MENTAL HEALTH & PSYCHOTROPIC DRUGS

THE BRAIN

Functions: Mental disturbances can affect any of these functions of the brain:

• Regulation of skeletal muscle contraction;

• Initiation and regulation of basic drives (sex, hunger, thirst, aggression);

• Conscious sensation;
• Memory;
• Mood;
• Thought;

• Regulation of sleep cycle;

• Language
Structure: Since all of these brain functions are carried out by similar mechanisms and are
often in similar locations, mental disturbances are often associated with
alterations in other brain functions as are the drugs used to treat them.

Cerebral Cortex White Matter

PARIETAL LOBE
Sensory & Motor
Abstract Thought
Proprioception
Reading/Math
Right/Left Orientation

OCCIPTAL LOBE
Vision
Visual Association
Visual Memory
Language Formation

TEMPORAL LOBE
Auditory Processes
Language
Memory
Connects with Limbic

CEREBELLUM
FRONTAL LOBE Balance & Coordination
Thought Processes Maintains Equilibrium
Intelligence Coordinates Skeletal Muscle
Social Judgment Contraction
MIDBRAIN
Voluntary Motor Ability
Pupilary reflexes
Eye movement

PONS
Auditory Pathway MEDULLA OBLONGATA
Reflex Centers
Balance
Heart rate
Respirations
Cough, swallow, sneeze
Page 1 of 12 Blood pressure
Vomiting
NERVOUS SYSTEM

Sympathetic Dominant division of the autonomic nervous system in stress situations.

Norepinephrine is the primary neurotransmitter of the sympathetic nervous
system.
“Fight or Flight”
Effects:
• Dilated pupils
• Increased salivary flow
• Increased heart rate
• Constricted arterioles
• Dilated bronchi
• Decreased digestion and intestinal motility
• Decreased urinary bladder activity

Parasympathetic Acetylcholine is the primary neurotransmitter of the parasympathetic

nervous system.
“Feed and Breed” or “Rest and Digest”
Effects:
• Undilated pupils
• Decreased salivary flow
• Decreased heart rate
• Dilated arterioles
• Undilated bronchi
• Increased digestion and intestinal motility
• Increased urinary bladder activity
Mental Disturbances May affect sympathetic and/or parasympathetic nervous systems in non-
normal ways.
Stress: Sympathetic nervous system initiates the release of CRH
(corticotropin-releasing hormone), which causes the pituitary to
release ACTH (adrenal corticotropin hormone), which causes the
adrenal cortex to release cortisol. However, all three hormones
influence the functions of the nerve cells in the brain. In mental
illness, depression and anxiety, the normal negative feedback
loop for these hormones does not appear to work.
Anxiety: May activate both parasympathetic nerves (hypermotility of GI,
diarrhea) and sympathetic nerves (vasoconstriction,
hypertension) simultaneously.
Nerve Communication

Communication of information between neurons is accomplished by movement of chemicals across a

small gap called the synapse. Chemicals, called neurotransmitters, are released from one neuron at the
presynaptic nerve terminal. Neurotransmitters then cross the synapse where they may be accepted by
the next neuron at a specialized site called a receptor. The action that follows activation of a receptor site
may be either depolarization (an excitatory postsynaptic potential) or hyperpolarization (an inhibitory
postsynaptic potential). A depolarization makes it MORE likely that an action potential will fire; a
hyperpolarization makes it LESS likely that an action potential will fire. (Chudler, University of Washington)

There are four elements involved in nerve-to-nerve or nerve-to-muscle communication:

(1) Production or existence of a neurotransmitter;
(2) Release of the neurotransmitter;
(3) Reception of the neurotransmitter by another nerve or cell; and
(4) Inactivation of the neurotransmitter
Changing any one of the four elements can change the results.

Neurotransmitter (NT): Definition: A chemical that modifies or results in the transmission of nerve
impulses between two synapses. (Mosby’s Dictionary, 7th ed., 2006)

Different types of chemicals may act as neurotransmitters: small molecules (like

the monoamines such as serotonin), amino acids (such as GABA), neuroactive
peptides (such as endorphins), and soluble gases (such as nitric oxide).

NT Release: Neurotransmitters are made in the cell body of the neuron and then transported
down the axon to the axon terminal. Molecules of neurotransmitters are stored in
small "packages" called vesicles. Neurotransmitters are released from the axon
terminal when their vesicles "fuse" with the membrane of the axon terminal,
spilling the neurotransmitter into the synaptic cleft. (Chudler, University of Washington)

Reception of NT: The NT will only bind to post-synaptic cell receptors that recognize them. If these
receptors are altered or blocked, then the NT will not bind and the NT action will
be prevented.

