10 - CNS Pharmacology 2 Flashcards
1
Q
Seizure VS. Epileptic Seizure VS. Non- Epileptic Seizure
A
Seizure: A sudden alteration of behaviour that is caused by CNS dysfunction.
→ Seizures are sudden and transient.
Epileptic Seizure: A seizure that is caused by primary CNS dysfunction
→ due to excess depolarization and hypersynchronization of neurons.
Non-Epileptic Seizure – A seizure-like episode that is not the result of abnormal electrical activity in the brain
Epilepsy: A tendency for recurrent spontaneous epileptic seizures.
Status Epilepticus: A single unremitting epileptic seizure of duration longer
than 30 minutes OR frequent seizures without recovery of awareness in
between.
→Status epilepticus is an emergency
2
Q
What is Epilepsy?
A
Epilepsy: a neurological disorder that
produces brief disturbances in the normal electrical activity in the brain.
- characterized by sudden, brief seizures
- nature and intensity of seizures vary from person to person
3
Q
Types of Seizures
A
1) Focal/Partial Seizures
→ Simple Partial
→ Complex Partial
2) Generalized Seizures
→ Absence
→ Myoclonic
→ Atonic
3) Secondary Generalized Seizures
4
Q
1) Focal/Partial Seizures
A
These seizures arise in one area of
the brain.
→ The terms focal seizure and partial
seizure are interchangeable.
→ 2 types of focal/partial
seizures:
1. Simple partial seizure
2. Complex partial seizure
5
Q
a. Simple partial seizure
A
Involve no loss of consciousness.
- Sudden, transient, and brief
- Symptoms depend on where the seizure activity is arising from.
Ex Case.
→45 year old man
→Clonic movements of right arm
→ Progression to right face then
right leg (seizure is in L side of brain)
→No impairment of consciousness
→ Lasting ~ 45 seconds
→ MRI – L motor strip oligodendroglioma
6
Q
b. Complex partial seizure
A
- A complex partial seizure involves loss of consciousness
- Patients may appear to be awake, but are not aware of surroundings.
- Symptoms depend again on where the seizure activity is taking place.
Ex Case:
→37 year-old man with right temporal lobe epilepsy.
→ Whistling; bicycling movements in left leg (activity of seizure is in L side of body)
→ Rising epigastric sensation with nausea.
→Normal ictal speech.
→No memory of the events post-ictally (i.e. after seizure).
→Duration: 30 – 45 seconds.
7
Q
2) Generalized Seizure
A
- These seizures have a bilateral,
diffuse onset, seeming to arise
from all areas of the brain at once.
5 types of
generalized seizures:
1. Absence seizures
2. Tonic/Clonic seizures
3. Myoclonic seizures
4. Tonic seizures
5. Atonic seizures
8
Q
a. Absence seizures
A
- Also called “petit-mal” (an older name).
- Involve loss of consciousness
- Typical Symptoms: behavioural arrest and staring
- Are usually brief but may occur in clusters and can recur multiple times in a day.
- Rarely associated with automatisms (unusual purposeless movements), usually minor if there are any
- More common in childhood
→ can be misdiagnosed as a child staring into space - can measure the activity in the brain with an EEG
9
Q
b. Tonic/Clonic seizures
A
Tonic clonic seizures involve:
- An abrupt loss of consciousness
- at the beginning of the seizure, A tonic period (muscles become rigid), lasting ~ 1 minute
- A clonic period (involuntary muscle contractions), lasting and additional 2-3 minutes
- Patients may become incontinent and have tongue biting.
- In the post-ictal phase patients may be drowsy, confused and frequently
complain of headaches. - Used to be called “Grand-mal seizure”
10
Q
c. Myoclonic seizures
A
- These seizures involve sudden, brief muscle contractions that can involve
any muscle group. - Usually there is no loss of consciousness.
- Sometimes they are associated with a later development of generalized
tonic-clonic seizures.
11
Q
d. Tonic seizures
A
- Often involve sudden muscle stiffening (rigidity).
- Often involve impaired consciousness.
12
Q
e. Atonic seizures
A
- Involve sudden loss of muscle tone.
- Usually brief, around 15 seconds.
- Also known as “drop seizures”, as patients typically drop to the ground.
