Ch 18 Psychiatric Disorders
Psychiatric Disorders
 Disorders of psychological function sufficiently
severe to require treatment
 Diagnosis can be difficult
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Patients with the same disorder can display different
symptoms
Patients with different disorders can display many of the
same symptoms
 Diagnosis based on info from the DSM (Diagnostic
& Statistical Manual of the American Psychiatric
Association)
Psychiatric Disorders
 Schizophrenia
 Affective Disorders: Depression & Mania
 Anxiety Disorders
 Tourette Syndrome
Schizophrenia
 Means “splitting of psychic functions”
 The disorder most commonly associated with
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madness
Affects 1% of the population
Typically begins in adolescence or early adulthood
Complex & diverse symptoms that overlap with those
of other disorders
Symptoms frequently change during progression of
the disorder
No single symptom appears in all cases
Schizophrenia
 Symptoms split into 2 categories:
1. Positive:

Symptoms that seem to represent an excess or distortion of
normal function
2. Negative:
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Symptoms that seem to represent a reduction or loss of
normal function
Positive Symptoms of Schizophrenia
 Delusions
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Delusions of being controlled, persecution, or grandeur
 Hallucinations
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Imaginary voices making critical comments or telling the
individual what to do
 Inappropriate affect
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Failure to react with the appropriate emotion to events
 Incoherent speech or thought
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Illogical thinking, echolalia (vocalized repetition of some or all of
what was heard), peculiar associations among ideas, belief in
supernatural forces
 Odd behavior
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Difficulty performing everyday tasks, lack of personal hygiene,
talking in rhymes, catatonia (remaining motionless, often in
awkward positions)
Negative Symptoms of Schizophrenia
 Affective flattening
 Reduction or absence of emotional expression
 Alogia
 Reduction of absence of speech
 Avolition
 Reduction or absence of motivation
 Anhedonia
 Inability to experience pleasure
Causal Factors in Schizophrenia
 Genetic component
 But experience also plays a role
 Some people inherit a potential for the disorder & it
may or may not be activated based on experience
 Factors that can contribute to the development of
schizophrenia
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Birth complications, early infections, autoimmune reactions,
toxins, traumatic injury & stress
Dopamine Theory of Schizophrenia
 First suggested by the fact that early antipsychotic
drugs (chlopromazine & reserpine) caused
motor effects like those of Parkinson’s
 Theory that schizophrenia is caused by the presence
of too much dopamine
 Amphetamine & cocaine, which increase dopamine,
can cause schizophrenic episodes in healthy people
Dopamine Theory of Schizophrenia
 Discovery that there are 5 subtypes of dopamine
receptors (D1-D5)
 Drugs worked in different ways because they acted
on different receptor subtypes
 Schizophrenia is caused by hyperactivity specifically
at D2 receptors
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Widely accepted, but still doesn’t explain the whole picture
 Neuroleptics: antischizophrenic drugs
 Higher affinity for D2 correlates to effectiveness
Limitations of the Dopamine Theory
 4 key discoveries that cannot by explained by the D2
version of the theory:
1. Receptors other than D2 are involved
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Glutamate, GABA & 5-HT
Atypical neuroleptics developed to act on these non-D2
receptors (ex: clozapine)
2. It takes weeks of neuroleptic therapy to alleviate
symptoms
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Despite the fact that neuroleptics can block activity at D2
receptors within hours
Limitations of the Dopamine Theory
3. Schizophrenia is associated with widespread brain
damage
Not just limited to dopaminergic circuits
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4. Neuroleptics are only marginally effective
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Not effective in all cases
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When they do have an effect, it is generally only on some of
the symptoms
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More effective in treating the positive symptoms
Affective Disorders: Depression & Mania
 Affective Disorders: Any psychiatric disorder
characterized by disturbances of mood or emotion
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Aka mood disorders
Depression
 Experiencing periodic depression is a normal
reaction to loss
