1. VAISHNAVI SURESH NAIR
MADNESS

2. A PROGRESSIVE DETERIORATION OF
INTELLECT, BEHAVIOUR & PERSONALITY DUE
TO DIFFUSE DISEASE OF CEREBRAL
HEMISPHERE, MAXIMALLY AFFECTING THE
CEREBRAL CORTEX & HIPPOCAMPUS.
DEMENTIA
COMMON SIGNS & SYMPTOMS
-MEMORY LOSS
-IMPAIRED JUDGEMENT
-DIFFICULT WITH ABSTRACT
THINKING
-FAULTY REASONING
-INAPPROPRIATE BEHAVIOUR
-LOSS OF COMMUNICATION SKILLS
-DISORIENTATION TO PLACE & TIME
-GAIT, MOTOR & BALANCE PROBLEMS
-NEGLECT OF PERSONAL CARE & SAFETY
-HALLUCINATIONS,PARANOIA &
AGITATION

3. RISK FACTORS FOR DEMENTIA
AGE (ABOVE 65)/
SEX (MALE)/
GENETIC
OVER WEIGHT/
DRUG/SMOKING/
ALCOHOL
BLOOD PRESSURE/
BLOOD SUGAR/
CHOLESTEROL
DEPRESSION/
STRESS
HEART DISEASES/
DIABETES/
VASCULAR DISEASES
HEAD INJURY/
INFLAMMATORY STRESS/
TUMOR
HIV INFECTION/
SOME
IMMUNOLOGICAL
DISORDERS
POOR EDUCATION/
LOW PHYSICAL
ACTIVITY/
POOR NUTRITION

4. • SYMPTOM RATHER THAN A SINGLE DISEASE ENTITY.
• OCCURS IN ANY AGE,MORE COMMON IN ELDERLY AGE (ABOVE 65
YEARS).
• IF OCCURRED UNDER 65, IT IS TERMED AS PRE-SENILE DEMENTIA.
• INCIDENCE RATE: 187/100,000 PERSONS.
• ACCELERATED BY CHANGE OF ENVIRONMENT, INTERCURRENT
INFECTIONS, SURGICAL PROCEDURES.

5. INTEROSPECTIVE:
UNSURE OF SELF
DIFFICULTY IN COPING
WITH WORK & DAILY
ROUTINE
(RETAINED INSIGHT)
LOSS OF INSIGHT,
BEHAVIOURAL CHANGES,
LOSS OF INHIBITION
LONG TERM CARE;
CAN’T BE UN-ATTENDED
MUTISM
INCONTINENCE,
DEATH.
DEVELOPMENT OF SYMPTOMS

6. CLASSIFICATION -BASED ON CAUSE
1)ALZHEIMER’S DISEASE (60% OF ALL CASES)
2)CEREBRO VASCULAR DISEASES (20% OF ALL CASES)
- MULTI INFARCT (ATHEROSCLEROTIC) DEMENTIA
- SUBCORTICAL VASCULAR DISEASE ( BINSWANGER’S DISEASE)
3)NEURO DEGENERATIVE - PICK’S DISEASE ; HUNTINGTON’S CHOREA ; PARKINSON’S DISEASE
4)INFECTIONS- CREUTZFELD-JACKOB’S DISEASE ; HIV(AIDS DEMENTIA COMLEX) ; VIRAL ENCEPHALITIS ;
PROGRESSIVE MULTIFOCAL LEUCOENCEPHALOPATHY
5)NORMAL PRESSURE HYDROCEPHALUS
6)NUTRITIONAL -WERNICKE KORSAKOFF (THIAMINE DEFICIENCY); B12 DEFICIENCY; FOLIATE DEFICIENCY
7)METABOLIC- HEPATIC DISEASE; THYROID DISEASE; PARATHYROID DISEASE; CUSHING’S SYNDROME
8)CHRONIC INFLAMMATORY – COLLAGEN VASCULAR DISEASE & VASCULITIS, MULTIPLE SCLEROSIS
9)TRAUMA – HEAD INJURY; PUNCH-DRUNK SYNDROME
10)TUMOR - eg: SUBFRONTAL MENINGOMA
SOME CASES ARE TREATABLE ; 10-15% ARE REVERSIBLE.

