DELIRIUM AND DEMENTIA

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					Confusion, Delirium and
      Dementia
   Samira Khazravan, M.D.
       Geriatric Fellow
   Department of Geriatrics
   Mary Immaculate Hospital
DELIRIUM
“Acute Confusional State”
                      DELIRIUM
   Word delirium is derived from Latin term meaning "off
    the track“.
   Not a disease but a syndrome with multiple causes that
    result in a similar constellation of symptoms.
   The clinical hallmarks are ed attention span & a
    waxing & waning type of confusion.
   A transient, usually reversible, impairment of
    consciousness with a ed ability to focus, sustain or
    shift attention.
   Should be treated as a medical emergency (early
    diagnosis & resolution of symptoms are correlated with
    the most favorable outcomes).
      CRITERIA FOR DIAGNOSING
              DELIRIUM
   A ∆ in cognition or development of a perceptual
    disturbance that is not better accounted for by a
    preexisting, established or evolving Dementia.
   Develops over a short period of time & tends to
    fluctuate during the course of the day.
   There is evidence that the disturbance is caused by
    a medical condition, intoxication or med use.
   There is no clear evidence of any underlying
    pathologic process.
                 EPIDEMIOLOGY
 14-56% of hospitalized elderly patients.
 Delirium is present in 10-22% of elderly patients at the time of
  admission, with an additional 10-30% of cases developing after
  admission.
 found in 40% of patients admitted to ICU.
 Extremely common among nursing home residents.
 Can occur at any age.
 MC in pts who are elderly & have compromised mental status.
 ed risk in pts w/dementia (2/3 of cases of delirium occur in pts
  w/dementia).
 Delirium due to physical illness is MC among very young & those
  older than 60 years.
 Delirium due to drug & alcohol intoxication or withdrawal is most
  frequent in persons aged mid teens to the late 30s.
                 RISK FACTORS
   Advanced age
   Dementia
   Functional impairment in ADLs
   Medical co morbidity
   History of alcohol abuse
   ♀ > or < ♂
   MC whites than in other races
   Sensory impairment – decreased vision & hearing
   Acute cardiac/pulmonary events
   HIV/AIDS
         MORBIDITY/MORTALITY
   10-fold risk of death.

   3-5-fold increase risk of nosocomial complications.

   Poor functional recovery & ed risk of death up to 2 years

   Some causes of delirium (Delirium Tremens,
    Severe Hypoglycemia, CNS infx, Heat stroke, Thyroid
    storm) may be fatal or result in severe morbidity if
    unrecognized & untreated.

   With some exceptions, such as OD of TCAs, drug
    intoxications generally resolve fully with supportive care.
           PATHOPHYSIOLOGY
 Exact pathophysiological mechanisms unclear.
 The main hypothesis is reversible impairment of cerebral
  oxidative metabolism & multiple NT abnormalities
  (Acetylcholine, Dopamine, Serotonin, GABA)
 Postulated mechanisms:
   – Interruption of BBB
   – Inflammatory mechanism [cytokines (interleukin-1 &
     6) are ed following infx, inflammation, toxic insults,
     head trauma & ischemia]
   – Stress rxn mechanism [psychosocial stress and sleep
     deprivation facilitate the onset of delirium].
    ETIOLOGY  Intracranial causes
   Neurodegenerative
    – Dementia w/Lewy bodies [only dementia that features
      transient episodes of impaired consciousness as a typical
      feature].

