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DELIRIUM, DEMENTIA,

AND AMNESTIC DISORDERS


 Delirium is marked by short-term
confusion and changes in cognition.

 Dementia is marked by severe


impairment in memory, judgment,
orientation, and cognition.

 Amnestic disorder is marked by


memory impairment and forgetfulness.
Delirium
 defined by the acute onset of fluctuating
cognitive impairment and a disturbance
of consciousness.

 a syndrome, not a disease, and it has


many causes, all of which result in a
similar pattern of signs and symptoms
relating to the patient's level of
consciousness and cognitive impairment
Delirium
 hallmark symptom of delirium is an
impairment of consciousness.

 Abnormalities of mood, perception, and


behavior are common psychiatric
symptoms;

 tremor, asterixis, nystagmus,


incoordination, and urinary incontinence
are common neurological symptoms.
Delirium

 Classically, delirium has a sudden onset


(hours or days), a brief and fluctuating
course, and rapid improvement when the
causative factor is identified and
eliminated

 poor prognostic sign


Delirium

Intensive care unit psychosis


Acute confusional state
Acute brain failure
Encephalitis
Encephalopathy
Toxic metabolic state
Central nervous system toxicity
Paraneoplastic limbic encephalitis
Sundowning
Cerebral insufficiency
Organic brain syndrome
Delirium
 point prevalence in the general
population is 0.4 % for people 18 years
of age and older and 1.1 % for people 55
and older.

 10 to 30 percent of medically ill patients


who are hospitalized exhibit delirium

 highest rate of delirium is found in post-


cardiotomy patients, more than 90
percent
FACTORS THAT PREDISPOSE PATIENTS TO
DELIRIUM:
Vision impairment hypertension Use of bladder catheter

Medical illnesses COPD Preoperative cognitive


(severity and quantity) impairment
Cognitive impairments Alcohol abuse Functional limitations

>70 years old Smoking history History of delirium

Any iatrogenic event Abnormal sodium level Abnormal sodium,


potassium or glucose test
Use of physical restraints Abnormal glucose level Preoperative use of
benzodiazepines
Malnutrition Abnormal bilirubin level Preoperative use of
narcotic analgesics
More than 3 medications BUN:CREA >18 Epidural use
added
Major causes of delirium :

1. central nervous system disease (e.g.,


epilepsy)

2. systemic disease (e.g., cardiac failure)

3. either intoxication or withdrawal from


pharmacological or toxic agents
COMMON CAUSES OF DELIRIUM:
1. CNS disorders – seizure, migraine, head
trauma, brain tumor, nonhemorrhagic stroke,
transient ischemia
2. Metabolic disorder- electrolyte imbalance,
hypoglycemia, hyperglycemia, insulin
resistance
3. Systemic illnesses - infections, trauma, burns,
heatstroke
4. Medications – morphine, steroids,
antihypertensives, anesthesia, neuroleptic
malignant syndrome, serotonin syndrome
COMMON CAUSES OF DELIRIUM

5. Over-the-counter preparations – herbals, teas,


nutritional supplements
6. Botanicals – jimsonweed, oleander, foxglove,
Amanita phalloides
7. Drugs of abuse – intoxication and withdrawal
8. Toxins – heavy metals and aluminum
Core features of Delirium:
1. altered consciousness
2. altered attention
3. impairment in other realms of cognitive
function
4. relatively rapid onset (usually hours to
days)
5. brief duration (usually days to weeks)
6. often marked, unpredictable fluctuations
in severity and other clinical
manifestations during the course of the
day,
Associated Clinical Features:

 Disorganization of thought process


 Perceptual disturbances
 Psychomotor hypo/hyper activity
 Disruption of sleep-wake cycle
 Mood alterations
 Autonomic hyperactivity or instability
 Myoclonic jerking
 dysarthria
 The major neurotransmitter hypothesized
to be involved in delirium is acetylcholine
decreased acetylcholine activity

 the major neuroanatomical area is the


reticular formation. (attention and
arousal)

 major pathway implicated in delirium is the


dorsal tegmental pathway
 One of the most common causes of
delirium is toxicity from too many prescribed
medications with anticholinergic activity.

 delirium associated with alcohol withdrawal


has been associated with hyperactivity of
the locus ceruleus and its noradrenergic
neurons

 Other neurotransmitters: serotonin and


glutamate
 physical examination often reveals clues to
the cause of the delirium.
 Examples:
Bradycardia – Hypothyroidism, Stokes-Adams
syndrome, Increased intracranial pressure
Tachycardia – Hyperthyroidism, Infection, Heart
failure
Fever – Sepsis, Thyroid storm, Vasculitis
Laboratory Workup of the Patient with Delirium
Standard studies
Blood chemistries (including electrolytes, renal and
hepatic indexes, and glucose)
Complete blood count with white cell differential
Thyroid function tests
Serologic tests for syphilis
Human immunodeficiency virus (HIV) antibody test
Urinalysis
Electrocardiogram
Electroencephalogram
Chest radiograph
Blood and urine drug screens
Additional tests when indicated
Blood, urine, and cerebrospinal fluid (CSF) cultures
B12, folic acid concentrations
Computed tomography or magnetic resonance imaging
brain scan
Lumbar puncture and CSF examination
DIFFERENTIAL DIAGNOSES:

