PSYCHOPHARMACOLOGY

PRESENTER-YANGO MLAGWA, LUCAS

RESIDENT IMED YR 3
18/04/2023

FACILITATOR-DR CATHERINE .
1
outlines 2
 Basic principles
 Antipsychotics
 Antidepresants
 Mood stabilizers
 Anxiolytics and sedative hypnotics
 Anticonvulsants
 Prescribing for special groups (elderly,pregnant,pt with other medical
conditions)
Basic principles. 3

 Psychopharmacology is the study of the effects of drugs on affect,

cognition, and behavior

 In psychiatric disorders, treatments,includes pharmacological and non

pharmacological.
 Pharmacological treatments includes-Antipsychotics
Antidepresants,Mood stabilizers,Anxiolytics and sedative hypnotics and
Anticonvulsants
 The non pharmacological treatments of psychiatric disorders includes-
Interpersonal therapy,Supportive psychotherapy ,Family therapy ,Group
therapy,Couple therapy,Cognitive behavioural therapy
 4

Pharmacokinetics is the study of drug

absorption, distribution within body, and drug
elimination
 Absorption depends on the route of administration
 Drug distribution depends on how soluble the drug
molecule is in fat (to pass through membranes) and
on the extent to which the drug binds to blood
proteins (albumin)
 Drug elimination is accomplished by excretion into
urine and/or by inactivation by enzymes in the liver
 Drug Effectiveness 5

Dose-response (DR) curve: Depicts

the relation between drug dose and
magnitude of drug effect
The effectiveness of a drug is
considered relative to
its safety (therapeutic index)
Neuromodulators

Neurotransmitter binding to receptors produces either EPSPs or IPSPs

 Glutamate produces EPSPs
 GABA produces IPSPs
Neurotransmitters Go through 7 steps
1. Synthesis
2. Storage
3. Enzymatic destruction if not stored
4. Exocytosis
5. Termination of release via binding with autorecptors
6. Binding to receptors
7. Inactivated
Drugs are developed that address these actions as an AGONIST (mimic
the NT ) or ANTAGONIST (block the NT)
 Choice of drugs 8

 Decision on choice of drug dependent on:

 what effects are needed from drug e.g. sedation
 Previous experience on use of drug
 Sensitivity to EPSE and other sideffects.
 Low doses of drug required
 Whether refractory type of illness or not: Clozapine use
 When refractory type of illness and there is fear of
agranulocytosis: Risperidone
 Equal efficacy though different potency
 More potent antipsychotic medications have higher EPSE
 s .
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 10
Antipsychotics.
INDICATION FOR ANTIPSYCHOTIC
Treatment with neuroleptics not disorder specific but symptom
specific,therefore important to know the target symptoms
1.Psychotic symptoms includes:
-Schizophrenia-Brief reactive psychosis,
-Schizophreniform disorder,-Affective disorders,
-Organic mental disorders,-Mild anxiety and Delusional disorder
Target symptoms and syndromes
Antipsychotics
 Antipsychotic are classified as
1.Typical/1st generation = D2 receptor antagonist
Effective against +ve > -ve
Examples-Chlorpromazine,Thioxanthenes:
Thiothixene,Butryrophenones: Haloperidol
2.Atypicals/2nd generation = Serotonin-dopamine antagonists
Effective against both +ve & -ve sx
Examples- Clozapine,Benzisoxazole:
Risperidone,olanzapine,quetiapine
3.Oral vs injectable(depot preparation ie-Fluphenazine decanoate
(modicate),Haloperidol decanoate,Zuclopethixol
decanoate,Flupenthixol decanoate
Requires ~ one month for significant antipsychotic effects.
Antipsychotics
Average Daily Doses in mg
Typicals Atypicals

Risperidone (4-8)
Haloperidol (5-15)
Thioridazine(100-300) Olanzapine (10-20)

Chlorpormazine (50-400) Quetiapine (600-1200)

Clozapine (100-600)

Lower numbers indicate higher potency

 Compliance to treatment 17

 Health education of paramount importance on the

compliance/adherence to medications.
 Non use of drug on regular basis causes relapse
 Non compliance due to side effects associated with neuroleptic
drug use
Slowed thinking
Slowed motor activity
 May need use of DEPOT medication, given at 2 weekly to
monthly intervals
Additional risk of NMS as drug can not be
withdrawn quickly
 Adverse effects 18

 Anticholinergic-Dry mouth, difficult urinating,

constipation, blurred vision, toxic-confusional state
 Alpha adrenergic blockade-Orthostatic
hypotension, impotence, failure to ejaculate
 Dopaminergic blockade-EPSE,
galactorrhea, amenorrhea, impotence, tardive
dyskinesia, weight gain
 Antihistaminic effects-Sedation
Dealing with EPSE 19

 EPSE:
 Pseudo parkinsonism -2 weeks of use
 Akathisia-2 weeks of use
 Acute dystonia-immediate effect on use
 Reduce dose of drug the patient is using
 Use of anticholinergic agents if symptoms
persist or if has acute dystonic reactions
 Use benzotropine, procyclidine,
chlorpheniramine
Therapeutic guidelines 20

 Initiating therapy
 Prior treatments, effects and side effects
 Lowest effective dose
 Dose increments
 Every 2-5days if non response to arousal symptoms
 Regulation of dose dependent on resolution or non
resolution of target symptoms
 No blood levels are available for neuroleptics
 If treatment failure and in advanced setting where
blood monitoring not an issue give
Dibenzoxazepines-Clozapine
Antidepressants

 Used in many psychiatric disorders other than

Depression.

 Full clinical response in 6-8 weeks in major

depression, up to 6/12 in obsessive compulsive
disorder.
Examples:
Fluoxetine & Paroxetine (20-60 mg/d)
Fluovoxamine & Sertraline (50-200 mg/d)
Imipramine(200-300 mg/d)
Antidepressants 23
Drug groups Specific drugs Dose range (mg)
Heterocyclics Amitriptyline 50 – 150 (150-300)
Imipramine 50 – 150 (150-300)
Amoxapine 150-200
Maprotiline 150-225

Monoamine Phenelzine 45-90

oxidase inhibitors Tranylcypromine 30-50
selegiline
Phenyl Trazodone 300-600
piperazines Nefazodone 300-600

SSRI’s Fluoxetine 10-80

Fluvoxamine 100-300
Citalopram,escitalopram
THREE PHASES OF TREATMENT
Remission Recovery
Normal

Relapse Recurrence
Symptom Severity

Response
Relapse
> 50%
STOP 65 to 70%
Rx STOP
Rx
Acute Continuation Maintenance
Phase (3 months+) Phase (6-12 months) Phase (years)
Time
Antidepressants and the Cytochrome
P450 System
 Antidepressants and mood stabilizers may be
inhibitors, inducers or substrates of one or more
cytochrome P450 isoenzymes
 Knowledge of their P450 profile is useful in
predicting drug-drug interactions
 When some isoenzymes are absent of inhibited, others
may offer a secondary metabolic pathway
 P450 1A2, 2C (subfamily), 2D6 and 3A4 are
especially important to antidepressant metabolism and
drug-drug interactions
 29

