COGNITION:

NEUROCOGNITIVE
ØMemory
ØLanguage
ØOrientation

DISORDERS ØJudgment
ØConducting interpersonal relationships
ØPerforming actions (praxis)
ØProblem solving

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DELIRIUM
• Marked by short term
confusion and changes in
cognition;
• DELIRIUM • Subcategories:
• GMC (infection)
• DEMENTIA • Substance-induced
• Multiple causes
• OTHER AMNESTIC DISORDER • Other or multiple
etiologies (sleep
deprivation, meditation)
• MILD COGNITIVE IMPAIRMENT
DEMENTIA
• Major Neurocognitive
Disorder
• Marked by severe
impairment in memory,
judgment, orientation and
cognition.
• Subcategories:
• Alzheimer’stype
• Vascular dementia
• HIV dementia
• Head trauma
• Pick’s disease
• Prion disease
• Substance-induced
• Multiple etiologies
• Not specified
AMNESTIC
DISORDERS
• Major Neurocognitive
Disorder caused by other
medical conditions
• Marked primarily by
memory impairment in
addition to other
cognitive symptoms.
• Causes:
• Medical conditions
(hypoxia)
• Toxins and medications
• Unknown causes

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CLINICAL EVALUATION: CLINICAL EVALUATION:

I. HISTORY TAKING II. MENTAL STATUS EXAMINATION

Ødetailed rendition of patient’s changes in daily routine: self care, job ØA means of surveying functions and abilities to allow a definition of personal
responsibilities, meal preparations, shopping and personal support, interaction strengths and weaknesses.
with friends, ability to maintain personal finances ØRepeatable, structured assessment
ØPromotes effective communication among physicians
ØParticular pursuit that is central to patient and impact of illness ØEstablishes basis for future comparison
ØEssential for documenting therapeutic effectiveness
ØPatient-specific baseline for monitoring the effects of future therapies. ØAllows comparisons between different patients

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 CLINICAL EVALUATION: CLINICAL EVALUATION:
A. General Description D. Mood and Affect
III. COGNITION 1.
2.
General Appearance, dress, sensory aids
Level of consciousness and arousal
1.
2.
Internal mood state; sense of humor
Future outlook
3. Attention to environment 3. Suicidal ideas and plans
4. Posture(standing and seated) 4. Demo emotional status
ØMemory 5. Gait E. Insight and Judgment
6. Movements of limbs, trunk, and face 1. Self appraisal and self esteem
ØVisuospatial and constructional abilities 2. Understanding of current circumstances
7. General demeanor
ØReading, writing and mathematical abilities 8. Response to examiner 3. Ability to describe personal psychological and physical
status
9. Native or primary language
ØAbstraction B. Language and Speech
4. Appraisal of major social relationships
5. Understanding of personal roles and responsibilites
1. Comprehension F. Cognition
2. Output 1. Memory 8. Finger gnosis
3. Repetition 2. Visuospatial skills 9. Right-left orientation
4. Other aspects: object naming, color naming, body
part identification, ideomotor praxis go command 3. Constructional ability 10. executive functions
4. Mathematics 11. abstraction
C. Thought
5. Reading
1. Form
6. Writing
2. Content
7. Fine sensory function

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CLINICAL EVALUATION: CLINICAL EVALUATION:

IV. SCREENING LABORATORY TESTS V. NEUROPSYCHOLOGICAL TESTING
GENERAL TESTS ANCILLARY LABORATORY TESTS
CBC Blood cultures Nocturnal penile tumescence
Erythrocyte sedimentation rate Rapid plasma regain test CSF glucose, protein
ØProvides a standardized, quantitative, reproducible evaluation of a patient’s
Electrolytes HIV testing CSF cell count
cognitive abilities
Glucose Serum heavy metals CSF culture
BUN, Crea Serum copper Cryptococcal antigen
ØFor initial evaluation and periodic assessment
Liver function tests Ceruloplasmin VDRL test
Serum calcium and phosphorus Serum B12 RBC folate levels CT scan
Thyroid function tests Urine culture MRI
Serum protein Urine toxicology PET
Drugs levels Urine heavy metal screen SPECT
Urinalysis EEG
Pregnancy test Evoked potentials
ECG polysomnography

