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?

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

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

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

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

NEURON

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

HOW NEURONS WORK

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.

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

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

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

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

EQUASYM XL

50% immediate release

CONCERTA XL Methylphenidate Water 22% Immediate Release Outer Coating

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

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

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

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

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%)

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