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Drugs Affecting the Central Nervous System


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Title: Drugs Affecting the Central Nervous System

Drugs Affecting the Central Nervous System
Disease states of Central Nervous System
  • Typically caused by too much, or too little
  • Too much
  • Hyperexcitable neurons fire in absence of stimuli
    (e.g. seizure disorders)
  • Too many neurotransmitter molecules binding to
    post-synapse receptors
  • psychoses

  • Too little
  • Too few neurotransmitters binding to post-synapse

Major Parts of the Brain
  • Cerebrum
  • Brainstem
  • Cerebellum

  • Largest and uppermost part of the brain
  • Divided into right and left hemispheres
  • Controls all the higher intellectual and motor
    functions of the body
  • Cerebrum composed of an outer cortex and an inner

Cerebral Cortex
  • Contains neuronal cell bodies (gray matter) that
    control all voluntary activities of the body
  • Divided up into 4 lobes frontal, parietal,
    temporal, and occipital, each controlling
    specific brain functions
  • Electroencephalogram (EEG) is a recording of the
    electrical activity of the cortex

Cerebral Medulla
  • Referred to as the white matter and is composed
    of myelinated nerve axons
  • Functions to conduct nerve impulses to and from
    different parts of the nervous system
  • Basal ganglia are neuronal cell bodies (gray
    matter) located within the cerebral medulla that
    function in the regulation of motor activity

Brainstem and Spinal Cord
  • Located below the cerebrum and is continuous with
    the spinal cord
  • Brainstem divided into the thalamus,
    hypothalamus, pons, and medulla oblongata
  • Spinal cord is a collection of all the sensory
    and motor nerves going to and from the brain

Reticular Formation
  • A network of nerves and brain areas involved in
    regulating alertness, wakefulness, and sleep
  • Composed of both inhibitory and excitatory nerves
  • Excitatory nerves collectively referred to as the
    reticular activating system (RAS)
  • Many stimulants (amphetamines) and depressants
    (alcohol, barbiturates) affect the RAS

Limbic System
  • Network of nerves and brain areas involved in
    emotional and behavioral responses
  • Associated with emotional responses to fear,
    anger, anxiety, sexual behavior, and reward and
  • Affected by drugs of abuse and involved in the
    development of drug dependency

  • Adrenergic hormone released at the effector organ
    by sympathetic neurons
  • Monamine
  • Depression thought be caused by impaired
    monoamine transmission
  • Drugs that stimulate monoamine release are
    indicated for ADD or narcolepsy

  • Another monoamine derived from the amino acid
  • Binds dopamine receptors (D1 or D2)
  • Antipsychotics prevent signals activated by
    dopamine binding
  • Parkinsons disease also caused by altered
    dopamine binding

Serotonin (5-HT)
  • Monoamine hormone derived from the amino acid
  • Typically released by inhibitory neurons
  • Lysergic acid diethylamide binds to serotonin
  • Depression, ADD and headaches associated with
    serotonin imbalance

Gamma-amino butyric acid (GABA)
  • Inhibitory neurotransmitter of the brain and
    central nervous system
  • Synthesized from the amino acid glutamate
  • Cause Ca2 influx into the neuron resulting in
  • More difficult to excite
  • Benzodiazepines and barbituates enhance GABA

Excitatory Amino Acids
  • Amino acid glutamate or structurally related
  • Important for learning and memory
  • Abnormal increased activity will result in
  • Alzheimers, ALS, stroke, Huntingtons

Mental Depression
  • Exogenous or reactive depression usually occurs
    in response to some external factor or adverse
    life event
  • Endogenous depression usually originates from
    within the psyche of the individual and the
    causes are less well understood
  • Bipolar mood disorder involves alternating cycles
    of depression and mania

Causes of Mental Depression
  • Exact causes not well understood
  • Mental depression appears to involve the
    development of low levels of the brain monoamine
    neurotransmitters, serotonin (SER) and
    norepinephrine (NE)
  • This explanation is referred to as the Monoamine
    Theory of Mental Depression