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DELIRIUM: DELIRIUM:
Ø characterized by an acute decline in both the level of consciousness and
cognition with particular impairment of attention.
ØIntensive care unit psychosis ØCentral nervous system
ØHallmark symptom: IMPAIRMENT OF CONSCIOUSNESS ØAcute confusional state toxicity
ØAcute brain failure ØParaneoplastic limbic
ØLife threatening, potentially reversible encephalitis
ØEncephalitis
ØSundowning
ØEncephalopathy
ØAbnormalities of mood, perception, and behavior are common psychiatric ØCerebral insufficiency
symptoms; ØToxic metabolic state
ØOrganic brain syndrome

Øtremor, asterixis, nystagmus, incoordination, and urinary incontinence are

common neurological symptoms

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 DELIRIUM: EPIDEMIOLOGY DELIRIUM: EPIDEMIOLOGY
ØIn community studies: 1% of ØGeneral surgery: 10-15%
elderly age 55 years and above
ØOpen heart surgery: 30% CAUSES OF POST-OP DELIRIUM:
Ø (13% of these are in the 85 years or
older group) ØHip fractures : >50% 1. Stress of surgery
ØElderly Emergency dept patients: ØICU patients: 70-87% 2. Postoperative pain
10% reported to have delirium ØEnd of life care: 83% 3. Insomnia
ØAt the time of admission to ØNursing home or postacute care
medical wards: b/w 15 and 21% of 4. Pain medications
settings: 60%
older patients meet criteria for 5. Infection
ØSevere burns: 21%
delirium 6. Fever
ØAIDS during hospitalization: 30-40%
ØFor patients with no delirium at 7. Blood loss
time of admission : 5-30% with ØTerminally ill patients: 80%
subsequent cases of delirium
during hospitalization

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DELIRIUM: EPIDEMIOLOGY DELIRIUM: EPIDEMIOLOGY

P R E D I S P O S I N G FA C TO R S
DEMOGRAPHIC CHARACTERISTICS
• Male, 65 yrs and older
COGNITIVE STATUS : Dementia, cognitive
impairment, history of delirium, depression
FUNCTIONAL STATUS : functional dependence,
immobility, hx of falls, low level of activity
SENSORY IMPAIRMENT: hearing, visual
DECREASED ORAL INTAKE: dhn, malnutrition
DRUGS: psychoactive, anticholinergics, alcohol abuse
COEXISTING MEDICAL CONDITIONS:
severe medical diseases metabolic derangement
Chronic renal/hepatic dse HIV; terminal dses.
Stroke; neurologic disease fractures;trauma
P R E C I P I TAT I N G FA C TO R S
• DRUGS : sedative hypnotics, narcotics, ØPoor prognostic sign
anticholinergics, multiple drugs; alcohol or drug ØRates of institutionalization increased threefolds for patients 65 years and
withdrawal
older who exhibit delirium while in the hospital
• PRIMARY NEURO DSES: stroke, nondominant
hemisphere; IC bleeding; meningitis/ encephalitis ØMortality rates:
• INTERCURRENT ILLNESSES: infections, – 23 – 33 % - 3-month mortality rate
iatrogenic complications, severe acute illness, hypoxia,
shock, anemia, dhn, poor nutritional status, – 50% - 1 year mortality rate
hypoalbuminemia, metabolic derangements – 20 – 75 % - mortality rate during that hospitalization for elderly patients
• SURGERY: orthopedic, cardicac, prolongedCP • After discharge – 15% 1 month mortality rate
bypass, noncardiac surgery
• 25% within 6 months
• ENVIRONMENTAL: ICU, physical restraints,
bladder catheter, multiple procedures, pain,
emotional stress, prolonged sleep deprivation.

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DELIRIUM: ETIOLOGY DELIRIUM: ETIOLOGY

Major causes of delirium : Common causes of delirium :

