1. A D H D So what do we know? Huge amount of research
No clear indication of cause
Huge amount of research
Various theories & indicators
Lots more work to be done
So what do we know?

2. HEREDITY & GENES Research reveals it runs in families
Mainly genetically inherited condition
Number of genes involved
Genes linked to neurotransmitters (chemicals) in the brain
Other possible causes include:
Pre-natal and birth difficulties; alcohol/drug abuse, brain injury (cerebral palsy), lead toxicity, thyroidism

3. Neurobiology of ADHD
The Frontal Cortex is involved mainly with executive functions These include:
problem solving
attention & concentration
reasoning
planning
learning and remembering
inhibiting behaviours
Frontal Cortex

4. Neurobiology of ADHD
The Limbic System controls our emotions. If over-activated it can cause:
mood swings
temper outbursts
over-activity
hyper-vigilance
abnormal sleep routine
difficulties coping with stress
poor motivation
problems with thoughts & feelings

5. Neurobiology of ADHD
The Recticular Activating System, connected to the spinal cord, is the control centre where external signals meet internal thoughts. It is the ‘key’ to turning on the brain and provides the neural connections for:
filtering & processing information
motivation
motor activity
self control
paying attention to correct task

6. NEURON

7. HOW NEURONS WORK
Electrical signals (nerve impulses) carried by neurons (brain cells) are passed on to other neurons at junctions called synapses allowing incoming stimuli to pass from cell to cell.
The signals are carried across the synapse by chemicals called neurotransmitters. Neurotransmitters fit into tailor-made receptors of the target neuron, like a key in a lock. This docking process converts the chemical signal back into an electrical nerve impulse.
The brain uses over 50 different neurotransmitter chemicals. The ones affected in ADHD are Dopamine and Noradrenaline

8. HOW NEURONS WORK

9. NORMAL versus ADHD
An enzyme called a Transporter Gene recycles unused neurotransmitters. This is known as re-uptake.
In ADHD this is overactive and results in a shortage of neuro- transmitters at the synapse so transmission of stimuli (information) is restricted.
For a few people the receptors are less active than they should be and do not receive the transmitted information efficiently.

10. BRAIN DIFFERENCES
Overactive Transporter Gene(s) cause re-uptake of chemicals (neurotransmitters) - or
Receptors not working efficiently
EEG = less mature pattern of electrical activity
FMRI scans = revealed under-developed areas of brain
Extensive research has found smaller brain volume
Difficulty filtering incoming information and prioritising
Result: auditory and visual overload

12. HOW MEDICATION WORKS
Prescribed psychostimulant medications slow or block the re- uptake action of the Transporter Gene(s).
More neurotransmitters allow information to pass from cell to cell more normally
Where required non-stimulant guanfacine works to improve receptor efficiency

13. TYPES OF MEDICATION Psycho-stimulants (available in UK)
Methylphenidate Hydrochloride
Short-acting: Ritalin, Equasym, Medikinet, Tranquilin
Designed to be effective for 3-4 hrs
Slow Release (XL): Equasym, Medikinet, Concerta
Designed to be effective for 8 hrs & 12 hrs respectively
Dexamfetamine
Short-acting: Dexedrine - Effective for 3-4hrs
Lisdexamfetamine
Slow Release: Elvanse – Effective for 12hrs

14. TYPES OF MEDICATION Non-stimulants Atomoxetine Guanfacine
Sustained Release: Strattera (24hrs)
Only targets Neurotransmitter Noradrenaline
Guanfacine
Sustained Release: Intuniv (24hrs)

15. EQUASYM XL

16. 50% immediate release

17. CONCERTA XL
Methylphenidate
Water
22% Immediate Release Outer Coating

18. SIDE EFFECTS Methylphenidate Hydrochloride
Initial side effects may include:
Headache, upset stomach, nausea
Longer-term side effects may include:
Reduced appetite
Difficulty falling asleep
Rare side effects may include:
Palpitations
Rash
Bruising or swelling

19. BENEFITS Increases: Decreases: Improves:
Attention span and concentration
Short-term memory
Decreases:
Hyperactivity
Impulse led behaviours
Improves:
Behaviour modification and management
Remedial support and therapies
Relationships and self-esteem

20. ENVIRONMENT-HOME Structure and routine Firm but fair discipline
Consistent approach
ADHD-friendly parenting style
Foster and encourage resilience
Be realistic in expectations

21. ENVIRONMENT-SCHOOL Positive ethos and mutual respect
Working knowledge of ADHD
Good attitude and approach
Determine and address cause of reaction

22. ADHD North West November 2006
COMORBIDITIES
Associated Conditions
Specific Learning Difficulties (45%)
Dyspraxia (50%)
Communication (60-80%)
Sensory Processing 40%)
Bipolar Disorder (20%)
Autistic Spectrum Disorder (60-80%)
Anxiety, Depression (30%)
Obsessive Compulsive Disorder (30%)
Mood Dysregulation Disorder (80%)
Tics & Tourette’s Syndrome (50%)
Oppositional Defiant Disorder (60%)
Epilepsy (30%)
Conduct Disorder (30%)
Sleep Issues (15-50%)
Asthma & Allergies (30%)

23. POSITIVE TRAITS Warm-hearted, caring, compassionate
Spontaneous, innovative, fun-loving
Energetic, imaginative, risk-taker
Persistent, tenacious, resourceful
Willing to try new things
Often highly intelligent
Usually good in crisis