2. PLAN OF PRESENTATION
• INTRODUCTION
• TYPES OF ANXIETY
• NEUROBIOLOGY OF ANXIETY DISORDERS
• SYMPTOMATOLOGY
• MANAGEMENT
• PHARMACOLOGICAL
• NON PHARMACOLOGICAL
• RECENT ADVANCES
3. WHAT IS ANXIETY ?
• ANXIETY IS A DIFFUSE, HIGHLY UNPLEASANT, OFTEN VAGUE FEELING OF
APREHENSION, ACCOMPANIED BY ONE OR MORE BODILY SENSATIONS-
PALPITATIONS, PERSPIRATIONS, HEADACHE ETC.
• PHILOSOPHERS AND THINKERS HAVE LONG WRITTEN ABOUT THE
CENTRALITY OF ANXIETY IN HUMAN LIFE AND EXPERIENCES.
• ON THE OTHERHAND, IT IS ONE OF THE NEWEST OF SUBJECTS AS THE
SCIENTISTS ARE UNDERSTANDING THE UNDERLYING PSYCHOBIOLOGY AND
ITS MANAGEMENT, EFFECTIVELY ONLY FOR LAST FEW DECADES.
4. DEFINITION
“Feeling of apprehension caused by anticipation of danger,
which may be internal or external”
“Anxiety isan emotional state commonly caused by the
perception of real or perceived danger that threatens the
security of an individual. It allows a person to prepare for or
react to environmental changes.”
• This is an adaptive response, and is transient in nature.
5. • ANXIETY IS A NORMAL EMOTION UNDER CIRCUMSTANCES OF THREAT AND IS
THOUGHT TO BE PART OF THE EVOLUTIONARY “FIGHT OR FLIGHT” REACTION OF
SURVIVAL.
• ANXIETY CAN PRODUCE UNCOMFORTABLE AND POTENTIALLY DEBILITATING
PSYCHOLOGICAL (E.G., WORRY OR FEELING OF THREAT) AND PHYSIOLOGICAL
AROUSAL (E.G., TACHYCARDIA OR SHORTNESS OF BREATH) IF IT BECOMES EXCESSIVE.
• SOME INDIVIDUALS EXPERIENCE PERSISTENT, SEVERE ANXIETY SYMPTOMS AND
POSSESS IRRATIONAL FEARS THAT SIGNIFICANTLY IMPAIR NORMAL DAILY
FUNCTIONING.
• THESE PERSONS OFTEN SUFFER FROM AN ANXIETY DISORDER.
6. TYPES OF ANXIETY
• AN INTEGRAL PART OF OUR DAY TO DAY LIFE
AND HELPS THE INDIVIDUAL IN COPING WITH
STRESS DEVELOPING
• BETTER ADAPTIVE SKILL
• PLANNING AHEAD
• BETTER PERFORMANCE
• INTENSED INTERNAL UNCOMFORTABLE
FEELING STATE LEADS TO MALADAPTIVE
BEHAVIOUR, THOUGHT AND COGNITONS
AND POORER PERFORMANCE.
NORMAL ANXIETY PATHOLOGICAL ANXIETY
ANXIETY DISORDER
7. CLASSIFICATION OF ANXIETY DISORDER
• PANIC DISORDER WITHOUT
AGORAPHOBIA.
• PANIC DISORDER WITH
AGORAPHOBIA.
• AGORAPHOBIA WITHOUT H/O PANIC
DISORDER.
• SPECIFIC PHOBIA.
• SOCIAL PHOBIA.
• OCD
• PTSD
• ACUTE STRESS DISORDER
• GENERALISED ANX- DISORDER.
• ANXIETY DISORDER DUE TO
• GENERAL MEDICAL CONDITION.
• SUBSTANCE INDUCED ANXIETY
DISORDER.
• ANXIETY DIS ORDER NOS.
8. • SEPARATION ANXIETY DISORDER
• SELECTIVE MUTISM NEW !!!
• SPECIFIC PHOBIA
• SOCIAL ANXIETY DISORDER
• PANIC DISORDERNEW !!!
• PANIC ATTACKNEW !!!
• AGORAPHOBIA NEW !!!
