This document provides information on organic brain syndrome, including dementia and delirium. It defines organic brain syndrome as brain dysfunction caused by pathology inside or outside the brain. Dementia is described as the acquired impairment of cognitive functions such as memory and orientation, while delirium is an acute impairment of consciousness and cognition. The document discusses the epidemiology, risk factors, pathologies, clinical features, investigations, and management of various types of organic brain syndrome including Alzheimer's disease and vascular dementia.

1. Organic brain syndrome
Tai Zu Huang
Teoh Wee Loon

2. Introduction
• Brain dysfunction caused by organic pathology
inside or outside of the brain
• Can be classified by:
– Global syndromes
• Delirium
• Dementia
– Specific syndromes
• Amnesic syndrome
• Organic mood disorder
• Organic delusional state
• Organic personality disorder

3. Dementia
DEFINITION:
•An acquired, generalized and usually
progressive impairment of cognitive
functions (ie
memory, recall, orientation, language, abst
raction etc)
•Content being affected but not level of
consciousness

4. Epidemiology
• Affect predominantly elderly people
• Prevalence increases with age:
– 15% >65y/o (different studies have different prevalence)
– 25% >85y/o
• F > M
• A community survey (n=223) amongst Malays age 60 years
and above in Selangor:24% were cognitively impaired
• Another study found the prevalence of dementia in urban
communities of Malays (>60y/o) in KL was 6%
• Study of elderly in Malaysia yielded a prevalence of organic
mental disorder (inconclusive of dementia) at 14.4%
• Down syndrome is also associated with the development of
dementia

5. Classification
Part of
brain
affected
Aetiology

6. Part of brain affected
• Brain damage affects the brain cortex
or upper layer
• Cause problem with
memory, language, thinking & social
behaviour
• Eg: Alzheimer’s & Creutzfeld –Jakob
disease
cortical
• Affects brain below the cortex
• Changes in emotion & movement
• Eg Huntington’s
disease, Parkinson’s disease & AIDS
subcortical

7. Aetiology
•Alzheimer’s disease
• Parkinson disease
•Lewy body dementia
Degenerative
•Pseudodementia of depression
• Cognitive decline in late life scizophreniaPsychiatric
•Multi infarct dementiaVascular
• multiple sclerosisDemyelinating
• Vitamin def (e.g vit
B12,folate), endocrinopathies (eg
hypothyroidism), abnormality of cortisol
metabolism
Metabolic

8. Aetiology
• Prion disease ( Creutzfeld –Jakob disease)
• AIDSInfection
• Alcohol, heavy
metals, irradition, pseudodementia d2
medication (anticholinergics), carbon monoxide
Drugs and
toxins
• Huntington disease, trauma(dementia pugilistica
in boxers), tumorOthers

9. VITAMIN D VEST
• V – Vitamin Deficiency [B12, folate and
thiamine(Wernicke-korsakoff)]
• I – Intracranial masses (tumour, abscess)
• T – Trauma (head injury, dementia pugilistica)
• A – Anoxia
• M- Metabolic (diabetes)
• I – Infection (HIV, syphilis, Creutzfeldt-Jakod)
• 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%)
• D – Degenerative
(Alzheimer’s, Hungtington’s, CJD)
• V – Vascular (multi-infarct dementia)
• E – Endocrine (hypothyroid)
• S – Space occupying lesion (subdural
hematoma)
• T – Toxic (alcohol)

11. Diagnosis of dementia
Dementia is diagnosed based on:
History (based on aetiology)
 Mental state examination including MMSE
Other lab investigation depend on aetiology
Most type of dementia can be diagnosed
based on criteria in DSM –IV

12. Clinical features:
• Personality changes: become more hostile, irritable and explosive
• Hallucination and delusions
– 20-30% pts have hallucinations
– 30-40% have delusions (delusion of paranoid or persecutory)
• Mood changes: depression and anxiety (40-50% of pts)
• Cognitive changes
• Thinking: slow and impoverished
• Insight: poor
• Catastrophic changes – when patient are taxed beyond their
restricted abilities, there maybe sudden change to anger and tears
• Sundowner syndrome – confusion, ataxia, drowsiness after
“sundown”