Inactivation of NT: There are three mechanisms for inactivating a NT.

(1) Diffusion: The unbound NT molecules drift away from the synaptic cleft to
sites that do not recognize them.
(2) Enzymatic Deactivation: Specific enzymes bind with the NT molecules and
change their shape so they will no longer be recognized by the receptors.
(3) Reuptake: The neuron that released the NT can take back the whole NT
molecule removing it from the cleft. The NT will then be destroyed by an
intracellular enzyme (such as monoamine oxidase) or be recycled for use
later.
Neurotransmitters

Neurotransmitter Receptor Action Decreased Elevated

MONOAMINES
Dopamine (DA) D1, D2 • Fine muscle movement • Parkinson’s • Schizophreni
(Synthesized from • Integration of emotions and thoughts • Depression a
Deactivated
Tyrosine) by • Mania
• Involved with decision-making
(Catecholamine) Monoamine
Oxidase • Stimulates hypothalamus to release hormones (sex, thyroid, adrenals)
Norepinephrine α1, α2 • Level in brain affects mood • Depression • Mania
(NE)
β1, β2 • Plays a part in sleep/wake cycle • Anxiety
(Synthesized from
Dopamine) Deactivated • Stimulates sympathetic branch of ANS for “fight or flight” • Schizophreni
by a
(Catecholamine)
Monoamine
Oxidase
Serotonin 5-HT • Actual name is “5-hydroxytryptamine” • Depression • Anxiety
(5-HT) Deactivated • Most of 5-HT’s function is vasoconstriction in cardiovascular, respiratory and GI systems.
(Synthesized from by
Tryptophan) Monoamine • Plays a role in sleep regulation, dreaming, hunger, mood, pain perception, aggression and
Oxidase sexual behavior
• Is found in platelets and plays a role in platelet aggregation

AMINO ACIDS
Glutamate NMDA • Most prevalent neurotransmitter in the Central Nervous System. Used by more that 50% of • Depression
(Derived from α- mGluR1,2 neurons • Suicide
ketoglutarate) • Glutamate is the most important excitatory (EPSP) neurotransmitter, exciting about 90% of
Deactivated • Multiple
by Glial Cells the postsynaptic terminals to which it contacts
sclerosis
in CNS
(Astrocytes)
• As an excitatory neutrotransmitter, it binds to ionotropic receptors, causing depolarization by
opening Na+ ion channels
• At metabotropic receptors, it is modulatory; Plays a major role in cellular metabolism
• Principle excitatory amino acid in CNS
Gamma- GABAA • The most important inhibitory (IPSP) neurotransmitter • Anxiety • Reduces
aminobutyric Acid GABAB Anxiety
• Present in high concentrations in the CNS, preventing the brain from becoming overexcited • Schizophrenia
(GABA)
•
(Synthesized directly • As an inhibitory neutrotransmitter, it binds to both ionotropic and metabotropic receptors,
Huntington’s
Chorea
from glutamate) causing hyperpolarization by opening Cl- ion channels
• Used by inhibitory interneurons in the spinal cord
• Plays a role in inhibition; reduces aggression, excitation and anxiety
• May play a role in pain perception
• Has anticonvulsant and muscle-relaxing properties
Neurotransmitter Receptor Action Decreased Elevated
 NEUROPEPTIDES
CRH Acts on • Plays a role in mental activity • Depression • Stress
Corticotropin Pituitary to
•
Releasing Hormone release • Initiates the CRH-ACTH-Cortisol reaction in stress
Anxiety
ACTH

Endorphins Opiate o Substance P and enkephalins: Active during inflammation and pain transmission in the PNS
receptors
o Endorphins: Endogenous opiates which cause euphoria, suppress pain, or regulate responses
(Derived from to stress
secretory proteins
formed in the cell • Are either excitatory or inhibitory, and can also act as neuromodulators, affecting the
body) amount of neurotransmitter released
• Some form part of the neuroendocrine system by functioning both as hormones and
neurotransmitters
• Plays a part in physiological processes including euphoric feelings, appetite modulation, and
the release of sex hormones.