• GENERELIZED ANXIETY DISORDER
• SUBSTANCE/MEDICATION INDUCED ANXIETY DISORDER
• ANXIETY DISORDER DUE TO ANOTHER MEDICAL CONDITION
• OTHER SPECIFIED ANXIETY DISORDER
• UNSPECIFIED ANXIETY DISORDER
10. ALL ANXIETY DISORDERS HAVE 2 COMPONENTS
TO UNDERSTAND THE NEUROBIOLOGY OF ANY ANXIETY DISORDER WE
NEED TO UNDERSTAND THE NEUROBIOLOGY OF BOTH
FEAR
WORRY
12. LINKING ANXIETY SYMPTOMS TO CIRCUITS
ANXIETY AND FEAR SYMPTOMS ARE REGULATED BY AN AMYGDALA-
CENTERED CIRCUIT.
WORRY, ON THE OTHER HAND, IS REGULATED BY A CORTICO-STRIATO-
THALAMOCORTICAL (CSTC) LOOP.
THESE CIRCUITS MAY BE INVOLVED IN ALL ANXIETY DISORDERS, WITH
THE DIFFERENT PHENOTYPES REFLECTING NOT UNIQUE CIRCUITRY BUT
RATHER DIVERGENT MALFUNCTIONING WITHIN THOSE CIRCUITS.
13. LOOKING AFRAID/ AFFECT OF FEAR
ORBITO FC
AMYGDALA
• FEELINGS OF FEAR ARE REGULATED BY
RECIPROCAL CONNECTIONS BETWEEN
THE AMYGDALA AND THE ANTERIOR
CINGULATE CORTEX (ACC) AND THE
AMYGDALA AND THE ORBITOFRONTAL
CORTEX (OFC).
ACC
• SPECIFICALLY, IT MAY BE THAT OVER
ACTIVATION OF THESE CIRCUITS
PRODUCES FEELINGS OF FEAR.
15. AVOIDANCE/FIGHT/FLIGHT/FREEZE MOTOR
RESPONSE
AMYGDALA
PAG
• FEELINGS OF FEAR MAY BE EXPRESSED
THROUGH BEHAVIORS SUCH AS AVOIDANCE,
WHICH IS PARTLY REGULATED BY RECIPROCAL
CONNECTIONS BETWEEN THE AMYGDALA AND
THE PERIAQUEDUCTAL GRAY (PAG).
• AVOIDANCE IN THIS SENSE IS A MOTOR
RESPONSE.
• OTHER MOTOR RESPONSES ARE TO FIGHT OR
TO RUN AWAY (FLIGHT) IN ORDER TO SURVIVE
THREATS FROM THE ENVIRONMENT.
17. CHANGES IN RESPIRATORY RATE
AMYGDALA
PBN
• CHANGES IN RESPIRATION MAY OCCUR DURING
A FEAR RESPONSE; THESE CHANGES ARE
REGULATED BY ACTIVATION OF THE
PARABRACHIAL NUCLEUS (PBN) VIA THE
AMYGDALA.
• INAPPROPRIATE OR EXCESSIVE ACTIVATION OF
THE PBN CAN LEAD NOT ONLY TO INCREASES IN
THE RATE OF RESPIRATION BUT ALSO VARIOUS
SYMPTOMS.
SHORTNESS OF BREATH
EXACERBATION OF ASTHMA, OR
A SENSE OF BEING SMOTHERED.
18. AUTONOMIC OUTPUT OF FEAR
ATHEROSCLEROSIS
CARDIAC ISCHEMIA
BLOOD PRESSURE
MYOCARDIAL INFARCTION
SUDDEN DEATH
“SCARED TO DEATH” MAY NOT ALWAYS BE
AN EXAGGERATION OR A FIGURE OF SPEECH!
19. AUTONOMIC OUTPUT OF FEAR
AMYGDALA
LC
• AUTONOMIC RESPONSES ARE TYPICALLY
ASSOCIATED WITH FEELINGS OF FEAR.
• THESE INCLUDE INCREASES IN HEART RATE
(HR) AND BLOOD PRESSURE (BP), WHICH
ARE REGULATED BY RECIPROCAL
CONNECTIONS BETWEEN THE AMYGDALA
AND THE LOCUS COERULEUS (LC).
• LONG-TERM ACTIVATION OF THIS CIRCUIT
MAY LEAD TO INCREASED RISK OF
ATHEROSCLEROSIS, CARDIAC ISCHEMIA,
CHANGE IN BP, DECREASED HR
VARIABILITY, MYOCARDIAL INFARCTION
(MI), OR EVEN SUDDEN DEATH.
