Delirium / Dementia



    Delirium, Dementia

    -       Cognitive Disorders:

    o   Delirium

    o   Dementia

    o   Amnestic Disorder







    Alzheimers – gradual

    Vascular - stepwise







    Worse in am







    Language/memory loss. Short-term memory first


    Neuro sx


    (Except Delirium Tremens)

    LB – Parkinsonism


    Afective sx






    (syndrome, not disease!!!!)


    -       Defined by disturbance of consciousness, impaired cognition, and attention.

    -       disorientation, confusion, and global cognitive impairment.

    -       Difficulty focusing, sustaining or shifting attention, impaired cognition, perceptual disturbance (Illusions).

    -       Other sx: sundowning: worse at night

    -       10-15% of hospital medical patients develop delirium.

    -       Risk factors:

    o   Elderly >80yo

    o   Pre-existing dementia

    o   Recent surgery, bone fractures,

    o   Infections

    o   Use of narcotics or antipsychotics

    -       40-50% of pts with delirium will die within 1 year.

    DSM-IV-TR Delirium

    A.     Disturbance of consciousness with reduced ability to focus, sustain and shift attention.

    B.     Change in cognition (memory, orientation, language) or perceptual disturbance not accounted for by potential dementia.

    C.     Develops rapidly (hours to days) and fluctuates throughout the day.

    D.     Evidence that disturbance caused by GMC

    -       Cause:

    o   Usually serious medical, surgical, or neuro condition or drug intoxication or w/d.

    • Anticholinergics
    • Opioids
    • Steroids

    o   Environment is NOT a CAUSE of delirium but can influence it

    -       Workup:

    • o   History, physical (Neuro exam)
    • o   Lab work CBC, Lytes, creatinine, BUN, LFTs, glucose, Thyroid
    • o   Panculture (urine, blood)
    • o   Chest Xray


    -       Temperature likely up from autonomic instability or infection

    -       DDx:

    o   Vs. Schizophrenia: Hallucinations in delirium are often fragmentary and disorganized and tend to be visual/tactile, as opposed to auditory

    o   Vs. EtOH withdrawal (need benzos)

    o   Dementia (long-onset, awareness not disturbed)

    -       Tx:

    o   Treat underlying condition

    o   If agitated, may need restraints, use strong antipsychotics

    §  (Haloperidol 0.5-1mg IM q2-4hrs or 0.5-2mg po) – no anticholinergics, but EPS (avoid in parkinsons, use Quetiapine)

    §  SGA (e.g. risperidone – no anticholinergic, mild EPS). 

    §  Avoid older drugs with anticholinergic effects (Chlorpromazine, thioridazine) can worsten effects.

    §  Anticholinergic levels correlate with delirium duration.

    o   benzos ONLY in ETOH w/d

    o   Modify environment:

    §  Keep in well-list quiet room

    §  Display reminders of day, date, time place and situation in the patient’s room –calendars, family photos, newspapers.



    -       Syndrome impaired cognitive function with a decline in social/occupational functioning.

    -       Cognitive impairment (4 a’s)

    -       Aphasia (language disturbance)

    -       Amnesia (Memory disturbance)

    -       Apraxia (complex motor activities)

    -       Agnosia (unable to identify objects despite normal sensory system)

    -       Earliest signs:subtle change in personality, decrease in interests, some apathy or shallow emotions.

    -       Intermediate: Intellectual skills gradually decline, person may be unaware.

    -       Advanced: cognitive impairment, mood, personality changes pronounced.  Psychotic symptoms may develop. Insight may be impaired.

    -       Severely Advanced: unable to care for self, forget names, sometimes cannot recognize close relatives, Eventually Mute, and dies within 1 year.

    -       Psueodementia– appears with depression (poor memory, calculation  etc…) however reversible with depression tx.  High risk of progressing to dementia

    -       Alzheimers Dementia:

    -       Half develop hallucinations or delusions.

    -       20% develop major depression

    -       Vascular Dementia

    -       Depression common

    -       Dx:

    -       History, physical (Neuro exam)

    -       Lab work CBC, TSH, lytes, Ca, Blood sugar, Creatining, B12

    -       Neuroimage only if:

    §  Age <60

    §  Duration <2 years, rapid unexplained decline

    §  Recent head trauma, bleeding disorder, neuro sx

    §  Hx of cancer etc..

    §  Suspicion of NPH

    -       Mild Cognitive Impairment (MCI)if individual scores low on memory tests, but no impairment in daily function (12%/year progression to dementia).


    Non-Treatable Dementias

    Alzheimers Disease

    -       50-60% of all cases of dementia

    -       Classified:

    o   <65yo early onset (likely familial) (5% Prevalence)

    o   >65 late onset (40% Prevalence)

    -       Onset insidious, death in 8-10 years after sx recognized

    -       Prevalence of illusions, hallucinations, or delusions associated with accelerated cognitive decline.

    -       Etiology:

    o   Histopathology

    o   Amyloid plaques (B-amyloid protein)-> inflammation + neuronal death

    o   Neurofibrillary tangles (tau protein) -> cell death  (not specific to alzheimers)  Can detect tau in CSF.