    -No other dementias feature impairment of consciousness
    unless complicated by a delirium (i.e. 2° to infx, anoxia,
    etc).
ETIOLOGY  Intracranial causes
 Space-occupying lesions
   – Tumor
   – Cyst
   – Abscess
   – Hematoma
 Head injury (esp. Concussion)
                ETIOLOGY
 INTOXICATION
   – Alcohol (Delirium tremens, Wernicke-Korsakoff
     encephalopathy).
   – Sedative-Hypnotic use/abuse.
 Poisons
       Heavy metals (Lead, Mercury, Manganese)

       Carbon monoxide
    ETIOLOGY  Drugs (ingestion or
            withdrawal)
– Amphotericin B               – Dopaminergic agents
– Anticholinergics             – Disulfiram
– Anticonvulsants              – Digoxin
                               – Insulin
– Antidepressants
                               – Lithium
– Antihistamines
                               – Opiates
– Antihypertensive drugs [-
                               – Phenytoin
    blockers]
                               – Salicylates
–   Antiparkinsonian drugs
                               – Steroids
–   Antipsychotics             – Sedatives (barbiturates
–   Cannabis                     & benzodiazepines)
–   H2 Blocker (Cimetidine)    – TCAs
    ETIOLOGY  Intracranial causes
 Infx
   – Meningitis & Encephalitis (Bacterial, Viral, Fungal,
     Parasitic or Tuberculosis organisms)
   – Neurosyphilis
   – Sepsis
 Epilepsy
 Cerebrovascular disorders
   – TIA
   – Cerebral thrombosis or Embolism
   – Intracranial or SAH
   – HTNive Encephalopathy
 Vasculitis (e.g. From SLE)
ETIOLOGY  Metabolic & endocrine
   – Electrolyte             – Thyrotoxicosis
       disturbances (Na+,   –  &  thyroidism
       Mg2+, Ca2+)
                             – &
   –   Acid-Base D/o             parathyroidism
   –   Renal Failure &       –   &
       Uremia                    adrenocorticism
   –   Hepatic                   (Cushing’s syndrome,
       encephalopathy            Addison’s disease)
   –   Hypoglycemia (DM)     –   Pheochromocytoma
   –   DKA                   –   Hypopituitarism
   –   Insulinoma            –   Wilson’s disease
                  ETIOLOGY
 Nutritional Deficiencies
  – Thiamine (Wernicke’s encephalopathy)
  – Vitamin B12 (Pernicious Anemia)
  – Vitamin B1 (Beriberi)
  – Folic acid
  – Niacin
 Anoxia
  – Respiratory failure (Hypoxia/Hypercarbia)
  – Heart failure
 MI, A. Fib
                ETIOLOGY

   Neoplasms (1 or metastatic lesions of
    CNS; CA induced HyperCa2+)

   Degenerative disease
    – Alzheimer’s, Pick’s Dz, Multiple Sclerosis,
      Parkinsonism, Huntington’s chorea, Normal
      Pressure Hydrocephalus)
              ETIOLOGY
 Major   causes of delirium – HIDE
  – Hypoxia
  – Infections
  – Drugs
  – Electrolyte disturbances
          SIGNS & SYMPTOMS
 Usually acute onset
 Fluctuating levels of consciousness (impairment
    usually least in AM)
 Perceptual disturbances (hallucinations or
  illusions)
 Impaired consciousness:
    – Reduced awareness of environment  clouding of
      consciousness  coma
    – Reduced ability to sustain attention (easily
      distracted)
       SIGNS & SYMPTOMS

   Impaired cognitive function
    – Impaired STM (1° memory) & recent memory.
    – Disoriented to time & often place [orientation
      to self seldom lost].
    – Language abnormalities [rambling, incoherent
      speech & impaired ability to understand]
      common.
       SIGNS & SYMPTOMS
   Perceptual & thought disturbance
    – Ranging from misinterpretations (e.g. A door
      slamming is mistaken for an explosion) 
      illusions (e.g. A crack in the wall is perceived
      as a snake)  hallucinations (especially visual)
   Psychomotor abnormalities
    – Patients may be hyper or hypoactive or
      fluctuate from one to the other
    – May also have an enhanced startle reaction
            SIGNS & SYMPTOMS
   Sleep-wake cycle disturbance
    – Daytime drowsiness  night-time hyperactivity 
      complete reversal of normal cycle
    – Nightmares of delirious patients may continue as
      hallucinations after awakening
   Mood disturbance (Emotional Liability)
    – Depression, euphoria, anxiety, anger, fear & apathy
    – Lack of initiative, impaired impulse control, inability
      to reason thru problems, confabulation
   A physical illness should always be ruled
      out whenever a patient presents with
    prominent visual hallucinations because
      patients with schizophrenia & other
     functional psychotic disorders usually
       experience auditory hallucinations.
      DIFFERENTIAL DIAGNOSIS
   Dementia

   Primary psychiatric illnesses – Depression, Mania,
    Schizophrenia.

