2. Introduction
โข Brain dysfunction caused by organic pathology
inside or outside of the brain
โข Can be classified by:
โ Global syndromes
โข Delirium
โข Dementia
โ Specific syndromes
โข Amnesic syndrome
โข Organic mood disorder
โข Organic delusional state
โข Organic personality disorder
3. Dementia
DEFINITION:
โขAn acquired, generalized and usually
progressive impairment of cognitive
functions (ie
memory, recall, orientation, language, abst
raction etc)
โขContent being affected but not level of
consciousness
4. Epidemiology
โข Affect predominantly elderly people
โข Prevalence increases with age:
โ 15% >65y/o (different studies have different prevalence)
โ 25% >85y/o
โข F > M
โข A community survey (n=223) amongst Malays age 60 years
and above in Selangor:24% were cognitively impaired
โข Another study found the prevalence of dementia in urban
communities of Malays (>60y/o) in KL was 6%
โข Study of elderly in Malaysia yielded a prevalence of organic
mental disorder (inconclusive of dementia) at 14.4%
โข Down syndrome is also associated with the development of
dementia
6. Part of brain affected
โข Brain damage affects the brain cortex
or upper layer
โข Cause problem with
memory, language, thinking & social
behaviour
โข Eg: Alzheimerโs & Creutzfeld โJakob
disease
cortical
โข Affects brain below the cortex
โข Changes in emotion & movement
โข Eg Huntingtonโs
disease, Parkinsonโs disease & AIDS
subcortical
7. Aetiology
โขAlzheimerโs disease
โข Parkinson disease
โขLewy body dementia
Degenerative
โขPseudodementia of depression
โข Cognitive decline in late life scizophreniaPsychiatric
โขMulti infarct dementiaVascular
โข multiple sclerosisDemyelinating
โข Vitamin def (e.g vit
B12,folate), endocrinopathies (eg
hypothyroidism), abnormality of cortisol
metabolism
Metabolic
9. VITAMIN D VEST
โข V โ Vitamin Deficiency [B12, folate and
thiamine(Wernicke-korsakoff)]
โข I โ Intracranial masses (tumour, abscess)
โข T โ Trauma (head injury, dementia pugilistica)
โข A โ Anoxia
โข M- Metabolic (diabetes)
โข I โ Infection (HIV, syphilis, Creutzfeldt-Jakod)
โข N- Normal pressure hydrocephalus
10. We must always think of treatable causes of dementia before we start to manage
them although it is very rare (10%)
โข D โ Degenerative
(Alzheimerโs, Hungtingtonโs, CJD)
โข V โ Vascular (multi-infarct dementia)
โข E โ Endocrine (hypothyroid)
โข S โ Space occupying lesion (subdural
hematoma)
โข T โ Toxic (alcohol)
11. Diagnosis of dementia
Dementia is diagnosed based on:
๏ฑHistory (based on aetiology)
๏ฑ Mental state examination including MMSE
๏ฑOther lab investigation depend on aetiology
๏ฑMost type of dementia can be diagnosed
based on criteria in DSM โIV
12. Clinical features:
โข Personality changes: become more hostile, irritable and explosive
โข Hallucination and delusions
โ 20-30% pts have hallucinations
โ 30-40% have delusions (delusion of paranoid or persecutory)
โข Mood changes: depression and anxiety (40-50% of pts)
โข Cognitive changes
โข Thinking: slow and impoverished
โข Insight: poor
โข Catastrophic changes โ when patient are taxed beyond their
restricted abilities, there maybe sudden change to anger and tears
โข Sundowner syndrome โ confusion, ataxia, drowsiness after
โsundownโ
13. Investigation:
โข Depend on suspected etiologies
โข CBC (note MCV), glucose, TSH, B12, folate
โข electrolytes, LFTs, renal function
โข CT head
โข MRI as indicated
โข as clinically indicated โ VDRL
(syphilis), HIV, ANA, anti-dsDNA
(SLE), caeruloplasmin, copper (wilsonโs
disease), cortisol, toxicology, heavy metals
14. Management of dementia:
โข Treat treatable causes
โข Treat the cause of superimposed delirium
โข Biological: medication
โข Psychosocial: home care, day care, inpatient
care, residential care, avoidance of driving
15. Management of dementia:
Non-
pharmacologica
l
Pharmacological Caregivers
InterventionCognition Behaviour Mood
Promoting
independence:
communication,
ADL skill
training,
exercise,
rehabilitation,
combination
Maintainence of
cognition:
reality therapy,
Validation, life
review
Cholinesterase
inhibitors:
donepezil
โขMild, moderate
and severe AD
โขVascular
dementia
โขDementia with
Lewy Body
(DLB)
Atypical
antipsycotics:
โขcan be used
agitation and
psychosis
โขAvoid in DLB
Antidepressants Evaluate
caregiver needs
Multicomponen
t intervention:
โขPsychotherapy
โขPsychoeducatio
n
โขSupportive
therapy
โขRespite/day
care
โขtraining
16. Non-
pharmacologic
al
Pharmacological Caregivers
interventionCognition Behaviour Mood
Challenging
behaviours
โขBehaviour
management
โขMusic
โขReminiscence
therapy
Reduction of
co-morbid
emotional
