2023 Sedative-Hypnotics D. Chanitos.N.ppt

CNS DRUGS
BY:
DANIEL CHANS.M (MPS)
BPharm, MScPHA, MPharm Clinical Pharm
Pharmacology and Therapeutics Dept
Daniel Chans. M 2022 1

Clinical Scenario…
• A 21-year-old college woman is involved in her
first serious dating relationship.
• Like many young women, she wants to look and
feel her best.
• While flipping through a clothing catalogue, she
notices the attractiveness of several female
models.
• She wonders anxiously if it means she is gay.
• She repeatedly asks her boyfriend for
reassurance, sometimes to his annoyance.

…
• The young woman avoids being alone with most
other women for fear of somehow losing self-
control and sexually acting out.
• She prays to God continually for forgiveness.
• When an obsessive idea is triggered, she tells
herself three times that she loves her boyfriend,
and mentally rehearses all the ways he makes
her feel good.
• WHAT DO YOU THINK IS WRONG??

• MINOR TRANQUILIZERS
– SEDATIVES-HYPNOTICS AND ANXIOLYTICS
• MAJOR TRANQULIZERS
– ANTIPSYCHOTICS/NUEROLEPTICS
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SEDATIVE-HYPNOTIC AND ANXIOLYTIC DRUGS
• A sedative is a drug that reduces a person’s response to
external stimuli and causes drowsiness.
• A hypnotic is a drug that induces sleep.
• An anxiolytic drug is an agent that reduces anxiety.
• ANXIETY is an adaptive response that prepares a person
to react to a threatening event.
• It is characterized by changes in mood (apprehension and
fear), physiologic arousal, and increased perceptual acuity
(hypervigilance).
• Chronic anxiety is a maladaptive response to psychological
stress and may impair a person’s ability to perform daily
activities.
6
Daniel Chans. M 2022

• Chronic anxiety contributes to organ dysfunction and may cause
diarrhea, tachycardia, sweating, tremors, and dizziness.
• Anxiety disorders include:
* Acute anxiety disorder (often self-limiting).
* Panic disorder (characterized by feelings of an impending
sense of doom, accompanied by sweating, tachycardia, tremor,
and other visceral symptoms).
* Phobic disorders (an individual becomes overly fearful
about a particular condition).
* Obsessive-compulsive disorder (obsessions are recurring
or persistent thoughts and impulses; compulsions are repetitive
behaviors in response to obsessions).
* Generalized anxiety disorder (a persistent state of fear and
apprehension concerning future events).
7

• SLEEP is a reversible state of reduced consciousness
accompanied by characteristic changes in the
electroencephalogram (EEG).
• Stages 1 – 3 of sleep are collectively called non-rapid eye
movement (NREM) sleep, and stage 4 is called rapid eye
movement (REM) sleep.
• Sleep disorders include:
* insomnia
* hypersomnia (difficulty awakening)
* narcolepsy (sleep attacks)
* sleep apnea (episodes of hypoventilation during sleep)
* nightmares and night terrors
8

SEDATIVES – HYPNOTICS
• Sedative: A drug that subdues excitement and calms the subject without
inducing sleep, though drowsiness may be induced.
• Sedation refers to the decreased responsiveness to any level of
stimulation; is associated with some decrease in motor activity and
ideation.
• A sedative shd reduce anxiety and exert a calming effect
• Hypnotic: A drug that induces sleep and/or maintain sleep, similar to
normal arousable sleep.
• The sedatives and hypnotics are more less general CNS depressants with
somewhat differing time-action and dose-action relationships.
• Those with quicker onset, shorter duration and steeper dose response
curves are preferred as hypnotics while more slowly acting drugs with
flatter dose response curves are employed as sedatives.
• a hypnotic at lower dose may act as sedative.
• Thus, sedation - hypnosis - general anaesthesia may be regarded as
increasing grades of CNS depression.
• Hypnotics given in high doses may produce general anaesthesia.
10

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Intermediate acting
CC: Slideshare
BZDS
• Hypnotic
• Anxiolytic
• Anticonvulsant

CLASSIFICATION of SEDATIVE-HYPNOTICS
• Barbiturates: classified on the basis of onset of
action and duration of action.
• Ultra -short acting e.g Thiopentone,
methohexital
• Short acting e.g Pentobarbitone, Secobarbitone
• Intermediate acting e. g Butabarbitone,
Aprobarbitone
• Long acting e. g Phenobarbital
13