Other drugs and adjuncts to antidepressants in the

treatment of depression e.g. thyroid related
hormones increase effectiveness of standard
ADs
Target symptoms and syndromes 30
Target symptoms Anticipated duration for outcome
oSomatic spx o 10 days to 2 weeks
oPsychomotor o 7-14 days after appropriate dose
level
oMood o Transitional mood, irritability/anger
3/4wks
oCognitive fx
o Improves with mood
o Improves with mood
oDepressive thought osocial and individual factors important
o Not ADs target symptoms; need
oPsychotic
neuroleptics
symptoms
oSocial impairment
o Rehabilitation/ psychotherapy
approaches also important
Diagnostic categories 31
 Major depressive disorder

 Depression with psychosis

 Dysthymic disorder

 Mood disorder due to a general medical condition

(depression)

 Adjustment disorder (with depressed mood)

 BPD (currently depressed)

 Cyclothymic disorder
Heterocyclic’s 32
 Indications
 Depressive disorders, anxiolytic properties
 Tri- and tetra cyclic antidepressants – 1950’s
 None of the newer drugs are more efficacious
 Desmipramine least anticholinergic effects
 Compliance major issue in treatment failure
 Side effects tolerability - 1/4th problems with side effects
 Poor therapeutic alliance
 Side effects: Anticholinergic, antihistamine, 5-HT activation,
adrenergic activation, drug interactions
 Heterocyclic's (2)
33
 Adverse effects
 Anticholinergic: dry mouth, blurred vision, constipation,
urinary hesitancy, toxic confusional states (limitations in
asthma and closed angle glaucoma – alt: SSRI’s,
Bupropion)
 Antihistamine: drowsiness, fatigue (hyper-somnia alt:
protriptyline)
 5-HT activation: drowsiness, restlessness (hyper-somnia
alt: protriptyline)
 Adrenergic activation: Tremor, excitement, palpitation,
orthostatic hypotension, weight gain, quinidinelike effects,
baseline ECG standard of care (limitations in cardiac
arrhythmias and CCF – alt: SSRI’s, Bupropion)
 Others: Seizures, decreased sexual performance,
triggering of mania, death when over dosed
 Monoamine oxidase inhibitors
34

 Indicated in:
 Atypical depression
 Panic disorder
 Non-responders with other drugs
 Irreversible non specific inhibition MAOA and B
 Adverse effects profile requires provision of more information when
prescribing and exploration of compliance.
 85% inhibition for effects (platelets monitoring)
 Adverse effects
 Share some of those of Heterocyclic's (anticholinergic, 5-HT and
adrenergic activation)
 MAOI (2) 35
 MAOI specific:
 Insomnia and day time stimulation
 Paraesthesia, insomnia and pedal edema
 Hypertensive crisis – Tyramine containing foods (Fava beans,
beer, red wines, liver, smoked meat, yeast etc) and
sympathomimetic amines (over the counters e.g.
Pseudoephedrine) should be avoided.
 Drug interactions: sympathomimetic amines; narcotics (stop
3/52 prior to elective surgery); fatalities reported with
meperidine and fluoxetine – Medic Alert Bracelets suggested.
 Chlorpromazine (50mg), phentolamine and other alpha blocking
agents good in MAOI related emergencies; peripheral vasodilators
also useful.
Monocyclics
36
 Indications
 Low tolerance of side effects of Heterocyclic's
 Bupropion (300-450 mg daily) – relative pure NE reuptake
inhibitor
 Advantage in absence of CVS effects and no significant
orthostatic hypotension
 Also no sexual SE, weight gain or day time drowsiness.
 Adverse effects:
 Restlessness, agitation, anxiety and insomnia – sufficient
to discontinue in about 2%
 Greater CNS lowering of seizure threshold effects hence
avoid in epileptics.
Phenylpiperazines
 37
Indications
 Agitation and aggression associated with AOBS
 Potent antagonists of 5-HT2 receptors; inhibit pre-
synaptic 5-HT reuptake, and NE for nefazodone .
 Lack quinidine effects on the heart. Safer when taken
alone in OD than the TCA’s, but synergistic effect with
CNS depressants including alcohol.
 Adverse effects
 Arrhythmogenic – premature VC’s, ventricular couplets
and episodic tachycardia – caution in heart block.
These adverse effects are less with nefazodone
 Sedation and orthostatic hypotension (the latter less so
with nefazodone)
 Drug interactions with some drugs metabolized thro.
Cyt. P450 system as they are inhibitory (more so
nefazodone)
SSRIs
38
 Indications
 Depressive, obsessive compulsive and eating disorders
 Widely prescribed, single dosing improves compliance
 Minimal effects adrenergic, muscarinic, histaminergic, of
serotonergic receptors – better side effects profile.
 Effective at low dose (75% respond)
 BUT expensive for Tanzania.
 Adverse effects
 Low risk of anticholinergic effects
 CNS and extra pyramidal effects of insomnia,
psychomotor agitation, tremor and headache
 GI effects of nausea and diarrhea
 Serotonin activation – palpitations, agitation, muscle
twitching, delirium
 Some inhibition of Cyt. P450 iso-enzymes contributes to
drug interactions
 Therapeutic strategies 39

 General issues
 Proper use of AD’s results in clinical improvement in 60-70% of
depressed patients compared to 30% if placebo used
 Onset of full antidepressant effects may take several weeks
 No way of predicting response or tolerance of side effects in first
episode users
 Generally AD ‘s have similar efficacy – distinguished by their
safety and side effect profiles
 Side effects are related to actions on various neurotransmitter
systems
 Therapeutic strategies (2)
40
 Know what you are treating!
 Accurate diagnosis and identification of target symptoms
 Drug choice
 History of prior responses to specific agents
 Patient
 Family member with depression
 Matching clinical condition to the drug
 presentation of depressive disorder (target symptoms Vs
patient problem list)
 Risk of drug interactions
 Risk of OD and toxicity profile (Venlafaxine [SSRI] and
nefazodone relatively safer)
 Side effects profile – before and after initiating medication
 Presence of concurrent medical conditions
 Other drugs used due to risk of drug interactions
 Therapeutic strategies (3)
41
 Prescribing practice
 Provide information about the illness
 Provide information about the treatment
 Realistic expectations of drug therapeutic effects
 Expectations of drug side effects
 Have a clear treatment plan – dosage, duration of
therapeutic trial (acute treatment and relapse
prevention), alternatives should the trial fail –
communicate to patient
 Other than for fluoxetine, start at low dose – determine tolerance
profile and minimize initial side effects. Increase dose to ½
recommended maximum dose by the end of one week
 Titrate dose versus therapeutic and side effects
 Prescribe adequate dose (3 weeks – 6 weeks for effects)
Therapeutic strategies (4)
 Duration of treatment 42

