is accompanied on the one hand by high (hormone) norepinephrine release in the sympathetic nervous system and on the other hand by high (neurotransmitter) norepinephrine and dopamine release in the central nervous system (= brain). Low levels are also likely to correlate. This could conclusively explain quite a few patterns of ADHD subtypes.

• Mesocortical / mesolimbic system (dopaminergic)
• Amygdala (serotonergic, acetylcholinergic)
• Hippocampus (serotonergic, acetylcholinergic)

A very large increase in norepinephrine / dopamine shuts down the PFC and shifts behavioral control to posterior brain regions.^2627282930 There are connections between cortisol and the stimulation of D1 receptors.⁷⁷
The PFC is very sensitive to its neurochemical environment. Too little (drowsiness) as well as too much (severe stress) catecholamine release in the PFC weakens the cognitive control of behavior and attention.¹¹⁵is the PFC remains permanently activated in ADHD-HI and ADHD-C - which is just too much at some point.

ADHD-I patients, on the other hand, suffer from an endocrinological overreaction to acute stress. Assuming the hypothesis that in ADHD-I not only the cortisol stress response but also the norepinephrine release in the brain to acute stress is excessive, the established finding that strongly increased norepinephrine levels block the PFC would explain why ADHD-I often suffer from thought blockades and excessive demands when making decisions.
The strong stress-cortisol response in ADHD-I, which occurs on the 3rd stage of the HPA axis some time after the noradrenaline release, leads to a strong brake of the noradrenaline release. The norepinephrine brake of the PFC is therefore relaxed again in ADHD-I and the PFC ramps up again after some time. Thus, the PFC does not remain permanently in a dysfunctional state (as in ADHD-HI/ADHD-C). Thus, a mere temporary underfunction of the PFC does not lead to a permanent dopamine surplus in the striatum, which is why striatal problems are not as severe in ADHD-I. (Excess as well as deficiency each cause disturbances in the communication of the nerves and can therefore cause different or almost the same symptoms in the same brain region, because only with optimal neurotransmitter levels is the communication of signals in the brain functioning properly).

The various subtypes can also be conclusively described as stress phenotypes, in agreement with the endocrinological / neurological characteristics described.
Stress phenotypes means a typed response to stress.

More on this below under 6.

PFC deactivation occurs through alpha 1-adrenoceptors, which have lower norepinephrine and cortisol affinity than alpha 2-adrenoceptors and are therefore only addressed at very high levels of norepinephrine and cortisol.

On this side, a strong dopamine/norepinephrine increase is thought to be the cause of the ADHD-I-typical underactivation of the PFC.
Since in ADHD-HI (and ADHD-C) there is a flattened cortisol response to an acute stressor, a parallel flattened norepinephrine/dopamine release would result in a permanent mild stress state that does not shut down the PFC but permanently overactivates it.

In any case, due to a weaker cortisol response to acute stress, cortisol levels at the end of a stress response in ADHD-HI and ADHD-C (and independent of the hypothesis on this side of a correlation of release levels) are worse able to shut down the stress systems of the HPA axis and norepinephrine release in the brain again.

2.3. ADHD subtypes according to EEG¶

Most studies find different EEG subtypes in ADHD sufferers.
Externalizing characters show a flattened error-related negativity (ERN), internalizing characters an increased ERN.¹¹⁶ The ERN is a component of the event-related potentials (qEEG). It occurs immediately after an incorrect motor response (given under time pressure). ERN is primarily measured above the PFC.
An attempt to automatically distinguish subtypes based on their EEG patterns using AI failed.⁵

The largest study known to us found a differentiation into 5 EEG subtypes and showed that externalizing symptoms (ADHD-HI, ADHD-C) were primarily associated with increased slow EEG activity in the theta and delta bands, whereas internalizing symptoms (ADHD-I) were associated with increased activity in the alpha and beta bands.¹¹⁷ In contrast, a study of 94 boys aged 6 to 9 years uniformly found increased total alpha activity with decreased alpha peak frequency, decreased alpha bandwidth, and decreased alpha amplitude suppression magnitude, as well as an increased alpha1 / alpha2 (a1 / a2) ratio, despite differentiation by subtype.¹¹⁸

2.3.1. ADHD-HI subtypes according to EEG¶

EEG abnormalities in ADHD-HI are primarily found in the striatum as well as the frontal-striatal area.¹¹⁹

2.3.1.1. Theta frontal increased, beta decreased (ADHD-HI with hyperactivity and impulsivity in hypoactive EEG)¶

A high theta-beta ratio defines a distinct EEG ADHD subtype.¹²⁰ This subtype was described in 24.5% of ADHD sufferers.¹²¹

