OCD, PTSD, and Panic Disorders

OCD Biological basis remains unknown But there seems to be some genetic component related to OCD and other anxiety disorders Meds ameliorate but do not eliminate symptoms in many patients Relapse is common after discontinuation of Medication

Anafranil/Clomipramine  Discovered to be effective in the mid 1980s  Is a potent nonselective serotonin reuptake inhibitor  Led to the 5HT theory for OCD  Led to the use and efficacy of SSRIs

Dopamine  Up to 40% of OCD patients do not respond to SSRIs  Cocaine worsens compulsions in Tourette syndrome  Family studies show OCD and Tourettes are linked leading  Use of older antipsychotics that block DA receptors added to ongoing SSRI tx reduces severity of symptoms in tx resistant clients (especially those with Tourettes)

Serotonin and Dopamine  Atypical antipsychotics Work SSRIs in some clients Have no effect on other clients And worsen symptoms in some clients

OCD and….  Tourettes = conventional antipsychotics and SSRIs  Depression = higher doses of SSRIs Longer delayed onset = weeks Results in depression=remission and in OCD are about 35% reduction, with relapse after discontinuation SSRIs appear to work via a different mechanism with OCD than Depression

OCD adjunct treatments  Handout of page 342 (hypothetic, not proven)  Augment with serotonergic agents  Add benzodiazepine (clonazepam) to help tolerate high dose of SSRI, to reduce anxiety, and enhance serotonin  Behavioral Therapy  Psychosurgery

Panic Attacks and Panic Disorder  Biological Theories Norepinephrine- dysregulation in this system (too much initially?) GABA- out of balance. The body produces natural benzos and these may be limited or inverse agonists may be excessive or receptors may be abnormal Abnormal Respiratory functioning and Lactate sensitivity

 False suffocation alarm theory- opposite disorder is Ondine’s Curse where one has diminished sensitivity of the suffocation alarm and they lack adequate breathing (esp. when asleep)

 Caffeine increases panic attacks  Alcohol can increase panic attacks  Pot can increase anxiety (even though it is often used initially to keep anxiety under control)

Treatments  SSRIs-First Line 3-8 weeks to work (same as antidepressant effects) Start with lower does due to Panic People being more sensitive to antidepressants Increase to same or higher doses as antidepressants to gain effects  Newer Antidepressants-Not approved, but promising Effexor and Reboxitine (how does this contradict the Norepinephrine theory?)-Second Line  Welbutrin may increase anxiety and agitation

Treatment  TCAs- Imipramine and Clomipramine-Third line  Benzodiazepines- adjunct treatment Rapid effect Cause cognitive slowing Addiction issues Withdrawal issues  High potency better (alprazolam, clonazepam) than low potency (diazepam, lorazepam) due to low potency benzos frequently resulting in sedation prior to adequate relief of panic and anxiety

Treatment  Bezos (cont) (can be used for immediate relief or build up in system) Alprazolam-very effective, short duration, administered 3-5x’s a day Clonazepam- longer duration, twice a day, less abuse potential, longer half lie so easier to taper. Weigh consequences of inadequate tx (physical, loss of social and occupational functioning, suicide) against risks for each individual

Treatment for Panic should include therapy  CT and CBT Educate about anticipatory anxiety Work with Catastrophizing Work with high attention to bodily signs Help cl understand use of medications and effects Help cl to regulate physiological system with deep relaxation training Exercise-inducing panic and reducing anxiety (Panic and GAD seem to develop from separate systems)

Relapse  Relapse rate is high when treatment is stopped  Panic disorder is a chronic disorder that most often requires maintenance treatment

Social Phobia  Paxil  SSRIs- first line  Effexor  Not a lot of evidence for TCAs  MAOs- 4 th line tx  Benzos- Clonazepam, a possibility  Beta Blockers  Buspar and Clonidine-no clear studies of efficacy

PTSD  Historically the focus has been on symptoms (depression, insomnia, etc)  SSRIs- First line  TCAs and MAOs –second line  Beta blockers and mood stabilizers- some clinical support  Benzos- with care, due to high concomitant A & D