 However, some people have an increased tendency
toward depression
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They repeatedly fall into deep despair & experience
anhedonia (inability to experience pleasure), often for no
apparent reason
Depression
 Depression can be so extreme that it is almost
impossible for them to complete necessary daily
tasks (keep a job, relationships, eating, personal
hygiene)
 Often have sleep issues & thoughts of suicide
 When this condition lasts over 2 weeks, it is
classified as clinical depression or major
depressive disorder
Mania
 Mania: Characterized by overconfidence,
impulsivity, distractibility & high energy
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Generally the opposite of depression
 During mild mania:
 Talkative, energetic, impulsive, positive & very confident
 Can be great at a job and/or very fun
 Full-blown mania:
 Unbridled enthusiasm, incessant talking that jumps topics,
grandiosity, high energy, distractability, impulsiveness
 Often leads to disaster, failed relationships, unfinished
projects
Major Categories of Affective Disorders
 Bipolar affective disorder:
 Depressive patients who experience periods of mania
 Unipolar affective disorder:
 Depressive patients who do not experience mania
 Reactive depression:
 Depression triggered by a negative experience (a death, job
loss)
 Endogenous depression:
 Depression with no apparent cause
 Probability of suffering from clinical depression
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during a lifetime is 10%
Women 2x more unipolar affective disorder than
men (bipolar equal)
Risk of suicide in clinically depressed individuals is
5%
Affects all ages
Affective disorders associate with heart disease
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And bone loss in women
Causal Factors in Affective Disorders
 Genetic factors
 Seasonal affective disorder (SAD):
 Attacks of depression & lethargy recur every winter
 Triggered by reduction of sunlight
 Light therapy can reduce symptoms
 Postpartum depression:
 Depression experienced by some women after giving birth
Antidepressant Drugs
 4 major classes of drugs for the treatment of
affective disorders:
1. Monoamine oxidase inhibitors
2. Tricyclic antidepressants
3. Selective monoamine-reuptake inhibitors
4. Mood stabilizers
Monoamine Oxidase Inhibitors (MAOIs)
 Monoamine agonist that increases the levels of
monoamines by inhibiting the activity of monoamine
oxidase (MAO), the enzyme that breaks down
monoamine NTs
 MAO inhibitors have several side effects, including
the cheese effect
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Consuming foods high in tyramine
(cheese, wine, pickles) have risk of stroke
from surges in blood pressure
Tricyclic Antidepressants
 Named for the 3 rings of their chemical structure
 Work by blocking the reuptake of serotonin &
norepinephrine
 Safer than MAOIs
Selective Monoamine-Reuptake Inhibitors
 Selective serotonin-reuptake inhibitors (SSRIs):
 Serotonin agonists that block the reuptake of serotonin from
the synapse
 Prozac, Paxil, Zoloft, etc.
 Few side effects
 Act against a wide range of
psychological disorders in addition
to depression
 Selective norepinephrine-reuptake inhibitors
(SNRIs)
Mood Stabilizers
 Developed because other antidepressants often
triggered mania
 Mechanism of action is unknown
 Ex: Lithium (a metallic ion)
Brain Pathology & Affective Disorders
 MRI studies have shown reductions in overall brain
size & in many different brain structures in bipolar
patients
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However, lots of variation
 2 structures are often abnormal:
 Amygdala
 Anterior cingulate cortex
 (and often the connections between them)
Monoamine Theory of Depression
 Depression is associated with underactivity at
serotonergic & noradrenergic synapses
 Largely based on the fact that many of the drugs
found to alleviate depression work as agonists of 5HT, NE or both
 Up-regulation: A compensatory increase in # of
receptors for a NT when there is an insufficient
amount of that NT released at a synapse
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Autopsies of clinically depressed individuals often have more
5-HT & NE receptors than normal
Diathesis-Stress Model of Depression
 Some people inherit a diathesis (genetic
susceptibility) & stress exposure in early life causes
them to be permanently sensitized, causing them to
overreact to mild stressors for the rest of their lives
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The diathesis alone cannot initiate the disorder
 Indirect evidence
 Depressed individuals release more stress hormones
Treatment of Depression with Brain Stimulation
 Significant therapeutic effects of chronic brain
stimulation through an implanted electrode
 Stimulates the anterior cingulate gyrus
 Permanently embedded under the skin to give