 No absolute rule
 Relapse rates in after successful treatment of acute
episode: 30% year 1; 50 % within 2 years; 70% within
3 years.
 Remission of symptoms 3-6 weeks, relapse
prevention 6-9 months of full therapeutic dose (10-
15% of non-compliant patients after remission may
relapse, a larger proportion do not respond as well
to the drug previously used) .
 Discontinue drugs gradually
 No evidence of benefits of longer term treatment (after 6-
9 months for relapse prevention)
 Treatment resistant cases
 Change to alternative chemically unrelated AD
 Augment with second drug – lithium (0.6-.8 mg/l; 600-900
mg daily), thyroid hormones, TCA with MAOI (caution
required)
 ECT an option
 43

Mood stabilizers
 44

Introduction
 Mood is pervasive and sustained feeling tone that is endured internally and
which impacts nearly all aspects of person’s behavior in the external world.
 Affect is the patient’s present emotional responsiveness
 Mood disorders are described by marked disruption in emotion ( severe lows
called depression and highs called hypomania or mania). These are common
psychiatric disorders leading to an increase in morbidity and mortality.
 Mood instability is the rapid change in low and high mood and also anxiety
and irritability
 Mood instability can be seen in patients with bipolar disorders, depressive
disorders and borderline personality disorders .
Introduction… 45

 Mood stabilizers are medications used to treat patients with bipolar

disorders. These medications help to prevent manic episodes and can
help prevent depression. Mood stabilizers are triple threats meaning
they are antimanic, antidepressant and prophylactic
 The cause of bipolar disorders is not well understood and the drugs
used to treat it are still not well understood.
Classification of Mood 46

stabilizers
 lithium
 Anticonvulsants eg; Carbamezapine and Valproic acid
(Sodium valproate)
 Antipsychotics (both first and second generation)
 ECT (electroconvulsive therapy)
Drugs regimen in Bipolar 1 and 2
BIPOLAR 1
 Mood stabilizer and
antipsychotics, because most
times they do present with
predominantly Manic
episodes, with less depressive
episodes.
47
BIPOLAR 2
 Antipsychotics, mood
stabilizer and anti depressant,
because they do present
predominantly with
depressive episodes than
manic episodes.
Common Mood Stabilizers

Carbamazepine Valproic Acid Lithium

40-100 mg/ml
4-12 mg/ml
Therapeutic Level Po- 0.5-1.2 mEq/L
Po-200mg-600mg/day
200mg,250,500,1g/day

Dizziness, sedation, nausea, diarrhea, nausea,

ataxia, leukopenia, ataxia, dysarthria, hypothyroidism,
Common S/E weight gain, slight tremors, dysarthria,
rash,
elevation of hepatic ataxia
transaminases

sinus node
Agranulocytosis, dysfunction, T-wave
teratogenicity (neural changes,
tube defect), induction teratogenic (neural
Dangerous S/E
of hepatic metabolism tube defects) teratogenic (cardiac
anomalies)
1. Valproic acid (Sodium 49

valproate) and dosage

 It is used to treat bipolar disorder, occasionally used to prevent
migraine and can be used to treat convulsions.
 Mechanism of action: Its mechanism of action is poorly
understood, postulated mechanism include blocking
(modulation) sodium channels which reduces neuron activity
and it also it increases activity of GABA.
 Its usually available in form of 200 mg, 250mg, and 500mg
tablets, given according to severity of the client's symptoms.Its
usually given BD/12 hrly for a long period of time, and tapered
down slowly as symptoms disappear. Maximum dose is
1000mg per day.
Side effects of sodium 50

valporate
 Teratogenicity (neural tube defects). So, for pregnant women,
folic acid supplementation is mandatory.
 GI effects (nausea, diarrhoea)
 Visual problems e.g. double vision and lazy eye.
 Hormonal disturbances, e.g. increased testosterone in women,
hair loss, &menstrual disturbances.
 Weight gain.
 Low red, and white blood cells, and platelets.
 It may also cause hepatitis, and pancreatitis.
 Hyperammonemia more common in combination with
carbamazepine
What to consider before 51
administering sodium valporate
Before starting the medication, do pregnancy test and routine
bloodwork followed by these routine investigations every 6
months;
CBC (complete blood count); since it may cause low red
blood cells, low white blood cells, and low blood platelets.
Liver Function Test (LFT); ALT and AST to check for liver
inflammation, as it may cause hepatitis.
Lipase blood test; it can cause pancreas inflammation,
especially if the patient is presenting with abdominal pain as a
sign pancreatitis.
Valproic acid toxicity 52

 Sleepiness (somnolence)
 Low blood Pressure (hypotension)
 Low respiratory rate (bradypnea)
 Seizures
 Low blood count on CBC blood test.
2. Carbamazepine 53

 Is an anticonvulsant drug used primarily to treat epilepsy

and neuropathic pain. Its an adjunctive treatment for
schizophrenia along with other medications and an agent for
bipolar disorder.
 Mechanism of action; Acts by binding to voltage-
dependent sodium channels in the inactive state and thus
prolonging their inactivation, thus reducing synaptic
transmission.
Dosage for Carbamazepine 54

 Its usually available as a one tablet of 200mg.

 It can be given OD/BD depending on severity of symptoms.
 Maximum dose being 600 mg per day.
 When given with benzyhexol or aminoglycosides or any
other drugs which lower their therapeutic levels maximum
dose can be raised to 800 mg.
Side effects of carbamazepine 55

 Lethargy
 Tremors (rhythmic, rapid, symmetrical, most prominent in
upper extremities, and may respond to dose change, also may
be treated with propranolol)
 Teratogenicity; harmful to fetus as it can also cause neuro-tube
defects(slight risk). Its safer than valproic acid, but less safe
than Lithium.
 Steven-Johnson syndrome is rare but can be deadly.
 GI (nausea and diarrhea)
 Aplastic anemia and agranulocytosis
 Neurologic; Dysarthria, ataxia, incoordination, diplopia, &
Nystagmus.
What to consider when using 56

Carbamazepine
 Before starting medication, perform pregnancy test,
Complete blood count and Liver function test.
 Then, after starting dose, perform Complete blood
count(CBC), ALT to check for liver inflammation every
after 6 months.
 If a patient presents with steven Johnson syndrome,
change to sodium valproate immediately.
3. LAMOTRIGINE 57

 It was developed as an anti-convulsant, but was later shown to be effective as a

maintenance treatment for bipolar disorders .
 Mechanism of Action: It blocks voltage-sensitive sodium channels, also modulates the
release of glutamate and aspartate. It also modestly increases plasma serotonin
concentrations by preventing its reuptake.
 It is available in 25,100 and 200mg tablets. In Bipolar disorder it can be given once daily
(OD) between 100 – 200mg daily.
 Lamotrigine has significant drug interaction with other drugs, the most serious interaction is
with valproic acid, in which when used concurrently, the serum levels of lamotrigine are
doubled.
 When used concurrently with carbamazepine, phenytoin or phenobarbital its concetration is
decreased by 40 to 50 percent.
SIDE EFFECTS 58

Lamotrigine is well tolerated. The most common adverse

effects include
Dizziness

Ataxia

Somnolence

CNS manifestation ( headache,diplopia, blurred vision)

Rash, which is common and occasionally severe and is a
source of concern and drug should be stopped immediately
since they can be a early manifestation of Stevens – Johnson
syndrome
4. Lithium Carbonate 59

