Transcript OCD, PTSD, and Panic Disorders

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 = 6-12+ 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 theoryopposite 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
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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)
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Relapse
 Relapse rate is high when treatment
is stopped
 Panic disorder is a chronic disorder
that most often requires maintenance
treatment
Social Phobia
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Paxil
SSRIs- first line
Effexor
Not a lot of evidence for TCAs
MAOs- 4th 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 stabilizerssome clinical support
 Benzos- with care, due to high
concomitant A & D