CHOLINERGICS
Acetylcholine Nicotinic • The only small molecule NT that is not an amino acid or derived from one • Alzheimer’s • Depression
(ACh) (N1, N2) • Precursor choline cannot be synthesized by the body and must be obtained from external • Huntington’s
food sources Chorea
(Synthesized from Muscarinic • Used by motor neurons as an excitatory neurotransmitter in the spinal cord • Parkinson’s
Choline)
(M1, M2) • Used at neuromuscular junctions as an excitatory neurotransmitter to influence muscle
activation
Deactivated • Used by the Autonomic Nervous System, such as smooth muscles of the heart, as an
by inhibitory neurotransmitter in preganglionic neurons and postganglionic parasympathetic
Cholinestera neurons
se • Used everywhere in the brain. For example, memory systems of the CNS (may be related to
Alzheimer's Disease).

• Most receptors for acetylcholine are ionotropic

• Plays a role in learning, memory
• Mood regulator: manic, sexual behavior

AMINO ACIDS DERIVATIVES

Histamine H1, H2W • Primary regulator of alertness • Female • Premature
• Used in control of smooth muscle, exocrine glands and vasculature. sexual ejaculation
dysfunction • Hyperactivit
(Synthesized from • High concentration in hypothalamus, which regulates hormone secretion
Histadine) • Paranoia y
• Inflammatory response (local blood flow)
• Ideas of • Obsessive-
• Stimulates gastric secretions grandeur compulsive
• Mania disorder
• Phobias
• Auditory
hallucination • Depression
• Suicidal
thoughts
www.columbia.edu/cu/psychology/courses/1010/mangels/neuro/transmission/transmission.html
http://faculty.washington.edu/chudler/chnt1.html
http://web.indstate.edu/thcme/mwking/nerves.html
Receptors

“Dopaminergic” Known as D1 or D2. (D2 is implicated in addiction.) They bind specifically with dopamine and are active in
many areas of the CNS:
Basal ganglia: MOVEMENT
Limbic: MOOD, EMOTIONS
Pituitary: INHIBITION OF PROLACTIN
Medulla Oblongata: VOMITING
Hypothalamus: ERECTION

“Adrenergic” Think “ADRENALIN”. They bind with the catecholamines (dopamine, norepinephrine, epinephrine) and are
active in the sympathetic response.
Alpha1: VASOCONSTRICTION; located on blood vessels in the skin, vas deferens and GI tract…
the effect is reduced blood flow to these areas.
Beta1: INCREASED HEART RATE; located in the heart where stimulation results in enhanced
myocardial contractility.
Beta2: BRONCHIAL DILATION; located in the lungs

“Serotonergic” Bind with serotonin. Serotonin affects mood, anxiety, arousal, aggression, impulse control, and thinking
abilities; but also contributes to physiological effects such as vasoconstriction, GI motility and smooth
muscle contractions.
5-HT1: CNS inhibitor affecting sleep, appetite, thermoregulation, anxiety, pulmonary vasoconstriction.
5-HT2: CNS excitation affecting behavior, learning and smooth muscle contraction (including stomach
contraction)
5-HT3: Affects anxiety and vomiting mechanism in the intestines
5-HT4 Increases GI motility

“Cholinergic” Bind with acetylcholine. The effects of cholinergic receptor stimulation include: vasodilation of blood
vessels; slower heart rate; constriction of bronchioles and reduced secretion of mucus in the respiratory
tract; intestinal cramps; secretion of salvia; sweat and tears; and constriction of eye pupils.

Nicotinic: Located at the neuromuscular junction and affect skeletal muscles.

Muscarinic: Located throughout the CNS and PNS and affect smooth muscles.

M2: In parasympathetic fibers, it reduced heart rate; in sympathetic fibers it causes

vasodilation in skeletal muscle

“Histaminergic” Bind with histamine. Histamine is a chemical involved in local immune responses as well as regulating
physiological function in the gut and acting as a neurotransmitter. New evidence also indicates that
histamine plays a role in chemotaxis of white blood cells. It also maintains ALERTNESS.

H1: Found on smooth muscle, endothelium, and central nervous system tissue; causes vasodilation,
bronchoconstriction, smooth muscle activation, and separation of endothelial cells (responsible for
hives), and pain and itching due to insect stings; the primary receptors involved in allergic rhinitis
symptoms and motion sickness. In stomach, it stimulates secretion of gastric acid.

H2: Located on parietal cells, which primarily regulate gastric acid secretion

H3: Decreases neurotransmitter release of histamine, acetylcholine, norepinephrine, serotonin

PSYCHOTROPIC DRUGS

Pharmacokinetics

“Agonists”: Drugs that enhance or potentiate the effects of a neurotransmitter or hormone. May be
accomplished by mimicking the effects, activating the receptors, increasing the amount of NT in the
synapse, or inhibiting the deactivation of the NT.