   Sundowning (mild to mod delirium @ night—MC in pts
    w/preexisting dementia & may be precipitated by
    hospitalization, drugs & sensory deprivation)disturbance
    in circadian rhythm.

 Focal syndromes – Wernicke’s aphasia, Anton’s
  syndrome & Bi-frontal lesions.
 Non-convulsive status.
DIFFERENTIAL DIAGNOSIS
   Delirium often is unrecognized or
    misdiagnosed & commonly is mistaken for
    dementia, depression, mania, an acute
    schizophrenic reaction or part of old age
    (patients who are elderly are expected to
    become confused in the hospital).
    FEATURE          DELIRIUM         DEMENTIA
ONSET              Acute         Gradual
DURATION           Hours –       Months – years
                     weeks
COURSE             Fluctuating   Progressive
                                   deterioration
CONSCIOUSNESS      Impaired      Normal
PERCEPTUAL         Common        Occurs in late
  DISTURBANCE                     stages
SLEEP-WAKE CYCLE   Disrupted     Usually normal
PROGNOSIS         Potentially    Not reversible
                    reversible
PRIMARILY AFFECTS Attention      Memory
MEDICAL            Yes           No
  EMERGENCY?
                       DIAGNOSIS
   Under-recognition is a major problem – nurses recognize &
    document <50%; DSM-IV criteria is precise but difficult to apply.

   History & Physical – focus on time course of cognitive changes,
    especially their association w/other symptoms or events; Note
    recently started meds, overdose, alcohol use, previous history,
    concurrent medical problems, signs of organ failure & infx (occult
    UTI is common in elderly), general medical evaluation, neurologic
    & mental status examination.

   Remember: Delirium is not a final diagnosis: this syndrome
    indicates the presence of a very serious medical condition that
    should be managed on medical not psychiatric, ward.
                         DIAGNOSIS
   Any pt who presents w/AMS needs a complete PE, w/particular attn
    to:
     – General appearance (unkempt, tattooed &/or malnourished) may
        suggest the possibility of drug or alcohol abuse)
     – Vital signs
     – Hydration status
     – Evidence of physical trauma
     – Evidence of neurological signs

