Transcript Psychiatric DOs

Rene M. Samaniego, M.D., FPPA
Makati Medical Center
Consultation-Liaison Psychiatry
Cognitive-Behavioral Therapy
Psychiatric DOs (?)
GMC (?)
Substances (?)
(prescription, nonprescription,
illegal)
‘Nonorganic’ or
‘Functional’ or ‘Primary’
Psychiatric DOs (?)
‘Organic’
GMC (?)
Substances (?)
(prescription, nonprescription,
illegal)

Evidence from history, P.E., or laboratory findings
that disturbance is the direct physiological
consequence of a GMC
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30-year old female
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Psychiatric: depressed affect; lethargy; difficulty in
concentration; psychomotor retardation
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Medical: cold intolerance, dry skin, constipation,
weight gain, brittle hair
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TFT: TSH; FT4
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Evidence from history, P.E., or laboratory findings
that disturbance is the direct physiological
consequence of a GMC
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Require two things: 1) presence of a GMC; 2) the
psychiatric disorder is etiologically related to the
GMC through a physiological mechanism
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The GMC may be part of the psychiatric
disturbance, but not the sole etiology of it
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Temporal association between the onset,
exacerbation, or remission of the GMC & mental
DO
E.g., symptoms of anxiety in parathyroid adenoma that
resolve after surgical excision & restoration of a normal serum
calcium level
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Treatment of GMC that alleviates the psychiatric
symptomatology may provide stronger evidence
of an etiological relationship
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Some psychiatric disorders may emerge several
years after the onset of the medical problem
E.g., psychosis secondary to epilepsy
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Signs and symptoms of a psychiatric DO can be
among the first to appear before the detection of
the underlying GMC
E.g., depression preceding choreiform movements in
Huntington’s disease; depression before detection of
pancreatic CA
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A psychiatric DO due to a GMC can be amenable
to symptomatic treatment even while the GMC
remains active
E.g., depression in epilepsy
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Presence of atypical features of the primary mental
DO
Atypical onset or course  e.g., acute
schizophrenic-like symptoms in a 75-y.o. individual
 Unusual associated features or symptoms  e.g.,
visual or tactile hallucinations in major depression
 Features disproportionately more severe than
would be expected given the overall presentation
 e.g., a 50-pound weight loss in a mildly
depressed individual
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The co-occurrence of a psychiatric DO and a
GMC may also be just coincidental
E.g., Depressive episode precipitated by stroke acting as a
psychosocial stressor, rather than resulting from the direct
physiological effects of the stroke
E.g., Patient with a history of depressive episodes suddenly
developed signs and symptoms of hypothyroidism
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The disturbance should not be better
accounted for by another mental disorder
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The disturbance does not occur exclusively
during the course of a delirium
First, exclude syndromes in which
psychotic symptoms may be
present in association with
cognitive impairment (e.g.,
delirium, dementia, and amnestic
disorder)
Psychosis is usually NOT
associated with changes in the
level of sensorium
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Etiology: Cerebral or systemic disease that affects
brain function
Infections
Intracranial Masses
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Tumors
Subdural masses
Brain abscess
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Trauma
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Head injury
Neurodegenerative DOs
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Parkinson’s Disease
Huntington’s Disease
Pick’s Disease
Amyotropic Lateral Sclerosis
Wilson’s Disease
Creutzfield-Jakob Disease
AIDS
Viral encephalitis
Neurosyphilis
Meningitis
Nutritional DOs
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Wernicke-Korsakoff syndrome
(thiamine deficiency)
Vitamin B12 deficiency
Folate deficiency
Pellagra
Substances
Metabolic DOs
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Hypothyroidism & Hyperthyroidism
Renal insufficiency, severe
Cushing’s syndrome
Hepatic insufficiency
Parathyroid disease