1. central nervous system disease (e.g., epilepsy) CNS DISORDERS Seizure (postictal, nonconvulsive status, statuse
epilepticus);Migraine; Head trauma, brain tumor, SAH, subdural
hematoma, abscess, IC hge, cerebellar hge, nonhrgic stroke,
transient ischemia
2. systemic disease (e.g., cardiac failure) METABOLIC DISORDERS Electrolyte abnormalities, DM, hypoglycemia, hypergycemia, or
insulin resistance
SYSTEMIC ILLNESSES Infection(e.g. sepsis, malaria, erysipelas, virl, plague,Lyme dse.,
3. either intoxication or withdrawal from pharmacological or syphilis, or abscess); Trauma, dhn or vol overload, nutritional def.,
toxic agents burns, uncontrolled pain, heat stroke, high altitude (>5000m)
MEDICATIONS Pain meds(Demerol, or morphine), antibiotics, antivirals, and
antifungals; antihypertensives; steroids, anesthesia, cardiac meds,
antineoplastics, anticholinergics, NMS, serotonin syndrome
OVER THE COUNTER PREPS Herbals, teas, nutirtional supplements

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 DELIRIUM: ETIOLOGY DELIRIUM: DSM V DIAGNOSTIC
Common causes of delirium :
CRITERIA
A. A disturbance in attention(i.e., reduced ability to focus, direct, sustain, and shift attention), and
BOTANICALS Jimsonweed, oleander, foxglove, hemlock, dieffenbachia, Amanita awareness (reduced orientation to the environment).
phalloides B. The disturbance develops over a short period of time, represents a change from baseline
CARDIAC Cardiac failure, arrythmia, MI, cardiac assist device, cardiac sx attention and awareness, and tends to fluctuate in severity during the course of the day.
PULMONARY COPD, hypoxia, SIADH, acid-base disturbance C. An additional disturbance in cognition (e.g. memory deficit, disorientation, language, Visuospatial
ability, or perception)
ENDOCRINE Adrenal crisis/failure, thyroid abn, PTH abn
D. The disturbance not better explained by another preexisting, established or evolving
HEMATOLOGICAL Anemia, leukemia, blood dyscrasia, stem cell transplant neurocognitive disorder and do not occur in the context of a severely reduced level of arousal,
RENAL Renal failure, uremia, SIADH such as coma.
HEPATIC Hepatitis, cirrhosis, hepatic failure E. There is evidence from the history, , PE, and lab findings that the disturbance is a direct
physiological consequence of another medical condition, substance intoxication or withdrawal, or
NEOPLASMS Primary brain, metastases, neoplastic syndromes exposure to a toxin, or is due to multiple etiologies.
DRUGS OF ABUSE Intoxication and withdrawal
TOXINS Intoxication and withdrawal; heavy metals and aluminum

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DELIRIUM: CLINICAL FEATURES DELIRIUM: CLINICAL FEATURES

Core features of Delirium: Associated Clinical Features:

1. altered consciousness 1. Disorganization of thought process

2. altered attention 2. Perceptual disturbances

3. impairment in other realms of cognitive function 3. Psychomotor hypo/hyper activity

4. relatively rapid onset (usually hours to days) 4. Disruption of sleep-wake cycle (fragmented sleep at night)
5. Mood alterations
5. brief duration (usually days to weeks)
6. often marked, unpredictable fluctuations in severity and other clinical manifestations during 6. Autonomic hyperactivity or instability
the course of the day, 7. Myoclonic jerking
8. dysarthria

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DELIRIUM: CLINICAL FEATURES DELIRIUM: CLINICAL FEATURES

• The major neurotransmitter hypothesized to be involved in delirium is • One of the most common causes of delirium is toxicity from too many prescribed
acetylcholine (decreased acetylcholine activity) medications with anticholinergic activity.

• delirium associated with alcohol withdrawal has been associated with hyperactivity of
• the major neuroanatomical area is the reticular formation. (attention and the locus ceruleus and its noradrenergic neurons
arousal)
• Other neurotransmitters: serotonin and glutamate
• major pathway implicated in delirium is the dorsal tegmental pathway
• beclouded dementia – when delirium occurs in a patient with dementia

• sundowning – worsening of clinical manifestations at night

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 DELIRIUM: CLINICAL FEATURES DELIRIUM: CLINICAL FEATURES
ØBedside diagnosis; char. By sudden onset of symptoms

ØMini-Mental Status Examination

ØEEG – generalized slowing of activity; focal areas of hyperactivity

ØPhysical examination often reveals clues to the cause of the delirium.