1. Dementia
2. Schizophrenia –hallucinations and
delusions are more constant and better
organized; no change in level of
consciousness or orientation;
3. Depression –
4. Dissociative Disorders
5. Factitious Disorders
DEMENTIA VS. DELIRIUM
FEATURE DEMENTIA DELIRIUM

ONSET slow rapid

DURATION Months to years Hours to weeks

ATTENTION preserved fluctuates

MEMORY Impaired remote memory Impaired recent and


immediate memory
SPEECH Word-finding difficulty Incoherent (slow or rapid)

SLEEP-WAKE CYCLE Fragmented sleep Frequent disruption (e.g.


day-night reversal)
THOUGHTS Impoverished Disorganized

AWARENESS Unchanged Reduced

ALERTNESS Usually normal Hypervigilant or reduced


vigilance
 beclouded dementia – when delirium
occurs in a patient with dementia

 sundowning – worsening of clinical


manifestations at night
Treatment :
 The primary goal is to treat the
underlying cause

 The other important goal of treatment is


to provide physical, sensory, and
environmental support (black – patch
delirium)

 The two major symptoms of delirium that


may require pharmacological treatment
are psychosis and insomnia.
 Anticholinergic toxicity – Physostigmine
salicylate (Antilirium) 1-2 mg IV or IM
with repeated q 15 – 30 minutes

 Psychosis - Haloperidol

 Insomnia – Benzodiazepines
(Lorazepam 1 -2 mg at bedtime)
Dementia

 is defined as a progressive impairment


of cognitive functions occurring in clear
consciousness.

 Global impairment of intellect is the


essential feature
Dementia
 prevalence of moderate to severe
dementia in different population groups:
 approximately 5% in the general
population >65 years of age
 20 – 40% in the general population
>85 years of age
 15 – 20% in outpatient general
medical practices
 50% in chronic care facilities.
 dementia of the Alzheimer's type - most
common (50 – 60%)

 vascular dementia – second most


common; causally related to
cerebrovascular diseases. (15 – 30 %)

 mixed vascular and Alzheimer's


dementia (10 – 15%)
DEMENTIA OF ALZHEIMER’S TYPE
(DAT)
 Final diagnosis requires neuropathological
examination of the brain
 Amyloid deposits are hallmark
 Gross: diffuse atrophy with flattened cortical
sulci and enlarged cerebral ventricles.
 Micro: senile plaques, neurofibrillary tangles,
neuronal loss (particularly in the cortex and the
hippocampus), synaptic loss (perhaps as much
as 50 percent in the cortex), and
granulovascular degeneration of the neurons.
 Acetylcholine and norepinephrine
Other Causes:
1. Head Trauma
2. Alcohol-related dementias
3. Parkinson’s Disease
4. Lewy Body Dementia
5. Pick’s Disease
6. Normal Pressure Hydrocephalus
7. Carbon Monoxide poisoning
8. Vitamin deficiencies
9. AIDS Dementia complex
10. Epilepsy
SUBCORTICAL VS. CORTICAL DEMENTIA

CHARACTERISTICS SUBCORTICAL CORTICAL

LANGUAGE No aphasia (anomia, if Aphasia early


severe)

MEMORY Impaired recall (retrieval) Recall and recognition


> recognition (encoding) impaired

ATTENTION AND Impaired Impaired


IMMEDIATE RECALL
VISUOSPATIAL SKILLS Impaired Impaired

CALCULATION Preserved till late Involved early


EXECUTIVE FUNCTIONS Disproportionately Degree of impairment
affected consistent with other
involvement
SUBCORTICAL VS. CORTICAL DEMENTIA
CHARACTERISTICS SUBCORTICAL CORTICAL

SPEED OF COGNITIVE Slowed early Normal until late in


PROCESSING disease
PERSONALITY Apathetic, inert unconcerned
MOOD Depressed Euthymic

SPEECH Dysarthric Articulate till late in


disease
POSTURE Bowed or extended upright
COORDINATION impaired Normal until late
Dementia

 Sundowner syndrome - is characterized


by drowsiness, confusion, ataxia, and
accidental falls ; overly sedated or
adverse reaction to even a small dose of
a psychoactive drug.