    -       Risk factors:

    o   Head injury

    o   Down Syndrome

    o   Low education/occupation level

    o   First-degree relative with Alzheimer’s disease (if 1st degree relative, 50% will have disease at age 90)

    DSM-IV-TR Dementia of Alzheimer’s Type

    A.     Multiple cognitive deficits both:

    1.     Memory impairment

    2.     One or more:

                                                   i.     Aphasia (language)

                                                  ii.     Apraxia (complex motor activities)

                                                iii.     Agnosia (recognize objects)

                                                iv.     Executive Functioning (planning, organizing)

    B.     Criteria A1 and A2 cause impairment of function and different from before.

    C.     Course: gradual onset, continuing decline

    D.     Cognitive deficits A1 and A2 are not due to

    1.     Other CNS illnesses (Parkinsons, CVA, Huntington, hematoma, tumor)

    2.     GMC (hypothyroid, B12, folic acid, neurosyphilis, HIV)

    3.     Substance

    E.     Not in delirium

    F.     Not better accounted for by Axis I disorder (MDD, schizophrenia)

    Without Behavioural Disturbance

    With Behavioural Disturbance (wandering, agitation, etc..)

    With Early Onset (<=65yo)

    With Late Onset (>65yo)


    Dementia with Lewy Bodies

    -       25% of Dementia

    -       Sx similar to Alzheimers

    -       Differentiated by early appearance of:

    o   Visual Hallucinations

    o   Parkinsonian Features

    o   More rapid progression

    -       Very sensitive to EPS side effects (use SGA if needed, not 1st gen)


    Frontotemporal Dementia

    -       Tau positive inclusions

    -       Parkinsonian features

    -       Two clinical syndromes:

    -       Disinhibition and shallow affect

    -       Early severe loss of expressive language and severe naming difficulties.


    Huntington’s Disease

    -       Neuropsychiatric, autosomal dominant

    -       Mild: depression, anxiety, irritability

    -       Moderate/Severe: Frank hallucinations and delusions

    -       Severe: Choreiform movements + dementia

    o   Dementia: impaired cognition w/o language problems.


    Creutzfeldt-Jakob Disease

    -       Virulent and irreversible caused by prions

    -       Rapidly progressive dementing illness causing death within a few months.

    -       Myoclonus, cerebellar, extrapyramidal

    -       Either inherited or transmitted by brain electrodes, transplants, human growth hormone, and gonadotropin.

    -       No treatment


    Non-treatable Dementias in general:

    -       Tx:

    o   Medical: cholinesterase inhibitors:

    Covered if MMSE 10-26


    1.  Donepezil (Aricept) od


    o   2.  Rivastigmine (Exelon) bid, or od of patch

    o   3.  Galantamine. (Remenyl)

    o   Meds S/E:

    §  Gi Upset (N/V/D/wt loss)

    §  Bradycardia (Syncope)

    o   Equally effective, slow cognitive decline.

    o   4.  Memantine (NMDA blocker) (receptor mediates learning/memory). 

    o   Effectiveness varies tremendously, best if early in disease

    o   Also slows inevitable decline.

    o   Keep all drug doses low

    o   SGA for agitation, do not use 1st gen due to EPS

    o   Trazodone (25-100mg) helps sundowning

    o   Behavioural

    o   Socialize and calm talking to prevent agitation

    o   Regular and predicable daily schedules, activities

    o   Avoid EtOH, caffeine, diuretics

    o   (Driving, cooking, waqndering, finances/fraud, caregiver support)


    Treatable Dementias:

    Vascular Dementia

    -       2nd most common after Alzheimers (15-30%)

    -       Accumulation of cerebral infarcts in pts with atherosclerotic disease.

    -       Rapid onset, stepwise deterioration

    -       May have Neuro sx.

    -       Often have Cardiac risk factors, prior strokes “silent”

    -       Tx: give aspirin, modify risk

    -       Subdural hematomafalls under this, clots in brain, need burr hole to remove.


    Normal Pressure Hydrocephalus (NPH)

    -       Increased CSF production or outflow obstruction, dilates ventricles, but pressure normal.

    -       Triad: dementia, gait disturbance, and urinary incontinence.

    -       Cause: unknown (worse with trauma)

    -       Some respond well to shunting.


    Other dementias:

    -       Infections (Whipple’s disease, fungi, syphilis, AIDS)

    -       Metabolic disorders (Parathyroid, thyroid, adrenal, pituitary, renal failure, liver failure, hypoglycemia).

    -       Nutritional (Thiamine def Wernike’s Encephalopathy, amnestic disorder, folate deficiency reversible if recognized early, niacin def).


    Amnestic Disorder

    -       Inability to learn new information or recall previous info leading to significant impairment.

    -       Usually oriented, and alert, but unable to recall stuff from hours earlier.

    -       Etiology: trauma, tumor, infection, infarction, seizures, drugs, most common is EtOH)

    -       May be due to Wernike’s encephalopathy in EtOH pts (along with opthalmoplegia, ataxic gait, nystagmus etc..).  May not improve when stop EtOH

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