Organizational and executive function problems in ADHD - neurophysiological correlates

Organizational problems are an essential part of executive functions.
A description of the executive functions can be found at ⇒ Organizational difficulties / executive problems In the article ⇒ Complete list of ADHD symptoms according to manifestations in the chapter ⇒ Symptoms.

Executive functions are primarily controlled by working memory.

ADHD is characterized by 3 pathways (according to Sonuga-Barke) that cause neurophysiological symptoms:

• Dopamine deficiency (among others) in dlPFC (working memory)
  • Executive functions
    • Disorganization
    • Forgetfulness
• Dopamine deficiency (among others) in the striatum (reinforcement center)
  • Motivation problems
  • Impulsiveness
  • Hyperactivity
• Changes in the cerebellum
  • Time perception problems

• 1. The working memory
  • 1.1. Working memory and dopamine
  • 1.2. Working memory and noradrenaline
  • 1.3. Working memory and CRH
• 2. Working memory problems with ADHD
• 3. Measurement of working memory problems
  • 3.1. Measuring working memory problems with the N-back test
• 4. Other executive functions
• 5. Cerebellum damage as a cause of executive problems
• 6. Insufficient use of neuronal resources

1. The working memory¶

Working memory supports the ability to temporarily store and manipulate information in order to control goal-oriented behavior.
Goldman-Rakic defined working memory as the ability to recall events in the absence of direct stimulation.¹ For this purpose, reciprocal feed-forward inhibition between groups of pyramidal neurons is used.
The working memory consists of three memory units that are coordinated by a central instance:

• Processing processor unit (“central executive”)
  • DlPFC
  • Processes information that is stored in the two memory stores
• Visual-spatial memory
  • Right posterior parietal lobe
• Acoustic-linguistic (“phonological”) memory
  • Lower left parietal lobe
• Short-term memory
  • Episodic buffer for visual-spatial and acoustic-linguistic information for processing by the central executive. Memory capacity on average 7 (+/-2) units (Miller’s number)

Transferred to a PC, the central executive could be described as the main processor, the short-term memory as the working memory (RAM) and the memory storage as different segments of the hard disk.

Working memory in the dlPFC is primarily dopaminergic and noradrenergic.
Both dopamine and noradrenaline influence working memory in an inverted-U form. Too little dopamine or noradrenaline impair the working memory just as much as too much dopamine or noradrenaline.²

1.1. Working memory and dopamine¶

The processes of working memory appear to be controlled predominantly by phasic rather than tonic dopamine.³ For example, DA neurons react phasically to stimuli that are to be memorized and show no tonic activity during the retention interval, i.e. the time during which the information is kept active.⁴
D1 agonists improve, D1 antagonists impair the function of working memory.⁵ Excessive D1 stimulation, such as during acute stress, leads to working memory deficits, as does insufficient D1 stimulation.⁶⁷⁸
D2 receptor agonists improve, D2 antagonists impair spatial (not non-spatial) working memory and thus executive functions in healthy adults.⁹

1.2. Working memory and noradrenaline¶

Working memory is also noradrenergically controlled in humans and rats, for example.¹⁰¹¹¹²
Activation of postsynaptic α1-adrenoceptors by stress impairs working memory via activation of the phosphatidylinositol protein kinase C (PKC) pathway.¹³ Guanfacine and clonidine improved spatial working memory in aging or younger PFC-lesioned monkeys.¹⁴
The amount of noradrenaline released in the PFC determines which type of adrenoreceptor is addressed. Moderate levels of noradrenaline activate high-affinity a-2A receptors (Gi coupled, cAMP inhibitory), while higher levels of noradrenaline, as released during stress, activate low-affinity a-1 receptors (phosphotidyl inositol coupled) and low-affinity b-1 receptors, which increases cAMP signaling. Moderate levels of noradrenaline improve working memory in the PFC via the high-affinity a-2A adrenoreceptor, whereas stimulation of the D1 receptor, a-1 adrenoreceptor and b-1 adrenoreceptor (low-affinity for noradrenaline) impairs working memory.⁵⁸

1.3. Working memory and CRH¶

CRH in general and in PFC in particular impairs visual-spatial working memory in a dose-dependent manner, which is particularly impaired in ADHD.¹⁵ Non-specific CRH receptor antagonists such as selective CRH-1 receptor antagonists remedied the impairment of working memory and were therefore considered by the authors as possible starting points for treatment of ADHD.

