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Parkinsonism & Alzheimer's disease

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Page 1: Parkinsonism & Alzheimer's disease
Page 2: Parkinsonism & Alzheimer's disease

History & epidemiology

Anatomy & physiology

Pathology of Parkinsonism

Clinical features & diagnosis of Parkinsonism

Management of Parkinsonism

Pathology of Alzheimer’s disease

Clinical Feature & Diagnosis of Alzheimer’s

- Introduction and Conclusion

Management Of Alzheimer’s Disease

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Neurodegenerative diseases

Parkinson’s DiseaseAlzheimer’s DiseaseHuntington’s DiseaseAmyotrophic lateral sclerosis (ALS)Spinocerebellar Ataxia

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PARKINSON’S DISEASENeurodegenerative disorder which effects the extrapyramidal system

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ALZHEIMER’S DISEASE

Neurodegenerative disease affecting the cerebral cortex & hippocampus

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Case Presentation

Surendra Kshetri

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Began to experience tremors and stiffness of his left arm while he walked

Changes in his posture and unusual movements of his left arm.

Sleep disturbances Gait problems- stooped posture Symptoms gradually worsened with time

Case 1Mr Poudel, 65 years old man, a retired university professor……

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Case 2Mrs Ellis Grey, 76 years old woman

Lived alone for several years Brought to the neurological department,

MTH by her daughter, memory impairment General and neurological examinations-

normal Speech – highly anomic , paraphasic Unable to provide birth month, year, current

year Cognitive domain – below average

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HISTORY & EPIDEMIOLOGY

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History of Parkinson’s Disease

First clear medical description: James

Parkinson in An Essay on the Shaking Palsy (1817)

Jean-Martin Charcot- Influential in refining and expanding this

early description & in disseminating information internationally

Named the disorder as Parkinson’s disease

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William Gowers- Slight male predominance of the disorder, joint deformities typical of the disease.

Richer and Meige Babinski - Babinski sign Brissaud Greenfield and Bosanquet- Clear delineation of

the brain stem lesions

Page 12: Parkinsonism & Alzheimer's disease

Epidemiology of Parkinson’s disease

Prevalence Crude prevalence -15 per 100,000 population

(China) to 657 (Argentina)

Incidence Crude annual incidence rates- 1.5 per 100,000

population (China) in 1986 to 14.8 (Finland) through 1968 to 1970.

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Gender differences Slightly more common in men than in women Male to female ratio- 1.2:1 to 1.5:1

Geographic distribution Crude prevalence

• China - 15 per 100,000 • India - 328 per 100,000 • Mississippi, USA - 131 per 100,000 • Argentina - 657 per 100,000

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Ethnic distribution

White people in Europe and North America have a higher prevalence, around 100 to 350 per 100,000 population.

Asians in Japan & China and Africans have lower rates, around one-fifth to one-tenth of those in whites.

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Age Distribution

Less common before 50 years of age & increases steadily with age thereafter up to the ninth decade.

~1 in every 200 persons aged 60–69 had PD in the United States (US) and Western Europe.

For people in their 70’s, this increased to ~1 person with PD in every 100 people,

For people in their 80’s, ~1 in every 35 had PD

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History of Alzheimer's disease

Ancient Greek and Roman

philosophers and physicians associated old age with increasing dementia.

Alois Alzheimer- Identified the first case of what became known as Alzheimer's disease

Emil Kraepelin- First described as a distinctive disease

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Epidemiology of Alzheimer’s disease

Prevalance: Globally estimated number:

• 2013 - 44 million. • By 2030 - 76 million • By 2050 - 135 million

In the Asia Pacific Region, will increase from 23 million in 2015 to almost 71 million by 2050.

By 2050 more than half of the people with dementia worldwide (135 million) will live in this region.

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Incidence

“Every four seconds, a new case of dementia occurs somewhere in the world.”

Cohort longitudinal studies  provide rates between 10 and 15 per thousand.

Advancing age -primary risk factor Women- higher risk of developing AD particularly

in the population older than 85

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Basal Ganglia

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GRAY MATTER(COLLECTION)

•CORPOUS STRATUM•AMYGDALOID •CLAUSTRUM•SUBTHALAMIC NUCLEI•SUBSTANTIA NIGRA

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Corpus striatum

Lentiformnucleus

putamen

Globus pallidus

Caudatenucleus

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caudate

putamen

Globus pallidus

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Cognition(caudate circuit) eg:A person seeing a lion approach ????