Benzodiazepines: May be divided according to
primary use—
• Hypnotic e. g Diazepam, flurazepam, nitrazepam,
flunitrazepam, temazepam, triazolam, midazolam.
• Antianxiety e. g Diazepam, oxazepam, lorazepam,
alprazolam, chlordiazepoxide
• Anticonvulsant e. g Diazepam, clonazepam, clobazam
, nitrazepam, midazolam
Newer non benzodiazepine hypnotics
• Eszopiclone, zaleplon, Zolpidem, zopiclone (Z-
drugs)
• Ramelton (a melatonin MT1 and MT2 receptor
agonist)
• Buspirone (slow-onset anxiolytic agent )

Other classes of drugs that exert sedative effects
• Antipsychotics, opioid analgesics
• Antidepressant drugs (eg TCAs, used widely in
management of chronic anxiety disorders.)
• Certain antihistaminic (H1) agents including hydroxyzine
and promethazine are also sedating.
• Glutethimide and meprobamate are of distinctive
chemical structure but are practically equivalent to
barbiturates in their pharmacologic effects.
• Their clinical use is rapidly declining.
• ALSO ethanol and chloral hydrate, paraldehyde..etc
• Some anticonvulsants (eg pregabalin, Gabapentin, etc)

• BARBITURATES
• Barbiturates - Prototype of CNS depressants.
• Barbiturates are substituted derivatives of barbituric
acid (malonyl urea).
• Barbiturates have variable lipid solubility, the more
soluble ones are more potent and shorter acting.
• They are insoluble in water but their sodium salts
dissolve yielding highly alkaline solution.
• PHARMACOLOGICAL ACTIONS
• Barbiturates are general depressants for all
excitable cells, the CNS is most sensitive where the
effect is almost global, but certain areas are more
susceptible. 17

• CNS Barbiturates produce dose dependent effects:
sedation —> sleep —> anesthesia —> coma.
 Hypnotic dose of a short acting barbiturate shortens
the time taken to fall asleep and increases sleep
duration.
 Barbiturates can impair learning, short term memory
and judgment.
 They can produce euphoria in addicts.(feeling of
extreme happiness).
 They have no analgesic action; small doses may
even cause hyperalgesia

• Barbiturates depress all areas of the CNS, but the reticular
activating system is most sensitive; its depression is
primarily responsible for inability to maintain wakefulness.
Mechanism of action
• Barbiturates appear to act primarily at the GABA : BZD
receptor - C1- channel complex and potentiate
GABAergic inhibition by increasing the life time of Cl-
channel opening induced by GABA. (GABA facilitatory)
• At high concentrations, barbiturates directly increase Cl-
conductance (GABA-mimetic action; contrast BZDs
which have only GABA-facilitatory action) and inhibit Ca2+
dependent release of neurotransmitters.
• In addition they depress glutamate induced neuronal
depolarization through AMPA receptors.
• At very high concentrations, barbiturates depress Na+ and
K+ channels also. 19

GABA RECEPTOR
20

GABA-A RECEPTOR
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• Other Systems
• Respiration Is depressed by relatively higher doses.
Neurogenic, hypercapneic and hypoxic drives to respiratory
centre are depressed in succession.
• Barbiturates do not have selective antitussive action
• CVS Hypnotic doses of barbiturates produce a slight decrease
in BP and heart rate: magnitude of change not differing from
that during normal sleep.
• Toxic doses produce marked fall in BP due to ganglionic
blockade, vasomotor centre depression and direct decrease in
cardiac contractility.
• Skeletal muscle Hypnotic doses have little effect but
anaesthetic doses reduce muscle contraction by depressing
excitability of neuromuscular junction.
• Smooth muscles Tone and motility of bowel is decreased
slightly by hypnotic doses; more profoundly during intoxication.
• Kidney Barbiturates tend to reduce urine flow by decreasing
BP and increasing ADH release.
• Oliguria attends barbiturate intoxication. 22

• Barbiturates-PK
• Barbiturates are well absorbed from the GIT.
• They are widely distributed in the body.
• The rate of entry into CNS is dependent on lipid
solubility: highly lipid soluble thiopentone has
practically instantaneous entry while less lipid
soluble ones (pentobarbitone, secobarbitone) take
longer; phenobarbitone enters very slowly.
• Plasma protein binding varies with the compound,
e.g. thiopentone 75%, pentobarbitone 35%,
phenobarbitone 20%.
• Barbiturates cross placenta and are secreted in
milk; can produce effects on the foetus and
suckling infant.
23