Treatment of Depression
  • Treatment involves a combination of psychotherapy
    and antidepressant drugs
  • Antidepressant drugs act to increase NE and SER
    levels in the brain
  • Tricyclic antidepressants (TCA) and selective
    serotonin reuptake inhibitors (SSRI) are the two
    most important antidepressant drug classes
  • Monoamine oxidase inhibitors (MAOI) are less
    frequently used and require dietary restriction

Monoamine Oxidase Inhibitors (MAOI)
  • Monoamine oxidase is the enzyme that metabolizes
    the monoamines NE and SER
  • Inhibition of MAO increases SER and NE levels and
    functional activity in the brain
  • Requires 24 weeks for maximum effects
  • Foods containing tyramine must be avoided
  • Tyramine stimulates the release of NE and may
    cause a hypertensive crisis
  • MAOIs are indicated for patients who cannot
    tolerate TCAs and SSRIs

Tricyclic Antidepressants (TCA)
  • Mechanism of action of TCAs is to block reuptake
    of NE and SER into nerve endings
  • Blockage of reuptake increases NE and SER levels
    and stimulation of NE and SER receptors
  • Requires 24 weeks for maximum effect
  • TCAs are divided into secondary amines which
    increase NE more than SER and are less sedating
    than tertiary amines which increase SER more than

Autonomic Effects of TCAs
  • TCAs possess anticholinergic activity which can
    cause dry mouth, visual disturbances,
    constipation, and urinary retention
  • TCAs also possess alpha blocking activity that
    can lower blood pressure
  • TCAs can also affect cardiac rhythm and may cause
    cardiac arrhythmias

Selective Serotonin Reuptake Inhibitors (SSRI)
  • Selectively block the reuptake of SER
  • Cause little if any anticholinergic and alpha
    blocking effects
  • Are generally not sedating, and in some cases
    cause CNS stimulation
  • Common adverse effects include nausea, agitation,
    restlessness, and less frequently seizures

Psychomotor Stimulants
  • Generally referred to as the amphetamines
  • Produce CNS stimulation more than an
    antidepressant effect, little used for depression
  • Act by increasing NE and DA activity
  • Clinical use for narcolepsy and treatment of
    hyperkinetic children
  • Amphetamines have a high abuse potential
  • Adverse effects due to excessive CNS and
    autonomic stimulation

  • Lithium is an elemental ion similar to sodium
  • Acts to depress nerve excitability that helps
    prevent mood swings and manic behavior
  • Common adverse effects include nausea, diarrhea,
    tremors, increased thirst, ringing in the ears
    (tinnitis), and more seriously kidney and heart
  • Periodic blood levels to prevent overdosage

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Sedatives and Hypnotics
  • Sedatives are drugs used to induce a mild state
    of CNS depression characterized by both mental
    and physical calmness
  • Hypnotics are drugs used to induce and maintain
  • The same drugs are used to induce both sedation
    and hypnosis however, the dosage for inducing
    sedation is lower

Classification of Sedative- Hypnotic Drugs
  • Barbiturates a drug family of chemically
    similar drugs with similar actions and features
  • Benzodiazepines a drug family of chemically
    similar drugs with similar actions and features
  • Miscellaneous nonbarbiturates a group of drugs
    with dissimilar chemical structures and
    pharmacologic features

Pharmacology of Barbiturates
  • Drugs classified as short, intermediate, and
    long-acting sedative-hypnotics
  • At low doses they increase the inhibitory effects
    of GABA
  • At high doses they act like general anesthetics,
    and can cause profound CNS depression and death
    in overdosage
  • Barbiturates are also anticonvulsants

Effects of Barbiturates on the Sleep Cycle
  • Decrease stage 1, falling asleep
  • Increase stage 2, a lighter stage of sleep
  • Decrease stages 3 and 4 referred to as deep sleep
    or slow-wave sleep
  • Decrease REM sleep, and may cause REM rebound

Adverse Features of Barbiturates
  • Cause drug tolerance with chronic use and drug
    dependency with abuse
  • Can cause a severe type of physical drug
    addiction when chronically abused
  • The withdrawal reaction from barbiturates can be
    serious, resulting in convulsions and death
  • Drug interactions, induce microsomal enzymes to
    increase the rate of drug metabolism of all drugs
    metabolized by the microsomal enzymes