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Chronic Inflammatory DOs
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Systemic Lupus Erythematosus
Multiple Sclerosis
Whipple’s Disease
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Alcohol
Amphetamines
Cocaine
Phencyclidine
Hallucinogens
Sedative, hypnotic, & anxiolytics
Cannabis
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Course & Prognosis: depend largely on the etiology
E.g., psychotic symptoms secondary to head trauma improve
dramatically during recovery
E.g., infectious process causing irreversible CNS tissue
damage, psychotic symptoms may not improve despite
treatment of the infection
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Treatment: Basic principles involve rapid
identification and treatment of the underlying
cause
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Standard treatments for symptomatic relief (e.g.,
anti-psychotics)
Characterized by:
1)depressed
mood - prominent,
persistent, distressing, & functionally
impairing
2)elevated, expansive, or irritable
mood
The mood manifestation can either
be depressed, manic, or mixed
Fully or partly fulfill criteria
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Epidemiology: unknown
Depression in medically ill slightly higher in men
Illnesses in which depressive episodes are common: strokes,
Parkinson’s disease, Huntington’s disease, HIV infection, & MS
Manic symptoms less prevalent in neurological disease than
depression
Trauma
Drug Intoxication
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Alcohol or sedative-hypnotics
Antipsychotics/Antidepressants
Metoclopramide, H2 blockers
Antihypertensives
Sex steroids
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Drug Withdrawal
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Nicotine, caffeine, alcohol or
sedative-hypnotics, cocaine,
amphetamines
Tumors
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1* cerebral
Systemic neoplasm
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Cerebral contussion
Subdural hematoma
Infection
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Cerebral (e.g., HIV, meningitis,
encephalitis, syphilis)
Systemic (e.g., sepsis, UTI, PN)
Cardiac & Vascular
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Cerebrovascular (e.g., infarcts,
hemorrhage, vasculitis)
Cardiovascular (e.g., low-output
states, CHF)
Demyelinating Diseases
Physiological or Metabolic
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Hypoxemia
Electrolyte disturbances
Renal or hepatic failure
Hypo- or hyperglycemia
Post-ictal states
Endocrine
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Thyroid or glucocorticoid
disturbances
Nutritional
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Vitamin B12 deficiency
Folate deficiency
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Multiple sclerosis
Neurodegenerative Diseases
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Parkinson’s disease
Huntington’s disease
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Depressive symptoms: depressed mood; decrease interest in
activities; poor sleep & appetite; lethargy; psychomotor
agitation/retardation; feelings of worthlessness, excessive
guilt; poor concentration & indecisiveness; recurrent thoughts
of death or suicidal ideations
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Manic symptoms: mood persistently elevated, expansive,
irritable; inflated self-esteem; decreased need for sleep; more
talkative than usual; flight of ideas or racing thoughts;
distractibility; increase in goal-directed activities
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Course & Prognosis: Secondary depressive
disorders have poorer prognosis than primary
depression; usually runs a chronic course,
characterized by remissions & recurrences, and
sometimes by continuous illness
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Prognosis will depend on the etiology
E.g., depression secondary to hypothyroidism has a better
outcome than depression in metastatic pancreatic
carcinoma
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Treatment: resolving the underlying medical cause
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Standard treatments: antidepressants (SSRIs,
tricyclics, MAOIs, & psychostimulants)
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Psychotherapy: an adjunctive approach
The concept of psychiatric disturbance secondary
to a medical illness difficult for many patients to
grasp
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Key feature: presence of
anxiety symptoms
(generalized anxiety, panic
attacks, obsessivecompulsive symptoms, or
phobias)
Endocrinopathies
Substance Intoxication
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Caffeine
Amphetamines, cocaine, & other