2. Working memory problems with ADHD¶

ADHD correlates with working memory problems,¹⁶ unlike tic disorders.¹⁷

The various components of working memory in ADHD appear to be impaired with varying degrees of frequency (and very differently from individual to individual). Around 70% of those affected showed an impairment in one of the 3 areas:¹⁸

• Reorganization of the working memory (very common)
  • Retaining and rearranging information
• Updating the working memory (frequent)
  • Actively monitoring incoming information and replacing outdated information with relevant information
  • 8% of those affected showed particular strength in this area
• Dual processing (rare)
  • Maintaining information while performing a secondary task
  • 20% of those affected showed particular strength in this area

In the dlPFC, sustained attention to solving problems is mapped. The ADHD symptoms caused by impaired sustained attention therefore correlate with a disorder of the dlPFC.¹⁹ Selective attention (distractibility), on the other hand, is located in the dorsal nucleus accumbens.

Working memory problems in ADHD do not diminish in adulthood. In some cases, a deterioration in distractibility has been observed.²⁰

Another study surprisingly found that language acquisition and arithmetic math skills, which require working memory, were not significantly impaired in children with ADHD. However, performance dropped significantly when those affected believed they were less gifted.²¹

In addition to executive problems, one study also found problems with the Theory of Mind (ToM) in children with ADHD (in contrast to other studies). However, these did not correlate with the executive problems, so that an involvement of the working memory seemed unlikely.²² Another study found reduced Theory of Mind abilities in adults with ADHD, which correlated with executive problems.²³

In children with ADHD, a correlation was found between impaired working memory and eye movement abnormalities during reading. Visual scanning of words during reading was discontinuous, uncoordinated and chaotic. ADHD groups showed higher entropy index among the four categories of saccades than non-affected groups.¹⁶
With ADHD, it takes 250 ms for an error in sentence structure to be detected. For non-affected people, it only takes 100 ms.²⁴

Organizational difficulties (disorganization) are often associated with time perception problems.²⁵ However, this is not consistent with the neurophysiological correlates of organizational problems / executive problems described here (deficits in working memory, which is located in the dlPFC), while the neurophysiological correlates of time (perception) problems are primarily located in the cerebellum.

One study found evidence that the cognitive deficits of patients with ADHD that can be measured with the N-back task are not due to a deficit in working memory, but to a disturbance of the cognitive state (memory load, task duration and new stimuli). ADHD patients and controls showed no significant differences in terms of reaction time and accuracy:²⁶

• Spatially, adult ADHD patients showed significantly higher activation levels of oxyHb in the left orbitofrontal area and left frontopolar area (channels 4 and 11) in the 2-back task and lower activation levels of deoxyHb in the 3-back task than healthy controls (corrected p < 0.05).
• In terms of time, adults with ADHD reached their peak ROIs earlier than healthy controls.

3. Measurement of working memory problems¶

The problem-solving skills and sustained attention items associated with working memory can be measured with tests.

3.1. Measuring working memory problems with the N-back test¶

Working memory and sustained attention can be tested with the N-back test.²⁷

Find out more at ⇒ N-back test In the subsection ⇒ Attention and reaction tests in the section ⇒ Tests in the article ⇒ ADHD - diagnostic methods in the chapter ⇒ Diagnostics.

4. Other executive functions¶

Inhibition (control of reaction inhibition)²⁸

• PFC right inferior²⁹
• Basal ganglia
  • Subthalamic nucleus³⁰

Error detection

• PFC medial²⁹
• ACC rostral and the temporoparietal junction³¹

Control of interference (a component of reaction inhibition)

• ACC³²
• PFC lateral³²
• Parietal cortex²⁸

Planning and solving problems²⁸

• DlPFC³¹
• ACC³¹
• OFC³¹
• Motor/premotor areas³¹

correct execution of working memory tasks²⁸

• DlPFC
• VlPFC
• Rostral PFC
• Parietal cortex (bilateral and medial-posterior)

Word fluency:²⁸

• Phonemic word fluency
  Number of words with a certain initial letter that a test band can form:

  • Frontal regions³³
    • Left motor/premotor regions
    • Left or bilateral opercular regions
    • Left lateral orbitofrontal regions
    • Right dorsolateral regions

• Semantic / categorical word fluency
  Number of words that a respondent can form from a certain semantic category (e.g. animals), regardless of the initial letter

  • Temporal regions³³

cognitive flexibility²⁸

• Cortex inferior parietal
• Superior colliculus
• Posterior lateral thalamus
• Medial frontal regions
• Pre-supplementary motor area

5. Cerebellum damage as a cause of executive problems¶

Children with tumor-related damage to the cerebellum showed significantly more frequent executive problems and social-emotional problems.³⁴

6. Insufficient use of neuronal resources¶

One study investigated the access to brain capacities during a more resource-intensive task in patients with ADHD. It was found that executive dysfunction during a more resource-intensive task could be due to insufficient utilization (allocation) of neuronal resources.³⁵ The difference was shown in a reduced pupil dilation.