ØBradycardia – Hypothyroidism, Stokes-Adams syndrome, Increased intracranial pressure
Ø Tachycardia – Hyperthyroidism, Infection, Heart failure
Ø Fever – Sepsis, Thyroid storm,Vasculitis

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DELIRIUM: DIFFERENTIAL DIAGNOSIS DELIRIUM: DIFFERENTIAL DIAGNOSIS

1. Dementia
2. Schizophrenia –hallucinations and delusions are more constant and better
organized; no change in level of consciousness or orientation;
3. Depression – distinguished on basis of EEG
4. Dissociative Disorders
5. Factitious Disorders- inconsistencies in MSE and on basis of EEG

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DELIRIUM: TREATMENT DELIRIUM: TREATMENT

I. TREAT THE UNDERLYING CAUSE III. PHARMACOTHERAPY
Ø Anticholinergic toxicity – Physostigmine salicylate (Antilirium) 1-2 mg IV or IM with repeated q ØPSYCHOSIS : Haloperidol initial dose 2- 6 mg IM repeated in an hour if patient remains
15 – 30 minutes
agitated. Oral medication, the dose approx..1.5x the IM dose (liquid or tablet) twice daily,
with 2/3 of the dose given at bedtime.
II. PROVIDE PHYSICAL, SENSORY AND ENVIRONMENTAL SUPPORT ØDroperidol – alternative IV formulation
Ø To prevent accidents ØPhenothiazines should be avoided because of significant anticholinergic activity
Ø Neither sensory deprived or overstimulated (black patch delirium)
Ø Regular sitter;friend or relative in the room
ØINSOMNIA : best treated with short- or intermediate-acting BDZ
Ø Familiar pictures and decorations
Ø Clock orcalendar
Ø Regular orientations ØIf with severe pain or dyspnea : should not hesitate to prescribe opioids

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 DEMENTIA DEMENTIA : EPIDEMIOLOGY
ØMajor neurocognitive disorder • 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
ØA disease process marked by progressive cognitive impairment in a
clear consciousness. – 15 – 20% in outpatient general medical practices
– 50% in chronic care facilities.

ØDementia of Alzheimer’s is the most common type • dementia of the Alzheimer's type : 50 – 60%
• vascular dementia :15 – 30 %
ØSecond most common in Vascular Dementia • mixed vascular and Alzheimer's dementia: 10 – 15%

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DEMENTIA : ETIOLOGY DEMENTIA : ALZHEIMER’S TYPE

DEGENERATIVE DEMENTIAS
Alzheimers, frontotemporal, Parkinson’s disease, Lewy
body dementia, idiopathic cerebral ferrocalcinosis
(Fahr’s dse.), progressive supranuclear palsy
MISCELLANEOUS
Huntington’s dse.,Wilson’s dse., metachromatic
leukodystrophy, neuroacathocytosis
PSYCHIATRIC
Pseudodementia of depression, cognitive decline in late
life schizophrenia
PHYSIOLOGIC
Normal pressure hydrocephalus
METABOLIC
Vitamin deficiencies, endocrinopathies, chr. metab. dist.
TUMOR primary or metastatic
TRAUMATIC
• Commonly diagnosed in the clinical setting after other causes of dementia has
Dementia pulingistica, posttraumatic dementia, SDH
been excluded
INFECTION
Prion dse., AIDS, syphilis • Amyloid precursors are hallmark
CARDIAC,VASCULAR, ANOXIA
Infarction, Biswanger dse., hemodynamic insufficiency
• GENETIC FACTORS:
DEMYELINATING DSE – 40% of patients have a family history of dementia of the Alzheimer’s type
Multiple sclerosis
– Concordance rate higher among monozygotic twins (43%) than dizygotic twins (8%)
DRUGS AND TOXINS – Autosomal dominant transmission; rare
Alcohol, heavy metals, irradiation, anticholinergics
(pseudodementia), carbon monoxide – Gene for amyloid precursor protein : long arm of chromosome 21

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DEMENTIA : ALZHEIMER’S TYPE DEMENTIA : ALZHEIMER’S TYPE

• NEUROPATHOLOGY: • NEUROTRANSMITTERS:
– GROSS: diffuse atrophy with flattened sulci and enlarged cerebral ventricles
– MICRO: – Hypoactivity of Acetylcholine and norepinephrine
1. senile plaques – amyloid plaques* ; more strongly indicate Alzheimers dse. – Specific degeneration of cholinergic neurons in nucleus basalis of Meynert
2. neurofibrillary tangles- cytoskeletal elements; primarily phosphorylated tau protein; not – Decreased acetylcholine and choline acetyltransferase concentrations in the brain
unique to Alzheimers dementia
– Decrease NE containing neurons in the locus ceruleus
3. neuronal loss (particularly in cortex and hippocampus) – Decreased concentrations of somatostatin and corticotropin (neuroactive peptides)
4. synaptic loss (as much as 50% in the cortex)
5. granulovascular degeneration of the neurons