21. ENDOCRINE OUTPUT OF FEAR
AMYGDALA
HYPOTHALAMUS
• THE FEAR RESPONSE MAY BE
CHARACTERIZED IN PART BY ENDOCRINE
EFFECTS SUCH AS INCREASES IN CORTISOL,
WHICH OCCUR BECAUSE OF AMYGDALA
ACTIVATION OF THE HYPOTHALAMIC–
PITUITARY–ADRENAL (HPA) AXIS.
• PROLONGED HPA ACTIVATION AND
CORTISOL RELEASE CAN HAVE SIGNIFICANT
HEALTH IMPLICATIONS, SUCH AS INCREASED
RISK OF CORONARY ARTERY DISEASE, TYPE 2
DIABETES, AND STROKE.
22. STRESS AND THE HPA AXIS
ADULT STRESSORS
DISINHIBITION
OF HPA AXIS BY HIPPOCAMPUS
CRF
RELEASE
ACTH
RELEASE
GLUCO-
CORTICOID
RELEASE
HIPPOCAMPAL
ATROPHY
ABNORMAL STRESS RESPONSE
MDD ANXIETY DISORDER
CRF
RELEASE
GLUCOCORTICOIDS
INHIBIT CRF
RELEASE
ACTH RELEASE
GLUCO-
CORTICOID
RELEASE
NORMAL STRESS RESPONSE
23. PATHOPHYSIOLOGY
• DATA FROM BIOCHEMICAL AND NEUROIMAGING STUDIES INDICATE
THAT THE MODULATION OF NORMAL AND PATHOLOGIC ANXIETY
STATES IS ASSOCIATED WITH MULTIPLE REGIONS OF THE BRAIN AND
ABNORMAL FUNCTION IN SEVERAL NEUROTRANSMITTER SYSTEMS,
INCLUDING
• NOREPINEPHRINE (NE)
• SEROTONIN (5-HT)
• γ –AMINOBUTYRIC ACID (GABA)
24. NORADRENERGIC MODEL
• THIS MODEL SUGGESTS THAT THE AUTONOMIC NERVOUS SYSTEM OF ANXIOUS PATIENTS IS
HYPERSENSITIVE AND OVERREACTS TO VARIOUS STIMULI.
• THE LOCUS CERULEUS MAY HAVE A ROLE IN REGULATING ANXIETY, AS IT ACTIVATES
NOREPINEPHRINE RELEASE AND STIMULATES THE SYMPATHETIC AND PARASYMPATHETIC
NERVOUS SYSTEMS.
5-HT MODEL
• GAD SYMPTOMS MAY REFLECT EXCESSIVE 5-HT TRANSMISSION OR OVERACTIVITY OF THE
STIMULATORY 5-HT PATHWAYS.
• PATIENTS WITH SAD HAVE GREATER PROLACTIN RESPONSE TO BUSPIRONE CHALLENGE,
INDICATING AN ENHANCED CENTRAL SEROTONERGIC RESPONSE.
• THE ROLE OF 5-HT IN PANIC DISORDER IS UNCLEAR, BUT IT MAY HAVE A ROLE IN
DEVELOPMENT OF ANTICIPATORY ANXIETY.
• PRELIMINARY DATA SUGGEST THAT THE 5-HT AND 5-HT2 ANTAGONIST
METACHLOROPHENYLPIPERAZINE CAUSES INCREASED ANXIETY IN PTSD PATIENTS.
25. γ-AMINOBUTYRIC ACID (GABA) RECEPTOR MODEL
• GABA IS THE MAJOR INHIBITORY NEUROTRANSMITTER IN THE CNS.
• MANY ANTIANXIETY DRUGS TARGET THE GABA RECEPTOR.
• BENZODIAZEPINES (BZS) ENHANCE THE INHIBITORY EFFECTS OF GABA,WHICH
HAS A STRONG REGULATORY OR INHIBITORY EFFECT ON SEROTONIN (5-HT),
NOREPINEPHRINE, AND DOPAMINE SYSTEMS.
• ANXIETY SYMPTOMS MAY BE LINKED TO UNDERACTIVITY OF GABA SYSTEMS OR
DOWNREGULATED CENTRAL BZ RECEPTORS.