- Potential for falling injuries
13
Q
3) Secondary Generalized Seizure
A
- A seizure that begins in one area
of the brain (like a focal seizure)
and then spreads throughout the
brain. - The preliminary focal phase is
sometimes referred to as an
“aura”.
14
Q
Localizing Focal Seizures
A
- The location of a focal seizure can be determined by evaluating the patient’s symptoms and what we know about the various regions of the brain.
15
Q
Frontal Lobe
A
- Simple repetitive motor movements
involving a localized muscle group are
associated with seizure activity in the
contralateral (opposite side of the brain) primary motor cortex
→ movements in R side of body are linked to seizure activity in the L side of brain - Tonic posturing affecting the entire side of the body are associated with seizure activity in the contralateral Supplemental Motor Area (SMA) and other higher level motor structures.
- Very complex behavioural automatisms that involve bilateral movement (swimming or bicycle riding movements) are associated with seizure activity in higher areas of the frontal cortex.
- These behaviours often involve vocalizations, laughter and/or crying.
16
Q
Temporal Lobe
A
- Emotions such as anger, fear,
euphoria and psychic symptoms
such as déjà vu, jamais vu or
amnesia are associated with seizure
activity in the temporal lobe. - Auditory (hearing) hallucinations of
buzzing or voices talking, and
olfactory (smell) and gustatory
(taste) hallucinations are associated
with the temporal lobe. - More complex sensory phenomena,
involving visual distortions,
paresthesias (i.e. numbness) and
autonomic disturbances can also be
associated with temporal lobe
seizures.
17
Q
Parietal Lobe
A
- Localized paresthesias, such as
numbness and “pins and needles”,
are associated with seizure activity
in the contralateral somatosensory
cortex
. - More complex and widespread paresthesias are associated with
seizure activity in the somatosensory association cortex
. - Seizure activity in the higher order
sensory association areas in the
parietal lobe can be associated
with complex multi-sensory
hallucinations and illusions
→ Can be hard to distinguish from
temporal lobe seizure activity, which is more common
18
Q
Occipital Lobe
A
- Visual hallucinations, such as flashing
or a repeated pattern in the
environment, are associated with
seizure activity in the occipital lobe. - The hallucinations are less likely to be
of organized objects such as people
or faces. - Seizure activity in the occipital lobe
can also produce temporary blindness
or decreased vision, as well as the
sensation of eye movement. - Patients can have reflex nystagmus
(involuntary eye movement). - Simple partial seizures in the occipital lobe can be mistaken for migraine
headaches, as many of the symptoms are similar to common migraine auras.
19
Q
Epileptogenesis
A
3 main classifications for the etiology of epilepsy:
- Symptomatic epilepsy
→Epilepsy arising from an identified physical cause, such as a brain tumor, stroke, infection, or other injury. - Idiopathic Epilepsy
→Epilepsy that does not have an identifiable cause; there is often a family history of seizures, and genetics likely play a role - Cryptogenic epilepsy
→Epilepsy that is likely to have an underlying cause that has not been identified classified as cryptogenic until healthcare professional can determine the underlying cause
20
Q
The Seizure Threshold
A
- Seizures are caused by spontaneous, uncontrollable discharges from
hyperexcitable areas of the brain. - The seizure threshold can be thought of as the balance between excitable
and inhibitory forces in the brain. - Everybody has a seizure threshold and the seizure threshold affects how
susceptible a patient is to having a seizure. - Keep in mind that seizures are mediated by changes in electrical activity, so the ability to reach threshold and fire an action potential is important in the generation of a seizure.
- Factors that affect seizure threshold are: stroke, head injury, drug/alcohol withdrawal, infection, tumour, severe fever, visual stimuli (flashing lights)
21
Q
Antiepileptic Drugs (AED’S)
A
- Antiepileptic drugs work by four distinct mechanisms of action:
- Blocking sodium channels.
- Blocking voltage-dependent calcium channels.
- Glutamate antagonists
- Potentiating the actions of GABA
22
Q
1) Blocking sodium channels
A
- Sodium influx into the cell is a critical step in the generation of an action potential (excess firing of AP’s causes a seizure)
- After sodium enters the cell, the sodium channel enters an inactive state
during which time further sodium entry to the cell is prevented (another AP can not fire) - In normal cases, the sodium channel very quickly returns to the active
state to allowing more sodium to enter the cell to generate another action
potential - Sodium channel blocker AEDs act to prolong the inactivation state of the
sodium channel and therefore don’t allow neurons to fire at a high frequency
23
Q
Phenytoin
A
- the most widely used AED and
acts by blocking sodium channels. - Phenytoin is useful in the
treatment of all types of epileptic
seizures except absence seizures. - The metabolic capacity of the liver
to metabolize phenytoin is limited.