Executes Learned Patterns of Motor Activity

FUNCTIONS

eg:writing of letters of the alphabet. hammering nails, shooting a basketball through a hoop,

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Control of movement

Nigrostriatal

pathway

Indirectpathway

Direct Pathway

Planning of movement

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GlobuspallidusInternal

&substantianigra parsreticulata

Globuspallidusexternal

Striatum

Cortex

Subthalamic nucleus

Thalamus

Motor Cortex

BasalGanglia

Direct Pathway(decreases inhibition of thalam

us)

Functional organization of the Basal Ganglia

Excitatory

Inhibitory

Indire

ctpa

thway

Direct

pathway

Indi

rect

Pat

hway

(incr

ease

s in

hibi

tion

of th

alam

us)

Substantianigra parscompacta

D1D2

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PATHOLOGY OF PARKINSON’S DISEASE

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Parkinsonism is a clinical syndrome characterized by motor symptoms like bradykinesia,tremor and rigidity.

Classification of the Parkinsonism Primary parkinsonism (Parkinson’s disease)

• Sporadic• Genetic

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Secondary parkinsonism (environmental etiology)• Drugs (Antipsychotic medications, Reserpine,

Tetrabenazine)• Postencephalitic• Toxins: MPTP, cyanide• Heavy metal (iron, manganese)• Vascular• Brain tumors• Head trauma• Normal-pressure hydrocephalus

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Parkinsonism-plus syndromes• Progressive supranuclear palsy• Multiple system atrophy• Cortical-basal ganglionic degeneration• Progressive pallidal atrophy• Diffuse Lewy body disease (DLBD

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Etiology

Idiopathic Genetic

Parkinson’s disease

Results due to reduction in the striatal dopamine content due to damage of nigrostriatal pathway.

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Idiopathic

Ageing Usual occurrence in late middle age,

and increases in its prevalence at older ages

Loss of striatal dopamine and dopamine of cells in the SN with age

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Genetic factors

PD may be multifactorial in etiology with genetic contributions

The younger the age of symptom onset, the more likely genetic factors play a dominant role

At least ten single gene mutations identified

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Mutations in gene coding Alpha synuclein and LRRK2 (leucine rich repeat kinase 2) - Autosomal dominant PD

Mutations in gene coding Parkin,DJ-1and PINK1- Autosomal recessive PD

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Pathogenesis Three major mechanisms in dopaminergic neuron

loss

Mitochondrial dysfunction

Oxidative and nitrosative stress

Ubiquitin proteosome system dysfunction

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Morphology Macroscopic:

Pallor or depigmentation of neurons in substantia nigra and locus ceruleus

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Microscopic

Loss of pigmented ,catecholaminergic neurons Intraneuronal Lewy bodies within the

pigmented neurons of the substantia nigra. Lewy bodies are cytoplasmic eosinophilic round

to elongated inclusions that often have a dense core sourrounded by halo.

Lewy bodies are composed of Alpha –synuclein

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NORMAL PARKINSONS DISEASE

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Clinical Features & Diagnosis of Parkinsonism

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Motor symptomsNon-motor symptoms

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Motor symptoms

Characterized by Four cardinal features : Bradykinesia (or Hypokinesia ) Tremor at rest Rigidity Postural instability

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Bradykinesia

Slowness of movements with a progressive loss of amplitude or speed.

Difficulty with planning, initiation and execution of movements.

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Clinical Manifestations of Bradykinesia  Difficulties with tasks requiring fine motor control: Loss of spontaneous movements and gesturing  Hypomimia (decreased facial expression)

MASK LIKE FACE Decreased spontaneous blinking  Hypophonia   Micrographia  Sialorrhoea

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Why Bradykinesia in Parkinsonism??

“Driving while stepping on the brakes”

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Rest Tremor

Tremor : Rhythmical & involuntary shaking, trembling or quivering movements of the muscles.