• IN PATIENTS WITH GAD, BZ BINDING IN THE LEFT TEMPORAL LOBE IS REDUCED
ABNORMAL SENSITIVITY TO ANTAGONISM OF THE BZ BINDING SITE AND
DECREASED BINDING WAS DEMONSTRATED IN PANIC DISORDER.
• ABNORMALITIES OF GABA INHIBITION MAY LEAD TO INCREASED RESPONSE TO
STRESS IN PTSD PATIENTS.
26. NEUROTRANSMITTER IN CIRCUITS
• 5HT
• GABA
• GLUTAMATE
•CRF/HPA
• NE
• VOLTAGE GATED ION CHANNELS.
AMYGDALA CENTRED CIRCUIT CSTC [WORRY LOOP]
[ FEAR LOOP]
• 5HT
• GABA
• GLUTAMATE
•DA
• NE
• VOLTAGE GATED ION CHANNEL.
28. GENERALIZED ANXIETY DISORDER
• THE DIAGNOSTIC CRITERIA FOR GAD REQUIRE
PERSISTENT SYMPTOMS FOR MOST DAYS FOR AT LEAST
6 MONTHS.
• THE ESSENTIAL FEATURE OF GAD IS UNREALISTIC OR
EXCESSIVE ANXIETY AND WORRY ABOUT A NUMBER OF
EVENTS OR ACTIVITIES OR OTHER IMPORTANT AREAS
OF FUNCTIONING.
29.
30. PRESENTATION OF GENERALIZED ANXIETY DISORDER
• PSYCHOLOGICAL AND COGNITIVE SYMPTOMS :
• EXCESSIVE ANXIETY
• WORRIES THAT ARE DIFFICULT TO CONTROL
• FEELING KEYED UP OR ON EDGE
• POOR CONCENTRATION OR MIND GOING BLANK
• PHYSICAL SYMPTOMS :
• RESTLESSNESS
• FATIGUE
• MUSCLE TENSION
• SLEEP DISTURBANCE
• IRRITABILITY
31. PANIC DISORDER
• PANIC DISORDER BEGINS AS A SERIES OF UNEXPECTED
(SPONTANEOUS) PANIC ATTACKS INVOLVING AN INTENSE,
TERRIFYING FEAR SIMILAR TO THAT CAUSED BY LIFE-
THREATENING DANGER.
• DURING AN ATTACK, PATIENTS OFTEN DESCRIBE AN
OVERWHELMING SENSE OF DOOM, A FEAR OF DYING OR
LOSING CONTROL.
• PANIC ATTACKS USUALLY LAST NO MORE THAN 20 TO 30
MINUTES,
• WITH THE PEAK INTENSITY OF SYMPTOMS WITHIN THE
FIRST 10 MINUTES.
• SECONDARY TO THE PANIC ATTACKS, MANY PATIENTS
EVENTUALLY DEVELOP AGORAPHOBIA.
32.
33. SYMPTOMS OF A PANIC ATTACK
• DEPERSONALIZATION
• DEREALIZATION
• FEAR OF LOSING CONTROL
• FEAR OF GOING CRAZY
• FEAR OF DYING.
• PSYCHOLOGICAL SYMPTOMS • PHYSICAL SYMPTOMS :
• ABDOMINAL DISTRESS
• CHEST PAIN OR DISCOMFORT
• CHILLS
• DIZZINESS OR LIGHT-HEADEDNESS
• FEELING OF CHOKING
• HOT FLUSHES
• PALPITATIONS
• NAUSEA
• SHORTNESS OF BREATH
• SWEATING
• TACHYCARDIA
• TREMBLING OR SHAKING.
34. SOCIAL ANXIETY DISORDER
• SAD IS CHARACTERIZED BY AN INTENSE, IRRATIONAL, AND
PERSISTENT FEAR OF BEING NEGATIVELY EVALUATED OR
SCRUTINIZED IN ATLEAST ONE SOCIAL OR PERFORMANCE
SITUATION.
• EXPOSURE TO THE FEARED CIRCUMSTANCE USUALLY
PROVOKES AN IMMEDIATE SITUATION-RELATED PANIC
ATTACK.
• ADULTS WITH SAD USUALLY RECOGNIZE THEIR FEAR IS
EXCESSIVE AND UNREASONABLE; HOWEVER, THEY ARE
UNABLE TO OVERCOME IT WITHOUT TREATMENT.
