Attention deficit disorder (ADD) is a neurodevelopmental disorder characterized by inattention, impulsivity, and hyperactivity. ADD is one of the most commonly diagnosed mental health conditions in children, with around 9.4% of children in the United States having been diagnosed with ADD as of 2016. While the exact causes of ADD are still being researched, scientists believe that there are multiple factors that contribute to the development of ADD, including genetics, environment, brain chemistry and structure. Understanding the neurological basis of ADD can help improve diagnosis and allow for the development of more targeted treatments.
Symptoms of ADD
The core symptoms of ADD include:
- Inattention – Difficulty focusing, wandering attention, lacking persistence, difficulty organizing tasks
- Impulsivity – Impatience, difficulty taking turns, interrupting others, difficulty thinking before acting
- Hyperactivity – Excessive motor activity, restlessness, constant motion, fidgeting
These symptoms must be chronic, impairing, and inconsistent with the child’s developmental level to meet diagnostic criteria for ADD. However, the way these symptoms manifest can vary greatly from person to person. Some individuals with ADD may be predominantly inattentive, while others are more hyperactive and impulsive. The severity of symptoms can also differ significantly.
Genetic Factors
Research suggests that genetics play a major role in ADD. ADD has a high heritability rate, with estimates ranging from 60% to 90%. This means that differences in genes account for 60% to 90% of the differences between people with and without ADD. Having a parent or sibling with ADD greatly increases an individual’s risk of also developing the disorder. Specific genes associated with dopamine and norepinephrine regulation in the prefrontal cortex have been linked to ADD risk. The exact genes involved are still being investigated.
Some of the specific genes implicated in ADD include:
- DAT1 – Regulates dopamine reuptake
- DRD4 – Dopamine D4 receptor
- DRD5 – Dopamine D5 receptor
- 5-HTT – Serotonin transporter
- HTR1B – Serotonin receptor
However, variations in these genes only account for a small amount of the genetic risk, suggesting that ADD likely involves the combined effects of multiple genes.
Brain Structure
Structural and functional brain imaging studies have identified some key brain differences that may underlie ADD symptoms:
Prefrontal Cortex
The prefrontal cortex controls high-level executive functions like attention, planning, inhibition, and working memory. Multiple studies have found that individuals with ADD tend to have slightly smaller prefrontal cortex volumes compared to those without the disorder. They also show altered neural activity in regions of the prefrontal cortex.
Corpus Callosum
The corpus callosum connects and facilitates communication between the brain’s hemispheres. Research indicates the corpus callosum tends to be smaller and less developed in those with ADD. This could impair coordination between the hemispheres.
Cerebellum
The cerebellum is involved in motor control and some cognitive functions. Some studies have found impairments in this region, which could contribute to hyperactivity and cognitive symptoms of ADD.
Basal Ganglia
The basal ganglia play an important role in cognition and motor control. Research has found links between changes in the basal ganglia and symptoms of inattention and hyperactivity in ADD.
Overall Brain Volume
Some studies have found that children with ADD tend to have a 3-4% smaller total brain volume compared to other children. However, findings have been mixed overall.
Neurotransmitter Imbalances
Neurotransmitters are chemicals that transmit signals between neurons in the brain. Several key neurotransmitters have been implicated in ADD:
Dopamine
Dopamine signaling is critical for cognitive functions like attention, motivation, and impulse control. Most ADD medications target the dopamine system. Both too much and too little dopamine signaling can impair function and lead to ADD-like symptoms. Genetic differences in dopamine receptors and transporters have been linked to ADD risk.
Norepinephrine
Norepinephrine is also involved in attention regulation and response to stimuli. Some research has found individuals with ADD have higher baseline norepinephrine levels. Certain medications used to treat ADD, like atomoxetine, target the norepinephrine system.
Serotonin
Serotonin impacts mood, anxiety, inhibition, and impulsivity. Some studies have found associations between serotonin dysfunction and symptoms of impulsivity and hyperactivity in those with ADD.
Environmental Factors
While genetics and neurobiology contribute significantly to the development of ADD, research suggests environmental factors also play an important role, likely by interacting with genetic vulnerabilities:
- Prenatal environment – Exposure to nicotine, alcohol, toxins, stress during pregnancy increase ADD risk.
- Traumatic brain injury – Even mild injuries can increase risk of developing ADD symptoms.
- Chemical exposure – Lead and organophosphate pesticide exposure has been linked to increased ADD risk, likely due to effects on dopamine systems.
- Prematurity – Being born prematurely (less than 37 weeks) seems to increase ADD risk.
Environmental influences during key stages of brain development may disrupt normal development in ways that result in ADD. The exact mechanisms are still being investigated.