13. Investigation:
• Depend on suspected etiologies
• CBC (note MCV), glucose, TSH, B12, folate
• electrolytes, LFTs, renal function
• CT head
• MRI as indicated
• as clinically indicated – VDRL
(syphilis), HIV, ANA, anti-dsDNA
(SLE), caeruloplasmin, copper (wilson’s
disease), cortisol, toxicology, heavy metals

14. Management of dementia:
• Treat treatable causes
• Treat the cause of superimposed delirium
• Biological: medication
• 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
•Mild, moderate
and severe AD
•Vascular
dementia
•Dementia with
Lewy Body
(DLB)
Atypical
antipsycotics:
•can be used
agitation and
psychosis
•Avoid in DLB
Antidepressants Evaluate
caregiver needs
Multicomponen
t intervention:
•Psychotherapy
•Psychoeducatio
n
•Supportive
therapy
•Respite/day
care
•training

16. Non-
pharmacologic
al
Pharmacological Caregivers
interventionCognition Behaviour Mood
Challenging
behaviours
•Behaviour
management
•Music
•Reminiscence
therapy
Reduction of
co-morbid
emotional
problem (eg
depression and
anxiety)
Memantine
(glutamate
NMDA
antagonist)
•Severe AD
Cognitive
enhancers:
•Cholinesteras
e inhibitors
•Memantine
(NMDA
receptor
antagonist)
Antidepressant
in fronto-
temporal
dementia

17. Alzheimer disease
• First described by Alois Alzheimer in 1907
• Although cause remains unknown, progress had been made to try
to understand molecular basic of amyloid deposits
• genetic factors
– a minority (<7%) of AD cases are familial, autosomal dominant
– 3 major genes for autosomal dominant AD have been identified:
• amyloid precursor protein (chromosome 21)
• presenilin 1 (chromosome 14)
• presenilin 2 (chromosome 1)
– the E4 polymorphism of apolipoprotein E is a susceptibility genotype (E2 is
protective
• Biochemical factors
– Neurotransmitter such as Ach and Norepinephrine become hypoactive
– Neuroactive peptides somatostatin and corticotrophin also decreased in concentration

18. DSM-IV-TR diagnostic criteria for dementia of
Alzheimer’s type
• A. Development of multiple cognitive deficits
manifested by both:
– 1) memory impairment
– 2) ≥1 of the following cognitive disturbances:
• Aphasia
• Apraxia
• Agnosia
• Disturbances in executive functioning

19. • 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
• C. gradual onset and continuing cognitive decline
• D. not due to any other
– CNS conditions
– Systemic conditions
– Subtance-induced conditions
• E. Deficits do not occur during the course of
delirium
• F. Disturbance is not better accounted by other
Axis-I disorder (MDD, Schizophrenia)

20. Risk factors
• Aging (elderly people > 65 years of age)
• Female
• Family history
-Defective genes on chromosomes 1,14,21
• Hypothethical risk factor : aluminium toxicity
• Having history of head injury
• Low education level
• Smoking
• Down syndrome (y?)

21. Pathology
• Macroscopic appearance of brain : diffuse
atrophy, esp frontal, parietal and temporal
lobes, flattened sulci & enlarged cerebral
ventricles
• Microscopic findings : senile plaques (amyloid
plaques – 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

23. Course, prognosis & treatment
• Slowly progress memory impairment
• Aphasia, apraxia and agnosia also present
• May later develop motor & gait disturbances;
may become bedridden
• Mean survival is 7 years from onset
• Treatment : cholinesterase inhibitor (eg:
galantamine, rivastigmine, donepezil)

24. • There is a new case of dementia every 7
seconds in our world
• Alzheimer is the most common cause of
dementia and is not part of aging process
• There are currently no prevention and cure
for it

25. Vascular dementia
• Caused by blockage of in brain’s blood supply
• Leading to progressive decline in memory &
cognitive functioning
• > ,affects people between the ages of 60 and
75, HTN or CV dss
• Approximately 10-15% have coexisting vascular
dementia and dementia of Alzheimer’s type
• Pathology : a/w multiple infarcts coz by
thromboembolism fr extracranial arteries
arteriosclerosis in main vessels

26. Vascular dementia
• 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
• Diagnosis, other signs and symptoms are as according to DSM-
IV diagnostic criteria
• Prognosis
-lifespan averages is 4-5 years from time of diagnosis

27. Delirium
acute generalized impairment of
mental disorder
Hallmark symptoms :impairment
of consiousness, in association with
global impairment of cognitive
functions
Common psychiatric symptoms:
abnormalities of
perception, mood, behaviour
Common neurological symptoms:
tremor, nystagmus, incoordination, ur
inary incontinence, asterixis.