WHY CAN’T I
TALK TO
PEOPLE ?
35.
36. SOCIAL ANXIETY DISORDER
• IN INDIVIDUALS UNDER 18 YEARS OF AGE, THE DURATION OF
SYMPTOMS IS AT LEAST 6 MONTHS. THE FEAR OR AVOIDANCE IS NOT
CAUSED BY A DRUG OR OTHER SUBSTANCE (E.G., COCAINE), OR A
GENERAL MEDICAL OR PSYCHIATRIC DISORDER.
• THE MEAN AGE OF ONSET OF SAD IS DURING THE MID-TEENS. RATES
OF SAD ARE SLIGHTLY HIGHER AMONG WOMEN THAN MEN AND
MORE FREQUENT IN YOUNGER COHORTS. IT IS A CHRONIC DISORDER
WITH A MEAN DURATION OF 20 YEARS.
38. POSTTRAUMATIC STRESS DISORDER (PTSD)
• POSTTRAUMATIC STRESS DISORDER (PTSD) IS A CONDITION MARKED BY
THE DEVELOPMENT OF SYMPTOMS AFTER EXPOSURE TO TRAUMATIC LIFE
EVENTS.
• THE PERSON REACTS TO THIS EXPERIENCE WITH FEAR AND HELPLESSNESS,
PERSISTENTLY RELIVES THE EVENT, AND TRIES TO AVOID BEING REMINDED
OF IT.
• PTSD CAN OCCUR AT ANY AGE, AND THE COURSE IS VARIABLE.
• ONE-THIRD OF PATIENTS WITH PTSD HAVE A POOR PROGNOSIS, AND
ABOUT 80% HAVE A CONCURRENT DEPRESSION OR ANXIETY DISORDER.
39.
40. THE HIPPOCAMPUS AND RE-EXPERIENCING
AMYGDALA
HIPPOCAMPUS
• ANXIETY CAN BE TRIGGERED NOT ONLY BY AN
EXTERNAL STIMULUS BUT ALSO BY AN
INDIVIDUAL’S MEMORIES. TRAUMATIC
MEMORIES STORED IN THE HIPPOCAMPUS CAN
ACTIVATE THE AMYGDALA, CAUSING THE
AMYGDALA, IN TURN, TO ACTIVATE OTHER
BRAIN REGIONS AND GENERATE A FEAR
RESPONSE.
• THIS IS TERMED RE-EXPERIENCING, AND IT IS A
PARTICULAR FEATURE OF POSTTRAUMATIC
STRESS DISORDER.
41. PTSD SYMPTOMS
RE-EXPERIENCING SYMPTOMS
AVOIDANCE SYMPTOMS
• RECURRENT, INTRUSIVE DISTRESSING MEMORIES OF THE
TRAUMA
• RECURRENT, DISTURBING DREAMS OF THE EVENT
• FEELING THAT THE TRAUMATIC EVENT IS RECURRING (E.G.,
DISSOCIATIVE FLASHBACKS)
• PHYSIOLOGIC REACTION TO REMINDERS OF THE TRAUMA
• AVOIDANCE OF CONVERSATIONS ABOUT THE TRAUMA
• AVOIDANCE OF THOUGHTS OR FEELINGS ABOUT THE
TRAUMA, AVOIDANCE OF ACTIVITIES THAT ARE REMINDERS
OF THE EVENT
• AVOIDANCE OF PEOPLE OR PLACES THAT AROUSE
RECOLLECTIONS OF THE TRAUMA
• INABILITY TO RECALL AN IMPORTANT ASPECT OF THE
TRAUMA
• ANHEDONIA
• RESTRICTED AFFECT
• SENSE OF A FORESHORTENED FUTURE (E.G., DOES NOT
EXPECT TO HAVE A CAREER, MARRIAGE)
42. • HYPER-AROUSAL SYMPTOMS
• DECREASED CONCENTRATION
• EASILY STARTLED
• HYPERVIGILANCE
• INSOMNIA
• IRRITABILITY OR ANGRY OUTBURSTS
• SUBTYPES
• ACUTE: DURATION OF SYMPTOMS IS LESS THAN 3 MONTHS
• CHRONIC: SYMPTOMS LAST FOR LONGER THAN 3 MONTHS
• WITH DELAYED ONSET: ONSET OF SYMPTOMS IS AT LEAST 6 MONTHS
POSTTRAUMA
44. OBSESSIVE-COMPULSIVE DISORDER (OCD)
• OBSESSIVE-COMPULSIVE DISORDER (OCD) IS ONE OF THE TEN LEADING
CAUSES OF DISABILITY.