Pharmacology of Benzodiazepines
  • Drugs classified as short, intermediate, and
    long-acting sedative-hypnotics
  • Drugs also produce antianxiety, skeletal muscle
    relaxing, and anticonvulsant effects
  • Act by increasing the inhibitory effects of GABA
  • Drugs do not induce the drug metabolizing
    microsomal enzymes

Effect of Benzodiazepines on the Sleep Cycle
  • Decrease stage 1, falling asleep
  • Increase stage 2
  • Decrease stages 3 and 4
  • Do not significantly decrease REM sleep
  • Benzodiazepines are considered safer drugs than
    the barbiturates, especially in overdosage

Miscellaneous Nonbarbiturates
  • Zolpidem and zaleplon are short-acting hypnotics
    that do not disrupt the sleep cycle
  • These drugs increase the inhibitory effects of
    GABA but differently than other drugs
  • Both drugs are considered to be safer than other
    hypnotics and are at low risk for abuse
  • Side effects include dizziness, headache, GI
    disturbances, and mental confusion

  • Classified as a CNS depressant drug
  • Unlike other drugs, alcohol provides nutritional
  • Like other drugs of abuse, alcohol causes
    development of drug tolerance, dependency, and
    withdrawal reactions
  • Most of the pharmacology of alcohol centers
    around its chronic use, abuse, and toxicology

  • Used to treat alcoholism and deter drinking
  • Disulfiram inhibits metabolism of alcohol,
    allowing acetaldehyde to accumulate
  • Increased acetaldehyde produces severe nausea,
    vomiting, headache, and hypotension
  • Alcoholics take the drug on a daily basis,
    knowing that if they drink any alcohol they will
    become violently ill

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Parkinsons Disease
  • A neurological movement disorder of the brain
    involving the basal ganglia
  • Symptoms include tremor, muscular rigidity, and
    disturbances of movement
  • Major cause is a deficiency of the inhibitory
    neurotransmitter dopamine (DA) and the resulting
    excessive activity of the excitatory
    neurotransmitter acetylcholine (ACH)

Drug Therapy
  • Primary therapy is the administration of drugs
    that increase the levels of DA in the basal
  • Secondary therapy is the administration of
    anticholinergic drugs that decrease ACH activity
    in the basal ganglia
  • Goal is to restore the balance between DA and ACH

Drugs that Increase Dopamine
  • Levodopa
  • Dopamine agonists
  • Amantadine
  • Enzyme inhibiting drugs that slow the metabolic
    breakdown of dopamine

  • The precursor of DA that is taken orally and
    converted into DA in the basal ganglia
  • Administered in combination with carbidopa that
    increases the amount of DA that enters the brain
  • Levodopa and carbidopa drug combination known as
  • Levodopa is considered the most effective drug
    for the treatment of Parkinsons disease

Adverse Effects of Levodopa
  • Nausea, vomiting, and loss of appetite
  • Hypotension, and rapid/irregular heart rate
  • Dystonias, slow or weak movements that usually
    occur when levels of DA are low
  • Dyskinesias, uncontrolled or involuntary
    movements when DA levels are too high
  • On-off phenomenon when drug effects suddenly
    increase or decrease due to fluctuating levels of
    DA in the basal ganglia
  • Behavioral and mental disturbances

Dopamine Agonists
  • Drugs bromocriptine, pergolide, pramipexole, and
  • Stimulate DA receptors in the basal ganglia
  • Used alone or in combination with levodopa
  • Adverse effects similar to levodopa nausea,
    hypotension, dyskinesias, and mental disturbances

Amantadine (Symmetrel)
  • An antiviral drug that additionally increases the
    release of DA in the brain
  • Used in early stages of treatment and in
    combination with other drugs
  • Effectiveness usually decreases in 612 months
  • Adverse effects include nausea, mental
    disturbances, and occasionally skin discoloration