• Three processes are involved in termination of action of
barbiturates: the relative importance of each varies with the
compound.
(a) Redistribution It is important in the case of highly lipid
soluble thiopentone and other ultrashort acting
barbiturates.
(b) After their i.v. injection, consciousness is regained in 8-12
mins due to redistribution while the ultimate disposal
occurs by metabolism (t½ of elimination phase is 9 hours).
• Effect of single dose of short acting barbiturate may last
just 6-10 hours due to redistribution, while elimination t½ is
15-50 hours.
(b) Metabolism: drugs with intermediate lipid solubility
(short acting barbiturates) are metabolized in the liver by
oxidation, dealkylation and conjugation.
(c) Excretion: Barbiturates with low lipid solubility (long
acting agents) are significantly excreted unchanged in
urine.
24

NB: Barbiturates induce hepatic microsomal
enzymes and increase the rate of their own
metabolism as well as that of many other drugs.
• USES
• Phenobarbitone is used in epilepsy and
thiopentone in anaesthesia.
• They are occasionally employed as adjuvants in
psychosomatic disorders. (read from Goodman and
Gillman)
• The enzyme inducing property of phenobarbitone
can be utilized to hasten clearance of congenital
non-haemolytic jaundice and kernicterus.
• Convulsions in neonates
25

• ADVERSE EFFECTS
• Side effects Hangover is common after the use of barbiturates as
hypnotic, because they have long plasma t½.
• On repeated nightly use they accumulate in body—produce tolerance
and dependence. Mental confusion, impaired performance and traffic
accidents may occur.
• Idiosyncrasy In an occasional patient barbiturates produce excitement.
This is more common in the elderly.
• Precipitation of porphyria in susceptible individuals.
• Hypersensitivity Rashes, swelling of eyelids, lips etc—more common in
atopic individuals.
• Tolerance and dependence: Tolerance develops on repeated use.
• However, fatal dose is not markedly increased: addicts may present with
acute barbiturate intoxication. There is partial cross tolerance with other
CNS depressants.
• Psychological as well as physical dependence occurs and barbiturates
have considerable abuse liability—one of their major disadvantages.
• Withdrawal symptoms are—excitement, hallucinations, delirium,
convulsions; deaths have occurred.
• Induction of CYP-450 (phenobarbital) 26

• Contraindications/precautions
1. Acute intermittent porphyria.
2. Liver and kidney disease.
3. Severe pulmonary insufficiency, e.g. emphysema.
4. Obstructive sleep apnoea.
• Interactions
1. Barbiturates induce the metabolism of many drugs and reduce their
effectiveness - warfarin, steroids (including contraceptives),
tolbutamide, griseofulvin, chloramphenicol, theophylline.
2. Additive action with other CNS depressants - alcohol,
antihistamines, opioids etc.
3. Sodium valproate has been found to increase plasma
concentration of phenobarbitone.
4. Phenobarbitone competitively inhibits as well as induces phenytoin
and imipramine metabolism: complex interaction.
5. Phenobarbitone decreases absorption of griseofulvin from the GIT
27

PROPERTIES OF SELECTED DRUGS

BENZODIAZEPINES
• BZDs are the most frequently prescribed sedative hypnotic
agents, this class has proliferated and has gained
popularity over barbiturates as hypnotics and sedatives.
Read the reason as to why?
Site and Mechanism of action:
• Benzodiazepines act preferentially on midbrain ascending
reticular formation (which maintains wakefulness) and on
limbic system (thought and mental functions).
• Muscle relaxation is produced by a primary medullary site
of action and ataxia is due to action on cerebellum.
• BZDs act by enhancing presynaptic/postsynaptic inhibition
through a specific BZD receptor which is an integral part of
the GABAA receptor - Cl- channel complex.
• The subunits of this complex form a pentameric
transmembrane anion channel gated by the primary ligand
(GABA), and modulated by secondary ligands which
include BZDs. Daniel Chans. M 2022 29