sympathomimetic agents
Alcohol
Cannabis
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Metabolic Derangements
Substance Withdrawal
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Caffeine
Nicotine
Alcohol
Sedative-hypnotics
Pheochromocytoma
Hyperthyroidism &
hyperparathyroidism
Hypercortisolemic states (adrenal
dysfunction)
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Hypoxemia
Hypercalcemia
Hypoglycemia
Caffeine
Caffeine
Caffeine
 1 cup of coffee = 100–150mg
caffeine
 Caffeine Intoxication –
consumption of caffeine in
excess of 250mg at one time
Caffeine Intoxication
 Tachycardia or cardiac
arrythmia
 Diuresis
 GI disturbances
 Restlessness, nervousness
or excitement
 Rambling flow of thought &
speech
 Insomnia; etc
Caffeine
Beverage
Caffeine
Regular brewed coffee
170-200 mg
Decaffeinated brewed coffee
10 mg
Instant coffee
90-140 mg
Brewed tea
60-100 mg
Canned iced tea
25-35 mg
Cola drinks
40-60 mg
Dark chocolate
20 mg
Milk chocolate
6 mg
***Daily limit of 200 mg  recommended by the AMA
Caffeine
 Caffeine withdrawal –
results from a prolonged daily
intake of caffeine followed by
an abrupt cessation, or
reduction in the amount of
use
 Usually lasts 4 to 5 days
Nicotine
Nicotine
 A ‘psychostimulant’
 Associated with chronic
obstructive pulmonary
disease, cancers,
coronary heart disease,
peripheral vascular
disease
Nicotine Withdrawal
 Nicotine craving
 Frustration, irritability, &
anger
 Anxiety
 Difficulty concentrating
 Restlessness
 Bradycardia
 Increased appetite
Alcohol
Alcohol Intoxication
 A ‘depressant’
 Can hasten onset of
sleep, BUT can disrupt
normal sleep cycle
 Sedative effect & ready
availability  used to
relieve anxiety,
insomnia, & depression
Alcohol Intoxication
 Maladaptive behavioral
changes
 Mild intoxication:
relaxed, talkative,
euphoric, disinhibited
Alcohol Intoxication
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Slurred speech
Incoordination
Unsteady gait
Memory impairment
Stupor
‘Blackouts’
Alcohol Withdrawal
 Begins within several
hours after cessation of,
or reduction in,
prolonged heavy alcohol
consumption
Alcohol Withdrawal
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Autonomic hyperactivity
Hand tremor
Insomnia
Nausea & vomiting
Transient illusions or
hallucinations
 Anxiety
 Seizures
Endocrinopathies
Substance Intoxication
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Caffeine
Amphetamines, cocaine, & other
sympathomimetic agents
Alcohol
Cannabis
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Metabolic Derangements
Substance Withdrawal
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Caffeine
Nicotine
Alcohol
Sedative-hypnotics
Pheochromocytoma
Hyperthyroidism &
hyperparathyroidism
Hypercortisolemic states (adrenal
dysfunction)
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Hypoxemia
Hypercalcemia
Hypoglycemia
Neurologic DOs
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Vascular (cerebrovascular
disease, subarachnoid
hemorrhage, migraine)
Trauma (cerebral trauma & postconcussive syndromes)
Degenerative types (Huntington’s
disease)
Systemic Conditions
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Hypoxia (cardiovascular diseases,
cardiac arrhythmia, pulmonary
insufficiency, anemia)
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Course & Prognosis: Depend on the specific cause
E.g., anxiety due to hyperthyroidism remits well with treatment
E.g., anxiety due to cardiomypathy with a low-output state
may run a more chronic course
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Treatment: Treat the underlying cause
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Symptomatic treatment with benzodiazepines &
antidepressant medications (like SSRIs) to treat
specific symptoms (panic attacks or obsessivecompulsive symptoms)
Insomnia: deficiency of sleep
Hypersomnia: excess of sleep
Parasomnia: abnormal
behavior or activity during
sleep
Circadian Rhythm Sleep
Disorder: disturbance in the
timing of sleep
Condition
Sleep Symptoms
Parkinsonism
Frequent awakenings,
disturbance of circadian
rhythm
Dementia
Sundowning, frequent
awakenings
Epilepsy
Diff. initiating sleep, frequent
awakenings, parasomnias
Cerebrovascular Disease
Diff. initiating sleep, frequent
awakenings
Huntington’s Disease
Frequent awakening
Kleine-Levin Syndrome
Hypersomnia
Uremia
Restless legs, nocturnal
myoclonus
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Treatment: Identification and treatment of the
cause
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Symptomatic treatments:
1) sedative-hypnotics for insomnia
2) stimulants for hypersomnia
3) benzodiazepines for restless leg syndrome or
nocturnal myoclonus
4) antidepressants (tricyclics) for regulation of REM
sleep for circadian rhythm sleep disorders
1.
Female or male
hypoactive sexual desire
DO
1.
Male erectile DO
2.