   The delirious or obtunded patient should be evaluated for Pupillary,
    Fundoscopic & extraocular abnormalities; nuchal rigidity; thyroid
    enlargement & heart murmurs or rhythm disturbances.
                      DIAGNOSIS
   Other clues to etiology on PE:
    – A pulmonary exam  wheezing, rales or absent breath
      sounds
    – An abdominal exam  Hepato/Splenomegaly
    – A cutaneous exam  rashes, icterus, petechiae,
      ecchymosis, track marks or Cellulitis (often hidden under
      clothing, particularly pants & socks; checking these areas
      in pts with diabetes is critical; any serious infx can lead
      to mental status ∆s)
       CLUES TO DIAGNOSIS
 Smell for alcohol
 Musty odor of Fetor Hepaticus
 Fruity smell of DKA
 Icterus &/or asterixis  liver failure w/ serum ammonia
 Agitation & tremulousness  sedative or A/C withdrawal
 Fever  infx, heat illness, thyroid storm, ASA toxicity or
  extreme adrenergic overflow of certain drug overdoses &
  withdrawal syndromes (Esp. delirium tremens)
 Extreme hyperthermia (w/pinpoint pupils)  pontine strokes
 BP = common in delirium b/c of resulting adrenergic
  overload
 Hemotympanum, battle sign, raccoon eyes or otorhinorrhea 
  basilar skull fracture (2° to occult head trauma)
                     DIAGNOSIS
 A rapid RR  DKA (Kussmaul respiration), sepsis, stimulant
  drug intoxication & ASA OD
 A slow RR  narcotic OD, CNS insult or various sedative
  intoxications
 A rapid PR  fever, sepsis, dehydration, thyroid storm & cardiac
  dysrhythmias & stimulants, anticholinergics, quinidine,
  theophylline, TCAs or ASA OD
 A slow PR   ICP, asphyxia, complete heart block, CCBs,
  Digoxin & beta-blockers
 Pupillary dilation  intoxication w/ hallucinogen, amphetamine,
  cocaine or anticholinergic med
 Pupillary constriction  narcotic intoxication
 Pupillary inequality  late sign of uncal herniation
 A funduscopic examination:
   – Loss of venous pulsations  early  ICP elevation
   – Papilledema  severe  ICP
    DIAGNOSIS -- Special cases:
 In pts w/delirium & severely  BP, check ocular fundi for
  arteriolar spasm, disc pallor, papilledema, flame
  hemorrhages & exudates ( Malignant HTN).
 In pregnant pts w/diastolic pressure >75 mm hg in 2nd
  trimester or >85 mm hg in 3rd trimester  Pre-eclampsia
  (Hyperreflexia, Edema, Proteinuria).
 In pts w/HTN & Bradycardia   ICP
 With Delirium & Hypotension  dehydration, diabetic
  coma, hemorrhage due to trauma, aneurysmal rupture, GI
  bleeding, adrenergic depletion (2° to cocaine, amphetamine
  or TCA OD) & Addisonian crisis (particularly in steroid
  dependent pts).
                 DIAGNOSIS
 A brief bedside neurologic exam, to include mental
  status testing, is essential for workup of delirium
  when a rapidly treatable cause (hypoglycemia or
  narcotic OD) is not immediately apparent
 The mini-mental status examination (MMSE) (a
  formalized way of documenting severity & nature of
  mental status ∆s)
 In addition, or as an alternative to the MMSE,
  correctly drawing the face of a clock (to include the
  circle, numbers & hands) is a sensitive test of
  cognitive function
 Other simple screening tests include "serial 7's,"
    LABORATORY/RADIOLOGICAL
   CBC, electrolytes, BG levels, BUN/Cr
   Also helpful – UA, LFTS (serum ammonia & PT), toxicology
    screen, ABG, CXR, O2 Sat & cultures
   Consider: Vitamin B-12 & Folate levels, VDRL test (r/o
    Neurosyphilis) & thyroid function studies
   Head CT scan [done b/f LP to r/o CNS infx, trauma, CVA, SAH,
    hematomas, toxoplasmosis or abscess (especially in pts w/HIV
    who present w/H/A)]
   LP (CSF studies including India ink prep & VDRL)
   Plain abdominal x-ray  swallowed bags of drugs ("body
    packing") or radiodense substances (iron tablets)
   EKG (MI or a. fib; low voltages  Hypothyroidism &
    pericardial effusion; Tachycardia, widened QRS or prolonged QT
    interval  TCA overdose)
                    MANAGEMENT
   ABC’s + Normalize fluid & electrolyte status
   Provide Thiamine when administering glucose [or else may lead to acute
    Wernicke syndrome (ataxia, confusion, oculomotor palsies in the setting of
    malnutrition)]
   Physical or pharmacologic restraints (may be necessary to prevent pts from
    harming self or others)
   Low dose Haloperidol (Typical Antipsychotic doc for severe agitation,
    acute psychosis & severe delirium when no CIs exist) [sedative qualities +
    effect on DA-Ach balance; Assess for akathisia & EPS; Avoid in elderly
    w/parkinsonism; in ICU, monitor for QT prolongation, torsades,
    neuroleptic malignant syndrome & withdrawal dyskinesias; antidote:
    Dantrolene]
   Avoid sedative meds if possible [use Benzodiazepines Lorazepam (Ativan)
    -- doc in ED (if unable to control a dangerous patient; may obscure the
    MMSE)]
   Treat underlying cause
   Multi-factorial approach is most successful
                   MANAGEMENT
 Highly distressing for pts & anxiety provoking for medical ward
  staff.
 Hospitalization is essential.
 To limit confusion, foster trust & provide reassurance, try to ensure
  that pt is nursed by same staff consistently.
 Maximize visual acuity (e.g. Glasses, appropriately lit
  environment) & hearing ability (e.g. Hearing aid, quiet
  environment) to avoid misinterpretation of stimuli.
 Involve friend or family member to remain w/pt to help comfort &
  orientate them.
 Avoid complications of delirium – remove indwelling devices
  ASAP, prevent or treat constipation, urinary retention & encourage
  proper sleep hygiene.
      COURSE & PROGNOSIS
 Average duration of delirium is 7 days
 Inpatients who develop delirium have an ed
  mortality, with elderly pts having up to a 75%
  chance of dying during that admission
 Delirium is fully reversible in most cases with
  proper recognition & treatment of the etiology
 Failure to dx & manage delirium is costly, life-
  threatening & can lead to loss of function
DEMENTIA
      WHAT IS DEMENTIA?
 An acquired syndrome of decline in
  memory and other cognitive functions
  sufficient to affect daily life in an alert
  patient
 Progressive and disabling
 NOT an inherent aspect of aging
 Different from normal cognitive lapses
                    Dementia
  DSM IV criteria:
Development of cognitive deficits manifested by both
  -impaired memory
  -aphasia, apraxia, agnosia and disturbed executive
   function
Significantly impaired social and occupational
   function
Gradual onset and continuing decline
Not due to CNS and other physical or psychiatric
   conditions
                   Prevalence
 10% percent of persons over age 70

