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ADHD Medication explained
Clinical Studies on effectiveness of long acting stimulant medication for ADHD
These medicines are called stimulants because they increase the brain
chemicals dopamine and norepinephrine.
They are a central nervous system stimulant prescription medicine.
These medications are Schedule 8 medicines which are subject to strict legislative controls due to their high potential for misuse, abuse and dependence.
They come in 2 forms; long acting & short acting
Long acting
Takes from 45-90 mins to work
Lasts from 8-12 hours
One a day
Doses from 20mg to 70mg
This medication is Vyvanse
Vyvanse Patient Information
Vyvanse Clinical Information
Detailed medication data can be found here
Covered on PBS $31.60 for 30 days
Short acting
Takes around 30 mins to work
Lasts from 3-4 hours
Multiple doses per day, upto a max of 8 tablets per day
5mg dose
This medication is Dexamphetamine
Clinical trials highlighting effectiveness and safety
Long-lasting medicines are usually the most practical option because people with ADHD may have trouble remembering to take their medicine.
They also provide steady symptom relief throughout the day. By contrast, if you use short-acting stimulants, your symptoms may return between doses. Some people “crash” as their short-acting dose wears off, meaning their energy and mood drop.
How ADHD medication works
Stimulant medication increases attention and decrease impulsiveness and hyperactivity in patients with ADHD
They help reduce severity of ADHD symptoms by increasing the levels of the neurotransmitters dopamine and norepinephrine in the brain.
Neurotransmitters are chemicals produced by the nerve cells that help neurons communicate with one another.
Studies on Safety of Vyvanse medication:
How ADHD medication works: click here for more details
Mechanism of action of long acting Vyvanse
Amphetamines are non-catecholamines, sympathomimetic amines with central nervous system (CNS) stimulant activity. Amphetamines increase dopamine and norepinephrine in the synaptic space by promoting the release of catecholamines from the presynaptic nerve terminals.
They also block norepinephrine and dopamine reuptake into the presynaptic neuron by competitive inhibition. Released norepinephrine affecting both alpha-adrenergic receptor sites and beta-adrenergic receptor sites.
Stimulation of beta-adrenergic receptor sites by these medications increases heart rate, stroke volume, and skeletal muscle blood flow.
Alpha-adrenergic stimulation causes vasoconstriction and an increase in total peripheral resistance, leading to elevations of both systolic and diastolic blood pressures, a weak bronchodilator, and respiratory stimulant action.
ADHD is a neurodevelopmental disorder that manifests in something called executive dysfunction.
Executive dysfunction causes your brain to have difficulty selecting and monitoring your
behaviour to reach your goals.
It affects task management, scheduling, awareness of time, goal setting, and concentration.
The part of your brain responsible for executive functions is called the prefrontal cortex.
You can think of this as the manager of your brain.
It is responsible for decision making, goal setting, moderating social behaviour.
ADHD is not a breakdown of the brain in one spot. It is a breakdown in the connectivity, the communication networks, and an immaturity in these networks.
These brain networks are interrelated around emotion, attention, behaviour and arousal.
People with ADHD have trouble with global self-regulation, not just regulation of attention,
which is why there are attentional and emotional issues.
Stimulant medications, such as methylphenidates and dexamphetamines, work by targeting the areas of the brain that release dopamine, a chemical (i.e., neurotransmitter) known to be abnormally low in levels within ADHD patients.
ADHD was the first disorder found to be the result of a deficiency of a specific neurotransmitter — in this case, norepinephrine — and the first disorder found to respond to medications to correct this underlying deficiency.
Like all neurotransmitters, norepinephrine is synthesized within the brain. The basic building block of each norepinephrine molecule is dopa; this tiny molecule is converted into dopamine, which, in turn, is converted into norepinephrine.
ADHD involves impaired neurotransmitter activity in 4 functional regions of the brain:
Prefrontal Cortex, Limbic System,
Basal Ganglia & Reticular Activating System.
Causes of ADHD
For most people with ADHD, many genetic and environmental risk factors accumulate to cause the disorder (Faraone et al., 2015).
The environmental risks for ADHD exert their effects very early in life, during the fetal or early postnatal period. In rare cases, however, ADHD-like symptoms can be caused by extreme deprivation early in life (Kennedy et al., 2016), a single genetic abnormality (Faraone and Larsson, 2018), or traumatic brain injury early in life (Stojanovski et al., 2019).
These findings are helpful to understand the causes of ADHD but are not useful for diagnosing the disorder.
The associations between aspects of the environment and the onset of ADHD have attained a very high level of evidential support. Some have strong evidence for a causal role but, for most, the possibility remains that these associations are due to correlated genetic and environmental effects.
For this reason, we refer to features of the pre- and post-natal environments that increase risk for ADHD as correlates, rather than causes.