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 DEMENTIA : VASCULAR DEMENTIA DEMENTIA : PICK’S DISEASE

• Formerly multi-infarct dementia • Frontotemporal dementia

• Primary cause presumed to be multiple areas of cerebral vascular disease
• Most commonly seen in men, esp. with preexisting hypertension
• Infarction of small and medium-sized cerebral vessels; multiple parenchymal
lesions spread over wide areas of the brain
• P.E.: carotid bruits, fundoscopic abnormalities, enlarged cardiac chambers
• BISWANGER’S DSE: subcortical arteriosclerotic encephalopathy
– Presence of many small infarctions of the while matter that spare the cortical regions
• Neuronal loss, gliosis, and neuronal Pick’s bodies(cytoskeletal elements)
• Cause is unknown; approx. 5% of irreversible dementias
• Most common in men, with first degree relatives with the disorder
• Early stages are more often characterized by personality and behavioral
changes, with relative preservation of other cognitive functions
• Features of Kluver-Bucy syndrome more common

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DEMENTIA : HUNTINGTON’S DSE. DEMENTIA : PARKINSON’S DSE.

• Subcortical type; more motor abnormalities and fewer language abnormalities
• Psychomotor slowing and difficulty with complex tasks, but memory, language
and insight remain intact in the early and middle stages
• Classic choreoathetoid movements
• High incidence of depression and psychosis
• Subcortical type
• 20-30% of patients with Parkinson’s dse have dementia
• Bradyphrenia: slow movements paralleled in slow thinking

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DEMENTIA : HIV-RELATED DEMENTIA : HEAD TRAUMA-RELATED

• AIDS dementia complex or HIV dementia • Dementia pugilistica – punch-drunk syndrome; occurs in boxers
• Annual rate of 14% • Emotional lability, dysarthria, and impulsivity
• Development of dementia often paralleled by the appearance of parenchymal • Repeated concussion also seen in football players
abnormalities in MRI scans.
• Other infectious dementias are caused by Cryptococcus or Treponema
pallidum
• Personality changes: apathy, emotional lability or behavioral disinhibition.

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 DEMENTIA : DEMENTIA : CLINICAL FEATURES
DSM V DIAGNOSTIC CRITERIA
A. Evidence of significant cognitive decline from a previous level of performance • Memory impairment is typically an early and prominent feature; early in the
in one or more cognitive domains based on: course it is mild and usually most marked for recent events.
1. Concern of the individual, a knowledgeable informant, or the clinician that there has • As it progresses, memory impairment becomes severe, and only the earliest
been a significant decline in cognitive function; and learned information is retained
2. A substantial impairment in cognitive performance, preferably documented by • Orientation progressively affected
standardized neuropsychological testing or another quantified clinical assessment. • Language abilities esp in cortical dementias
B. The cognitive deficits interfere with independence in everyday activities • Changes in personality
C. The cognitive deficits do not occur exclusively in the context of a delirium. • Hallucination and delusion
D. The cognitive deficits are not better explained by another mental disorder. • Depression and anxiety
• Aphasia, apraxia, agnosia, seizures, primitive reflexes, sleep disturbances

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DEMENTIA : CLINICAL FEATURES DEMENTIA : CLINICAL FEATURES

• ACCORDING TO KURT GOLDSTEIN: • SUNDOWNER SYNDROME:

– Reduced ability to apply “abstract attitude”
• Generalizing from a single instance, forming concepts, grasping similarities and – Characterized by drowsiness, confusion, ataxia, and accidental falls.
differences
– Occurs in older people who are overly sedated and in patients with dementia wo
– Catastrophic reaction : agitation secondary to the subjective awareness of react adversely to even a small dose of a psychoactive drug;
intellectual deficits under stressful circumstances
– Also occurs in demented patients when external stimuli, such as light and
• Patient attempts to compensate by using strategies to avoid demonstrating failures:
interpersonal orienting cues, are diminished.
change subject, make jokes, divert the interviewer.
• Coarse language, inappropriate jokes, neglect of personal appearance and hygiene,
general disregard for the conventional rules of social conduct.