 20 to 40% of individuals over age 85

 Affects more than 4 million Americans

 Costs more than $50 billion annually
      Causes of Dementia & the
        differential diagnosis:
 Alzheimer’s disease
 Vascular (multi-infarct) dementia
 Dementia associated with Lewy bodies
 Delirium
 Depression
OTHER:
 ETOH, exposure to heavy metals (arsenic, antimony, bismuth)
 Parkinson’s disease, Pick’s disease, frontal lobe dementia
 Infectious diseases: These infections may be caused by viruses
  (HIV, viral encephalitis); spirochetes (Lyme disease,
  neurosyphilis); or prions (Creutzfeldt-Jacob disease)
 Abnormal brain structure: Hydrocephalus, subdural hematoma
 Most common REVERSIBLE
          causes
 Hypothyroidism
 Vitamin B-12
 Folate deficiency
 Dementia of depression
 Drugs
 Alcoholism
                     Assessment
History
Onset and Duration of the memory loss

A) Elderly person with slowly progressive memory loss
  over several years AD

B) Change in personality with disinhibition and
  intact memory may suggest FTD

C) History of sudden stroke with an irregular
   stepwise progression suggests Multi-infarct
  dementia

D) Rapid progression with rigidity and
   myoclonus suggests CJD
            Assessment (cont.)
E) Gait disturbances+memory problems+resting
   tremors may suggest PD

F) Multiple sex partners or intravenous drug use
   may indicate CNS infection

G) Hx of Recurrent head trauma suggests
   Subdural Hematoma

H) Alcoholism Thiamine deficiency

I) Gait disturbances,urinary incontinence and
   memory problems suggest NPH
             Assessment (cont.)
Physical Examination

•    Cogwheel rigidity, bradykinesiaPD

•    Inability to initiate and coordinate stepsNPH

•    Myoclonic jerks are present in CJD

•    Hemiparesis or other focal neurologic deficits
     MID

•    Dry cool skin,hair loss,bradycardia
     Hypothyroidism
          Cognitive assessment
   MMSE
    – most widely used screening exam
    – used in assessment and follow up
    – score interpretation depends on patients age
      and education level
   Clock drawing
    – test of visuospatial skills
    – draw numbers within a pre-drawn circle 3
      inches in diameter to make that circle look like
      the face of a clock
    – Normal score 0-3
    – Dementia 4-7
                                        MMSE
Orientation
Name: hospital/floor/town/state/country                       5 (1 for each name)