• Total power increased overall¹²¹
• Relative theta increased, especially frontal¹²¹
  • Elevated theta frontal has been found in several EEG studies in ADHD¹²²
  • This is considered representative of frontal lobe problems, especially hyperactivity¹²³
• Relative and absolute theta increased¹²⁴
• Beta activity reduced overall¹²¹
  • Lower amplitude at relative beta measured at electrode discharge points Cz on Pz-O1 and Pz-O2 and paramedian¹²⁴
• Consequence: theta-beta ratio increased (theta high, beta low)¹²⁴
• Delta central and posterior reduced¹²¹
• Alpha frontal and rear reduced¹²¹
• Increased slow waves, decreased fast waves¹²⁵
• Behavioral type¹²¹
  • Most typical ADHD symptom picture of all EEG subtypes
  • Hyperactivity
  • Enjoyable
  • Less anxious

Therapy Goals:

• Increase SMR (12 to 15 Hz)
• Decrease theta (4 to 8 Hz)
• Decrease theta while increasing beta: addresses tonic aspects of cortical activation to achieve attentive, focused, yet serene state¹²⁶

Effectiveness:

• Theta down and alpha up (at the same time, if necessary)
  The latter two training methods (train down theta, train up beta or train down theta / train up alpha) differed little in their results in 7-10 year olds. Both protocols alleviate symptoms of ADHD-HI in general (p <0.001) as well as symptoms of hyperactivity (p <0.001), inattention (p <0.001), and omission errors (p <0.001), but not oppositional and impulsive symptoms.¹²⁷
• Of 19 participants with ADHD-HI according to DSM III-R 12, 11 responded very well to neurofeedback training in which beta was trained up and theta was trained down (40 sessions). The other 7 showed smaller improvements. In the responders, IQ improved by 10 points at the same time as symptomatology (from 112 to 122). However, N = 19 is too small for a reliable statement.¹²⁸

2.3.1.2. Beta overactivated (“Overactivated” ADHD-HI)¶

Beta subtype is reported to be present in approximately 23.2%¹²⁹ of ADHD sufferers.

Findings:¹²⁴¹³⁰

• Amplitude of beta (13 to 30 Hz)¹³¹ or (18-26 Hz) increased, frontally and at the back of the head
• Beta dominates relative and absolute power
• Occurrence throughout the cortex
  • Frontal¹²⁴
  • Posterior¹²⁴
• Increased frontal overall performance¹²⁹
• Increased beta activity over the entire top of the skull¹²⁹
• Theta activity in fronto-central regions reduced¹²⁹
• Alpha activity in the frontal regions reduced¹²⁹
• Behavioral type¹²⁹
  • Symptomatic:
    • Increased aggression
    • Increased vandalism
    • Increased antisocial behavior.
  • Subtype-specific:
    This neurological abnormality is not seen in ADHD-I, but only in a subgroup of the mixed type, which is also said to differ from the rest of ADHD-C by a greater tendency to develop other symptoms ¹³²¹²⁵
    • Tantrums
    • Moody mood swings
    • Increased delinquency

However, ADHD sufferers with excessive beta are not hyperactive. Compared to non-affected individuals, be typical:¹³³

• Beta increased overall
• Delta is significantly reduced centrally posteriorly
• Alpha is reduced overall
• Significantly reduces the overall posterior power
• Reduces the theta / beta ratio overall.
• Skin conductance is significantly reduced (just as in sufferers with excessively elevated theta)

From this, the authors conclude that the theta / beta ratio is not associated with arousal.

Therapy Goals:

• Increase SMR (12 to 15 Hz)
• Reduce beta 2 (21 to 35 Hz)
• Reduce gamma (35 to 45 Hz)

A renowned group of researchers reported that ADHD sufferers with very low EEG theta values were more often nonresponders with respect to stimulants.¹³⁴ However, we know beta-type sufferers who benefited greatly from methylphenidate and even more from amphetamine medication.

2.3.2. ADHD-I subtypes in the EEG¶

EEG abnormalities in ADHD-I are reported to occur primarily in the PFC as well as in the frontal-paretic area.¹¹⁹

2.3.2.1. Delta and theta increased, beta decreased¶

One study found this subtype in 24.5% of ADHD sufferers.¹³⁵ Characteristic is:

• Delta increased overall¹²⁴¹³⁵
• Theta increased overall¹²⁴¹³⁵
• Abnormal increase of slow frequencies (delta/theta) primarily in central and centro-frontal areas¹³⁶
• Alpha reduced overall¹³⁵
• Beta reduced¹²⁴
• Total power posterior reduced¹³⁵
• Behavioral type¹³⁵
  • Enthusiastic
  • Impulsive
  • Requires close supervision to complete tasks
  • Less need for sleep
  • Swears, uses obscene language
  • No social behavior disorder (Conduct disorder, CD)
  • Prefers to surround himself with younger children
  • Developmental delay
• ADHD sufferers with high front-midline theta often showed
  • High and steep power peaks when discharged to Fz
  • At high FMT activity in the higher FMT frequencies:
    • Problems with emotion regulation and memory control.
  • At high FMT activity in the lower FMT frequencies:
    • Learning difficulties or memory problems.
  • Anxiety
  • Affect Breakthroughs