 Catastrophic reaction - marked by


agitation secondary to the subjective
awareness of intellectual deficits under
stressful circumstances.
DIFFERENTIAL DIAGNOSIS:

 Age-associated memory impairment


(normal aging) - benign senescent
forgetfulness

 Depression – “pseudodementia”

 Delirium
DEMENTIA VS. PSEUDODEMENTIA

Clinical course and history


PSEUDODEMENTIA DEMENTIA
Family always aware of Family often unaware of
dysfunction and its severity dysfunction and its severity
Onset can be dated with some Onset can be dated only within
precision broad limits
Symptoms of short duration Symptoms usually of long
before medical help is sought duration before medical help is
sought
Rapid progression of symptoms Slow progression of symptoms
after onset throughout course
History of previous psychiatric History of previous psychiatric
dysfunction common dysfunction unusual
DEMENTIA VS. PSEUDODEMENTIA
Complaints and clinical behavior
PSEUDODEMENTIA DEMENTIA
Patients usually complain much of Patients usually complain little of
cognitive loss cognitive loss
Patients' complaints of cognitive Patients' complaints of cognitive
dysfunction usually detailed dysfunction usually vague
Patients emphasize disability Patients conceal disability
Patients highlight failures Patients delight in accomplishments,
however trivial
Patients make little effort to perform Patients rely on notes, calendars,
even simple tasks etc., to keep up
Patients struggle to perform tasks
DEMENTIA VS. PSEUDODEMENTIA
Complaints and clinical behavior

PSEUDODEMENTIA DEMENTIA
Patients usually communicate Patients often appear
strong sense of distress unconcerned

Affective change often pervasive Affect labile and shallow


Loss of social skills often early Social skills often retained
and prominent
Behavior often incongruent with Behavior usually compatible with
severity of cognitive dysfunction severity of cognitive dysfunction
Nocturnal accentuation of Nocturnal accentuation of
dysfunction uncommon dysfunction common
DEMENTIA VS. PSEUDODEMENTIA
Clinical features related to memory, cognitive, and
intellectual dysfunctions
PSEUDODEMENTIA DEMENTIA
Attention and concentration Attention and concentration
often well preserved usually faulty
”Don't know answers typical Near-miss answers frequent
On tests of orientation, patients On tests of orientation, patients
often give don't know answers often mistake unusual for usual

Memory loss for recent and Memory loss for recent events
remote events usually severe usually more severe than for
remote events
Memory gaps for specific Memory gaps for specific
periods or events common periods unusual
Marked variability in Consistently poor performance
performance on tasks of similar on tasks of similar difficulty
difficulty
 The first step in the treatment of
dementia is verification of the diagnosis;

 Preventive measures : changes in diet,


exercise, and control of diabetes and
hypertension
General treatment approach:
1. to provide supportive medical care

2. emotional support for the patients


and their families
3. pharmacological treatment for
specific symptoms, including
disruptive behavior.
Pharmacotherapy
 benzodiazepines for insomnia and
anxiety, antidepressants for depression,
and antipsychotic drugs for delusions
and hallucinations

 should be aware of possible idiosyncratic


drug effects in older people

 drugs with high anticholinergic activity


should be avoided.
 CHOLINESTERASE INHIBITORS
 Donepezil (Aricept)
 Rivastigmine (Exelon)
 Galantamine (Remiryl)
 Tacrine (Cognex)

 MEMANTINE –acts on glutamate receptors


Amnestic Disorders

 defined primarily by impairment in the


ability to create new memories.

 Amnesia is most commonly found in


alcohol use disorders and in head injury.
 major neuroanatomical structures :
 dorsomedial and midline nuclei of the
thalamus
 Hippocampus
 the mamillary bodies
 the amygdala
 The benzodiazepines are the most
commonly used prescription drugs
associated with amnesia.

 Thiamine deficiency, hypoglycemia,


hypoxia (including carbon monoxide
poisoning), and herpes simplex
encephalitis ;
 anterograde amnesia - impairment in the
ability to learn new information

 retrograde amnesia - inability to recall


previously remembered knowledge

 Short-term and recent memory are


usually impaired
 Korsakoff's syndrome is an amnestic
syndrome caused by thiamine deficiency

 alcoholic blackout -conscious awareness


of being unable to remember a period
the night before during which they were
intoxicated.
 Electroconvulsive therapy (ECT)
treatments are usually associated with
retrograde amnesia for a period of
several minutes before the treatment
and anterograde amnesia after the
treatment.
 Transient global amnesia - is
characterized by the abrupt loss of the
ability to recall recent events or to
remember new information.

 last from 6 to 24 hours


Characteristic Alzheimer's Dementia Amnestic Disorder
Onset Insidious Can be abrupt

Course Progressive Static or


deterioration Improvement

Anterograde memory Impaired Impaired

Retrograde memory Impaired Temporal gradient

Episodic memory Impaired Impaired

Semantic memory Impaired Intact

Language Impaired Intact

Praxis or function Impaired Intact


 The primary approach to treating
amnestic disorders is to treat the
underlying cause.
 1st phase of recovery - clinicians serve as a
supportive auxiliary ego who explains to a
patient what is happening and provides missing
ego functions
 2nd phase of recovery- build a therapeutic
alliance with patients by explaining slowly and
clearly what happened and by offering an
explanation for a patient's internal experience.
 3rd phase of recovery - integrative
- help the patient form a new identity by
connecting current experiences of the self with
past experiences

-Grieving over the lost faculties may be an


important feature