7. CLASSIFICATION -BASED ON SITE
# FRONTAL PREMOTOR
CORTEX.
#BEHAVIOURAL
CHANGES,
LOSS OF INHIBITION,
ANTI-SOCIAL
BEHAVIOUR,
FACILE &
IRRESPONSIBLE
#Eg: NORMAL PRESSURE
HYDROCPHALUS,
HUNTINGTON’S
CHOREA,
METABOLIC DISEASE
ANTERIOR POSTERIOR
#PARIETAL & TEMPORAL
LOBES.
#DISTURBANCE OF
COGNITIVE FUNCTION
(MEMORY &
LANGUAGE)
WITHOUT MARKED
CHANGE IN BEHAVIOUR.
#Eg: ALZHEIMER’S
DISEASE.
SUB-CORTICAL CORTICAL
#APATHETIC
#FORGETFUL & SLOW,
POOR ABILITY TO USE
KNOWLEDGE
#ASSOCIATED WITH
OTHER NEUROLOGICAL
SIGNS & MOVEMENT
DISORDERS.
#Eg: PARKINSON’S
DISEASE,
AIDS DEMENTIA
COMPLEX.
# HIGHER CORTICAL
ABNORMALITIES
#DYSPHASIA,
AGNOSIA,
APRAXIA
#Eg:ALZHEIMER’S
DISEASE

8. Alzheimer’s disease:
• Most common type of dementia; accounts for an estimated 60 to 80 percent of cases.
Symptoms:
 Difficulty remembering names and recent events is often an early clinical symptom.
 apathy and depression are also often early symptoms.
 Later symptoms include impaired judgment, disorientation, confusion, behaviour
changes and difficulty speaking, swallowing and walking.
Brain changes:
=>Hallmark abnormalities are deposits of the protein fragment beta-amyloid (plaques) and
twisted strands of the protein tau (tangles) as well as evidence of nerve cell damage and
death in the brain.

9. Cerebrovascular dementia:
 Previously known as multi-infarct or post-stroke dementia, vascular dementia is the second
most common cause of dementia after Alzheimer's disease.(20% Of all cases)
Eg:MULTI INFARCT DEMENTIA (ATHEROSCLEROTIC) , SUBCORTICAL VD (BINSWANGER’S
DISEASE-SUBCORTICAL LEUCOENCEPHALOPATHY)
Symptoms:
 Impaired judgment or ability to plan steps needed to complete a task is more likely to
be the initial symptom, as opposed to the memory loss often associated with the initial
symptoms of Alzheimer's.
 Occurs because of brain injuries such as microscopic bleeding and blood vessel
blockage.
 The location of the brain injury determines how the individual's thinking and physical
functioning are affected
Brain changes:
 Brain imaging can often detect blood vessel problems implicated in vascular dementia.

10.  As Parkinson's disease progresses, it often results in a progressive dementia similar to
dementia with Lewy bodies or Alzheimer's.
Symptoms:
 Problems with movement are a common symptom early in the disease. If dementia develops,
symptoms are often similar to dementia with Lewy bodies.
 RESTING TREMOR, AKINETIC RIGIDITY,BENT POSTURE,HYPOMIMIA
Brain changes:
 Alpha-synuclein clumps are likely to begin in an area deep in the brain called the
substantia nigra. These clumps are thought to cause degeneration of the nerve cells that
produce dopamine.
Parkinson’s disease
Eg: PICK’S DISEASE , HUNTINGTON’S CHOREA , PARKINSON’S
DISEASE
NEURO DEGENERATIVE DEMENTIA:

11. Pick’s disease
 presents with impairment of recent memory associated with entorhinal cortex and hippocampal
dysfunction, Pick disease typically affects the frontal and/or anterolateral temporal lobes.
 A TYPE OF FRONTO-TEMPORAL DEMENTIA.
 Emotional & behavioral changes, mutism, aphasia, echolalia(repeating whatever spoken to them), rigidity,
apraxia, weakness, memory loss.
BRAIN CHANGES:
 Pick disease is defined pathologically by severe atrophy, neuronal loss, and gliosis.
 Frequently, Pick disease is accompanied by the occurrence of tau-positive inclusions.
 Swollen (ballooned) neurons (Pick cells) and argentophilic neuronal inclusions, known as
Pick bodies, can disproportionally affect the frontal and temporal cortical regions. Fewer Pick
bodies may be present in these regions if the primary symptoms are behavioral (behavioral
variant), compared with the primary symptoms of aphasia.

12. Dementia caused by infections
 CJD is the most common human form of a group of rare, fatal brain disorders affecting people and certain
other mammals. Variant CJD (“mad cow disease”) occurs in cattle, and has been transmitted to people under
certain circumstances.
Symptoms:
 Rapidly fatal disorder that impairs memory and coordination and causes behavior changes.
Brain changes:
 Results from misfolded prion protein that causes a "domino effect" in which prion protein throughout the
brain misfolds and thus malfunctions.
Eg: CREUTZFELD-JACOB DISEASE , HIV INFECTION (AIDS-DEMENTIA COMPLEX) , VIRAL ENCEPHALITIS ,
PROGRESSIVE MULTIFOCAL LEUCOENCEPHALOPATHY
CREUTZFELD-JACOB DISEASE

13. HIV Infection (AIDS-Dementia complex)
 A condition that leads to the loss of intellectual abilities such as memory, judgment, and abstract
thinking. It can also cause changes in personality.
 AIDS Dementia Complex (or ADC) is a type of dementia that occurs in advanced stages of AIDS (acquired
immunodeficiency syndrome).
These are some of the first signs and symptoms of ADC:
•Short attention span
•Trouble remembering
•Poor judgment
•Slowed thinking and longer time needed to do tasks
•Irritability
•Unsteady gait, tremor, or trouble staying balanced
•Poor hand coordination
•Social withdrawal or depression
In later stages, you may have more severe symptoms:
•Extreme mood swings
•Psychosis
•Loss of bladder and bowel control

14. Normal Pressure Hydrocephalus
Symptoms:
 Symptoms include difficulty walking, memory loss and inability to control urination.
Brain changes:
 Caused by the build up of fluid in the brain. Can sometimes be corrected with surgical
installation of a shunt in the brain to drain excess fluid.
Nutritional
Eg: WERNICKE-KORSAKOFF (THIAMINE DEFICIENCY), B12 DEFICIENCY , FOLIC ACID
DEFICIENCY
 Korsakoff syndrome is a chronic memory disorder caused by severe deficiency of thiamine
(vitamin B-1). The most common cause is alcohol misuse.
Symptoms:
 Memory problems may be strikingly severe while other thinking and social skills seem
relatively unaffected.
Brain changes:
 Thiamine helps brain cells produce energy from sugar. When thiamine levels fall too low, brain
cells cannot generate enough energy to function properly.
WERNICKE KORSAKOFF SYNDROME

15. By Metabolic disorders
 Eg: HEPATIC DISEASES, THYROID DISEASES, PARATHYROID DISEASES, CUSHING’S SYNDROME
Chronic inflammatory
 Eg: COLLAGEN VASCULAR DISEASE, VASCULITIS, MULTIPLE SCLEROSIS
Trauma
 Eg: HEAD INJURY, PUNCH-DRUNK SYNDROME
Punch-Drunk Syndrome
A condition seen in boxers and alcoholics, caused by repeated cerebral concussions and
characterized by weakness in the lower limbs, unsteadiness of gait, slowness of
muscular movements, hand tremors, hesitancy of speech, and mental dullness.
 Boxer's encephalopathy, dementia pugilistica. A syndrome affecting 10–20% of professional boxers, which
is the cumulative result of recurrent brain damage and progressive communicating hydrocephalus due to
extrapyramidal and cerebellar lesions that translate into dysarthria, ataxia, tremors, pyramidal lesions–
causing mental deterioration and personality changes–eg, rage reaction and morbid jealousy–
'Othello syndrome'