problem (eg
depression and
anxiety)
Memantine
(glutamate
NMDA
antagonist)
โขSevere AD
Cognitive
enhancers:
โขCholinesteras
e inhibitors
โขMemantine
(NMDA
receptor
antagonist)
Antidepressant
in fronto-
temporal
dementia
17. Alzheimer disease
โข First described by Alois Alzheimer in 1907
โข Although cause remains unknown, progress had been made to try
to understand molecular basic of amyloid deposits
โข genetic factors
โ a minority (<7%) of AD cases are familial, autosomal dominant
โ 3 major genes for autosomal dominant AD have been identified:
โข amyloid precursor protein (chromosome 21)
โข presenilin 1 (chromosome 14)
โข presenilin 2 (chromosome 1)
โ the E4 polymorphism of apolipoprotein E is a susceptibility genotype (E2 is
protective
โข Biochemical factors
โ Neurotransmitter such as Ach and Norepinephrine become hypoactive
โ Neuroactive peptides somatostatin and corticotrophin also decreased in concentration
18. DSM-IV-TR diagnostic criteria for dementia of
Alzheimerโs type
โข A. Development of multiple cognitive deficits
manifested by both:
โ 1) memory impairment
โ 2) โฅ1 of the following cognitive disturbances:
โข Aphasia
โข Apraxia
โข Agnosia
โข Disturbances in executive functioning
19. โข B. cognitive deficits in criteria A1 and A2 cause
significant impairment in social and occupational
functioning and represent a significant decline from
a previous level of functioning
โข C. gradual onset and continuing cognitive decline
โข D. not due to any other
โ CNS conditions
โ Systemic conditions
โ Subtance-induced conditions
โข E. Deficits do not occur during the course of
delirium
โข F. Disturbance is not better accounted by other
Axis-I disorder (MDD, Schizophrenia)
20. Risk factors
โข Aging (elderly people > 65 years of age)
โข Female
โข Family history
-Defective genes on chromosomes 1,14,21
โข Hypothethical risk factor : aluminium toxicity
โข Having history of head injury
โข Low education level
โข Smoking
โข Down syndrome (y?)
21. Pathology
โข Macroscopic appearance of brain : diffuse
atrophy, esp frontal, parietal and temporal
lobes, flattened sulci & enlarged cerebral
ventricles
โข Microscopic findings : senile plaques (amyloid
plaques โ amount indicates
severity), neurofibrillary tangles (composed of
cytoplasmic skeleton, mainly phosphorylated tau
protein), neuronal loss(in cortex &
hippocampus), synaptic loss ( 50 % in cortex) &
granulovascular degeneration of neurons
22.
23. Course, prognosis & treatment
โข Slowly progress memory impairment
โข Aphasia, apraxia and agnosia also present
โข May later develop motor & gait disturbances;
may become bedridden
โข Mean survival is 7 years from onset
โข Treatment : cholinesterase inhibitor (eg:
galantamine, rivastigmine, donepezil)
24. โข There is a new case of dementia every 7
seconds in our world
โข Alzheimer is the most common cause of
dementia and is not part of aging process
โข There are currently no prevention and cure
for it
25. Vascular dementia
โข Caused by blockage of in brainโs blood supply
โข Leading to progressive decline in memory &
cognitive functioning
โข > ,affects people between the ages of 60 and
75, HTN or CV dss
โข Approximately 10-15% have coexisting vascular
dementia and dementia of Alzheimerโs type
โข Pathology : a/w multiple infarcts coz by
thromboembolism fr extracranial arteries
arteriosclerosis in main vessels
26. Vascular dementia
โข Clinical features:
-sx are fluctuating & episodes of confusion are common esp at
night
-Neurological signs is common
-in some cases emotional & personality changes may be
apparent b4 impairment of memory & intelect
โข Diagnosis, other signs and symptoms are as according to DSM-
IV diagnostic criteria
โข Prognosis
-lifespan averages is 4-5 years from time of diagnosis
27. Delirium
๏ถacute generalized impairment of
mental disorder
๏ถHallmark symptoms :impairment
of consiousness, in association with
global impairment of cognitive
functions
๏ถCommon psychiatric symptoms:
abnormalities of
perception, mood, behaviour
๏ถCommon neurological symptoms:
tremor, nystagmus, incoordination, ur
inary incontinence, asterixis.
28. Epidemiology:
โข general population: 1.1%
โข medically ill patient who are hospitalized: 10-30%
โข surgical intensive unit: 30%
โข cardiac intensive care unit: 40-50%
โข AIDS: 30-40%
29. Risk factor
โข Hospitalization
โข Nursing home resident
โข Childhood (example: febrile illness)
โข Old age especially male
โข Severe illnesses like cancer, AIDS
โข Pre-existing cognitive impairment or brain pahtology
โข Recent anesthesia
โข Substance abuse
30. Etiology:
โข Common pathway to any brain insult.