→ phenytoin displays nonlinear kinetics (a small increase in dose may produce a large increase in plasma concentration)
→ drugs with linear kinetics: increasing dose of drug linearly = linear increase of steady state plasma concentration - Phenytoin has a narrow therapeutic range and undergoes therapeutic drug monitoring.
- Adverse effects of phenytoin include sedation, gingival hyperplasia, skin
rash. - Phenytoin is teratogenic
→ should not be used in pregnant women
24
Q
2) Blocking voltage-dependent calcium channels.
A
- Influx of calcium through voltage-dependent calcium channels promotes
neurotransmitter release from the pre-synaptic nerve terminal - AP opens Ca channels = release of NT = activation of next neuron
- Inhibition of calcium channels suppresses neurotransmitter release
- Ca channel blockers inhibit Ca from entering pre-synaptic nerve terminal and does not allow release of NT to activate next neuron
→ prevents uncontrollable firing of AP’s; which prevents seizures
25
3) Glutamate antagonists
- Glutamate is an excitatory CNS neurotransmitter
- Blocking glutamate decreases CNS excitation and is therefore a treatment
target for AED’s.
- Glutamate mediates its effects by binding to either: 1) the NMDA receptor
or 2) the AMPA receptor
- Glutamate antagonists (used to treat epilepsy) block both the NMDA and
AMPA receptors and therefore prevent excitation in the CNS.
26
4) Potentiating the actions of GABA
The GABA Receptor
- GABA is an inhibitory CNS
neurotransmitter.
- Binding of GABA to its receptor
causes negatively charged Cl- ions
to rush into the cell.
- Increased negative charge in the
cell will make it more difficult for
threshold to be reached and
therefore more difficult to have an
action potential
→ resting membrane potential (-70), if GABA is open, it causes negative charges to enter the cell and causes threshold to decrease further (-90)
27
Potentiating the Actions of GABA
- Drugs that potentiate the actions of GABA increase inhibitory stimuli in the
CNS and therefore suppress seizure activity.
- Drugs that potentiate the actions of GABA can mediate their effect 4 ways:
1. Enhancing binding of GABA to its receptor.
2. Stimulating GABA release.
3. Inhibiting GABA reuptake.
4. Inhibiting GABA metabolism.
28
Antiepileptic Drugs
- AEDs can be classified as
1) traditional
→ phenytoin
→valproic acid
2) newer AEDs
→ lamotrigine
- The effectiveness of traditional vs. newer AEDs appears to be similar.
- Newer AEDs tend to have decreased side effects and a decreased
propensity to induce hepatic drug metabolizing enzymes (less susceptible to drug-drug interactions)
29
Depression
- Occasional feelings of depression are
normal, as are grief and sadness following any form of loss.
- When these symptoms are prolonged and interfere with everyday life, depression may be diagnosed.
- Depression occurs in 1/3 of
people at some time in their life.
30
Types of Depression
- Depression can be classified into 2 major types: exogenous or endogenous.
Exogenous depression
→triggered by external stimuli
Endogenous depression
→may or may not be related to external events.
31
Diagnosis of Depression
- For a diagnosis of depression, at least 5 of the following symptoms must
occur for at least 2 weeks:
→Depressed mood most of the day, nearly everyday.
→Loss of interest or pleasure in all or almost all activities.
→Significant weight loss (without dieting) or weight gain.
→ Insomnia or hypersomnia.
→Psychomotor agitation or retardation.
→Fatigue and energy loss.
→ Feelings of worthlessness or excessive guilt
→ Decreased ability to think, concentrate, or excessive
indecisiveness.
→ Recurrent thoughts of death or suicidal ideations.
32
Exogenous Depression
1) Pathological grief
→Prolonged grieving
coupled with excessive guilt.
→ Psychotherapy is usually a more effective treatment
2) Adjustment disorder
→Prolonged depression following failure or rejection (i.e. losing your job, failing out of school).
→ Common symptoms include hypersomnia (excess sleep) and hyperphagia (overeating). →Psychotherapy is often more
effective than drug therapy.