Dyspareunia
Local Disease Processes that
Affect 1* or 2* Sexual Organs
Medications
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Cardiac drugs (anti-hypertensives
e.g., β-blockers, clonidine,
diuretics)
H2 blockers
Anti-cholinergics
Anti-convulsants
Anti-psychotics/Anti-depressants
Sedative-hypnotics
Substances of Abuse
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Alcohol
Opioids
Stimulants
Cannabis
Sedative-hypnotics
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Congenital anomalies or
malformations
Trauma
Tumors
Infection
Post-surgical or post-irradiation
neurological & vascular
pathology
Neurological
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CNS (e.g., strokes, multiple
sclerosis)
PNS (e.g., peripheral neuropathy)
Vascular
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Atherosclerosis
Vasculitis
Endocrine
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Diabetes Mellitus
Alterations in thyroid function,
adrenal cortex, gonadotropins,
gonadal hormones
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Course & Prognosis: Depends on the cause
E.g., Drug-induced syndromes generally remit with
discontinuation (or dosage reduction) of the offending
agent; endocrine-based dysfunctions also improve with
restoration of normal physiology
E.g., sexual dysfunctions due to neurological disease,
protracted or progressive
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Treatment: Varies widely
Address underlying pathology
 Symptom-based treatments: for male ED, you may
give pharmacological agents like sildenafil
(Viagra) or surgical implantation of a penile
prosthesis
 When reversal of underlying cause is not possible,
supportive and behaviorally oriented
psychotherapy (include both patient & partner);
psychoeducation & development of sexual
interactions not limited by dysfunction
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Motoric immobility (assuming fixed
postures & waxy flexibility)
Excessive motor activity (purposeless
& not influenced by external stimuli)
Extreme negativism or mutism
Peculiarities of voluntary movement
Echolalia or echopraxia
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Common causes: neoplasms, encephalitis, head
trauma, diabetes, metabolic disorders
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Course & prognosis: Depend on the etiology
Treatment: Resolve underlying cause; antipsychotic
medications may improve postural abnormalities
even though no effect on underlying disorder
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Note: Always rule out schizophrenia in patients with
catatonic symptoms
Personality change – the person’s
fundamental means of interacting &
behaving have been altered
If you have an adult individual who
suddenly develops significant
personality change, always suspect
a brain injury
Specific personality trait changes for
specific brain diseases: passive &
self-centered behaviors in
Alzheimer’s dementia; or apathy in
frontal lobe lesions
Head Trauma
Multiple Sclerosis (subcortical
white matter degeneration)
Hydrocephalus
Toxins
Frontal Lobe Tumors
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Meningiomas
Gliomas
Progressive Dementia
Syndromes
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AIDS Dementia complex
Huntington’s disease
Progressive supranuclear palsy
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Irradiation with a predilection to
the white matter
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Course & Prognosis: Depends on the etiology
E.g., correction of a hydrocephalus; surgery, chemotherapy,
or radiation therapy of mass lesions can improve the
personality change dramatically
E.g., head trauma, improvement in the personality change is
slow and gradual (months or years), may have residual
personality disturbances
E.g., degenerative processes, disruptive in early phase of
disease, then become more apathetic, unresponsive as
disease progresses
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Treatment: Correct underlying pathology,
symptomatic treatment
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For control of affective symptoms (impulsivity,
aggression, explosiveness): mood stabilizers such as
lithium carbonate, valproic acid, &
carbamazepine; also ß-adrenergic antagonists like
propranolol
For apathy & inertia, psychostimulants
For those whose cognitive & verbal skills are
preserved, psychotherapy
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In DSM-IV-TR classification, clustered
together & apart from the
secondary psychiatric disorders
Defined by impairment in cognition
(specifically memory, language, and
attention)  cognitive impairment is
their cardinal symptom
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Considered as a syndrome, not a disease entity
Underrecognized & underdiagnosed
A.k.a. acute confusional state, acute brain
syndrome, metabolic encephalopathy, toxic
psychosis, acute brain failure
Hallmark of delirium: impairment of consciousness
in association with global impairments of cognitive
functions
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Psychiatric symptoms
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Abnormalities in mood  irritability, dysphoria,
anxiety, or euphoria
Abnormalities in perception  illusions or
hallucinations
Decreased level of consciousness  diminished
ability to focus & sustain attention
Disorientation, especially to time & place
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Psychiatric symptoms
Disorganization in their thought process (mildly
tangential to frankly incoherent
Psychomotor hyperactivity or hypoactivity
Disruption of the sleep-wake cycle (fragmentation
of sleep at night with or without daytime
drowsiness)
Neurologically: tremor, asterixis, nystagmus,
incoordination, & unrinary incontinence
Intracranial Causes