“Antagonists: Drugs that decrease or limit the effects of a neurotransmitter or hormone. May be accomplished by
blocking the receptors, preventing the NT from binding with the receptors (changing its shape, for
example), preventing the NT’s release, or increasing the rate of the NT’s deactivation.

It is thought that some of the symptoms of psychosis are the result of too much or not enough neurotransmitter.
Therefore, drugs try to counter the effects of this imbalance by “correcting” or modulating the action. However,
because the nervous system is complex in its interconnectedness, changing the action at one transmission/receptor
site has effects in other areas. This is why psychotropic drugs have such debilitating side effects.

Modulation of NTs

Receptor Blocking (Decreases NT action)

Example: Dopamine Receptor Blocking

In schizophrenia, the victim suffers from excess Dopamine. Blocking the dopamine
receptors prevents the NT from binding with its receptors and thereby reduces the effects
of the NT with the goal of reducing the effects of the schizophrenia.

However…dopamine not only effects mood and thought processes, it also controls the
modulation and fine-tuning of motor activity and inhibits the release of prolactin in the
pituitary.

This results in the movement dysfunctions knows as extrapyramidal effects and

in galactorrhea (production of breast milk) in females and gynecomastia (female-
like breasts) in males.

Additionally, dopamine blockers also bind to the acetylcholine muscarinic receptors

(smooth muscle, cardiac muscle and exocrine glands used in the parasympathetic
response) and the norepinephrine alpha1 receptors (used in vasoconstriction).

This results in antiparasympathetic effects known as “anticholinergic” effects

(blurred vision, dry mouth, constipation, urinary retention) due to the blocking of
ACh and in orthostatic hypotension and failure to ejaculate due to the blocking of
NE.

Enzyme Inhibitors (Increases NT action)

Example: Monoamine Oxidase Inhibitors (MAOI)

Again, in depression, the goal of antidepressants is to elevate the level of NTs. Besides
blocking the reuptake, another strategy is to prevent the destruction of the NT once it has
been re-absorbed by the neuron that released it.

The monoamines (dopamine, norepinephrine, epinephrine and serotonin) are destroyed

by an enzyme called monoamine oxidase (MAO) inside the neuron. An enzyme inhibitor
prevents the MAO from destroying the NT.

However…MAOs are also located in the liver and are responsible for breaking
down all monoamines, including food substances and drugs. Tyramine, for
 example (found in aged cheese, pickled and smoked herring, and wine) is a
monoamine that must be broken down by MAOs. If not broken down, tyramine
can cause life-threatening hypertension.

Reuptake Inhibition (Increases NT action)

Example: Tricyclic Antidepressants

In depression, the NTs norepinphrine and serotonin are thought to be decreased. To

elevate the levels of NT in the synapse, reuptake inhibitors block the pre-synaptic
receptors preventing the reabsorption of the NT by the cell that released it.

However…the molecules that bind to the pre-synaptic receptors, also tend to bind with the
muscarinic receptors for acetylcholine, the alpha-1 receptors for norepinephrine and the
H-receptors for histamine.

This results in the anticholinergic effects of dry mouth, blurred vision, constipation
and urinary retention; the orthostatic hypotension and erectile dysfunction
associated with norepinephrine blockage; and sedation and weight gain
associated with histamine blockage.

Selective Reuptake Inhibition (Increases NT action)

Example: SSRIs (Selective Serotonin Reuptake Inhibitors)

To counter the side effects of general reuptake inhibition, some drugs preferentially block
the uptake of certain NTs. SSRIs target only serotonin pre-synaptic receptors and
therefore do not bind with the muscarinic, adrenergic or histaminergic receptors, and
thereby reduce the anticholinergic and antihistamine side effects.

However…in depression, a decrease in norepinephrine is accompanied by the

decrease in serotonin. SSRIs do not elevate levels of NE, and are therefore not
as effective as other antidepressants that elevate levels of both NTs.

