Dementia and Amnesia

8/6/2019 Dementia and Amnesia

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Dementia and Amnesia


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Cerebral Cortex

Sensory and Motor

Memory

Emotions Neurochemistry ofMemory

Frontal Lobe

Foresight, imagination and intuition


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Organic brain syndrome

Dementia

Deterioration ofmental function

Thought and memory Feeling and conduct

Delirium

Acute dementia Amnesia

Loss ofmemory without change in character


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Epidemiology

Dementia affects 1725 million people

worldwide

affects predominantly elderly people Prevalence in people > 65 is 5% and in > 80, it

is 20%


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Aetiology ofdementia

Degenerative disorders: Alzheimers disease (AD); fronto-temporal dementias (FTD);

dementia with Lewy bodies (DLB); Parkinson disease dementia; Huntingtons disease;

progressive supranuclear palsy.

Vascular causes: multi-infarct dementia (MID); lacunar infarcts; Binswangers disease;

cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy

(CADASIL); vasculitis (eg, lupus erythematosus).

Trauma: major head injury; subdural haematoma; boxing.

Intracranial tumours: primary tumours; metastatic tumours.

Hydrostatic causes: hydrocephalus (obstructive or communicating); normal pressure

hydrocephalus (NPH).

Toxic, endocrine and metabolic causes: heavy metals; drug intoxication; hypothyroidism;

hypercalcaemia; B12 and folate deficiencies; hepatic and renal failure; paraneoplastic/limbic

encephalitis; inherited metabolic disorders (eg, Wilsons disease, leukodystrophies). Infection: bacterial (eg, Spirochetalspp. causing Lyme disease and syphilis); fungal (eg,

Cryptococcus); viral (eg, subacute sclerosing panencephalitis [SSPE]; progressive multifocal

leukoencephalopathy; post-encephalitic HIV). Other infectious agents (eg, Creutzfeldt-Jakob

disease [CJD], variant CJD [vCJD]; neurocysticercosis; tuberculosis).

Anoxia: post-cardiac arrest; carbon monoxide poisoning.


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Types ofdementia

Alzheimers disease (60%; ofcases)

Vascular dementia (3040%; including about

20% where dual pathology exists) Dementia with Lewy bodies (15% ofcases)

Fronto-temporal dementia (5%)


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Vascular Dementia

multi-infarct dementia

diffuse white matter disease (alsocalled leukoaraiosis,

subcortical arteriosclerotic encephalopathyor Binswanger's

disease). The occurrence ofdementia depends partly on the total

volume ofdamaged cortex, but it is also more common in

individuals with left-hemisphere lesions

multi-infarct dementia patients have a history of

hypertension, diabetes, coronary artery disease, or other

manifestations ofwidespread atherosclerosis.

Aging -> accumulation ofamyloid in cerebral blood vessels


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Vascular Dementia

Diffuse white matter disease (Binswanger's disease)

MRI shows involvement ofperiventricular white

matter

chronic ischemia due toocclusive disease ofsmall,

penetrating cerebral arteries and arterioles

Mitochondrial disorders can present with strokelike

episodes and can selectively injure basal ganglia or

cortex


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Vascular dementia

Clinical features with a score of7 and

more

Abrupt decline in cognitive function

Impairment ofmemory History ofstroke or CVD

Large vessel infarcts visible by imaging

(MRI and CT)

Single infarct placed strategicallyaffecting a particular cognitive

function


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Early stages: inability to acquire new memories

Advanced stages: confusion, irritability and aggression, mood

swings, language breakdown, long-term memory loss

No treatment as ofyet

Non invasive therapy (mental stimulation and exersise)

Pharmacological

Anticholinestrases (donepezil, gelantamine, rivastigmine) ,

NMDA antagonist (memantine)

and secretase inhibitors that diminish the production ofA


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Characteristics ofAlzheimers

Aphasia loss or impairment of

language caused by brain dysfunction

Apraxia inability to execute learned

movements on command Agnosia inability to recognize or

associate meaning to a sensory

perception

Acalculia inability to perform

arithmetical calculations

Agraphia inability to write

Alexia inability to read


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Cortical Dementia

Alzheimer's, Pick's disease, Binswanger's

disease and Creutzfeldt-Jakob disease

characteristic problems with memory, theinability to recall words and as the disease

progresses to understand what others are

saying (aphasia).


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Subcortical Dementia

dementias believed to result in structures below the

cortex. Huntington's disease, Parkinson's and AIDS

dementia complex are three examples.

It is more common to see changes in personality anda slowing down ofthought processes with this

classification ofdementia.