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DEMENTIA : DIFFERENTIAL DIAGNOSIS DEMENTIA : DIFFERENTIAL DIAGNOSIS

1. Dementia of Alzheimer’s type vs Vascular dementia 1. Depression

– Decremental deterioration that can accompany CVD over time; focal neurological – Depression-related cognitive dysfunction (pseudodementia)
symptoms are more common in vascular dementia 2. Factitious disorder
2. Vascular Dementia vs Transient Ischemic Attack – Erratic and inconsistent
– TIAs are brief periods of focal neurological dysfunctions lasting <24 hours 3. Schizophrenia
3. Delirium – Less severe symptoms
– Rapid onset, brief duration, cognitive impairment fluctuation during course of the day, 4. Normal Aging
nocturnal exacerbation of symptoms, marked disturbance in sleep-wake cycle, and – Benign senescent forgetfulness; minor severity and no significant interference with social
prominent disturbances in attention and perception and occupational behaviors
5. Other disorders: Malingering, Intellectual disability, amnestic disorder

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 DEMENTIA : DIFFERENTIAL DIAGNOSIS DEMENTIA : DIFFERENTIAL DIAGNOSIS

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DEMENTIA : DIFFERENTIAL DIAGNOSIS DEMENTIA : DIFFERENTIAL DIAGNOSIS

51 52

DEMENTIA : TREATMENT DEMENTIA : TREATMENT

II. PHARMACOTHERAPY
I. The first step in the treatment of dementia is verification of the diagnosis • benzodiazepines for insomnia and anxiety, antidepressants for depression, and antipsychotic
drugs for delusions and hallucinations
Ø Preventive measures : changes in diet, exercise, and control of diabetes and • should be aware of possible idiosyncratic drug effects in older people
hypertension • drugs with high anticholinergic activity should be avoided.
Ø General treatment approach:
• CHOLINESTERASE INHIBITORS
1. to provide supportive medical care
– Donepezil (Aricept)
2. emotional support for the patients and their families – Rivastigmine (Exelon)
3. pharmacological treatment for specific symptoms, including disruptive behavior. – Galantamine (Remiryl)
– Tacrine (Cognex)

¢ MEMANTINE –acts on glutamate receptors

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 AMNESTIC DISORDERS AMNESTIC DISORDERS
Ødefined primarily by impairment in the ability to create new memories. ØThe benzodiazepines are the most commonly used prescription drugs
associated with amnesia.
ØAmnesia is most commonly found in alcohol use disorders and in head injury
ØThiamine deficiency, hypoglycemia, hypoxia (including carbon monoxide
poisoning), and herpes simplex encephalitis ;
ØMajor neuroanatomical structures :
Ødorsomedial and midline nuclei of the thalamus Øanterograde amnesia - impairment in the ability to learn new information
ØHippocampus
ØThe mamillary bodies Øretrograde amnesia - inability to recall previously remembered knowledge
Øthe amygdala

ØShort-term and recent memory are usually impaired

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AMNESTIC DISORDERS
ØKorsakoff's syndrome is an amnestic syndrome caused by thiamine deficiency

Øalcoholic blackout -conscious awareness of being unable to remember a period the

night before during which they were intoxicated.

ØElectroconvulsive therapy (ECT) treatments are usually associated with retrograde

amnesia for a period of several minutes before the treatment and anterograde
amnesia after the treatment.

ØTransient global amnesia - is characterized by the abrupt loss of the ability to recall
recent events or to remember new information.
Ølast from 6 to 24 hours

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AMNESTIC DISORDERS MILD COGNITIVE IMPAIRMENT

qThe primary approach to treating amnestic disorders is to treat the underlying 1. Memory complaint, preferably qualified by an informant’
cause. 2. Memory impairment for age and education
q1st phase of recovery - clinicians serve as a supportive auxiliary ego who 3. Preserved general cognitive function
explains to a patient what is happening and provides missing ego functions
4. Intact activities of daily living
q2nd phase of recovery- build a therapeutic alliance with patients by explaining
5. Not demented
slowly and clearly what happened and by offering an explanation for a patient's
internal experience.
q3rd 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

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