33
Endogenous Depression
1) Major depression
→ Common symptoms include loss of interest and lack of response to positive stimuli
→Symptoms are usually worse in the
morning
→Insomnia and weight loss are also typical.
2) Severe depression
→Similar symptoms to major depression
→addition of severe suicidal ideation and psychoses.
3) Atypical depression
→ Similar symptoms to major depression but patients have the atypical symptoms of hypersomnia and hyperphagia
→ patients with atypical depression are obese
4) Dysthymia
→The patient’s mood is regularly low but symptoms are not as severe as major depression
→Symptoms are usually more noticeable to family members/close friends than they are to the patient. →Usually responds better to psychotherapy than to drugs.
5) Seasonal Affective Disorder (SAD)
→ Mild or moderate symptoms of depression related to the
lack of sunlight
→Usually only affects people in the
winter months.
6) Postpartum Depression
→Moderate to severe depression in women after they give birth
→Usually occurs within 3 months of delivery but may occur up to a year after birth.
7) Bipolar Disorder
→Alternating periods of elevated
or irritable mood and periods of depression.
34
The Monoamine Hypothesis
- The exact cause and pathophysiology of depression are unknown
- The major hypothesis for depression
is the monoamine hypothesis.
- This hypothesis suggests that altered monoamine release, receptor
sensitivity, or post-synaptic function lead to symptoms of depression.
Ex in support of this hypothesis:
→ Jim, a 20 year old university student goes to a rave Saturday night and takes ecstasy, a drug that depletes the neurotransmitter serotonin (5-HT). Jim has a great time at the rave. The next week Jim lacks motivation to study for his classes, doesn’t leave his couch, and thinks his life is going nowhere
→ drugs that increase serotonin are effective at treating depression symptoms
35
Antidepressants
- Antidepressant drugs act to increase the synaptic levels of one or more
monoamine neurotransmitters.
- The efficacy of antidepressants is difficult to assess since it often takes
months for effects to occur
- Results from placebo-controlled clinical trials suggest that 40% of the effects observed may be attributed to the placebo effect.
- Antidepressant drugs mediate their effects by 2 mechanisms:
1. Inhibiting monoamine reuptake (into pre-synaptic nerves)
2. Inhibiting monoamine metabolism (more monoamine are able to be released)
36
Classes of Antidepressant Drugs
There are 4 major classes of drugs used to treat depression:
1. Tricyclic Antidepressants
2. Selective Serotonin Reuptake Inhibitors (SSRIs)
3. Selective Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs)
4. Monoamine Oxidase Inhibitors (MAOIs)
37
1) Tricyclic Antidepressants
- Their name stems from their chemical structure which has 3 rings, hence tricyclic.
- TCAs act by inhibiting the reuptake of both serotonin and norepinephrine
→ if AP is fired and NT is released, it blocks reuptake of NT and allows it stay in synaptic cleft longer and mediate effect
→ TCA's increase serotinergic and norepinephrin neurotransmission
- Effective in the treatment of major depression
38
Adverse Effects of Tricyclic Antidepressants
- Anticholinergic effects
- Sedation
- Orthostatic hypotension
- Decreased seizure threshold
- Cardiac toxicity – rare but potentially serious (can cause death)
- Weight gain
- Sexual dysfunction
39
2) Selective Serotonin Reuptake Inhibitors (SSRIs)
- Similar mechanism of action to TCA’s
but they only block serotonin reuptake.
- SSRIs have similar efficacy to TCA’s but the incidence of side effects is lower.
- SSRIs are the most commonly used
treatment of depression and are most
commonly used in major depression.
40
Adverse Effects of Selective Serotonin Reuptake Inhibitors
(SSRIs)
- Weight gain
- Sexual dysfunction
- Insomnia
- Serotonin syndrome
→ increased serotonin transmission which results in agitation, confusion, anxiety, hallucinations and incoordination.
- Symptoms may appear within 3 days of initial therapy and disappear when the drug is stopped
41
3) Selective Serotonin/Norepinephrine Reuptake Inhibitors (SNRIs)
- SNRIs block the re-uptake of both norepinephrine and serotonin and are
effective treatments of major depression.
- main advantage is faster onset of action (faster at treating symptoms)
- How are they different than TCAs? →They do not have the characteristic
3 ring structure that TCAs have
→ but the MOA of SNRIs is very similar to TCAs.