Autoreceptor Blockage (Increases NT action)

Example: Buspirone

Another way to elevate levels of NT at the synapse is to deactivate the mechanism for
shutting off its release. Pre-synaptic cells contain an autoreceptor that binds with the NT.
When the autoreceptor is bound, the release of the NT is stopped. Autoreceptor blockers
prevent the NT from binding with the autoreceptors, and as a result, the NT continues to
be released into the synapse.
DRUG CLASSES

ANTIPSYCHOTICS

Traditional: Phenothiazides, thioxanthenes, butyrophenones

 All block dopamine receptors (and muscarinic, alpha-1, and H receptors)
 Treat positive symptoms of schizophrenia
 All cause extrapyramidal (EPS) side effects that may not be reversible
 Parkinsonism, akinesia, alcathisia, dyskinesia, tardive dyskinesia

Atypical: Block serotonin and dopamine receptors. Have fewer side effects than traditional.
• Clozapine (Clozaril)
• Blocks dopamine in the limbic system only (no motor dysfunction)
• Side Effects: Bone marrow suppression (agranulocytosis); convulsions;
myocarditis; sedation, hypersalivation, tachycardia, dizziness.
• Not a first choice drug because of side effects.
• Risperidone (Risperdal)
• Treats both positive and negative symptoms of schizophrenia.
• No motor dysfunction at normal doses.
• Elderly at increased risk of CVA with dementia and agitation
• Side Effects: weight gain, sexual dysfunction
• Quetiapine (Seroquel)
• Binds with broad range of receptors (dopamine, serotonin, histamine,
norepinephrine, acetylcholine)
• Best with Lewy Body Dementia
• Not for use with Alzheimer’s or vascular dementia
• Side effects: weight gain, sedation

• Olanzapine (Zyprexa)
• A derivative of clozapine
• Antagonist of serotonin, dopamine, histamine, norepinephrine and muscarinic
receptors.
• Side effects: anticholinergic effects, sedation, hyperglycemia and Type II
diabetes mellitus
• Ziprasidone (Geodon)
• Affects serotonin and norepinephrine
• Acts as both a reuptake inhibitor and binds serotonin, dopamine, norepinephrine
and histamine receptors
• Side effects: anticholinergic effects, sedation and can prolong the QT interval
(may be fatal with a history of arrhythmia).
• Aripiprazole (Abilify)
• Partial agonist at dopamine receptor site (stabilizes dopamine system)
• Can decrease dopamine if too much is released, or it can stimulate receptors to
increase dopamine levels if not enough.
• Side effects: sedation, hypotension, anticholinergic effects
ANTIDEPRESSANTS

All antidepressants carry an FDA warning for children/adolescents and suicide.

Tricyclic (TCA): Amitriptyline (Elavil); imipramine (Tofranil); nortriptyline (Pamelor)

 Block reuptake of norepinephrine and serotonin (to a lesser degree) preventing their
destruction and increasing their level at the synapse
 Also block muscarinic and histamine receptors
 Unsure about mechanisms for helping depression, but they do work.
 Side effects: sedation, anticholinergic effects, seizures, arrhythmias, heart block, CVA,
hypoglycemia.

MAOIs Isocarboxazid (Marplan); phenelzine (Nordil); tranylcypromine (Parnate)

• Prevents monoamine oxidase from destroying dopamine, norepinephrine, and serotonin
after reuptake.
• Increases synaptic level of neurotransmitters resulting in anti-depressant effects.
• Avoid foods containing tyramine because MAO is prevented from breaking down this
amino acid. May result in fatal hypertensive crisis.
• Prevents the liver from breaking down other drugs containing monoamines, thereby
increasing the risk for toxicity.

SSRIs Fluoxetine (Prozac); sertraline (Zoloft); paroxetine (Paxil); citalopram (Celexa); escitalopram
(Lexapro)
• Block the reuptake and destruction of serotonin only
• Has a decreased ability to block the muscarinic and histamine receptors than the TCAs,
therefore fewer anticholinergic/sedative effects MAOIs

Atypical/Novel Venlafaxine (Effexor); duloxetine (Cymbalta); mirtazapine (Remeron)

• SNRIs: Serotonin and norepinephrine reuptake inhibitors
Bupropion (Wellbutrin);
• Dopamine and norepinephrine reuptake inhibitor
• Seems to block nicotinic receptors
• Effective antidepressant and first-line smoking cessation drug
Trazodone (Desyrel)
• Probably a serotonin reuptake inhibitor
• Most common side effect is sedation
• Not used often because of it sedative effects.
• May potentiate digoxin.
ANTIANXIETY (“Anxiolytics”)

Benzodiazapines: Diazepam (Valium); clonazepam (Klonopin); alprazolam (Xanax)