Registration
Identify three objects by name and ask patient to repeat3     (1 for each object)

Attention and calculation
Serial 7s; subtract from 100 (e.g., 93-86-79-72-65)           5 (1 for each subtraction)

Recall
Recall the three objects presented earlier                    3 (1 for each object)

Language
Name pencil and watch                                         2 (1 for each object)

Repeat "No ifs, ands, or buts“                                1

Follow a 3-step command (e.g., "Take this paper,,
fold it in half and place it on the table")                   3 (1 for each command)

Write "close your eyes" and ask patient to obey               1
written command

Ask patient to write a sentence                               1

Ask patient to copy a design (e.g., intersecting pentagons)   1

TOTAL                                                                  30
Clock drawing
        Cortical dementias
 Alzheimer’s
 Vascular
 Diffuse Lewy body
 Pick’s disease
 Creutzfeldt-Jacob disease
                      Alzheimer’s
Slowly progressive dementing illness associated
with diffuse cortical atrophy, amyloid plaques and
neurofibrillary tangles

CLINICAL MANIFESTATIONS
• Progressive memory impairment (predominantly short term)
• Language impairment
• Complex deficits in visual and spatial abilities
• Acalculia
• Personality changes - progressive passivity to marked
  hostility
• Increased stubbornness & suspiciousness
• Delusions
• Hallucinations
• Symptoms of depression and anxiety
                          Alzheimer’s (cont.)




   PLAQUES                                      TANGLES




Brain slice: left from
Alzheimer's Disease,
right from normal brain                         CT SCAN
Alzheimer’s (cont.)

       A.   MRI BRAIN NORMAL 86-year-old
            male.

       B. MRI BRAIN 77-year-old male with
           Alzheimer's disease.

       c. Fluorodeoxyglucose PET scans of a
            normal control.

       D. A patient with Alzheimer's disease.


       Note that the patient
       has decreased activity in the parietal
           lobes bilaterally (arrows)
           Alzheimer’s (cont.)
   Management
    – KISS (keep it simple and short)
    – Maintain autonomy and independence
    – Establish routines
    – Safety issues: cooking, driving, community
      services referral, discuss legal issues, caregiver
      education
    – Medications: donepezil, tacrine
            Donepezil (ARICEPT)
Reversible cholinesterase (ChE) inhibitor
In Alzheimer's disease behavioral consequences (e.g., decline in
   memory and learning) that are partially related to cholinergic
   deficits
Used for the symptomatic management of mild to moderate forms of
   Alzheimer's disease

DOSAGE
5 to 10mg qd
CONTRAINDICATIONS
Liver disease, alcoholism, peptic ulcer disease, chronic
  obstructive pulmonary disease; and bradycardia
ADVERSE EFFECTS
N/V Diarrhea, Bradycardia Dizziness
      Memantine (Namenda)
 Non-competitive antagonist at N-methyl-
  D- aspartate receptors (NMDA)
 Indicated for moderate to severe
  Alzheimer’s disease.
 Dose: 5 or 10 mg PO QD
 Seizure disorder and renal disease are
  contraindications.
 HTN and Urinary Incontinence are the
  adverse effects
       Multi-infarct dementia
Results from an accumulation of discrete
cerebral strokes that produce disabling deficits
of memory, behavior, and other cognitive
  abilities

CLINICAL MANIFESTATIONS
Stepwise deterioration
Focal neurologic deficits
Brain imaging shows multiple areas of stroke
         Lewy Body Dementia
-Lewy bodies are intraneuronal inclusions that
  stain with periodic acid-Schiff stain.

-In addition to chronic progressive dementia,
  these patients often also have parkinsonian
  features.