continual pulses
 Extreme measure given to those who do not respond
to conventional treatments
Anxiety Disorders
 Anxiety: Chronic fear that persists in the absence of
any direct threat
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Psychological correlate of stress
Adaptive when it motivates effective coping behaviors
Maladaptive when it is so severe it disrupts normal functioning
(anxiety disorders)
 Anxiolytic: anxiety reducing
 Anxiogenic: anxiety provoking
Anxiety Disorders
 All anxiety disorders associated with feelings of
anxiety (fear, worry, despondency) & variety of
physiological stress reactions (tachycardia,
hypertension, nausea, breathing difficulty, sleep
disturbances, high glucocorticoid levels)
 Most prevalent psychiatric disorder
 17% of people have one at some point in their lives
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Women 2x
5 Classes of Anxiety Disorders
1. Generalized Anxiety Disorders:
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Characterized by stress responses & extreme feelings of
anxiety that occur in the absence of any obvious reason
2. Phobic Anxiety Disorders:
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Similar to GAD but triggered by a specific object (ex:
spiders, dogs) or situation (ex: flying, darkness)
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Agoraphobia: pathological fear of public places & open
spaces
3. Panic Disorders:
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Characterized by rapid-onset attacks of extreme fear &
severe symptoms of stress (choking, heart palpitations,
shortness of breath)
5 Classes of Anxiety Disorders
4. Obsessive-Compulsive Disorders:
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Characterized by frequently recurring, uncontrollable,
anxiety-provoking thoughts (obsessions) & impulses
(compulsions)
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The compulsive behavior is done to alleviate the anxiety
associated with the obsessions
5. Posttraumatic Stress Disorder:
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Persistent pattern of psychological distress following
exposure to extreme stress (ex: war, sexual assault)
Etiology of Anxiety Disorders
 Genetic component
 Large experiential component
 Because the anxiety often has an identifiable trigger, it is easier
to assess the influence of experience in these types of disorders
Pharmacological Treatment of Anxiety Disorders
 3 categories of drugs
1. Benzodiazepines
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Most widely prescribed psychoactive drugs
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Ex: Valium
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Several adverse side effects
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Highly addictive; so only for short-term use
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Thought to work by agonizing GABA receptors
2. Serotonin Agonists
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Advantage of specificity; doesn’t cause the side effects associated with
benzos
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But does have its own side effects
3. Antidepressant Drugs
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Common comorbidity (tendency to occur together in the same
individual) of depression & anxiety
Neural Bases of Anxiety Disorders
 Substantial overlap in brain areas involved in anxiety
& affective disorders
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Amygdala, anterior cingulate cortex
But with anxiety disorders, there is no gross damage (as
opposed to shrinkage with affective)
Increased activity in the amygdala of a phobic patient when
shown a picture of ex: a spider
Tourette Syndrome
 A disorder of tics
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Involuntary, repetitive, stereotyped movements of vocalizations
 Many people with this disorder have no symptoms other
than tics
 Typically begins in childhood with simple motor tics
(blinking), with symptoms growing more complex &
severe with age (hitting, hopping, lewd gestures)
 Verbal tics can include barking, grunting, cursing
(coprolalia), echolalia
 Symptoms usually reach a peak after a few years & often
subside as the patient matures
Tourette Syndrome
 0.7% of the population
 3x more frequent in males
 Major genetic component
 Some patients also have ADD/ADHD and/or OCD
 Although tics are involuntary, they can be
temporarily be suppressed with great effort from the
patient
Neuropathology of Tourette Syndrome
 Very difficult to study
 People with this disorder often have smaller caudate
nuclei
 Some evidence of thinning in sensorimotor cortex
areas that control the face, mouth & voice box
Treatment of Tourette Syndrome
 Tics usually treated with neuroleptics
 Can reduce tics by about 70%
 However, often patients won’t take them because of the
adverse side effects