• PATIENTS WITH OCD EXPERIENCE SIGNIFICANT IMPAIRMENT IN THEIR
QUALITY OF LIFE (QOL), WITH REDUCTIONS IN SOCIAL, FAMILY, AND
OCCUPATIONAL FUNCTIONING.
• BECAUSE OF THE NATURE AND POTENTIAL SEVERITY OF SIGNS AND
SYMPTOMS AND THE RESULTANT NEGATIVE EFFECTS ON QOL, OCD IS
CONSIDERED A MAJOR MEDICAL CONDITION.
45. NEURAL CIRCUITS OF OBSESSION/WORRY
THALAMUS
STRIA
TUM
DLPFC SHOWN HERE IS A CORTICO-
STRIATOTHALAMO- CORTICAL
(CSTC) LOOP ORIGINATING
AND ENDING IN THE
DORSOLATERAL PREFRONTAL
CORTEX (DLPFC).
OVERACTIVATION OF THIS
CIRCUIT MAY LEAD TO
WORRY OR OBSESSIONS.
46. PRESENTATION
• OBSESSIONS
• REPETITIVE THOUGHTS (E.G., FEELING CONTAMINATED AFTER TOUCHING AN OBJECT,
DOUBTING WHETHER THE STOVE WAS TURNED OFF)
• REPETITIVE IMAGES (E.G., RECURRENT SEXUALLY EXPLICIT PICTURES)
• REPETITIVE IMPULSES (E.G., NEED FOR SYMMETRY OR PUTTING THINGS IN SPECIFIC
ORDER, IMPULSE TO SHOUT OUT OBSCENITIES IN A TEMPLE)
• COMPULSIONS
• REPETITIVE ACTIVITIES (E.G., HAND WASHING, CHECKING, ORDERING, NEED TO ASK,
NEED TO CONFESS)
• REPETITIVE MENTAL ACTS (E.G., COUNTING, REPEATING WORDS SILENTLY, PRAYING)
50. INVESTIGATIONS
• BLOOD SUGAR – T2 DM
• LIPID PROFILE
• CORTISOL LEVEL
• URINE DRUG SCREEN: SHOULD BE ORDERED TO RULE OUT SUSPECTED STIMULANT ABUSE
• TFTS: RECOMMENDED IF THE PATIENT HAS SUSPECTED THYROID DISEASE (E.G., WEIGHT
LOSS, GOITRE)
• 24-HOUR URINE TEST FOR VANILLYLMANDELIC ACID AND METANEPHRINES: ORDERED TO
RULE OUT PHAEOCHROMOCYTOMA IF CARDIAC SYMPTOMS SUCH AS TACHYCARDIA
AND/OR HYPERTENSION ARE PRESENT
• ECG AND ECHOCARDIOGRAM: RECOMMENDED FOR PATIENTS WITH A HIGH RISK OF
CARDIAC DISEASE OR EVIDENCE OF CARDIAC DISEASE
• PULMONARY FUNCTION TESTS: SHOULD BE CONSIDERED FOR PATIENTS WITH SHORTNESS
OF BREATH AND EVIDENCE OF PULMONARY DISEASE
• EEG: USEFUL FOR EVALUATING PATIENTS WHERE ANXIETY IS SUSPECTED TO BE A SEIZURE
PRODROMAL SYMPTOM.
54. PHARMACOLOGICAL
• 3 MAJOR NEUROTRANSMITTERS ARE TARGETTED IN
PHARMACOLOGICAL TREATMENT OF ANXIETY DISORDERS
1. GABA -
2. SEROTONIN -
3. NOREPINEPHRIN -
A. BENZODIAZEPINES
B. SSRIs
C. SNRIs
55. A) BENZODIAZEPINES
• BENZODIAZEPINES, PERHAPS THE BEST-KNOWN AND MOST WIDELY USED
ANXIOLYTICS, ACT BY ENHANCING GABA ACTIONS AT THE LEVEL OF THE
AMYGDALA AND AT THE LEVEL OF THE PREFRONTAL CORTEX WITHIN CSTC
LOOPS TO RELIEVE ANXIETY.