 It is also a prescription medicine used to treat the symptoms

of Bipolar disorder. It belongs to class of drugs called
Bipolar Disorder Agents.
 It is not used in our setting.
 How it works; It works by increasing GABA, an
inhibitory neurotransmitter.
Lithium carbonate effects 60

 Teratogenic. It is harmful to fetus, although less riskier in

pregnancy than sodium valproate, and carbamazepine. It
may rarely cause ebstein’s anomaly (1 in 100 births).
 Metallic taste in the mouth
 Tremor
 Polyuria/polydipsia
 Weight gain
 Hypothyroidism
 ECG changes like that of hypokalemia
Lithium toxicity (levels above 61

1.5mmol/L)
 Severe GI symtopms (Nausea, vomiting, and diarrhea)
 Tremors and muscle twitching
 Ataxia
 Dyarthria (abnormal speaking)
 Seizures
 Coma
What to consider in using 62

Lithium carbonate.
 Perform pregnancy test before start of dosage.
 EKG is to be performed before starting Lithium and as
prn(as per needed)
 Then perform these tests every 6 months; Electrolytes
levels, renal function test(creatinine levels), TSH blood test
( since it can cause hypothyroidism), and Calcium levels
(since it may cause hyperparathyroidism).
Drug interactions 63

 Drugs which can increase lithium levels like; NSAIDs (e.g.

ibuprofen), and blood pressure medications like ACE
inhibitors, and diuretics should not be used together with
lithium medication.
 Also dehydration may cause increase in lithium dosage.
ANTIPSYCHOTICS 64
FIRST GENERATION (TYPICAL) ANTIPSYCHOTICS
Also known as DRAs dopamine receptors antagonists
The work by inhibiting dopaminergic neurotransmission.
They effective in treating psychotic symptoms of acute mania.
Since antimanic agents have a slower onset of action than antipsychotic
in managing acute symptoms it is standard practice to combine
antipsychotic with another antimanic such as lamotrigine.
Example of first generation antipsychotic used in managing acute
mania is haloperidol.
SECOND GENERATION (ATYPICAL) 65
ANTIPSYCHOTICS

 Also known as serotonin – dopamine antagonists (SDAs)

 They act by blocking both dopamine and serotonin
receptors.
 They are also effective in the treatment of acute mania.
 They may be used in treatment as monotherapy or
adjunctive therapy with other antimanic.
 Example of drugs used include olanzapine and risperidone.
Non pharmacological mood 66

stabilization
1. Exercise
2. Sleep-work cycle stabilization
3. Substance abstinence
4. Specific psychological interventions like; psychoeducation,
family focused therapy, cognitive behavioral therapy and
interpersonal-social rhythm therapy.
5. Non specific psychosocial intervention like; activities
scheduling, sleep hygiene, problem solving, social skills
training and compliance strategies.
ELECTROCONVULSIVE THERAPY 67
 This procedure is done under general anesthesia in which a
small electric current is passed through to the brain,
purposefully to trigger brief seizures.
 It causes changes in the brain that can quickly reverse
symptoms of certain mental health condition.
 As pharmacological agents are the first line treatment for
major psychiatric disorder, ECT is used when the patient
has resistance to pharmacological agents.
 It is used in major depressive disorders, manic episodes and
schizophrenia.
 The relative rapidity of ECT response indicates its
usefulness for patients whose manic behavior has produced
dangerous levels of exhaustion.
ANXIOLYTICS
AND
SEDATIVES
HYPNOTICS
ANXIOLYTICS AND 69

SEDATIVES HYPNOTICS.
 Anxiolytics: are drugs that reduce tension and produce a
sense of calm
 Hypnotics: are drug that cause drowsiness and
encourage the onset and maintenance of a state of
sleep
BENZODAIZEPINES: 70

 First benzodiazepine-introduced 1959 then in 1963

diazepam become available
 Because benzodiazepines have a rapid anxiolytic sedative
effect, they are most commonly used for acute treatment of
insomnia, anxiety ,agitation or anxiety associated with any
psychiatric disorder.
 Not used in long term treatment to avoid the risk of
psychological and physical dependence associated with
long term use of benzodiazepines
 In chronic anxiety disorders, antidepressant drugs such as
SSRI and SNRIs are now used as primary treatments with
benzodiazepines used as adjuncts.
Mechanism of action of BDZ 71

 BDZs act as agonists at the GABA-BDZ receptor complex

 Gamma-aminobutyric acid is the principle inhibitory
neurotransmitter in the CNS and acts via GABA A receptors
to increase the opening of chloride ion channels.
 An influx of Cl ions results in hyperpolarization of the post
synaptic neuron, making an action potential more difficult
to achieve.

 72

 In the GABA–BDZ receptor complex, which is GABAA

receptors are linked to benzodiazepine receptors made up
from five macromolecular subunits.
 These subunits are arranged around the chloride ion
channel Opening of the ion channel requires binding of two
GABA molecules to the two GABA receptors. When a
BDZ binds to its receptor site on the complex, the ion
channel opens for a longer period.
 Thus BDZs enhances the inhibitory effects of GABA.
73
Points to note are: 74

(1) BDZs act only to enhance the effect of GABA and will do nothing
in the absence of GABA or if the GABA receptor is blocked;
(2) the binding sites for GABA and BDZs are separate;
(3) the presence of a BDZ enhances the binding of GABA to its
receptor
 75

 Although the typical BDZ drugs, such as diazepam, act as

full agonists at the receptor, having sedative, anxiolytic
and anticonvulsant effects, other compounds may have
different effects(full inverse agonists have the opposite
effect, being pro-convulsant and anxiogenic. Such
compounds are of experimental interest only.)
 Neutral competitive antagonists block the effects of both
agonists and inverse agonists and have no intrinsic activity
of their own
 76

 Flumazenil acts as such a drug in most situations and is

thus used to reverse the effects of overdoses of BDZs.
Pharmacokinetics: 77

 Diazepam is the most widely used BDZs

 Absorption is good with oral use but is slow with intramuscular
administration.
 Lorazepam which has greater water solubility, is the BDZ
recommended for intramuscular use.
 The principle active metabolite, desmethyldiazepam has a very
long elimination half life.
 78

 Hence, gradual accumulation of active metabolites is one of

the main reasons for many of these drugs having ‘
Hangover’
 The elimination half life of diazepam is age dependent
resulting in greater hangover effects in older people.
 Some BDZ undergo phase I metabolism, which resulting in
production of active metabolites and some only phase II
metabolism resulting in inactivation.
Pharmacokinetic properties of 79

diazepam
Bioavailability Almost complete with oral dosing
Peak concentration 30-90min
Renal excreation Negligible for unchanged drug
Elimination half life Young adults 20hours

Elderly people: 30-100hours

Pharmacological actions of 80

BDZ
 All BDZs except clorazepate are completely absorbed after oral
administration and reach peak serum levels within 30minutes to 2hours.
 Metabolism of clorazepate in the stomach converts it to desmethyldiazepam
which is then completely absorbed.
 The absorption, the attainment of peak concentrations and the onset of action
are quickest for diazepam, lorazepam, alprazolam, triazolam and estazolam.
 The rapid onset of effects is vital to persons who take a single dose of BDZ
to calm an episodic burst of anxiety or a fall asleep rapidly.
Cont.… 81