16. Tumor
 Eg: SUBFRONTAL MENINGOMA
Dementia rarely may be due to intracranial tumour, especially when
tumours occur in certain anatomical sites.
Mental or behavioral changes occur in 50-70% of all brain tumours as
distinct from dementia which is associated with frontal lobe tumours,
III ventricle tumours and corpus callosum tumours.
Cognitive impairment also occurs as a non metastatic complication of
systemic malignancy.

17. DEMENTIA WITH LEWY BODY DISEASE (DLB)
Symptoms:
 People with dementia with Lewy bodies often have memory loss and thinking problems
common in Alzheimer's, but are more likely than people with Alzheimer's to have initial or early
symptoms such as sleep disturbances, well-formed visual hallucinations, and muscle
rigidity or other parkinsonian movement features.
Brain changes:
 Lewy bodies are abnormal aggregations (or clumps) of the protein Alpha- synuclein. When
they develop in the brain cortex, dementia can result. Alpha- synuclein also aggregates in the
brains of people with Parkinson's disease, but the aggregates may appear in a pattern that is
different from dementia with Lewy bodies.
Other causes:
DEMENTIA CAN OCCUR AS A SYMPTOM OF MORE WIDE SPREAD DEGENERATIVE DISORDERS
Eg: HUNTINGTON’S DISEASE, DIFFUSE LEWY BODY DISEASE, PROGRESSIVE SUPRANUCLEAR PALSY, MOTOR
NEURON DISEASE etc.

18. Huntington’s Disease
 Huntington’s disease is a progressive brain disorder caused by a single defective gene on
chromosome 4.
Symptoms:
 Include Huntington’s chorea, dysarthria, dysphagia, facial twitching, chameleon or
trombone tongue a severe decline in thinking and reasoning skills, and irritability,
depression and other mood changes.
Brain changes:
 The gene defect causes abnormalities in a brain protein that, over time, lead to worsening
symptoms.
Mixed Dementia
 In mixed dementia abnormalities linked to more than one type of dementia occur
simultaneously in the brain.
Brain changes:
 Characterized by the hallmark abnormalities of more than one type of dementia —most
commonly, Alzheimer's and vascular dementia, but also other types, such as dementia
with Lewy bodies.

19. HISTORY TAKING
NOTE:
1) RATE OF INTELLECTUAL DECLINE
2) IMPAIRMENT OF SOCIAL FUNCTION
3) GENERAL HEALTH & RELEVANT DISORDERS (Eg: STROKE, HEAD INJURY)
4) NUTRITION STATUS
5) DRUG HISTORY
6) FAMILY HISTORY OF DEMENTIA
- FROM PATIENT & RELATIVE
TESTS ASSIGNED TO CHECK INTELLECTUAL FUNCTIONS ARE DESIGNED TO CHECK:
1) MEMORY 2) ABSTRACT THOUGHT 3) JUDGEMENT 4) SPECIFIC HIGHER CORTICAL
FUNCTIONS
IN EARLY / PSEUDO DEMENTIAS, A FORMAL ASSESSMENT FROM A CLINICAL
PSYCHOLOGIST IS ADVISABLE