42
Adverse Effects of SNRIs
- Nausea
- Diastolic hypertension
- Sexual dysfunction
43
4. Monoamine Oxidase Inhibitors (MAOIs)
- Monoamine oxidase (MAO) is an enzyme that inactivates monoamine
neurotransmitters
- 2 types of MAO:
1) MAO-A: metabolizes serotonin and norepinephrine
2) MAO-B: metabolizes dopamine
- MAO inhibitors used to treat depression are non-selective and inhibit MAO-A and MAO-B.
- MAO inhibitors treat atypical depression and dysthymia
- MAO inhibitors mediate their effects by inhibiting the metabolism of
monoamines in the pre-synaptic neuron
→ MOA enzyme is blocked = does not metabolize MOA NT = more MOA NT remain in pre-synaptic nerve terminal = can be released and act when AP fires
44
Adverse Effects of MOI's
- CNS excitation – anxiety, insomnia, agitation.
- Orthostatic hypotension
- Hypertensive crisis if taken with tyramine containing foods
45
Bipolar Disorder
- severe illness characterized by recurrent fluctuations between
episodes of mania and depression.
- Symptoms usually begin in adolescence or early adulthood.
- The manic phase consists of symptoms such as:
→Irritation
→ Inflated self-esteem (delusions of grandeur)
→Little need for sleep
→ Poor control of temper
→ Reckless behaviour (binge eating, drinking, drug use)
→ Easily distracted
- The symptoms experienced during the depressive phase are similar to the
ones described in depression
46
Pattern of Mood Episodes
- Not all patients cycle repeatedly between episodes of mania and
depression
→ ppl can experience repeated mania with occasional depression and others may experience repeated depression with occasional mania.
- The duration of each episode can also vary substantially from a day to over a year.
- patients with bipolar disorder experience approximately 2
episodes every 5 years.
47
Drug Treatment of Bipolar Disorder
Bipolar disorder is treated with 3 major groups of drugs:
1. Mood Stabilizers
2. Antipsychotics
3. Antidepressants
48
1) Mood Stabilizers
Mood stabilizers are drugs used to:
1. Relieve symptoms during manic or depressive episodes
2. Prevent recurrence of manic or depressive episodes
3. Do not worsen symptoms of mania or depression and do not alter the
rate of cycling
- The primary drugs used as mood stabilizers are : 1) lithium and 2)
antiepileptic drug valproic acid
49
Lithium
- Although the mechanism of action of lithium is not clear, it is suggested to
work by altering the uptake and release of glutamate and blocking the binding of serotonin.
- Lithium has a narrow therapeutic range and plasma concentrations may
be altered by sodium
- Agents that increase sodium loss from the body (i.e. diuretics) increase
lithium concentrations and may produce toxicity including GI upset,
tremor, sedation and hypotension.
50
2) Antipsychotics
- used in bipolar disorder acutely to control symptoms during manic
episodes and long term to help stabilize mood.
- Antipsychotic drugs benefit patients with bipolar disorder even if they don’t
have psychotic symptoms.
- Atypical antipsychotics are preferred over conventional antipsychotics due to the their lower risk of extrapyramidal symptoms
51
3) Antidepressants
- Antidepressants are used in bipolar disease to treat depressive episodes.
- Antidepressants are always combined with a mood stabilizer.
- if antidepressants were used alone, they may precipitate a manic episode.
- there is no good evidence for which antidepressant works best in bipolar disorder
52
Anxiety
- Anxiety is a normal physiological response to stress.
- In contrast, an anxiety disorder exists when the symptoms of anxiety create
a functional impairment in a
patient’s daily living.
- Anxiety and depression are
closely linked; patients that have an anxiety disorder are likely to also suffer from depression
53
Types of Anxiety
Anxiety disorders fall in 7 general categories:
1)General anxiety disorder
2) Panic Disorder
3) Agoraphobia
4) OCD
5) Social anxiety disorder
6) Post-traumatic stress disorder
7) Simple Phobia
54
2) Panic Disorder
- Patients have a sense of impending doom that is unrelated to stressors.
- They experience panic attacks, which are sudden in onset
- symptoms include: heart palpitations,
chest pain, shortness of breath, dizziness
→ often confused for a heart attack
54
1) General anxiety disorder
- Patient is overwhelmed with
uncontrollable worrying.