Rest tremor ( 4 - 6 Hertz) : Maximal when the limb is at rest Disappears with voluntary movement and sleep

Alternating contraction of agonist and antagonist muscles at a rapid pace

Usually Unilateral at onset

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Involves the hands, lips, chin, jaw and legs . “Pill-rolling” Tremor:

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Rigidity Increased muscle tone felt during examination by

passive movement Both the agonist and antagonist muscles are

involved Rigidity :

Cogwheel rigidity Lead-pipe rigidity

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Postural instability Stooped Posture UNIVERSAL FLEXION :

Extreme neck flexion ,  Extreme anterior truncal flexion  (camptocormia) &

Flexion of elbows and knees.

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Festinating / Shuffling Gait:i) Difficulty to initiate walkingii) Shortened strideiii) Reduced arm swingiv) Rapid small steps (shuffling)

RUNNING AFTER THE CENTRE OF GRAVITY

Freezing phenomenon

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Non-motor symptoms Neuropsychiatric

Depression & Anxiety disorders Apathy

Autonomic disturbance (dysautonomia) Urinary dysfunction Constipation

Sensory symptoms

pain Restless legs syndrome Olfactory dysfunction

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Sleep disturbances REM behavior disorder excessive day time drowsiness

Cognitive impairment Dementia : In >80% of patients after 20 years of

disease 

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Diagnosis of Parkinsonism

Diagnosis is primarily clinical, based on history and examination

Confirmatory diagnosis : Histological demonstration of the  intraneuronal Lewy bodies on autopsy

CT scan & MRI  exclude other causes.

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Examination of signs Bradykinesia :

Ask patient to do repetitive movements as quickly and as possible

• opening and closing the hand• tapping thumb and index fingers• or tapping the foot on the ground

Rest tremor: Differentiate from the intentional tremor seen in

cerebellar disease Best observed while the patient is focused on a

particular mental task.

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Rigidity: Increased resistance to passive movements

Postural stability The “Pull test” is performed in order to assess

postural stability

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UK Parkinson’s Disease Society Brain Bank’s clinical criteria for the diagnosis of probable Parkinson’s disease

Step 1 Bradykinesia At least one of the following criteria:

• Rigidity• Rest tremor (4–6 Hz )• Postural instability (not caused by primary

visual, vestibular, cerebellar or proprioceptive dysfunction)

Step 2 Exclude other causes of parkinsonism

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Step 3 At least three of the following supportive

(prospective) criteria:• Unilateral onset• Rest tremor• Progressive disorder• Persistent asymmetry• Severe levodopa induced chorea (dyskinesia)• Clinical course of 10 years or more

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Management of Parkinsonism

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No definite cureRelief of cardinal signs- rigidity, tremor , &

akinesiaCorrection of mood changesTreatment of other symptoms such as

depression,sleep disturbance .Treatment of cause when possible

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Management

General Measures

Drug Therapy Surgery

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1.General Measures

Physiotherapy

Speech therapy

Dietary controls

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Physiotherapy

Helps to reduce rigidity Corrects abnormal posture Improves walking , turning

& balance

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Speech therapy

Helpful in patients where dysarthria and dysphonia interferes communication

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Dietary controls

Include high-fiber diet Choose foods low in saturated

fat  and cholesterol. Avoid high protein diet

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Drug Therapy

Does not prevent disease progression but improves quality of lifeDrug therapy

Dopaminergic

activity

Cholinergic activity

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Classification of drugs

Drugs affecting Dopaminergic system

Dopamine precursors: Levodopa Peripheral decarboxylase inhibitors: Carbidopa MAO-B Inhibitors: Selegiline COMT Inhibitors: Tolcapone Dopamine releasing drugs: Amantadine Dopamine receptor agonists: Bromocriptine

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Drugs affecting Cholinergic system

Central anticholinergic: Trihexyphenidyl Antihistaminics: Promethazine

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Levodopa

‘Gold-standard' treatment for Parkinson's.. Therapautic benefit is nearly complete in early stages

but declines as disease advances1-2% cross BBBImproves cardinal signs- tremor, rigidity and akinesia.

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Side EffectsAt the initiation of therapy

Nausea, vomiting, hypotension, cardiac arrhythmias, angina, taste alteration.