The genetic and environmental risks described below are not necessarily specific to ADHD.
ADHD can also be the result of rare single gene defects (Faraone and Larsson, 2018) or abnormalities of the chromosomes (Cederlof et al., 2014). When the DNA of 8000+ children with autism spectrum disorder (ASD) and/or ADHD and 5000 controls was analyzed, those with ASD and those with ADHD had an increased rate of rare genetic mutations compared with controls (Satterstrom et al., 2019).
A review of 37 twin studies from the United States, Europe, Scandinavia, and Australia found that genes and their interaction with the environment must play a substantial role in causing ADHD (Faraone and Larsson, 2018; Larsson et al., 2014a; Pettersson et al., 2019).
In a genomewide study, an international team analysed DNA from over 20,000 people with ADHD and over 35,000 without ADHD from the United States, Europe, Scandinavia, China, and Australia. They identified many genetic risk variants, each having a small effect on the risk for the disorder (Demontis et al., 2019).
This study confirmed a polygenic cause for most cases of ADHD, meaning that many genetic variants, each having a very small effect, combine to increase risk for the disorder. The polygenic risk for ADHD is associated with general psychopathology (Brikell et al., 2020) and several psychiatric disorders (Lee et al., 2019a,b
Family, twin, and DNA studies show that genetic and environmental influences are partially shared between ADHD and many other psychiatric disorders (e.g. schizophrenia, depression, bipolar disorder, autism spectrum disorder, conduct disorder, eating disorders, and substance usedisorders) and with somatic disorders (e.g. migraine and obesity) (Demontis et al., 2019) (Faraone and Larsson, 2018) (Ghirardi et al., 2018) (Lee et al., 2019a,b) (Lee et al., 2013) (Anttila et al., 2018; Tylee et al., 2018) (van Hulzen et al., 2017) (Vink and Schellekens, 2018) (Brikell et al., 2018) (Chen et al., 2019a) (Yao et al., 2019).
However, there is also a unique genetic risk for ADHD.
Evidence of shared genetic and environmental risks among disorders suggest that these disorders also share a pathophysiology in the biological pathways that dysregulate neurodevelopment and create brain variations leading to disorder onset.
Very large studies of families suggest that ADHD shares genetic or familial causes with autoimmune diseases (Li et al., 2019), hypospadias (Butwicka et al., 2015), and intellectual disability (Faraone and Larsson, 2018).
History of ADHD & ADD
The term “ADD” was used by the American Psychiatric Association in the Diagnostic and Statistical Manual (DSM), third edition, first published in 1980. At that time scientists believed attention difficulties are sometimes independent from impulse problems and hyperactivity.
By the release of DSM-IV in 1994, the name of the disorder had been replaced with “ADHD.”
Today, “ADHD” is considered the current term, while “ADD” is considered outdated.
Now ADHD is the current terminology for the condition and can be split into three subtypes.
- ADHD with predominantly inattentive presentation
- ADHD with predominantly hyperactive-impulsive presentation
- ADHD combined presentation
Combined presentation refers to someone who shows significant symptoms of both hyperactive-impulsive and inattentive ADHD presentations.
What is the difference between ADHD and ADD?
ADHD (attention-deficit hyperactivity disorder) and ADD (attention-deficit disorder) are often used interchangeably to describe a neurodevelopmental disorder that mainly affects an individual’s ability to concentrate.
No longer diagnosed as ADD, mental health professionals now use the term ADHD. In this article, we cover when and why ADD was changed to ADHD, the differences between both disorders, the symptoms of those who have ADHD, and more.
ADHD, or attention-deficit hyperactivity disorder, is a brain disorder that may impact a person’s functioning or development.
It can interfere with an individual’s ability to concentrate, and they can become easily distracted. Other common symptoms can include being hyperactive, and impulsive in decision-making and actions.
This can lead to difficulties in learning institutions, workplaces, and at home, as individuals may struggle with basic skills such as organisation, time management, diligence, and staying on task.
The most recent data shows that 1 in 20 Australians is affected by ADHD. Most prevalent in boys, studies suggest women and adults are underdiagnosed as the symptoms of ADHD can present in a more muted way that can go undetected. They are less likely to present with hyperactive symptoms – and so without the disruptive behaviours, they often fall under the radar.
ADD, or attention-deficit disorder is the prior term for ADHD, a condition that affects a person’s ability to focus.
In 1987, ADD was renamed to ADHD, reflecting a broader understanding of the condition, encompassing both inattentive and hyperactive-impulsive symptoms. This change aligns with international diagnostic manuals, ensuring consistency in terminology and diagnosis.
ADD is still a commonly used term, typically to discuss those who have inattentive ADHD, as the acronym does not include hyperactivity. However, this term is considered outdated – ADHD is the correct diagnostic term according to current medical standards.