Enzyme Inhibitors
  • Selegiline (Eldepryl) inhibits MAO-B enzyme that
    slows metabolism of DA in the brain, increases DA
    levels used alone or with levodopa
  • Tolcapone (Tasmar) and entacapone (Comtan)
    inhibit another enzyme, COMT, that also slows
    metabolism of DA usually used with levodopa

Anticholinergic Drugs
  • Used to decrease the activity of ACH and restore
    the normal balance between DA and ACH
  • Benztropine (Cogentin)and trihexyphenidyl
    (Artane) most widely used drugs
  • Antihistamine drugs, diphenhydramine (Benadryl),
    with high anticholinergic activity occasionally
  • Used alone early in treatment or in combination
    with other drugs

Central Analgesics
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Clinical Indication
  • Produce a state of unconsciousness to prevent
    painful stimulation during surgical and dental
  • Types of anesthetics
  • Inhalation gases volatile liquids
    chloroform, halothane, nitrous oxide
  • Injectable fentanyl, ketamine, midazolam,

  • Signs Stages of General Anesthetics
  • General anesthetics gradually depress the CNS
  • Stage I Depression of the cerebral cortex
    produces analgesia euphoria and
  • Stage II Excitement phase with increased
    sympathetic tone produces
    increase in blood pressure, heart rate,
    respiration, and muscle tone
  • Stage III Surgical anesthesia because blood
    pressure and respiration return
    to normal, spinal reflexes are
    inhibited and skeletal muscles relaxedStage IV
    Medullary paralysis, paralysis of the diaphragm
    circulatory collapse leading to

  • Action of General Anesthetics
  • Induction of anesthesia time required to
  • the patient from consciousness to Stage III
  • Maintainance of anesthesia ability to keep
  • patient safely in Stage III
  • Dissociative anesthesia anesthesia and loss
  • of memory without skeletal muscle relaxation
  • Neuroleptanalgesia inhibition of pain while
  • conscious from combination of a narcotic and a
  • tranquilizer

  • Other Effects
  • CNS Depression of voluntary (motor) and
    involuntary (autonomic) systems. Secretion of
    antidiuretic hormone causes postop urinary
  • VascularDecreased sympathetic tone causes
    vasodilation hypotension
  • CardiacMyocardial depression, ventricular
  • Salivary and bronchial secretions
  • Skeletal muscle relaxation
  • GastrointestinalNausea and vomiting during
    recovery. Decreased intestinal motility causes
  • Hepatotoxicity Jaundice, elevated serum liver
    enzymes, necrosis

Adjuncts to General Anesthesia
  • Drugs routinely used before and after
  • surgery to reduce anxiety, counteract the
  • side effects of general anesthetics, and
  • improve patient recovery.
  • Analgesics-relieve pain, produce sedation
  • Antianxiety drugs-relieve apprehension
  • Antiarrhythmics-control arrhythmias
  • Anticholinergics-decrease secretions
  • Cholinergics-decrease urinary retention
  • Tranquilizers-control nausea vomiting

Drug Interactions
  • Residual depression of the CNS
  • narcotic (opiate) analgesics
  • muscle relaxants
  • tranquilizers
  • Potentiate skeletal muscle relaxation, weakness
    and fatigue
  • antibiotics that promote potassium loss
    streptomycin, kanamycin, erythromycin

The Opioid System
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Clinical Indication
  • Prevent or interrupt moderate to severe pain of
    any origin without a loss of consciousness
  • Acute pain-during or after surgical procedures
  • Chronic pain-of any etiology from back pain to
    cancer pain

Source of Opioid Analgesics
  • Opioid analgesics are derivatives of the
  • naturally occurring plant substance opium
  • OR
  • synthetic substances that produce the same
    pharmacologic effects as opium


Types of Analgesics Opiates-opium,
heroin codeine, morphine, hydromorphone,
oxycodone, oxymorphone Opioids-synthetic
butorphanol, fentanyl, levorphanol,meperidine,
methadone, propoxyphene Central analgesics
Drug Schedule Federal Comprehensive Drug Abuse
Prevention and Control Act
  • Because of their liability to produce physical
  • dependence, opioid analgesics are included
  • in the class of controlled substances as Schedule
    II drugs
  • Restricted to prescription use
  • No refill without new written prescription
  • Regulated by the FDA (Food and Drug
    Administration) and DEA (Drug Enforcement Agency)