 Several BDZs are effective after IV injection but only lorazepam and
midazolam have rapid and reliable absorption after IM administration.
 Diazepam, chlordiazepoxide, clonazepam, clorazepate, flurazepam and
quazepam have plasma half lives of 30 to more than100 hours and are
described as long- acting BDZs.
 The plasma half-lives of these compounds can be as high as 200hours in
persons whose metabolism is genetically slow. Example Africans
 Because the attainment of steady-state plasma concentrations of the
drugs can take up to 2 weeks, person may experience symptoms and
sign of toxicity after only 7 to 10 days of treatment with a dosage that
seemed initially to be in the therapeutic range.
CLINICALLY: 82

 Half life alone does not necessarily determine the duration of therapeutic
action for the most of BDZs.
 The fact that all BDZs are lipid –soluble to varying degrees means that BDZs
and their active metabolites bind to plasma proteins.
 The extent of this binding varies from 70 to 90 percent.
 Distribution, onset and termination of action after single dose are thus
determined mainly by BDZs lipid solubility, not elimination half- life.
 Drugs with high lipid solubility such as diazepam and alprazolam are absorbed
rapidly from the GIT and distribute rapidly to the brain by passive diffusion
along the concentration gradient, result to rapid onset of action.
CLINICALLY CONT… 83

 However, as the concentration of the medication increase in

the brain and decrease in the bloodstream, the concentration
gradient reverses itself and these medications leaves the
brain rapidly resulting in fast cessation of drug effect.
 So the drugs with longer elimination half life such as
diazepam may remain in the bloodstream for a substantially
more extended time than their actual pharmacological action
at BDZ receptors because the concentration in the brain
decrease rapidly below the level necessary for a noticeable
effect.
CLINICALLY CONT… 84

 In contrast, lorazepam which has a shorter elimination half-

life than diazepam but is less lipid-soluble has a slower
onset of action after a single dose because the drug is
absorbed and enters the brain more slowly.
 However, the duration of action after a single dose is longer
because it takes longer for lorazepam to leave the brain and
for brain levels to decrease below the concentration that
produces an effect.
 85

Advantages of long- half Disadvantage of long-

life drugs over short half acting drugs over short-
life drugs acting drugs

 It require less frequent dosing  Increase risk of daytime

 psychomotor impairment
Less variation in plasma
concentration  Increased day time sedation
 Less severe withdrawal
phenomena
THERAPEUTIC 86

INDICATION OF BDZs
 Anxiety disorder
 1. Generalized anxiety disorder (GAD): BDZs are effective for
the relief of anxiety associated with GAD , because GAD is a
chronic disorder with high rate of recurrence some persons with
GAD may warrant long-term maintenance with BDZs
example: ALPRAZOLAM
 2. Panic disorder : alprazolam and clonazepam , both are high
potency BDZs , are commonly used medications for panic
disorder with or without agoraphobia.
 Although the SSRIs are also indicated for the treatment of
panic disorder
Cont.. 87

 BDZs have the advantage of working quickly and not

causing significant sexual dysfunction and weight gain.
 However, the SSRIs are still often preferred because they
target common comorbid conditions such as depression or
OCD
 BDZs and SSRIs can be initiated together to treat acute
panic symptoms, use of the BDZs can be tapered after 3 to 4
weeks once the therapeutic benefits of the SSRIs have
emerged
Cont… 88

 3. Social anxiety disorder:

 Clonazepam is an effective treatment for social anxiety
disorder
 Also several other BDZs such as Diazepam have been used
as adjunctive medications for the treatment of social anxiety
disorder.
 4. Other anxiety disorders
 BDZs are used adjunctively for treatment of adjustment
disorder with anxiety, pathologic anxiety, anxiety associated
with life events e.g. after accident, OCD and PTSD
. 89

 5. Anxiety associated with depression:

 Depressed patients often experience significant anxiety and
anti depressants drugs may cause initial exacerbation of
these symptoms.
 Accordingly, benzodiazepines are indicated for the
treatment of anxiety associated with depression.
Precautions and adverse 90

Reactions
 The most common adverse effect of BDZs is drowsiness,
because of this persons should be advised to be careful
while driving or using dangerous machinery when taking
these drugs.
 The most severe adverse effects of the BDZs occur when
other sedatives substances such as alcohol are taken
concurrently.
 BDZs are teratogenic, therefore their use during pregnancy
is not advised.
Adverse effects of 91

benzodiazepines
COMMON OCCASIONAL RARE
Drowsiness Ataxia Amnesia
Dizziness Headaches Restlessness
Psychomotor impairment Reduced blood pressure Skin rash

Dry mouth
Blurred vision
Gastrointestinal upset
Treatment of BDZs overdose 92

 Flumazenil is used to reverse the adverse psychomotor,

amnestic and sedative effects of BDZs receptor agonists.
 Flumazenil is administered IV and has a half life of 7 to 15
minutes.
 For the initial management of known or suspected BDZs
overdose, the recommended initial dosage of flumazenil is
0.2mg (2ml) administered IV over 30 seconds. If the desired
consciousness is not obtained after 30seconds, a further dose of
0.3mg (3ml) can be administered over 30seconds.
 Further doses of 0.5mg (5ml) can be administered over
30seconds at 1-minute interval up to cumulative dose of 3.0 mg
Cont.…

 Most persons with a BDZs overdose respond to cumulative

dose of 1 to 3 mg of flumazenil.
 If person has not responded 5minutes after receiving
cumulative dose of 5mg of flumazenil, the primary cause
of sedation is probably not BDZ receptor agonist.
 Adverse effects of flumazenil: nausea, vomiting, dizziness,
agitation, cutaneous vasodilation, injection site pain,
impaired vision and headache

93
Tolerance, dependence and 94

withdrawal of BDZs:
 When BDZs are used for short periods (1 to 2 week) in
moderate dosages, they usually cause no significant
tolerance, dependence or withdrawal effects.
 It depend on how long a person takes the drug, what dose,
how quickly they taper it, and the half life of the compound.
 Abrupt discontinuation of BDZs particularly those with
short half-lives is associated with severe withdrawal
symptoms which may includes, depression, paranoia,
delirium and seizure.
Drug interactions 95

 The most common and potentially severe BDZs receptor

agonist interaction is excessive sedation and respiratory
depression occurring when BDZs are administered
concomitantly with other CNS depressants such as alcohol,
barbiturates, opioids and antihistamine
 Cimetidine, isoniazid, estrogen and oral contraceptives increase
the plasma concentration of diazepam, chlordiazepoxide,
clorazepines and flurazepine.
 Antacids and food may decrease the plasma concentration of
BDZs
 Death have been reported when parental lorazepam is given
with parental olanzapine
Dosage and clinical guidelines 96