Long-term complications Dyskinesias Behavioural effects: hallucination, psychosis On –off effect Wearing-off effect

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LEVODOPA + CARBIDOPA

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Surgery

Deep Brain Stimulation

Thalamotomy

Pallidotomy

Neural Transplantation

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Treatment approaches to newly diagnosed PD

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ALZHEIMER’S DISEASE

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ALZHEIMER’S DISEASE Neurodegenerative disorder Most common form of dementia in the elderly

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Aβ Peptide

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AETIOLOGY Old age, Family history

Diabetes Mellitus Hypertension, Elevated cholesterol, Low levels

of exercise

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Genetic mutation (chromosome 21/14/1/19)

Sequential cleavage by β-secretase and ɣ-secretase

Formation of Aβ peptide (Aβ40 / Aβ42)

Aβ peptide is prone to aggregation•Initially to oligomers•Then to large aggregates and fibrils

PATHOGENESIS

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Aβ peptide deposition

Direct Neurotoxicity Synaptic Dysfunction Inflammatory

Response

•Blocks long term potentiation•Changes membrane properties

(by microglia and astrocytes) •secretion of mediators•oxidative injury•alterations in Tau phosphorylation

Biochemically,•Decrease in cortical levels of Ach, choline acetyltransferase•Decrease in cholinergic receptors•Also NA and serotonin depletion

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MORPHOLOGYGROSS Cortical atrophy

Widening of cerebral sulci Compensatory ventricular enlargement

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MORPHOLOGY

MICROSCOPIC Senile (neuritic) plaque:

Spherical collection dilated, tortuous,

neuritic processes Amyloid core with Aβ peptides Microglia and Astrocytes at periphery Visualized with silver stain,Congo red Hippocampus, amygdala & neocortex

Diffuse Plaques

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MORPHOLOGY Neurofibrillary Tangles

Bundles of filaments in cytoplasm of neurons Common in cortical neurons ,hippocampus . Ultrastructurally, composed of paired

and some straight filaments

Hyperphosphorylated tau proteins, MAP2

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Cerebral Amyloid Angiopathy Neuritic plaques in the walls

of small blood vessels in the brain Granulovacuolar degeneration

Small, clear intraneuronal cytoplasmic

vacuoles

Hirano bodies Elongated, glassy, eosinophilic bodies Major component- actin

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CLINICAL FEATURES AND DIAGNOSIS OF

ALZHEIMER’S DISEASE

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DEFINITION

It is a chronic neurodegenerative disease that usually starts slowly and gets worse over time.

It most often begins in people over 65 years of age, although 4% to 5% of cases are early-onset Alzheimer's which begin before this.

 The average life expectancy following diagnosis is three to nine years.

The most common cause of death of people with Alzheimer’s Disease is Aspiration Pneumonia.

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AREAS AFFECTED

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STAGES OF PROGRESSION

Some experts use a simple three-phase model (early, moderate and late)

The most common system, developed by Dr. Barry Reisberg of New York University, breaks the progression of Alzheimer’s disease into seven stages

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THE 7 – STAGE SYSTEM Stage 1: No ImpairmentMemory problems or other symptoms of dementia are absent

Stage 2: Very Mild Decline

Minor memory problems or lose things around the houseNormal-aged forgetfulness is probably the most satisfactory terminology

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Stage 3: Mild DeclineRepeat statements and questions over and overOccasionally misplace possessionsDifficulty in remembering names of people and everyday objects

Stage 4: Moderate DeclineHave difficulty with simple arithmeticForget details about life historiesHave poor short term memory

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Stage 5: Moderately Severe Decline

Increasing confusion and disorientation Memory problems will get worseDifficulty in dressing properlyDelusionsObsessive, repetitive or impulsive behaviorProblems with speech or language

Stage 6: Severe DeclineMajor personality changesProblems with eyesightDifficulty changing position or moving around without assistanceLoss of bowel and bladder controlWandering

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Stage 7: Very Severe Decline

Need assistance with all activities of daily livingLose their ability to swallowGradual loss of speechStart to neglect their personal hygiene

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DIAGNOSIS

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IMPORTANCE OF EARLY DIAGNOSIS A better chance of benefiting from treatment

More time to plan for the future

Increased chances of participating in clinical drug trials

An opportunity to participate in decisions about care, transportation, living options, financial and legal matters

Benefit from care and support services, making it easier for them and their family

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CONDITIONS THAT MIMIC EARLY

ALZHEIMER’S DISEASE Central nervous system and other degenerative

disorders

Metabolic ailments

Substance-induced conditions

Psychological factors

Infections

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There is no specific test to prove that a person has Alzheimer’s

A diagnosis is made through a complete assessment that considers all possible causes

1. Medical History2. Physical Exam3. Neurological Exam4. Mental Status Tests5. Brain Imaging

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MENTAL STATUS TESTS Mini-mental state exam (MMSE) During the MMSE, a health professional asks the patient series of questions designed to test a range of everyday mental skills.   