-Frequent fluctuations of behavior, cognitive
  ability,and level of alertness may occur.

-No specific treatment
-No response to L- DOPA
Lewy Body (cont.)
     Frontotemporal Dementia
Presents as disinhibition, apathy, or agitation.
Focal lobar atrophy of the frontal and/or temporal
lobes seen on MRI.

Pick's disease

Subcategory of FTD.

Microscopic findings include gliosis, neuronal loss,
and swollen or ballooned neurons, with Pick bodies.

Slowly progressive dementia ,bulimia, language
  disturbance, emotional disinhibition, irritability,
  and persistent aimless wandering,language
  disturbance.
          Huntington’s disease
-Autosomal dominant degenerative brain disorder.

-Chorea and behavioral disturbance.

-Attention, judgment, awareness, may be seriously
  deficient at an early stage.

-No specific treatment.

-Adventitious movements and behavioral changes
 may partially respond to phenothiazines.
Huntington’s (cont.)
     Creutzfeldt-Jacob disease
 Atypical infectious agents called “prions” cause
  the disease.
 It’s a transmissible neurodegenerative disorder.
 Manifests in the sixth and seventh decade of life
  as rapidly progressive dementia with myoclonus.
 Minimal help with neuroimaging, EEG and CSF
  analysis.
 CSF protein 14-3-3, may be diagnostic
but the gold standard is………?
                 CJD cont….
   Brain biopsy for premortem diagnosis.
   Universal precautions are recommended for
    routine patient care as the “prions” are very
    resistant for routine disinfection methods.
   The only known disease that can transmit through
    corneal transplant and growth hormone
    administration.
   The disease in animals is called “bovine
    spongiform encephalopathy”.
   No effective treatment.
           HIV dementia
Dementia in HIV occurs when the pt develops
  AIDS(AIDS dementia complex).
-This is a diagnosis of exclusion based on
  neuroimaging and spinal fluid analysis.
-Neuropsychiatric testing is helpful in
  distinguishing from depression.
          Clinical features…
 Pts have difficulty with cognitive tasks and have
  diminished motor speed. Dementia manifestations
  may wax and wane with periods of lucidity and
  confusion over the course of a day.
 First clinical symptom may be deterioration in
  hand writing.
 Many pts will improve with effective antiretroviral
  therapy.
    Other types of dementia
 Korsakoff’s syndrome
 Wernicke’s encephalopathy
 Parkinson’s disease
 Chronic metal intoxications
        Korsakoff’s syndrome
Caused by prolonged untreated thiamine deficiency

• Memory for new events is seriously impaired,
whereas memory of knowledge prior to the illness
is relatively intact
• Confabulation

-MRI Mammillary body atrophy

-No specific treatment
  Wernicke’s encephalopathy
-Thiamine (vitamin B1)deficiency damages the
thalamus, mammillary bodies.

SYMPTOMS
Confusion
Ataxia
Diplopia

-Administration of parenteral thiamine may
reverse the disease.
           Parkinson’s disease
Develops due to loss of dopaminergic neurons in
  substantia nigra.
Approximately 20% of patients develop dementia.

CLINICAL MANIFESTATIONS
• Resting tremors
• Rigidity
• Bradykinesia
• Gait disturbances

Treatment with L-dopa neither accelerates nor
prevents this process.
  Chronic metal intoxications
 Lead poisoning

 Mercury poisoning

 Arsenic intoxication

 Dialysis dementia syndrome
Dementia is part of normal
  processing of age…


        True?

        False?
  Dementia impairs physical
functioning of the individual…


         True?

         False?
Delirious patient may have
 auditory hallucinations…


       True?

       False?
A person with dementia may
    develop delirium…
   True?



   False?
A person with delirium will
   develop dementia…

   True?

   False?
A 70 YO man comes and tells you that
he has been forgetting certain things
and has difficulty of recollecting some
names.
He is having dementia….?
True ? False ?
THANK YOU

				
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posted:1/16/2013
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