20. PHYSICAL EXAMINATION
NOTE: FOCAL SIGNS
INVOLUNTARY MOVEMENTS
PSEUDO BULBAR SIGNS
PRIMITIVE REFLEXES
CHECK: POUT REFLEX (Tap lips with a tendon hammer, a pout reflex is observed)
GRASP REFLEX (Tapping in between eyes, patient can’t inhibit blinking in response to
stimulation)
GLABELLAR REFLEX (Stroking palm induces grip)
PALMOMENTAL REFLEX (Quick scratch on palm induces sudden contraction of
mentalis muscle in face)
PRIMITIVE REFLEXES ARE PRESENT IN INFANCY & IN AGED PEOPLE, AS WELL AS
IN DEMENTIA
NEUROPSYCHOMETRIC TEST (ASSESSMENT OF ONE’S COGNITIVE FUNCTIONS SUCH AS MEMORY,
CONCENTRATION, PROBLEM SOLVING SKILLS) IS PERFORMED TO:
-DIAGNOSE EARLY DEMENTIA
-SEPARATE TRUE DEMENTIA FROM PSEUDO DEMENTIA
-MONITOR PROGRESS / TRIALS OF TREATMENT

21. DIAGNOSTIC APPROACH:
IMAGING MAINLY INCLUDES MRI , CT-SCAN , SPECT , PET etc.
LAB STUDIES INCLUDES CBC , ESR , THYROID HORMONE TEST, VIT-B12
BLOOD TEST , LIVER FUNCTION TEST (ALT,AST,BLOOD TEST) , HIV TEST,
ELECTROLYTE TEST (TO CHECK KIDNEY FUNCTION), TOXICOLOGY SCREEN
(DRUG) , ANTINUCLEAR ANTIBODIES (AUTOIMMUNE DISEASE) , LUMBAR
PUNCTURE (To check some proteins in spinal fluid), LEAD TEST (to check heavy
metals in blood) etc.
CONFIRMATION: USUALLY WITH AUTOPSY,BIOPSY.

22. Specimen in end stage AD demonstrating
severe global atrophy.
The images show FDG-PET and axial FLAIR
images of a normal subject and of patients
with AD and FTD.
In AD there is a decreased metabolism of the
parietal lobes (yellow arrows), whereas in
FTD, there is frontal hypometabolism (red
Presenile AD with normal hippocampus
and severe parietal atrophy
AD

23. The images show a patient with a strategic PCA
infarction involving the hippocampus.
This type of infarct can result in sudden dementia
if located in the dominant hemisphere.
It will usually not result in dementia if it occurs in
the non-dominant hemisphere.
Vascular Dementia (VaD)
The images are of a patient who had VaD,
but the medial temporal lobe was normal.
MTA in a patient with VaD

24. End stage FTLD with striking atrophy of
frontal and temporal lobes. No artophy of
parietal and occipital lobes.
Cerebro Amyloid Angiopathy showing
multiple peripherally located micro bleeds.
images of the same patient show Fazekas 2
white matter hyprintensities.
Fronto-temporal Lobar Degeneration
Cerebral Amyloid Angiopathy

25. Differential diagnosis:
Dementia, delirium and depression are the 3 most prevalent mental disorders in the
elderly.
While dementia and depression are prevalent in the community, hospitals and nursing
homes, delirium is seen most often in acute care hospitals.
 The first step is to recognise which of the syndromes is present.
Dementia is defined by a chronic loss of intellectual or cognitive function of sufficient
severity to interfere with social or occupational function.
Delirium is an acute disturbance of consciousness marked by an attention deficit and
a change in cognitive function.(Hallucinations, autonomic over reactivity as a
consequence of toxic, metabolic or infective conditions.
Depression is an affective disorder evidenced by a dysphoric mood, but the most
pervasive symptom is a loss of ability to enjoy usual activities.
These syndromes are not mutually exclusive, as dementia frequently coexists with
delirium and depression.