Neurological Basis Summary
While more research is still needed, studies overall point to ADD having a complex neurological basis involving genetics, brain structure and function, neurotransmitter regulation, and environmental influences:
| Neurological Factor | Association with ADD |
|---|---|
| Genetics | High heritability indicating strong genetic component. Specific genes involved with dopamine/norepinephrine systems linked to ADD risk. |
| Brain structure | Alterations found in prefrontal cortex, corpus callosum, cerebellum, basal ganglia. Slightly smaller overall brain volume. |
| Neurotransmitters | Imbalances in dopamine, norepinephrine, serotonin associated with ADD symptoms. |
| Environmental factors | Prenatal exposures, brain injury, chemical toxins can increase risk of ADD, likely by interacting with genetic vulnerabilities. |
Understanding the neurological basis of ADD can help improve early identification, allow for more personalized treatment plans targeting specific deficits and brain mechanisms, and point toward new treatment approaches that directly address the underlying pathology. Continued research on the complex neurological factors contributing to ADD will be important for advancing care and improving quality of life for those with the disorder.
Diagnosing ADD
Because there is no single test that can diagnose ADD, clinicians must conduct a comprehensive medical and psychological evaluation to determine if symptoms and impairment meet the diagnostic criteria outlined in the American Psychiatric Association’s Diagnostic and Statistical Manual (DSM-5).
Some of the key components of an ADD assessment include:
- Clinical interview assessing current symptoms, developmental history, family history, etc.
- Input from parents, teachers, spouses on observable symptoms
- Standardized behavior rating scales like Conners rating scales
- Cognitive testing to identify strengths and weaknesses
- Evaluation for other conditions that overlap with ADD
- Medical exam to rule out underlying physical causes
Imaging and genetic tests are not part of a routine diagnosis but may provide supporting information in uncertain cases. Clinicians look for evidence that inattention and/or hyperactivity symptoms began in childhood, are impairing in multiple settings, and are not better explained by another disorder.
ADD vs. ADHD
ADD was previously classified as a subtype of ADHD in the DSM-IV. The DSM-5, published in 2013, reclassified ADD as a presentation of ADHD. Under the current terminology there are three ADHD presentations:
- ADHD Predominantly Inattentive Presentation (ADD)
- ADHD Predominantly Hyperactive-Impulsive Presentation
- ADHD Combined Presentation
However, many clinicians and researchers continue to conceptualize the two as distinct disorders. Some key differences:
| ADD | ADHD | |
|---|---|---|
| Main symptoms | Inattention, disorganization, forgetfulness | Impulsivity, hyperactivity, restlessness |
| Common comorbidities | Anxiety, depression | Oppositional defiant disorder, conduct disorder |
| Response to stimulants | Lower | Higher |
| Natural history | Symptoms persist into adulthood | Symptoms tend to improve with age |
These differences suggest somewhat distinct underlying causes and developmental courses for what is currently classified as presentations of ADHD.
ADD Treatments
ADD is typically treated with a combination of medication and behavioral interventions tailored to the individual’s symptoms and impairments.
Medication
Stimulant medications like methylphenidate (Ritalin) and amphetamine-based stimulants (Adderall) are usually the first line pharmacological treatments. They boost dopamine and norepinephrine signaling. Non-stimulants like atomoxetine and guanfacine are also used, especially when stimulants cause adverse effects or are ineffective.
Psychotherapy
Common types of therapy include:
- Cognitive behavioral therapy (CBT) – Helps identify and modify negative thinking/behavior patterns
- Behavioral therapy – Uses strategies like rewards, consequences to shape behavior
- Family therapy – Improves family dynamics and parenting strategies
Therapy provides skills to help manage ADD symptoms and improve functioning. It is often used alongside medication.
School/Work Accommodations
Accommodations like extended time, quiet testing rooms, frequent breaks, organization coaching, etc. can support academic and professional success.
Lifestyle Changes
Sleep hygiene, exercise, stress management, and dietary changes like limiting sugar can complement other ADD treatments.
While ADD persists into adulthood, treatments along with development of compensatory strategies can help manage symptoms and enable those with the disorder to reach their full potential.
Conclusion
ADD is a neurodevelopmental disorder with a multifaceted neurological basis. Genetic vulnerabilities, atypical brain structure and functioning, and neurotransmitter imbalances interact with environmental influences to give rise to ADD’s hallmark symptoms of inattention, disorganization, and impulsivity. ADD seems to have some distinct characteristics and causal pathways compared to ADHD, though currently they are classified as presentations of ADHD in the DSM-5. A comprehensive diagnostic assessment along with individually tailored treatment incorporating medication, therapy, school accommodations, and lifestyle changes can help manage ADD symptoms. Further research clarifying the neurological underpinnings of ADD will enable improvements in diagnosis, treatment, and quality of life for affected individuals.