Language and memory functions appear largely

unaffected.


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Clinical Differentiation ofthe Major

Dementias

Disease First Symptom Mental Status Neuropsychiatry Neurology Imaging

AD Memory loss Episodic memory loss Initially normal Initially normal Entorhinal cortex and

hippocampal atrophy

FTD Apathy; poor

judgment/insight,

speech/language;hyperorality

Frontal/executive,

language; spares

drawing

Apathy, disinhibition,

hyperorality, euphoria,

depression

Due to PSP/CBD

overlap; vertical gaze

palsy, axial rigidity,dystonia, alien hand

Frontal and/or

temporal atrophy;

spares posteriorparietal lobe

DLB Visual hallucinations,

REM sleep disorder,

delirium, Capgras'

syndrome,

parkinsonism

Drawing and

frontal/executive;

spares memory;

delirium prone

Visual hallucinations,

depression, sleep

disorder, delusions

Parkinsonism Posterior parietal

atrophy; hippocampi

larger than in AD

CJD Dementia, mood,

anxiety, movement

disorders

Variable,

frontal/executive, focal

cortical, memory

Depression, anxiety Myoclonus, rigidity,

parkinsonism

Cortical ribboning and

basal ganglia or

thalamus

hyperintensity ondiffusion/flare MRI

Vascular Often but not always

sudden; variable;

apathy, falls, focal

weakness

Frontal/executive,

cognitive slowing; can

spare memory

Apathy, delusions,

anxiety

Usually motor slowing,

spasticity; can be

normal

Cortical and/or

subcortical infarctions,

confluent white matter

disease

AD, Alzheimer's disease; FTD, frontotemporal dementia; PSP, progressive supranuclear

palsy; CBD, cortical basal degeneration; DLB, dementia with Lewy bodies; CJD,

Creutzfeldt-Jakob disease.


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Table 365-3 Evaluation ofthe Patient with Dementia

Routine Evaluation Optional Focused Tests OccasionallyHelpful Tests

History Psychometric testing EEG

Physical examination Chest x-ray Parathyroid function

Laboratory tests Lumbar puncture Adrenal function

Thyroid function (TSH) Liver function Urine heavy metals

Vitamin B12 Renal function RBC sedimentation rate

Complete blood count Urine toxin screen Angiogram

Electrolytes HIV Brain biopsy

CT/MRI Apolipoprotein E SPECT

RPR or VDRL PET


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The Mini-Mental Status Examination

Points

Orientation

Name: season/date/day/month/year 5 (1 for each name)

Name: hospital/floor/town/state/country 5 (1 for each name)

Registration

Identify three objects by name and ask patient to repeat 3 (1 for eachobject)

Attention and calculation

Serial 7s; subtract from 100 (e.g., 9386797265) 5 (1 for each subtraction)

Recall

Recall the three objects presented earlier 3 (1 for eachobject)

Language

Name pencil and watch 2 (1 for eachobject)

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 eachcommand)

Write "close your eyes" and ask patient toobey written command 1

Ask patient to write a sentence 1

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

Total 30


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Diagnostic Categories

Reversible Causes Irreversible/Degenerative Dementias Psychiatric Disorders

Examples Examples Depression

Hypothyroidism Alzheimer's Schizophrenia

Thiamine deficiency Frontotemporal dementia Conversion reaction

Vitamin B12 deficiency Huntington's

Normal-pressure hydrocephalus Dementia with Lewy bodies

Subdural hematoma Vascular

Chronic infection Leukoencephalopathies

Brain tumor Parkinson's

Drug intoxication


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Normal-pressure hydrocephalus: enlarged lateral

ventricles (hydrocephalus) with little or nocortical

atrophy

NPH is presumed to be caused by obstruction tonormal flow ofCSF

Prion disorders

Vitamin Deficiencies Infection (HIV, syphilis, toxoplasmosis)

Mental Illness


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Transient global amnesia

sudden onset ofa severe episodic memory deficit

Elicited by a sudden emotional stimulus or physical

exertion

patient may seem confused without cognitiveimpairment

The ability toform new memories returns after a period

ofhours

cerebrovascular disease, epilepsy (7% in one study),

migraine, or cardiac arrhythmias have all been

implicated.


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Psychogenic amnesia

event-specific amnesia

more likely tooccur after violent crimes

severe drug or alcohol intoxication

Prolonged PA leads tofugue states Elicited by emotionallstress

In contrast toorganic amnesia, fugue states are associated

with amnesia for personal identity and events closely

associated with the personal past. Ability to learn new tasks and new events is preserved

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Dementia and Amnesia