• The modulatory BZD receptor increases the frequency of
Cl- channel opening induced by submaximal
concentrations of GABA
• The GABAA antagonist bicuculline antagonizes BZD
action in a non- competitive manner.
• BZDs donot themselves increase Cl- conductance; have
only GABA facilitatory but no GABA mimetic action.
• This probably explains the low ceiling CNS depressant
effect of BZDs.
• BZD agonists: the BZD-agonists enhance GABA induced
hyperpolarization (due to influx of Cl- ions), and decrease
firing rate of neurones
• BZD –inverse agonists: compounds called BZD-inverse
agonists like dimethoxyethyl-carbomethoxy-13-carboline
(DMCM) inhibit GABA action and are convulsants.
• BZD antagonist: The competitive BZD-antagonist
flumazenil blocks the sedative action of BZDs as well as
the convulsant action of DMCM. (antidote to BZDs)
30

GABA RECEPTOR
31

GABA-A RECEPTOR
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• Pharmacological actions
• Virtually all effects of the benzodiazepines result
from their actions on the CNS.
• The most prominent of these effects are sedation,
hypnosis, decreased anxiety, muscle relaxation,
anterograde amnesia, and anticonvulsant activity.
• Only two effects of these drugs result from
peripheral actions:
• coronary vasodilation, seen after intravenous
administration of therapeutic doses of certain
benzodiazepines,
• Neuromuscular blockade, seen only with very high
doses.
33

• CNS actions: In contrast to barbiturates they are not general
depressants, but exert relatively selective anxiolytic, hypnotic,
muscle relaxant and anticonvulsant effects.
• Low doses are sedative, higher doses are hypnotic& anaesthetics
• Even when apparently anaesthetic dose of diazepam is
administered some degree of awareness is maintained, though
because of anterograde amnesia (interference with establishment of
memory trace) the patient does not clearly recollect the events on
recovery.
• The antianxiety action of BZDs is probably not dependent on their
sedative property: with chronic administration relief of anxiety is
maintained but drowsiness wares off due to development of
tolerance.
• While there are significant differences among different BZDs, in
general, they hasten onset of sleep, reduce intermittent awakening
and increase total sleep time (specially in those who have a short
sleep span).
• Some degree of tolerance develops to the action of BZDs on sleep
after repeated nightly use.
34

• BZDs produce centrally mediated skeletal muscle
relaxation without impairing voluntary activity.
• Clonazepam and diazepam have more marked muscle
relaxant property; very high doses depress neuromuscular
transmission.
• Clonazepam, diazepam, nitrazepam and flurazepam have
more prominent anticonvulsant activity than other BZDs.
• However, their utility in long term epilepsy is limited by
development of tolerance to the anticonvulsant action.
• Given iv., diazepam (but not others) causes analgesia.
• In contrast to barbiturates, BZDs donot produce
hyperalgesia.
• Other actions Diazepam decreases nocturnal gastric
secretion and prevents stress ulcers.
• BZDs donot significantly affect bowel movement.
35

Goodman and Gillman

Pharmacokinetics
• Benzodiazepines are usually given orally and are well absorbed
by this route.
• For emergency treatment of seizures or when used in
anesthesia, the BDZ also can be given parenterally and some
such as diazepam-rectally
• BDZs with greater lipid solubility tend to enter the central nervous
system more rapidly and thus tend to produce their effects more
quickly.
• Tissue redistribution of benzodiazepines is an important means
of terminating the actions of selected members of this class of
drugs, many benzodiazepines do undergo extensive
biotransformation.
• Clinical Uses
• Anxiety: Anxiety disorders are among the most common forms
of psychiatric illness.
• Anxiety often accompanies other psychiatric disease and such
medical illnesses as angina pectoris, gastrointestinal disorders,
and hypertension. Both acute and chronic anxiety can be
treated with benzodiazepines. 38

• Insomnia: All of the BDZs will produce sedative– hypnotic effects of
sufficient magnitude to induce sleep, provided that the dose is high
enough.
• However, the aim in the treatment of sleep disorders is to induce sleep that
is as close as possible to natural sleep so that the patient falls asleep
quickly, sleeps through the night, and has sleep of sufficient quality to
awake refreshed.
• Epilepsy and Seizures: e.g. Lorazepam, midazolam and diazepam
• Sedation, Amnesia, and Anesthesia: Benzodiazepine- induced sedation
and amnesia are deemed useful in the preparation of patients for
anesthesia, surgery, and other frightening or unpleasant medical and
dental procedures and diagnostic tests.
• Midazolam is a frequently used anesthetic benzodiazepine.
• Muscle Relaxation : BDZs, such as diazepam, are often prescribed for
patients who have muscle spasms and pain as a result of injury.
• In these circumstances, the sedative and anxiolytic properties of the drug
also may promote relaxation and relieve tension associated with the
condition.
39