28. Epidemiology:
• general population: 1.1%
• medically ill patient who are hospitalized: 10-30%
• surgical intensive unit: 30%
• cardiac intensive care unit: 40-50%
• AIDS: 30-40%

29. Risk factor
• Hospitalization
• Nursing home resident
• Childhood (example: febrile illness)
• Old age especially male
• Severe illnesses like cancer, AIDS
• Pre-existing cognitive impairment or brain pahtology
• Recent anesthesia
• Substance abuse

30. Etiology:
• Common pathway to any brain insult.
• Is thought to involve dysfunction of the reticular
formation & acetylcholine transmission.
• Reticular formation→attention & arousal
• Study shown decrease in acetylcholinergic activity
• Other neurotransmitter: serotonin & glutamate

31. INTRACRANIAL CAUSES
• Epilepsy and postictal states
• Brain trauma (especially concussion)
• Infections
• Meningitis
• Encephalitis
• Neoplasms
• Vascular disorders

32. EXTRACRANIAL CAUSES
• Drugs (ingestion or withdrawal) and poisons
(Anticholinergic, anticonvulsants, antihypertensives, antiparki
nsonians, antipsychotics, cardiac
glycosides, insulin, opiates, sedatives and
hypnotics, steroids, alcohol)
• Endocrine dysfunction (hypofunction or hyperfunction)
(Pituitary, Pancreas, Adrenal, Parathyroid, Thyroid)
• Diseases of nonendocrine organs
(Hepatic encephalopathy, Uremic encephalopathy, Carbon
dioxide narcosis, Hypoxia, Cardiac
failure, Arrhythmias, Hypotension )

33. • Deficiency diseases
(Thiamine, nicotinic acid, B12, or folic acid deficiencies)
• Systemic infections with fever and sepsis
• Electrolyte imbalance of any cause
• Postoperative states
(postoperative pain, insomnia, pain medication, electrolyte
imbalance, infection, fever, blood loss)
• Trauma (head or general body)

34. Impaired delivery (of brain substrate eg. vascular
insufficiency due to stroke)
Metabolic
Drugs
Endocrinopathy
Liver disease
Infrastructure (structural disease of cortical
neurons)
Renal failure
Infection
Oxygen
Urinary tract infection
Sensory deprivation

35. CLINICAL FEATURES OF DELIRIUM
• Impairment of consciousness – disorientation & poor
concentration, fluctuating course & often worse in the evening.
• Behavior – overactive or underactive, sleep is often disturbed.
• Thinking – slow, muddled, ideas of reference & delusions are
transient and poorly elaborated.
• Mood – anxious, irritable or depressed, often labile.
• Perception – is distorted, misinterpretations of
illusions, hallucination (mainly visual). Tactile and auditory
hallucination can occur but less frequent.
• Memory – impaired.
• Insight – impaired

36. Diagnosis
• 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
• Onset usually sudden.
• Symptoms persist as long as the causative factors are
present, although delirium generally lasts less than a
week.
• 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.
• The older a patient and the longer the patient has been
delirious, the longer the delirium takes to resolve.

38. Differential diagnosis:
• Dementia
• Schizophrenia & mania
– No rapidly fluctuating course, do not impair the level of
consciousness or significantly impair cognition
• Acute amnesic syndrome
• 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

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:
• Recent memory severely impaired
• Remote memory spared
• Disorientation in time
• Confabulation
• Other cognitive function preserved
Organic Brain syndrome

42. Korsakoff syndrome
• Amnesic syndrome accompany with acute neurological
symptoms caused by neuronal damage that results from
thiamine deficiency in association with chronic alcohol
abuse.
• 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.
• Confabulation is a hallmark finding of Korsakoff
syndrome (also called Korsakoff psychosis).
• Treatment: IV thiamine
Organic Brain syndrome

43. Organic personality disorder
• Frontal lobe damage
• 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:
• Impairment of consciousness
• Delirium
• Post-traumatic amnesia: transient amnesia with retrograde
(events prior to injury) and anterograde (events following
injury) features.
Long-term consequences:
• Personality changes
• 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

46. Thank you!