 The clinical decision to treat an anxious person with BDZs

should be careful considered.
 Medical causes of anxiety eg thyroid dysfunction, should
be ruled out.
 BDZs use should be started at a low dosage and the
person should be instructed regarding the drug’s
sedative properties and abuse potential.
 An estimated length of therapy should be decided at the
beginning of therapy
 Some drugs has high potency e.g. clonazepam while other
has low potency e.g. oxazepam.
BUSPIRONE 97

 It acts on two types of receptors, serotonin(5-HT) and

dopamine(D)
 It has high affinity for the 5-HT1a serotonin receptor ,
acting as an agonist or partial agonist and moderate affinity
for the D2 dopamine receptor, acting as both an agonist and
an antagonist.
 It was initially believed to be better alternative to the BDZ
drug group because buspirone does not posses
anticonvulsant and muscle relaxant effects.
 Also it has antidepressant effect
Pharmacological Actions: 98

 Well absorbed from the GIT, but absorption is delayed by

ingestin
 Peak plasma levels are achieved 40 to 90 minutes after oral
administration.
 Because of short half life (2 to 11 hours), is dosed three
times daily
 An active metabolite of buspirone, 1-pyrimidinylpiperazine
(1-pp)
 Elimination half life of 1-pp is 6hours
Cont.. 99

 Buspirone does not affect the GABA-associated chloride

ion channel or the serotonin reuptake transporter
 It has activity in both5-HT and Dopamine type 2 receptor
 At the D2 receptor , it has properties of both an agonist and
an antagonist.
Therapeutic indication of 100

Buspirone
 1. Generalized anxiety disorder:
 It is a narrow spectrum antianxiety agent with demonstrated
efficacy only in the treatment of GAD
 Its clinical response may take 2 to 4 weeks
 2. OCD
 Its augmented in SSRIs in treatment of OCD
 3. SSRIs-induced bruxism and sexual dysfunction, nicotine
craving and ADHD
Precautions and adverse 101

reactions
 The common adverse effects of buspirone are: headache,
nausea, dizziness (12%) , nausea (8%), headache (6%) ,
nervousness (5%) and insomnia (2%)

 Buspirone should be used with caution by persons with

hepatic and renal impairment, pregnant women and nursing
mothers.
Drug interaction 102

 Coadministration of buspirone and haloperidol result in

increased blood concentrations of haloperidol.
 Drugs or food that inhibit CYP3A4,eg. Erythromycin,
Iitraconazole, nefazodone and grape fruit juice, increase
buspirone plasma concentration.
 Buspirone should not be used with MAOIs to avoid
hypertensive episodes and 2-week washout period should
pass between the disconsolation of MAOI use and the
initiation of treatment with buspirone
Laboratory interferences: 103

 Single doses of buspirone can cause transient elevations in

growth hormone, prolactin and cortisol concentration,
although the effects are not clinically significant.
 Dosage and clinical guidelines: Buspirone should not be
used in past hypersensitivity to buspirone, in cases of
diabetes associated metabolic acidosis or patients with
severely compromised liver or renal function
BARBITURATES AND 104

SIMILARLY ACTTING
DRUGS
 First barbiturate to be used in medicine was barbital which was
introduced in 1903, it was followed by phenobarbital,
amobarbital, pentobarbital, secobarbital and thiopental.
 Many problem are associated with these drugs including ,
high abuse and addiction potential.
 The use of barbiturates and similar compounds such as
meprobamates has practically been eliminated by the BDZs and
hypnotics such as zolpidem, eszopiclone and zaleplon which
have a lower abuse potentials and high therapeutic index than
the barbiturates.
Cont…. 105

 Nevertheless, barbiturates still have a role in the treatment

of certain mental and convulsive disorder

 Pharmacological action:
 The mechanism of action of barbiturates its potentiate the
effect of GABAA receptors .which enhances the inhibitory
action of GABA
 Barbiturates are well absorbed after oral administration
 The individual barbiturates metabolized by the liver and
excreted by the kidney
Cont.. 106

 The half-lives of specific barbiturates range from 1 to 12o

hours
 The barbiturates may also induce hepatic
enzymes(cytochrome P450), there by reducing the levels of
both the barbiturates any other concurrently administered
drugs metabolized by the liver.
Therapeutic indications: 107

 1. Sleep
 The barbiturates reduce sleep latency and the number of
awakenings during sleep, although tolerance to these effects
generally develops within 2 weeks.
 Discontinuation of barbiturates often leads to worsening of
insomnia

 2. Seizures
 Phenobarbital, most commonly used barbiturates for treatment
of seizures, has indication for treatment of generalized tonic-
clonic and simple partial seizures.
Cont.… 108

 Parenteral barbiturates are used in the emergency

management of seizures independent of cause.
 Example, IV phenobarbital should be administered slowly
at 10 to 20 mg/kg for status epilepticus.

 3. Electroconvulsive therapy
 Methohexial is commonly used as an anesthetics for ECT.
 It has lower cardiac risk than other barbiturate anesthetics.
Precautions and Adverse 109

reactions
 Some adverse effects of barbiturates are similar to those of
BDZs including; paradoxical dysphoria, hyperactivity and
cognitive disorganization.
 Rare adverse effects associated with barbiturates use
include the development of Stevens-Johnson syndrome,
megaloblastic anemia and neutropenia.

 Note: A significant difference btn barbiturates and BDZs is

the low therapeutic index of the barbiturates and hence
associated with significant risk of abuse potential and easy
development of tolerance and dependence.
Cont.… 110

 Barbiturates intoxication is manifested by :

 confusion
 drowsiness
 irritability
 hyperreflexia or areflexia
 ataxia
 nystagmus
 respiratory depression
 111

Treatment of barbiturates overdose

 It include ; induction of emesis or lavage , activated

charcoal and saline cathartics

 Supportive treatment including; maintaining airway and

respiration and treating shock as needed; maintaining vitals
and fluid balance, alkalinizing the urine
Precautions 112

 Because of some evidence of teratogenicity, barbiturates

should not be used by pregnant women or women who
breastfeeding.
 Barbiturates should be used with caution by patients with a
history of substance abuse, depression, diabetes, hepatic
impairment, renal disease, severe anaemia, hyperthyroidism
or hypoadrenalism.
 Also barbiturates is contraindicated in patients with acute
intermittent porphyria, impaired respiratory drive
Drug interactions 113

 Barbiturates should be used with great caution with other

prescribed CNS drugs such as antipsychotic and antidepressants
and non prescribed CNS agents such as alcohol.