3 MAJOR TYPES
1,4 BENZODIAZEPINES
1,5 BENZODIAZEPINES
2,3 BENZODIAZEPINES
57. 1,5 BENZODIAZEPINE
• CLOBAZAM
• ADVANTAGES & DISADVANTAGES
• ANXIOLYTIC
• ANTIEPILEPTIC
• DECREASED SEDATION
• LOW DEPENDENCE
• LOW MUSCLE RELAXATION
• CAN BE USED IN EXECUTIVE GROUPS
• CAN BE CONTINUED FOR LONG PERIOD OF TIME
58. 2,3 BENZODIAZEPINES
• TOFISOPAM
• TOFISOPAM, A RACEMIC 2,3-BENZODIAZEPINE
COMPRISED OF R- AND S-ENANTIOMERS, IS
UNLIKE TRADITIONAL 1,4-BENZODIAZEPINES.
• ADVANTAGES
• LIKE OTHER BENZODIAZEPINES, IT POSSESSES
ANXIOLYTIC PROPERTIES BUT UNLIKE OTHER
BENZODIAZEPINES IT DOES NOT HAVE
ANTICONVULSANT*, SEDATIVE, SKELETAL MUSCLE
RELAXANT, MOTOR SKILL-IMPAIRING OR
AMNESTIC PROPERTIES.
*WHILE IT MAY NOT BE AN ANTICONVULSANT IN AND OF ITSELF, IT HAS BEEN SHOWN TO ENHANCE THE ANTICONVULSANT ACTION OF CLASSICAL 1,4-BENZODIAZEPINES SUCH AS
DIAZEPAM.
BETTER RESOLUTION OF ANXIETY & EXISTING
DEPRESSION WITHOUT SEDATION, MUSCLE
RELAXATION
CLIN.TRIAL SUGGEST IT TO BE USEFUL IN ANXIETY
DISORDERS, ANXIETY NEUROSIS, MIXED ANXIETY
DEPRESSION, SOMATOFORM DISORDER, ALCOHOL
WITHDRAWAL, MENOPAUSAL SYNDROME
BINDS TO 2,3 BDZS
SITES IN THE
SUBCORTICAL AREA.
IT DOES NOT BIND TO
GABA-A RECEPTOR
COMPLEX IN
CORTICAL AREAS
59. B) SELECTIVE SEROTONIN REUPTAKE INHINITOR
• SEROTONIN IS A KEY NEUROTRANSMITTER
THAT INNERVATES THE AMYGDALA AS WELL
AS ALL THE ELEMENTS OF CSTC CIRCUITS,
NAMELY, PREFRONTAL CORTEX, STRIATUM,
AND THALAMUS, AND THUS IS POISED TO
REGULATE BOTH FEAR AND WORRY.
• ANTIDEPRESSANTS THAT CAN INCREASE
SEROTONIN OUTPUT BY BLOCKING THE
SEROTONIN TRANSPORTER (SERT) ARE ALSO
EFFECTIVE IN REDUCING SYMPTOMS OF
ANXIETY AND FEAR IN EVERY ONE OF THE
ANXIETY DISORDERS
60. SOME WIDELY USED SSRIs
• FLUOXETINE
• PAROXETINE
• ESCITALOPRAM
• SERTRALINE
• FLUVOXAMINE
• SIDE EFFECTS: STOMACHACHE, INCREASED ACTIVITY
LEVEL, INSOMNIA, AGITATION/DISINHIBITION AT
HIGHER DOSES
• LESS OFTEN DIARRHEA, HEADACHES, TICS,
CRAMPS/TWITCHING, SEXUAL SIDE EFFECTS.
• START AT A LOW DOSE AND INCREASE SLOWLY
BASED ON TREATMENT RESPONSE AND SIDE EFFECTS
61. C) NOREPINEPHRINE REUPTAKE INHIBITOR
SYMPTOMS OF HYPERAROUSAL SUCH AS
NIGHTMARES CAN BE REDUCED AND WORRY
CAN BE REDUCED BY NOREPINEPHRINE
REUPTAKE INHIBITORS (ALSO CALLED NET OR
NOREPINEPHRINE TRANSPORTER INHIBITORS).