- Hallmark: an unrealistic or excessive
worry about several activities that lasts 6 months or longer
55
3) Agoraphobia
- An anxiety where the patient feels judged or a situational anxiety where escaping would be difficult or embarrassing.
56
4) Obsessive-compulsive disorder
- Persistent obsession and compulsions that interfere with daily life (i.e. handwashing, checking locks).
57
5) Social anxiety disorder
- Anxiety in social situations
- Patients may not be able to talk (or stop talking), eat in front of others, or use public washrooms.
58
6) Post-traumatic stress disorder
- Anxiety that occurs after experiencing a traumatic event
- Symptoms may include reexperiencing the event and severe insomnia.
59
7) Simple Phobia
- Symptoms are related to a specific fear (i.e. spiders, elevators).
60
Drug Treatment for Anxiety
1. Benzodiazepines (BDZs)
2. Buspirone
3. Antidepressants
61
1) Benzodiazepines (BDZs)
- Benzodiazepines are the 1st line therapy for anxiety.
- They act by potentiating the actions of GABA at the GABA receptor.
*Note that benzodiazepines are NOT GABA agonists.*
→They bind to a different site on the GABA receptor and cause increased binding of GABA to the receptor*
- When GABA binds to the receptor, it opens a channel and chloride ions
move into the cell. This causes CNS depression.
- Because BDZs amplify the actions of endogenous GABA and are not
GABA agonists, there is limit to how much CNS depression they may
produce
→makes them much safer than GABA agonist drugs (ie. barbiturates)
62
Therapeutic Uses of Benzodiazepines
Benzodiazepines have several therapeutic actions. They are used to treat:
1. Anxiety
2. Seizures
3. Insomnia
4. Alcohol withdrawal
5. Muscle spasm
- Different dosages are used to produce different effects
→ ex. a higher dose of BDZ is used to treat insomnia than anxiety
- In terms of anxiety, BDZs are effective in treating generalized anxiety
disorder and social anxiety disorder
63
Adverse Effects of Benzodiazepines
1) CNS depression – drowsiness, difficulty concentrating.
2) Anterograde amnesia – impaired memory of events that occur following
dosing.
3) Respiratory depression – is rare with BDZ’s however more common if
combined with alcohol.
4) Teratogenic
5) Tolerance
→occurs to some effects but not others
→No tolerance to anxiolytic effects or sedative effects but tolerance does develop to the effect on seizures.
6) Withdrawal
→the dose of BDZ’s should be tapered slowly to avoid withdrawal.
64
2) Buspirone
- Buspirone is not a CNS depressant
- acts to treat anxiety in a
mechanism distinct from BDZs (it is its own class)
- Although the mechanism of action for buspirone is unclear, it appears to
involve modulation of serotonergic and/or dopaminergic neurotransmission.
- Advantage: Since buspirone is not a CNS depressant, it is useful in treating anxiety in patients who use alcohol.
- Buspirone is used for the treatment of generalized anxiety disorder
→ ineffective in the treatment of other types of anxiety (i.e. panic disorder, obsessive compulsive disorder).
- Buspirone shows no signs of tolerance or physical dependence.
- Disadvantage: that its anxiolytic effects develop slowly
→ineffective at treating symptoms that require immediate relief
Adverse effects
→buspirone is well tolerated
→ is non-sedating.
→adverse effects: dizziness,
lightheadedness and excitement
65
Antidepressants
- Antidepressant drugs are useful in the treatment of certain types of
anxiety:
1) Generalized anxiety disorder
→SSRIs and SNRIs are effective, but like buspirone are slow to generate their effect.
2) Panic Disorder/Agoraphobia
→SSRIs, TCAs and MAO inhibitors are useful but effects take 6-12 weeks to appear
→SSRIs are preferred because they are better tolerated than TCAs and MAO inhibitors.
3) Obsessive Compulsive Disorder (OCD)
→SSRIs are the first line therapy.
→Patients with OCD also require behavioural therapy
4) Social Anxiety Disorder
→SSRIs are the first line therapy although BDZ’s may also be used
→BDZ’s provide immediate relief from symptoms whereas SSRIs require time for the effect to occur
5) Post-Traumatic Stress Disorder
→There is no good evidence that
antidepressants or other drugs are effective in treating PTSD.