Therapy Goals:

• Increase beta 1 (15 to 21 Hz)
• Decrease theta (4 to 8 Hz)

Kühle¹²⁴ describes that in ADHD-I, delayed brain development is often found. As far as we know, the brain maturation of some areas is delayed in all ADHD subtypes. Whether this is a neurological deficit or only a neurological correlate of ADHD is questionable. The maturation delay in ADHD patients corresponds quite exactly to the brain maturation delay in giftedness.
See more at ⇒ Giftedness and ADHD

2.3.2.2. Only alpha activity inflated¶

This type is reported to occur in about 16.8%¹²⁵ of ADHD sufferers.

• Excessive alpha activity¹³⁷¹²⁵
  • Posterior¹³⁸
  • Central¹³⁹
  • Fronto-central¹²⁵
  • Sometimes also frontal¹³⁷
• Delta reduced overall¹²⁵
• Theta fronto-central reduced¹²⁵
• Behavioral type¹²⁵
  • Hyperactive, fidgety
  • Confused, feels like in a fog
  • Mildly obsessive
  • Perfectionist, sets high goals
  • Only deals with one or two ideas or activities

The described behavioral type with echoes of compulsivity is said to find its counterpart in studies of autism sufferers, in whom very high alpha values were also found.¹⁴⁰¹⁴¹

Alpha activity occurs as a μ-rhythm (also called monkey face (Mu-rhythm)) centrally over the entire cortex in the posterior temporal and/or temporal areas.

A study of girls with ADHD-I found significant differences from nonaffected individuals only in the Alpha 2 band.¹⁴²

2.3.2.3. Theta posterior increased, alpha and beta decreased¶

This type is said to occur in about 11%¹²⁵ of ADHD sufferers.

• Total frontal power significantly increased¹³³
• Theta significantly increased¹³³
  • Especially posterior
• Theta / beta ratio significantly increased¹³³
• Alpha reduced across the entire skullcap¹³³
• Beta reduced across the entire skullcap¹³³
• Delta activity centrally reduced.¹³³
• Behavioral type¹³³
  • Sociable
  • Serene
  • Fewer behavioral problems than other ADHD sufferers
  • Significantly less hyperactivity
  • Age-appropriate behavior (no developmental delay)
  • No increased anxiety
  • No increased antisocial behavior
  • No ritualized behavior

2.3.2.4. Only theta frontal midline (FMT) increased¶

• Abnormal increase in frontal midline theta (FMT) (5.5 to 8 Hz),¹⁴³¹⁴⁴ especially under task stress
• Dysfunction: hippocampus, anterior cingulate cortex (ACC)¹⁴⁵
• Medication recommendation: no medication; small doses of methylphenidate¹⁴⁵
• Unaffected individuals have little FMT at rest
• ADHD sufferers with high FMT often exhibit
  • High and steep power peaks when discharged to Fz
  • At high FMT activity in the higher FMT frequencies:
    • Often problems with emotion regulation and memory control
  • At high FMT activity in the lower FMT frequencies:
    • Often learning difficulties or memory problems
  • Anxiety
  • Affect Breakthroughs

2.4. ADHD subtypes according to QEEG¶

A study of 69 participants found three QEEG subtypes:¹⁴⁶

• increased absolute and relative beta performance
  • K-ARS: 25.31
• increased relative fast alpha and beta performance
  • K-ARS: 21.67
• increased absolute slow frequency (delta and theta power)
  • K-ARS: 12.64, barely higher than non-affected at 11.07
  • WURS: 55.82 significantly higher than non-affected at 42.81

Consequently, the third group can only be identified with the WURS (Wender-Utah Rating Scale) and not with the K-ARS (Koranic ADHD Rating Scale, the most widely used scale in Korea).

2.5. Functional differences of nerve conduction pathways in the brain (?)¶

Studies suggesting specific functional differences in brain nerve conduction pathways for ADHD-HI and ADHD-I,¹⁴⁷¹⁴⁸ suffer from very low case numbers (n < 50), which affects the robustness of the results (for more details, see: ⇒ Studies prove-sometimes nothing at all).