โข Is thought to involve dysfunction of the reticular
formation & acetylcholine transmission.
โข Reticular formationโattention & arousal
โข Study shown decrease in acetylcholinergic activity
โข Other neurotransmitter: serotonin & glutamate
33. โข Deficiency diseases
(Thiamine, nicotinic acid, B12, or folic acid deficiencies)
โข Systemic infections with fever and sepsis
โข Electrolyte imbalance of any cause
โข Postoperative states
(postoperative pain, insomnia, pain medication, electrolyte
imbalance, infection, fever, blood loss)
โข Trauma (head or general body)
35. CLINICAL FEATURES OF DELIRIUM
โข Impairment of consciousness โ disorientation & poor
concentration, fluctuating course & often worse in the evening.
โข Behavior โ overactive or underactive, sleep is often disturbed.
โข Thinking โ slow, muddled, ideas of reference & delusions are
transient and poorly elaborated.
โข Mood โ anxious, irritable or depressed, often labile.
โข Perception โ is distorted, misinterpretations of
illusions, hallucination (mainly visual). Tactile and auditory
hallucination can occur but less frequent.
โข Memory โ impaired.
โข Insight โ impaired
36. Diagnosis
โข DSM-IV diagnostic criteria for delirium due to a general
medical condition
A. Disturbance of consciousness (i.e. reduced clarity of awareness
of the environment) with reduced ability to focus, sustain or shift
attention.
B. A change in cognition (such as memory
deficit, disorientation, language disturbance) or the development
of perceptual disturbance that is not better accounted for by a
preexisting, established or evolving dementia.
C. The disturbance develop over a short period of time (usually
hours to days) & tends to fluctuate during the course of the day.
D. There is evidence from the history, PE or laboratory findings
that the disturbance is caused by the direct physiologic
consequences of a general medical condition.
37. Course & prognosis
โข Onset usually sudden.
โข Symptoms persist as long as the causative factors are
present, although delirium generally lasts less than a
week.
โข After removal of the causative factors, the symptoms
of delirium usually recede over a 3- to 7-day
period, although some symptoms may take up to 2
weeks to resolve completely.
โข The older a patient and the longer the patient has been
delirious, the longer the delirium takes to resolve.
38. Differential diagnosis:
โข Dementia
โข Schizophrenia & mania
โ No rapidly fluctuating course, do not impair the level of
consciousness or significantly impair cognition
โข Acute amnesic syndrome
โข Depression
39. Investigation:
First line Other useful test
Blood test FBC, ESR,
Urea and electrolyte (BUSE)
Calcium, Magnesium
Liver function test
Thyroid function test
Cardiac enzyme
Vitamin B12
Anti-nuclear antibody
Tumour marker
Anti-thyroid antibody
Copper studies
CNS investigation Head imaging ( CT, MRI) Lumbar puncture
EEG
Others ABG
ECG
Infection screening (blood
culture, urine culture)
Viral screen
40.
41. Amnesic syndrome
Characterized by a prominent disorder of recent memory
in the absence of generalized intellectual impairment
(dementia) or impaired of consciousness (delirium)
Clinical features:
โข Recent memory severely impaired
โข Remote memory spared
โข Disorientation in time
โข Confabulation
โข Other cognitive function preserved
Organic Brain syndrome
42. Korsakoff syndrome
โข Amnesic syndrome accompany with acute neurological
symptoms caused by neuronal damage that results from
thiamine deficiency in association with chronic alcohol
abuse.
โข It usually is preceded by an episode of Wernicke
encephalitis (eg, ataxia, confusion, oculomotor palsy),
typically precipitated by administration of glucose to a
malnourished alcoholic without concomitant parenteral
thiamine.
โข Confabulation is a hallmark finding of Korsakoff
syndrome (also called Korsakoff psychosis).
โข Treatment: IV thiamine
Organic Brain syndrome
43. Organic personality disorder
โข Frontal lobe damage
โข Clinical features:
- behaviour is disinhibited
- overfamiliar
- overtalkative
- inappropriate jokes
- euphoria
- concentration and attention will be reduced
- insight impaired
Organic Brain syndrome
44. Head injury
major head injury has both immediate and long-term
neuropsychiatric consequences.
Acute psycholoqical effects of head injury:
โข Impairment of consciousness
โข Delirium
โข Post-traumatic amnesia: transient amnesia with retrograde
(events prior to injury) and anterograde (events following
injury) features.
Long-term consequences:
โข Personality changes
โข Emotional symptoms
Organic Brain syndrome
45. Dementia Delirium Pseudodementia of
depression
Onset gradual/step-wise
decline
acute(hours-days) subacute
Duration months-years days-weeks variable
Natural History Progressive , usually
irreversible
fluctuating,
Reversible, high
morbidity/mortality
in very old
recurrent,usually
reversible
Level of
consciousness
normal fluctuating(over
24hours)
normal
Orientation intact initially impaired(usually
time and place)
intact
Mood and Affect labile but no usually
anxious
anxious, irritable,
fluctuating
depressed,stable