Flunitrazepam: Date rape drug
• Used in insomnia, anaesthesia
• Surgery premedication
• Induces partial amnesia and aids in sexual
assault by abusers
• Victims may not recall the events
• May be crushed, snorted, dissolved in a liquid
• Illegal in the US
• Assn: Read about Club drugs

• Alcohol and Sedative–Hypnotic Withdrawal:
• Withdrawal from long-term high-dose use of alcohol or
sedative–hypnotic drugs can be life threatening if physical
dependence is present.
• BDZs, such as chlordiazepoxide and diazepam, are sometimes
used to lessen the intensity of the withdrawal symptoms when
alcohol or sedative–hypnotic drug use is discontinued.
• Benzodiazepines are also employed to help relieve the anxiety
and other behavioral symptoms that may occur during
rehabilitation.
ADVERSE EFFECTS
• These include drowsiness, excessive sedation, impaired
motor coordination, confusion, and memory loss.
• Less common adverse effects include blurred vision,
hallucinations, and paradoxical reactions consisting of
excitement, stimulation, and hyperactivity.

TOLERANCE & DEPENDENCE
• Tolerance and dependence do occur with the use of benzodiazepines.
• Discontinuation of drug administration, particularly abrupt withdrawal, can
be associated with a variety of symptoms, including rebound insomnia
and rebound anxiety.
• The level of insomnia or anxiety may even exceed that which preceded
the treatment.
• Usually, a gradual tapering of the dose until it is eventually discontinued
lessens the likelihood of a withdrawal reaction, although in some
individuals even this method of drug removal can result in anxiety,
apprehension, tension, insomnia, and loss of appetite.
• More severe symptoms may occur when an individual withdraws from a
supratherapeutic dose, particularly if the drug has been taken for months
or years.
• These symptoms can include, in addition to those already mentioned,
muscle weakness, tremor, hyperalgesia, nausea, vomiting, weight
loss, and possibly convulsions. 42

Newer sedative-hypnotics (Z-drugs)
• Eszopiclone, zaleplon, and zolpidem have efficacies
similar to those of the hypnotic benzodiazepines in the
management of sleep disorders.
• Favorable clinical features of zolpidem and the other
newer hypnotics include rapid onset of activity and modest
day-after psychomotor depression with few amnestic
effects.
• Zaleplon acts rapidly, and because of its short half-life, the
drug appears to have value in the management of patients
who awaken early in the sleep cycle.
• Zaleplon and eszopiclone causes less amnesia or day-
after somnolence than zolpidem or benzodiazepines.

• Zolpidem
• The hypnotic zolpidem is not a benzodiazepine in structure, but it acts
on a subset of the benzodiazepine receptor family, BZ1.
• Zolpidem has no anticonvulsant or muscle-relaxing properties.
• It shows few withdrawal effects, and exhibits minimal rebound insomnia,
and little or no tolerance occurs with prolonged use.
• Most widely used for insomnia
• Zolpidem is rapidly absorbed from the gastrointestinal tract, and it has a
rapid onset of action and short elimination half-life (about 2 to 3 hours).
• Zolpidem undergoes hepatic oxidation by the cytochrome P450 system
to inactive products.
• Thus, drugs such as rifampin, which induce this enzyme system, shorten
the half-life of zolpidem, and drugs that inhibit the CYP3A4 isoenzyme
may increase the half-life this drug.
Adverse effects of zolpidem include nightmares, agitation, headache,
gastrointestinal upset, dizziness, and daytime drowsiness.

GABA RECEPTOR
CC:Quizlet.com

Non pharmacological management of insomnia
• Proper diet and exercise
• Avoiding stimulants before retiring,
• Ensuring a comfortable sleeping environment
• Retiring at a regular time each night
• Relaxation training,
• Behavioral-modification approaches, such as sleep-restriction and
stimulus-control therapies
• In sleep-restriction therapy, the patient keeps a diary of the amount of
time spent in bed and then chooses a time in bed of 30 to 60 minutes less
than this time. This induces a mild sleep debt, which aids sleep onset.
• In stimulus-control therapy, the patient is instructed to go to bed only
when sleepy, to use the bedroom only for sleep and sex, to get up and
leave the bedroom if sleep does not occur within 15 to 20 minutes, to
return to bed again only when sleepy, to arise at the same time each
morning regardless of sleep quality the preceding night, and to avoid
daytime naps.
47