2.6. Subtypes and serotonin¶

Further, different serotonin levels in the different subtypes are discussed, which are thought to be related to the 5-HT 1B receptor in ADHD-I and to the 5-HT 2A/C receptors in ADHD-HI.¹⁴⁹

2.7. Neuro-auditory profiles of subtypes¶

One study demonstrated differences between ADHD-HI, ADHD-I, and controls in auditory brain regions, the Heschl’s gyrus (HG) and the planum temporale (PT).
ADHD-HI and ADHD-I revealed reduced gray matter volumes in the left Heschl’s gyrus, and thus reduced HG/PT ratios in the left hemisphere.
ADHD-HI showed a lower right HG/PT ratio in the right hemisphere, whereas ADHD-I did not differ from controls.
ADHD-HI showed left-right asynchrony, whereas ADHD-I and controls showed balanced hemispheric response patterns.¹⁵⁰

3. ADHD-HI/ADHD-C and ADHD-I as stress phenotypes¶

See ⇒ Stress theories and stress phenotypes: a possible explanation of ADHD subtypes In the chapter ⇒ Stress

4. Problem of subdivision into subtypes¶

One problem with subtyping is that some ADHD sufferers outsource brain activities from affected brain areas to other brain areas, that is, they “misappropriate” brain areas to substitute for the abilities of the affected brain areas.

This makes diagnosis by means of questionnaires and tests more difficult.

A more objective determination of the particular ADHD subtype could be made by a more accurate history by EEG or QEEG measurement and stress system reactance by the dexamethasone/ACTH/CRH test.

5. ADHD variants by dopamine level?¶

Most voices in the literature link ADHD to decreased dopamine levels. This description is likely to include that the level of dopamine is neutral but the sensitivity of receptors is decreased, or that the breakdown of dopamine is too rapid. The result is that there is too little dopamine (action).
Apart from the fact that this description usually does not differentiate more precisely in which brain region the dopamine deficit exists and whether it is a deficit of tonic or phasic dopamine output or of basal dopamine levels, there is contrary evidence that dopamine excess can also cause ADHD symptoms. See, among others, ⇒ ADHD in animal models In the chapter ⇒ Neurological aspects.
This is consistent with the inverted-U model, according to which an excess as well as a deficit of a neurotransmitter can cause confusingly similar symptoms because optimal signal transmission depends on a certain (“mean”) neurotransmitter level. Signal transmission is equally affected by excessive as well as decreased neurotransmitter levels.

As long as ADHD is defined and diagnosed purely on the basis of symptoms, this will inevitably lead to sufferers with dopamine deficiency being treated in the same way as sufferers with dopamine excess (even if the latter are likely to be rare, or at least rarer, according to our conjecture). Against this background, the question arises whether it would not make sense to either

• To define ADHD neurobiologically as a dopamine (effect) deficit and to name all forms (even with similar symptoms) with a dopamine excess differently,
  or
• ADHD neurobiologically to be divided into two dopaminergic variants*, the hypodopaminergic variant (dopamine deficiency) and the hyperdopaminergic variant (dopamine excess).

However, contrary to our initial expectation, findings on the effects of ADHD medications in both hypodopaminergic and hyperdopaminergic animal models indicate that the primary medications used to date appear to have comparable effects in both variants.
Stimulants act primarily as dopamine reuptake inhibitors, thereby increasing the level of dopamine available in the synaptic cleft. Nevertheless, stimulants reduce hyperactivity even in animal models with dopamine excess, such as the DAT-KO mouse, without reducing extracellular dopamine levels. Atomoxetine, on the other hand, appears to reduce hyperactivity only in animal models with dopamine deficiency but not in dopamine excess. Cognitive impairments such as inattention and learning deficits appear to be ameliorated by stimulants as well as atomoxetine in the presence of dopamine excess.
See more at ⇒ ADHD in animal models In the chapter ⇒ Neurological aspects.

Even though the medications used so far seem to work equally well for dopamine deficiency and dopamine excess, we thought it would be desirable to distinguish more consciously between these different ADHD variants. The fact that the medications used to date work equally in both cases could also be the result of the fact that the effect of medications has not previously been assessed separately for the two variants. It is quite conceivable that, with appropriate differentiation, individual medications that have so far been devalued because of a lower efficacy (compared to the stimulants primarily used so far) could prove to be effective for one of the variants and ineffective for the other - as seems to be the case with atomoxetine with regard to hyperactivity. In this case, efficacy would need to be re-evaluated in relation to the area of use.

The question of the ADHD variants (hypodopaminergic/hyperdopaminergic) is not likely to gain practical importance as long as there is no inexpensive, reliable and side-effect-free method to determine the dopamine (effect) level in certain brain regions of affected persons. However, in the scientific study of ADHD and in a more in-depth study of drug treatment of ADHD, we would like to see more consideration of this aspect as well as a consistent differentiation of study results according to subtypes.