26. Diagnostic criteria for delirium
- Altered mental status (AMS) not explained by dementia.
-AMS developed over a short period of time (hours to days) and fluctuates
-AMS could be explained by a drug, acute illness or metabolic disturbance
Diagnostic criteria for dementia
-Memory loss, impairment of language, praxis, recognition or abstract thinking
-Chronic and progressive
-Delirium ruled out
Delirium is attention disorder vs. dementia which is a memory disorder.
In alcoholism before leaping into the diagnosis- WERNICKE KORASKOFF SYNDROME,
we should also consider the chance of CHRONIC SUBDURAL HEMATOMA

27. PREVENTION
PEOPLE WHO HAVE DEMENTIA DUE TO STROKE,
MAY BE ABLE TO PREVENT FUTURE DECLINES BY
REDUCING THEIR RISK FOR HEART DISEASES.
FOR Eg: 1)TREAT OR PREVENT HIGH BP
2)DON’T SMOKE
3)STAY AT A HELTHY WEIGHT
(REDUCE RISK OF DIABETES)
4)KEEP YOUR CHOLESTEROL NORMAL RANGE
5)PROPER PHYSICAL ACTIVITY
6)STAY MENTALLY & SOCIALLY ACTIVE

28. TREATMENT
# Doctors use medicines to treat dementia in the following ways:
 correct a condition that's causing dementia, such as thyroid replacement
for hypothyroidism, vitamins for lack of vit-B12, or antibiotics for infections.
 To maintain mental functioning for as long as possible when dementia
cannot be reversed.
 To prevent further strokes in people who have dementia caused by stroke
(vascular dementia).
 To manage mood or behaviour problems, such as depression, insomnia,
hallucinations, and agitation.

29. =>CHOLINESTERASE INHIBITORS SUCH AS
DONEPEZIL (ARICEPT),GALANTAMINE (REMINYL),
& RIVASTIGMINE (EXELON) ARE DEVELOPED TO
TREAT PRIMARILY ALZHEIMER’S , BUT ARE ALSO
USED IN OTHER DEMENTIAS ESPECIALLY IN
VASCULAR DEMENTIAS.
=>MEMENTINE (NAMENDA) USED TO TREAT THE
SYMPTOMS OF ALZHEIMERS DISEASE, BUT MAY
ALSO HELP WITH MILD-MODERATE VASCULAR
DEMENTIA
=> IT IS NOT CLEAR THAT HOW LONG
THESE MEDICINES WORK.
# MEDICINES TO HELP MAINTAIN MENTAL FUNCTIONS:

30. # CHANGING WHAT YOU EAT CAN REDUCE DEMENTIA SYMPTOMS & IMPROVE MENTAL
CLARITY
=>Reduce intake of carbs & sugars ; Take enough protein , vitamins-C,D,E,B12 ,
omega 3s fatty acid, zinc @ prescribed amount).
# MEDICINES TO CONTROL MOOD/BEHAVIOUR PROBLEMS
=> ANTI-PSYCHOTIC DRUGS:
SUCH AS RISPERIDONE (RISPERDAL) , OLANZEPINE (ZYPREXIA)
=> ANTI-DEPRESSANTS:
ESPECIALLY SELECTIVE SERETONIN REUPTAKE INHIBITORS
# MEDICINES TO PREVENT FUTURE STROKES
=>DOCTORS PRESCRIBE MEDICINES FOR HIGH BP & CHOLESTEROL
(THESE CAN’T REVERSE EXISTING DEMENTIA;BUT PREVENT FURTHER
BRAIN DAMAGE DUE TO STROKES & HD)

31. Reference:
• NEUROLOGY AND NEUROSURGERY ILLUSTRATED
• http://www.webmd.com/alzheimers/tc/dementia
• http://www.aplaceformom.com/blog/2013-02-01-diet-and-dementia/
• http://www.recover101.com/dementia-treatment-long-short-term
• http://apt.rcpsych.org/content/7/1/24.full
• http://www.alz.org/dementia/types-of-dementia.asp
• http://www.radiologyassistant.nl/en/p43dbf6d16f98d/dementia-role-of-mri.html
• http://www.ncbi.nlm.nih.gov/pubmed/7858369