HYPERACTIVITY OF CSTC
NRI ACTION ON NE NEURONAL
OUTPUT TO CSTC
63. OTHER COMMONLY USED DRUGS
• GABAPENTIN AND PREGABALIN
• ALSO KNOWN AS α2δ LIGANDS
• BIND TO THE α2δ SUBUNIT OF PRESYNAPTIC N AND P/Q VSCCS, BLOCK THE
RELEASE OF EXCITATORY NEUROTRANSMITTERS SUCH AS GLUTAMATE WHEN
NEUROTRANSMISSION IS EXCESSIVE.
• THEY HAVE DEMONSTRATED ANXIOLYTIC ACTIONS IN SOCIAL ANXIETY
DISORDER AND PANIC DISORDER
• 5-HT1A RECEPTOR PARTIAL AGONIST - BUSPIRONE
64. OTHER COMMONLY USED DRUGS
• MONOAMINE OXIDASE INHIBHITORS
• HYDROXYZINE
• ANTI-PSYCHOTICS – HAS LIMITED EVIDENCE AND HIGH SIDE EFFECTS
• PROPRANOLOL & OXPRENOLOL- LICENSED TO TREAT ANXIETY
SYMPTOMS- USED IN PTSD
65. PSYCHOTHERAPY IN ANXIETY DISORDER
NUMEROUS STUDIES HAVE SHOWN THE IMPORTANCE OF
COMBINING PSYCHOTHERAPY WITH PHARMACOTHERAPY IN
ANXIETY DISORDERS.
66. Psychotherapy was significantly more efficacious than pharmacotherapy in obsessive-compulsive
disorder (g=0.64). Furthermore, pharmacotherapy was significantly more efficacious than non-directive
counseling (g=0.33), and psychotherapy was significantly more efficacious than pharmacotherapy with
tricyclic antidepressants (g=0.21).
67. There was sufficient evidence that combined treatment is superior for major depression, panic disorder, and
obsessive compulsive disorder (OCD). The effects of combined treatment compared with placebo only were
about twice as large as those of pharmacotherapy compared with placebo only, underscoring the clinical
advantage of combined treatment. The results also suggest that the effects of pharmacotherapy and those of
psychotherapy are largely independent from each other, with both contributing about equally to the effects of
combined treatment.
69. BEHAVIOUR THERAPY
• EXPOSURE AND RESPONSE PREVENTION
• SYSTEMATIC DESENSITIZATION
• IMPLOSIVE THERAPY/FLOODING
• ANXIETY MANAGEMENT
• RELAXATION TECHNIQUES – YOGA, ZEN, JPMR
• BIOFEEDBACK
• DESENSITIZATION OF THE STIMULUS
• EYE MOVEMENT DESENSITIZATION AND REPROCESSING
• SOCIAL SKILLS TRAINING
70. COGNITIVE BEHAVIOUR THERAPY
• CONTROL OF AUTOMATIC THOUGHTS
• CORRECTION OF COGNITIVE ERRORS
• BREAKING THE ASSOCIATION BETWEEN THE EVENTS, COGNITIVE
AROUSAL AND MALADAPTIVE BEHAVIOUR
71. PSYCHOANALYTIC PSYCHOTHERAPY
• THE PSYCHOANALYTIC PROCESS INVOLVES BRINGING TO THE SURFACE
REPRESSED MEMORIES AND FEELINGS BY MEANS OF A SCRUPULOUS
UNRAVELING OF HIDDEN MEANINGS OF VERBALIZED MATERIAL AND OF
THE UNWITTING WAYS IN WHICH THE PATIENT WARDS OFF UNDERLYING
CONFLICTS THROUGH DEFENSIVE FORGETTING AND REPETITION OF THE
PAST.
72. PSYCHOANALYTICALLY ANXIETY IS CLASSIFIED
INTO 4 TYPES
THE CLASSIFICATION IS BASED ON THE TYPES OF PRIMARY COMPLEX AND
THE SUBSEQUENT NATURE OF ITS CONFLICT WITH THE EGO (CONSCIOUS
MIND).
1. TRAUMATIC ANXIETY (PANIC ATTACK) – EGO BECOMES PARALYSED
2. SEPARATION ANXIETY – SEPARATION FROM LOVED/VALUABLE OBJECTS
3. CASTRATION ANXIETY – LOSS OF LOVED/VALUABLE OBJECT
4. SUPEREGO ANXIETY
DEPENDING ON THE TYPE OF ANXIETY PSYCHOANALYTIC METHODS ARE
ADAPTED.