Anxiety Disorders
• Generalized anxiety
• PTSD
• Phobias
• Panic attacks
• OCD

ANXIOLYTICS
• Anxiety disorders as recognized clinically include:
• Generalized anxiety disorder (an ongoing state of excessive anxiety
lacking any clear reason or focus)
• Excessive anxiety about several aspects of life e.g. work, social
relationships, financial matters, aspects of daily life (expecting the worst
when there is no apparent reason for concern and anticipate disaster.
• Panic disorder (sudden attacks of overwhelming fear occur in association
with marked somatic symptoms, such as sweating, tachycardia, chest
pains, trembling and choking, abdominal discomfort).
• Phobias (strong fears of specific objects or situations, e.g. snakes, open
spaces, flying, social interactions)
• Post-traumatic stress disorder (anxiety triggered by recall of past
stressful experiences)
• Obsessive compulsive disorder (compulsive ritualistic behavior driven
by irrational anxiety, e.g. fear of contamination).
• A disorder where people feel the need to check things repeatedly, perform
certain routines repeatedly (rituals) or have certain thoughts repeatedily
49

• CLASSIFICATION OF ANXIOLYTIC DRUGS
• Benzodiazepines. This is the most important
group, used as anxiolytic drugs.
• Buspirone. This 5-HT1A receptor agonist is
anxiolytic but not appreciably sedative.
• β-Adrenoceptor antagonists (e.g. propranolol).
• Antidepressants e. g Fluoxetine, paroxetine
– TCAS, SSRIS etc (To be covered later…)

• BUSPIRONE
• The first example of a class of anxiolytic agents that can relieve some
symptoms of anxiety in doses that do not cause sedation. Buspirone
is structurally unrelated to existing psychotropic drugs.
• Mechanism of Action: it appears that its clinically relevant effects are
mediated through interactions at the serotonin (5-hydroxytryptamine, 5-
HT) 5-HT1A receptor, where it acts as a partial agonist.
• Pharmacokinetics: Buspirone is well absorbed from the gastrointestinal
tract, and peak blood levels are achieved in 1 to 1.5 hours; the drug is
more than 95% bound to plasma proteins. Buspirone is extensively
metabolized, with less than 1% of the parent drug excreted into the urine
unchanged. At least one of the metabolic products of buspirone is
biologically active.
• Clinical Uses: Buspirone is effective in general anxiety and in anxiety
with depression.
• Adverse Effects: The most common side effects are dizziness, light-
headedness, and headache. Abuse, dependence, and withdrawal have
not been reported, Daniel Chans. M 2022 51

• β -Adrenoceptor Blocking Agents
• Propranolol have been widely used in the treatment of cardiovascular diseases
• These blockers also are useful in some forms of anxiety, particularly those that
are characterized by somatic symptoms or by performance anxiety (stage fright).
• There is general agreement that -blockers can lessen the severity and perhaps
prevent the appearance of many of the autonomic responses associated with
anxiety. These symptoms include tremors, sweating, tachycardia, and palpitations.
• Antidepressants
• Antidepressant drugs, such as the tricyclic antidepressants and the selective
serotonin reuptake inhibitors (SSRIs), are very important for the treatment of
psychotic depression.
• They have been shown to be effective when used in the treatment of several
anxiety disorders, including general anxiety, obsessive- compulsive disorder, and
several phobias, including agoraphobia.
• Because the SSRIs are less toxic than the tricyclic antidepressants, their use in
the treatment of anxiety is safer and less likely to produce serious side effects.
• They are now the drug of choice for anxiety disorders

CLASSIFICATION OF SEDATIVE-HYPNOTIC AND ANXIOLYTIC
DRUGS
SEDATIVE-HYPNOTIC DRUGS
Benzodiazepines Barbiturates Antihistamines Others
Alprazolam Pentobarbital Diphenydramine Chloral
hydrate
Chlordiazepoxide Phenobarbital Hydroxyzine Melatonin
Diazepam Thiopental Zolpidem
Flurazepam
Lorazepam
Midazolam
Oxazepam
Temazepam
Triazolam
NON-SEDATING ANXIOLYTIC DRUGS
Buspirone
Propranolol
53

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