Sensation of Pain
  • Pain is composed of at least two elements
  • localized stimulation of peripheral nerves
    through damage or inflammation
  • recognition of pain within the CNS that
  • can intensify the reaction to pain

  • Mechanism of Action
  • Opioid analgesics relieve pain by
  • selectively acting on receptors within the
  • CNS (rather than on peripheral nerve
  • endings) to
  • decrease anxiety
  • reduce the reaction to pain
  • interrupt pain signal transmission within the
    spinal cord

Mechanism of Action (continued)
  • Opioid analgesics mimic the action of endorphins
  • produced in the brain and spinal cord by
  • selectively stimulating receptors
  • mu (µ) receptors mediate analgesia, euphoria, and
    respiratory depression
  • kappa (?) receptors mediate sedation, dysphoria
  • delta (d) receptors mediate, hallucinations, and
    increased respiration and blood pressure

Pharmacological Effects
  • CNS
  • Change in mental alertness, sedation (µ, ?)
  • Change mood, euphoria (µ) or dysphoria (?)
  • Stimulation of chemoreceptor trigger zone
  • initiating nausea and vomiting
  • Dose dependent depression of the vomiting center
  • Depression of respiratory centers (µ)
  • Headache
  • Cough suppressant (antitussive)
  • Secretion of antidiuretic hormone

Pharmacological Effects (continued)
  • Tolerance
  • Decreased response to euphoria, sedation,
    respiratory depression and analgesia with chronic
    daily use
  • Response returns when the dose is increased
  • Physical dependence
  • Chronic use establishes an internal expectation
    within the body of receiving receptor activiation
  • Withdrawal symptoms (abstinence syndrome) occur
    when the drug is abruptly discontinued. (This can
    be minimized by gradual taper down)

Pharmacological Effects (continued)
  • Smooth Muscle (µ receptor mediated)
  • Spasmogenic
  • Intestine- constipation
  • Gall bladder common bile duct- increasepressure,
  • Bronchial constriction
  • Urinary sphincters- oliguria
  • Histamine release
  • Bronchial constriction
  • Vasodilation-orthostatic hypotension

Antitussive Activity
  • Natural opiates such as codeine, hydrocodone,
  • and hydromorphone suppress coughs by
  • inhibiting centers in the brain
  • At present, dextromethorphan is the only opioid
  • that is used in commercial over-the-counter
  • cough suppressant products
  • Usually OTC products include additional active
  • ingredients that treat other symptoms of cold

Adverse Effects
  • Mental confusion
  • Sedation
  • Headache
  • Nausea
  • Vomiting
  • Dry mouth
  • Constipation
  • Urinary retention
  • Itching, rash, anaphylaxis
  • Orthostatic hypotension
  • Physical dependence

Acute Opioid Poisoning
  • Accidental ingestion of a large dose by
  • children or attempted suicide may produce
  • Coma
  • Decreased respiration
  • Cyanosis
  • Hypotension
  • Drop in body temperature
  • Death

Opioid Antagonists
  • A pure opioid antagonist fits the opiate
  • receptor, cannot stimulate the receptor, and
  • blocks the opioid analgesic from attaching
  • to the receptor.
  • naloxone, naltrexone
  • A partial antagonist fits the opiate receptor and
  • weakly stimulates the receptor while it blocks
  • opioid analgesic from attaching to the receptor
  • butorphanol, nalbufene

Cautions and Contraindications
  • Opioid analgesics should not be used in patients
  • with
  • Bronchial asthma
  • Heavy pulmonary secretions
  • Convulsive disorders
  • Biliary obstruction
  • Head injuries
  • A history of allergy or sensitivity to this class
  • Used with caution in
  • Elderly patients
  • Pregnant women

Drug Interactions
  • Potentiate CNS depression of all Opioids
  • sedatives, hypnotics, general anesthetics,
  • Meperidine or dextromethorphan
  • MAO inhibitors- sweating, hypotension,
  • Methadone
  • Reduced plasma levels of methadone-rifampin,

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