• All bind to (benzodiazepine) receptors adjacent to GABA receptors, potentiating the
effects of GABA.
• Benzodiazapines do not inhibit neurons in the absence of GABA.
• Side effects: sedation
• Flurazepam (Dalmane) and triazolam (Halcion) create a hypnotic effect and
increase sedation
• Lorazepam (Ativan) and alprazolam (Xanax) decrease anxiety without sedation.
• Used alone, these drugs rarely result in respiratory depression, coma or death.
However, used in conjunction with other CNS depressants (alcohol, opiates), they
can be life-threatening.
Atypical: Buspirone (BuSpar)
• Seems to act as a serotonin autoreceptor blocker, thereby increasing synaptic level
of serotonin.
• Does not have a strong sedative effect.
• Is not a CNS depressant
• Does not have an addiction potential

Antidepressants: Some antidepressants may also treat anxiety disorders.

• Imipramine (Tofranil)—a TCA—is used to treat panic attacks.

• SSRIs are used to treat obsessive/compulsive disorder

• Sertraline (Zoloft)—an SSRI—is used to treat social phobias.

ATTENTION DEFICIT

Psychostimulants: Methylphenidate (Ritalin); dextroamphetamine (Adderall)

• Attention deficit results from an overactive limbic system.
• Drugs seem to work by increasing the release and blocking the reuptake of
monamines.
• Side effects: agitation; increased psychotic thought processes; hypertension; long-
term growth suppression; abuse potential.

Non-stimulant: Atomoxetine HCl (Strattera)

• Acts as a norepinephrine reuptake inhibitor
• May be used in children over 6 years of age
• Side effects: decreased appetite; weight loss; fatigue; dizziness

ALZHEIMER’S DISEASE

Anticholinesterase: Tacrine (Cognex); donepezil (Aricept); rivastigmine (Exelon); galantamine

(Reminyl)
• Memory loss in Alzheimer’s is related to decrease in acetylcholine, resulting in
plaques and nerve tangles in the brain.
• Drugs cannot cure the disease, but may slow the symptoms and increase memory
function
 • Work by disrupting the enzyme acetylcholinesterase (which destroys acetylcholine
in the synapse).
• Tacrine (Cognex) has lots of side effects: nausea, abdominal distress, increased
heart rate, liver toxicity. Need to perform liver function tests regularly.
• Donepazil (Aricept) has fewer side effects than tacrine. However, it causes
sedation, nausea and diarrhea.
NMDA Receptor Blocker: Memantine HCl (Namenda)
• Antagonizes N-methyl-D-aspartate (NMDA) receptors, the persistent activation of
which seems to increase Alzheimer’s symptoms.
• Is the only drug for moderate to severe dementia related to Alzheimer’s.
• Renal impairment may be a side effect.

MOOD STABILIZERS (BIPOLAR DISORDER)

Lithium: Lithium (Escalith; Lithobid)

• Lithium is a charged ion (electrolyte)
• It may act by affecting the electrical conduction of the neuron
• May interact with sodium and potassium
• Its interaction/disruption to normal sodium/potassium processes makes it a threat to
all body functions
• Cardiac contractions (arrhythmias)
• Brain conductivity (seizures)
• Nerve/muscle impulses (motor side effects like tremors or weakness)
• Can affect fluid balance (polyruia, edema)
• Long term use increases risk to kidneys and thyroid
• Has the lowest therapeutic dose of all psych drugs.
• Side effects: tremor, ataxia, confusion, convulsions, N/V, diarrhea, arrhythmias,
polyruia, polydipsia, edema, goiter, hyperthyroidism
• Monitor blood levels closely!
Anticonvulsants: Carbamazepine (Tegretol); valproic acid (Depakote); lamotrigine (Lamictal);
Lamotrigine
• All are used to calm the manic client before long-term stabilization with lithium
• Valproic acid and carbamazepine may be used long-term when lithium cannot be
tolerated.
• Carbamazepine is similar to TCAs in structure and serves as a neuron analgesic
(calms excited nerves).
• Side effects are nausea, sedation, ataxia, rash, possible liver effects
• Regularly check liver functioning, CBC, ECG and electrolytes
• Valproic acid is probably first choice over lithium and carbamazepine
because it is better tolerated.
• Is recommended for mixed episodes and rapid cycling
• Side effects: alopecia, tremor, weight gain, sedation
• Newest approved anticonvulsant for use for bipolar is Lamotrigine.
• Used for acute and long-term management of mania/bipolar
• Has well-tolerated side effects; but may have a rare life-threatening
dermatologic effect.
• Calcium channel blockers and thyroid hormones have also been used
to treat manic/bipolar disorder.