 Also caution must be exercised when prescribing barbiturates

to patients who are talking other drugs that are metabolized in
the liver.
 Drugs that have their metabolism enhanced by barbiturates
administration include; opioids, antiarrhythmic agents,
antibiotics, anticoagulants, anticonvulsants, antidepressants,
contraceptives and immunosuppressants.
 114

Clinical guidelines:
 Barbiturates begin to act within 1 to 2 hours of administration.
 Treatment should begin with the low doses that are
increased to achieve a clinical effect.
 Children and older people are more sensitive to the effects
of barbiturates than young adults
 115

Non selective beta-blockers

 Many symptoms of anxiety (palpitations, rise in blood pressure, shaking,
tremor, GI hurrying) are due to sympathetic over activity and these
symptoms reinforce anxiety.
 Propranolol and other non selective beta-blockers cut the vicious cycle and
provide the symptomatic relief.
 They do not affect psychological symptoms, such as fear, tension and
worry, but are valuable in acutely stressful situations (examination fear,
unaccustomed public appearance).
SSRIs (selective serotonin reuptake inhibitors) are effective in obsessive
compulsive disorder (OCD), phobias, panic and many types of severe
generalized anxiety disorders
References 11
7

 Clinical pharmacology in psychiatry, L. F Gram, L.P

Balant 7th edition.
 Basic notes in psychophamacology by Michael I Levi 5 th
edition
 History psychopharmacology by P. Lopez volume 2
 A manual clinical psychopharmacology Alan F.
Schatzberg. M.D Eighth edition
 Kaplan & Saddock 11th edition
11
8
11
9
 12
0

 Chapter 10 Psychotherapies
 these includes
 Interactions between psychotherapist and client Interpersonal therapy
 Supportive psychotherapy
 Family therapy
 Defence mechanisms
 Group therapy
 Psychodynamic psychotherapy
 Couple therapy
 Cognitive behavioural therapy
 Eye movement and desensitisation reprocessing
 Dialectical behavioural therapy
 Grief counselling
 Cognitive analytic therapy Motivational interviewing Mindfulness

 12
1

 Supportive psychotherapy


 Aim: Supportive psychotherapy is a unique psychotherapy solely focuses on the needs of the
patient.


 Techniques 1. Therapist listens, allows emotional release, provides information and

encourages hope. 2. Therapist helps client to develop insight into problems as needed to
improve adaptive responses. 3. Therapist encourages patients to develop positive feelings to
help maintain therapeutic alliance. 4. Transference is not discussed in supportive
psychotherapy.


 Indications: most situations (e.g. adjustment issues, acute stress reaction, relationship
problems etc).


 Contraindications: 1. When psychotherapy itself is contraindicated (e.g. advanced dementia

delirium and intoxication) 2. Poor motivation 3. When other psychotherapies are more
appropriate (e.g. cognitive behaviour therapy for obsessive compulsive disorder).
 12
2

 Psychodynamic psychotherapy


 Aims:


 The main aim of psychodynamic psychotherapy is to enable clients to improve their self-understanding and
enabling them to engage in a reflection of themselves. The therapeutic process enables clients to develop
better tolerance for frustration, and also helps to increase their awareness of their underlying maladaptive
defence mechanisms that would require modification. Therapy aims to help them improve their interpersonal
relationships and also helps them cope with their personal symptoms.


 Indications:


 Commonly used for individuals with depressive and anxiety related disorders, or for individuals who have
had experienced childhood abuse and trauma or who are dealing with relationship and personality problems.
Psychodynamic psychotherapy requires clients to have adequate ego strength and possess abilities to form
and sustain relationships. More importantly, the clients must be motivated to change, and receptive to
psychological therapy.
 12
3

 Contraindications:


 Individuals with schizophrenia, tendencies for serious self harm, or with addiction related problems are not
suitable for this modality of therapy. Those with extremely poor insight into their own conditions are also
excluded.


 Techniques:


 1) Establish working alliance where the client and therapist agree to work on an emotional or psychological
problem 2) Free association 3) Focus on identified conflict 4) Development of therapeutic alliance 5)
Transference interpretation 6) Working through involves drawing previous maladaptive patterns or defences
to conscious awareness 7) Enactment refers to playing out the psychological phenomenon such as regression
in a safe setting to facilitate understanding 8) Containment of anxiety 9) Resolution of conflicts and avoid
maladaptive defences 10) Addressing termination issues 11) Techniques used in supportive psychotherapy
may be appropriate in times.


 Phases:


 in the beginning but it is often a complex and powerful event. It can be examined at the intrapsychic,
behavioural, cognitive, interpersonal and social levels (e.g. legal implications).
 124

 The therapist engages in a discussion and clarification of the current problem when therapy commences. An
exploration into the nature and the origins of the problem is undertaken. Therapeutic alliance is established
between the therapist and the client, and the therapeutic relationship thus formed and enables the
identification and confrontation of defences. Underlying unconscious motives are identified during the
therapy itself and subjected to interpretation. The therapist helps the client in working through and resolves
existing conflicts. Once that it achieved over several sessions, the therapy is then terminated.


 Negative reactions:


 1) Acting out refers to the poor containment of strong feelings triggered by the therapy (e.g. anger towards
the therapist). 2) Acting in refers to the exploration of therapist’s personal and private information. 3)
Negative therapeutic reaction refers to the unexpected deterioration in the face of apparent progression (e.g.
premature termination of therapy without explanation after apparent engagement).


 Termination of psychodynamic therapy



 Termination is a point where therapeutic endeavour comes to a defined end date set by the contract
 12
5

 Cognitive behavioural therapy (CBT)



 Cognitive therapy: Beck proposed that negative thinking in depression originates in

earlier assumptions and plays central roles in the maintenance of depressive
symptoms. The Beck’s cognitive model of depression includes the effect of early
experiences, core beliefs, assumptions, cognitive distortions, automatic thoughts and
the negative cognitive triad. Depression can be treated by modifying one of the
components of Beck’s cognitive model.


 Behaviour therapy: Mowrer’s two factor model states that fear of specific stimuli is
acquired through classical conditioning and clients try to reduce fear by avoiding the
conditioned stimuli through operant conditioning. Ayllon and Azrin’s token economy
model is a ward environment where reinforcers were applied to systematically change
clients’ behaviour. Aim: The aim of CBT is to improve emotion by identifying and
changing dysfunctional thoughts and maladaptive behaviours by a present-oriented,
time limited and highly structured therapy
 12
6

 Dialectical behaviour therapy (DBT)



 Indications: borderline personality disorder (BPD) and client’s attempt repetitive self-harm


 Techniques: 1) CBT 2) Dialectical thinking: advise the client not to think linearly. Truth is an evolving
process of opposing views rather than extremes 3) Zen Buddhism: emphasize wholeness, see alternatives
and engulf alternatives. 4) Use of metaphors: enhancing effectiveness of communication, discovering one’s
own wisdom and developing therapeutic alliance.


 Components: 1) Individual sessions: 45-60 minutes on a weekly basis, to review diary cards in the past one
week and discuss life threatening behaviours; 2) Skills training group by a trainer: weekly group for 2 hours,
didactic in nature and manual-based; 3) Brief out-of-hours telephone contact as part of treatment contract 4)
Weekly consultation group between the individual therapist and the skills trainer.



 12
7

 Interpersonal therapy (IPT)



 Indications: Depressive disorder (equally effective as CBT), eating disorder (bulimia

nervosa), interpersonal disputes, role transition, grief and loss


 Techniques:


 1) To create a therapeutic environment with meaningful therapeutic relationship and

recognize the client’s underlying attachment needs. 2) To develop an understanding
of the client’s communication difficulties and attachment style both inside and
outside the therapy. 3) To identify the client’s maladaptive patterns of
communication and establishment of insight. The therapist can adopt three stances:
neutral stance, passive stance and client advocate stance 4) To assist the client in
building a better social support network and mobilise resources.