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Epilepsy & post-ictal states
Brain trauma (especially
concussion)
Infections (meningitis,
encephalitis)
Neoplasms
Vascular disorders
Extracranial Causes
Drugs (ingestion or withdrawal)
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Anticholinergic agents
Anticonvulsants
Antihypertensive agents
Antiparkinsonian agents
Antipsychotics
Cardiac glycosides
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Opiates
Sedatives
Steroids
Cimetidine, clonidine, disulfiram,
insulin, phenytoin, ranitidine
Poisons
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Carbon monoxide
Heavy metals & other indstrial
poisons
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Endocrine Dysfunction (hyperor hypofunction)
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Pituitary, pancreas, adrenal,
parathyroid, thyroid
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Non-endocrine Diseases
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Liver (hepatic encephalopathy)
Kidney (uremic encephalopathy)
Lung (carbon dioxide narcosis,
hypoxia)
Cardiovascular system (cardiac
failure, arrhythmias, hypotension)
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Deficiency States
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Thiamine, nicotinic acid, B12, or
folic acid deficiencies
Systemic infections (with fever and
sepsis)
Electrolyte imbalance of any
cause
Post-operative states
Trauma (head or general body)
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Course, Prognosis & Treatment
Usually has a sudden onset (hours or days)
 Prodromal symptoms (restlessness & fearfulness)
 Has a brief & fluctuating course, improves rapidly
(within 3 to 7 days) when causative factor is
identified & treated
 General rule: the older the patient and the longer
the patient has been delirious, the longer the
delirium takes to resolve
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Cardinal symptom is cognitive impairment
Unlike delirium, no impairment in consciousness; no
alteration and fluctuation in consciousness
Main manifestation is diminution in cognition:
general intelligence, learning & memory,
language, problem solving, orientation,
perception, attention & concentration, judgment,
& social abilities
Personality changes may also be noted
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Dementia of the Alzheimer’s type – most common
cause (50-60% of the cases); occurs in patients
over 65 y.o.; manifested by progressive intellectual
deterioration, delusions, or depression
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Vascular dementia – next most common cause is
(10-20% of the cases), caused by thrombosis or
hemmorhage
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Dementia secondary to other medical conditions
Neurodegenerative disorders: Parkinson’s or
Huntington’s disease
 Infectious: AIDS, CJD, viral encephalitis
 Nutritional disorders: Wernicke-Korsakoff syndrome
caused by thiamine deficiency
 Metabolic disorders: hypothyroidism &
hyperthyroidism, Cushing’s syndrome
 Chronic inflammatory disease: SLE, & MS
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Dementia can also be substance-induced, either
caused by a medication or toxins
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Dementia due to multiple etiologies
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Dementia, not otherwise specified, in which the
etiology is unknown
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Course & Prognosis: Varies
steady progression (Alzheimer’s dementia)
 incrementally worsening course (vascular
dementia)
 stable dementia (dementia secondary to a head
trauma)
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Treatment: identify the cause, determine whether
reversible or irreversible
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For the reversible dementias (hydrocephalus,
hypothyroidism, or brain tumors) the dementia may
be halted or reversed
For more progressive types (Alzheimer’s dementia),
employ symptomatic treatment  cholinesterase
inhibitors like donepezil (Aricept), rivastigmine
(Exelon); galantamine (Reminyl); tacrine (Cognex),
and memantine (Abixa)
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For psychiatric symptoms associated with
dementia
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Benzodiazepines for insomnia and anxiety
Antidepressants for depression
Antipsychotics for hallucinations and delusions
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Be aware of idiosyncratic effects in the geriatric
population (paradoxical excitement, confusion, &
increased sedation)
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There are a variety of substances (medications,
illegal substances, or toxins) that may cause
different psychiatric DOs
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Considerations: 1) determine that the symptoms
developed within a month of the substance
intoxication or withdrawal; 2) the substance is
etiologically related to the psychiatric DO
1)
2)
3)
4)
If the symptoms precede the onset of the substance or
medication use
If the symptoms persist for a substantial period of time (about
1 month) after the cessation of an acute withdrawal or
severe intoxication
If the symptoms are substantially in excess of what would be
expected, given the type, duration, or amount of the
substance used
If there are other evidence suggesting that there is an
existence of a non-substance-induced DO (history of
recurrent non-substance-related psychiatric episodes)

The psychiatric disorder may be caused by the
combined effects of a GMC and substance use 
dual diagnosis (e.g., Mood DO due to GMC and
Substance-Induced Mood DO)

When the presentation contains a mix of symptoms
(e.g., mood and anxiety) – assign a single diagnosis
based on which symptoms predominate in the
clinical presentation
Thank you!