 12
8

 Family therapy

 Commonly encountered family problems and strategies to resolve:

 1) Task accomplishment problems (e.g. developmental tasks): identifying the task, exploring alternative approaches, taking action, evaluating and adjusting. 2) Communication problems and triangulation: introduction of humour, demonstration of warmth and empathy, role play and modifying both verbal and non-verbal communication. 3) Role problems (e.g. family scapegoat, parental child): identify
problems and redefine roles. The same-sex parent functions as primary programmer and disciplinarian. This will promote maximum ego development by setting limits and higher level goals. The opposite-sex parent functions as the facilitator or mediator within the triangular relationship to correct inappropriate parenting from the same sex parent. 4) Behaviour control problems (e.g. conduct disorder in a
child): engage family to deliver BT in home environment. 5) Boundary issues between family members (e.g. enmeshment): to promote communication and emotional interchange in disengaged relationship; to create necessary separation and independence in case of enmeshment. 6) Suprasystem problems (high crime rate in neighbourhood and affecting the family): Strengthening the boundary between the
family and the suprasystem; to work with extended family and social agencies.

 Types of family therapy:

 Structural family therapy (Minuchin):

 It identifies the set of unspoken rules governing the hierarchy, sharing of responsibilities and boundaries. The therapist will present these rules to the family in a paradoxical way to bring about changes. The therapist is actively in control of proceedings.

 Systemic family therapy:

 1. Milan associates often involve more than two therapists working in a team to maintain the systemic perspective. One therapist is always with the family while the team observes through the one-way screen or video camera. The team offers input to the therapist via telephone or during intersession breaks to discuss the family system. There are pre- and post-session discussions.

 2. Reframing an individual’s problem as family problem (e.g. daughter’s borderline personality may be reframed as the parental; problem in providing care to the child). An internal problem can be reframed as external problem if there is unproductive conflicts in the family which exhausted everyone. (e.g. The family is under influence of anger rather than an individual member is an angry person).

 3. Exploring the coherence and understand the family as an organised coherent system.

 4. Circular questioning is used to examine perspective of each family member on inter-family member relationship. It aims at discovering and clarifying conflicting views. Hypothesis can be formed from the conflicting views and change can be proposed.

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 Strategic family therapy uses a complex plan rather than a simple directive to produce change in the family. It employs the following techniques:

 1. Positive connotation: It is a form of reframing by ascribing positive motives to the symptomatic behaviour.

 2. Metaphors allow indirect communication of ideas. (e.g. Relationship metaphors use one relationship between therapist and one family member as a metaphor for another relationship. Metaphorical object refers to the use of a concrete object to represent abstract ideas (e.g. a blank sheet of paper in an envelope to represent family secrets).

 3. Paradoxical interventions: This method is used when direct methods fail or encounter strong resistance in some family members. The therapist will reverse the vector (i.e. rather than a top-down approach from the parents, a bottom-up approach from the child to the parents is allowed). This therapist will also disqualify anyone who is an authority on the problems including the parents. (e.g. children are
allowed to challenge the parents and undesired behaviour is encouraged. Paradoxically, change and improvement will take place as family members cannot tolerate the paradoxical pattern).

 4. Prescribing family rituals: Rituals refer to membership, brief expression and celebration. (e.g. the therapist passes a metaphor object to the family and any family member can use this object to call for a meeting at home). Ritual prescription refers to setting up a time table which assigns one parent to take charge on an odd day and a child to take charge on an even day. Ritual prescription is useful for family
with parental child.

 5. Other strategies include humour, getting help from a consultation group which observes through the one way mirror to offer advice and debate among family members.


 12
9

 Group therapy


 Types of group therapy:



 1. Milieu group therapy: Main developed therapeutic community where the whole
community (e.g. the ward) is viewed as a large group. Rapaport described four characteristics
in milieu GT: democratisation (equal sharing of power), permissiveness (tolerance of others’
behaviour outside the setting), reality confrontation (confront with the views from others) and
communalism (sharing of amenities).


 2. Supportive group therapy: for clients with chronic psychiatric disorders such as
schizophrenia to attend a day hospital with GT. It involves empathy, encouragement and
explanation. (e.g. Schizophrenia Fellowship).


 3. Outpatient group therapy: It may involve a self help group targeting at homogenous group
of clients focusing on one disorder (e.g. for anxiety disorders or AA). It is short term and
involves direct didactic instruction
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 Couple therapy


 Couple therapy involves the therapist (or sometimes two therapists) seeing two clients who are in a relationship. It aims
to sort out interpersonal and marital/partnership difficulties. Couple therapy works on issues such as grief in a couple
and/or sexual problems. Couple therapy follows one of the following psychotherapeutic models: CBT (identifying
reinforcement of undesirable behaviour in the couple), psychodynamic (understanding one’s own emotional needs and
how to relate to the needs of the partner), transactional (behaviours are analysed in terms of the child, adult and parent
within the client and how the client reacts with the partner in the relationship) and family-based therapies.


 Techniques of couple therapy:



 1) Reciprocity negotiation: the couple develops ability to express their offers and understand the partner’s request. This
promotes exchange of positive behaviours and reactions.


 2) Communication training: This encourages mutual exchange of emotional messages.



 3) Structural moves involve the following techniques. Experiment of disagreement focuses on a topic where one partner
always dominates while the other habitually gives in to avoid disagreement. This exercise will help the passive partner to
express an opinion forcefully and the other needs to value the expression. Role reversal helps one partner to understand
the viewpoints and experiences of the other.
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 Eye movement and desensitisation reprocessing (EMDR)

 EMDR is indicated for post-traumatic stress disorder. EMDR focuses on traumatic experiences and the negative cognitions and affective responses associated with these. The aim is to desensitise the individual to the affective responses. This is accompanied
by bilateral stimulation by inducing rapid eye movement as the client is asked to follow the regular movement of the therapist’s fore finger.

 The procedural phases of EMDR include: 1) assessment of target memory of image; 2) desensitisation by holding the target image together with the negative cognition in mind and bilateral stimulation continues until the memory has been processed with the
chains of association; 3) installation of positive images; 4) scanning of body to identify any sensations; 5) closure and debriefing on the experience of the session.

 Grief counselling

 Grief counselling allows client to talk about the loss, to express feelings of sadness, guilt or anger and to understand the course of grieving process. This will allow the client to accept the loss, working though the grief process and adjust one’s life without the
deceased.

 Motivational interviewing

 Indications: to enhance motivation to quit substance misuse or other forms of addiction (e.g. internet or gambling).

 Techniques: 1) Express empathy of patient’s substance abuse by reflective listening 2) Rolls with resistance and understand why patient is reluctant to give up a substance or a habit. 3) Develop discrepancy between one’s addiction and goals. 4) Support self-
efficacy to quit a drug or bad habit and to provide a menu of treatment options.

 Mindfulness

 This is largely a cognitive and behavioural program which uses a combination of: -Mindfulness mediation -Body awareness -Yoga

 It aims to help people become more mindful and help to reduce stress.