Mini-cog  During the mini-cog, a person is asked to complete two tasks: Remember and repeat the names of three common objects

after a few minutes Draw the face of a clock showing all 12 numbers in the right

places and a time specified by the examiner The results of this brief test can help a physician determine if

further evaluation is needed.

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BRAIN IMAGING

Structural imaging with MRI or CT.

Primarily done to rule out other conditions that may cause symptoms similar to Alzheimer's

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FUTURE OF DIAGNOSIS

Scientists are investigating a number of disease markers and diagnostic tests, such as genes, disease-related proteins and imaging procedures, which may accurately and reliably indicate whether you have Alzheimer's disease and how much the disease has progressed.

However, more research on these tests is necessary.

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MANAGEMENT OF ALZHEIMER’S DISEASE

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There is no known cure for Alzheimer's disease - the death of brain cells in the dementia cannot be halted or reversed

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Management of Alzheimer’s Disease

PHARMACOLOGICAL

NON PHARMACOLOGICAL

Managecognitive symptoms

Manage secondary symptoms

Modification&Support

patient/family

Increased quality

of life for

patient

1.

2.

3.

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Pharmacologic Options Cognitive enhancers

2 classes

• Donepezil• Galantamine• Rivastigmine• Tacrine [not used due to frequent side

effects and Hepatotoxicity]

Cholinesterase inhibitors

(ChEIs)

• MemantineNMDA-

receptor antagonist

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Mechanism of action: Cholinesterase inhibitors

Blocks acetylcholinesterase in Brain

Increase in Ach level in Brain

Increased communication between the nerve cells that use acetylcholine as a chemical messenger

Improve the symptoms of Alzheimer's disease

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Mechanism of action : Memantine

Blocks Glutamate ;released in excessive amounts when brain cells are damaged by Alzheimer's disease

Better tolerated than ChEIs Used either to replace or

supplement ChEIs

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Cholinesterase inhibitors(Donepezil, Galantamine, Rivastigmine)

NMDA-receptor antagonist(Memantine)

• Nausea• Vomiting• Diarrhea• Weight loss• Loss of appetite• Muscle weakness• Vivid dreams/nightmares

(donepezil)

• Dizziness• Headache• Constipation• Confusion

.

Common Side Effects

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Treatment

Agent Starting Dose

Titration Schedule

Metabolism

Donepezil 5 mg OD by 5 mg every 4 weeks

hepatic

Galantamine 4 mg BD by 4 mg every 4 weeks

hepatic

Rivastigmine 1.5 mg BD by 1.5 mg e every 4 4 weeks

Non hepatic

Memantine 5 mg OD by 5 mg e every weeks

Non hepatic

• Mild/Moderate AD: Cholinesterase inhibitors Moderate/Severe

• Memantine

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Managing Secondary symptoms

Mood stabilizers[anticonvulsant] may be effective in some patients Carbamazepine

Antidepressants are generally well tolerated in persons with dementia like Citalopram Fluoxetine

The antipsychotics, especially the second generation agents, are

the most commonly prescribed medications like Aripiprazole Olanzapine

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NON PHARMACOLOGIC

•Life style and Diet•Regular appointments•Communication with family, caregivers•Environmental modification•Attention to safety

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Advice & Life style A caregiver; to meet their

requirements. Remove excess furniture so

they can get around more easily.

Install handrails on the stairs and in the bathroom.

A 30 minute walk each day Reduce the number of mirrors:

They may find images in mirrors confusing or frightening.

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Diet

Omega 3 Fatty Acids ; help to improve cognitive abilities,

Nutritious diet is also important with high calorie drinks like milkshakes.

The patient should not drink caffeine or alcoholic beverages.

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New Treatment For A.D (Under trial)

By Purdue University researcher, The molecule, called a beta-secretase inhibitor,

prevents amyloid plaque formation in the brain

This plaque formation creates fibrous clumps of toxic proteins that are believed to cause the devastating symptoms of Alzheimer's.

2. NIC5-15, by Mount Sinai School of Medicine

effective treatment to stabilize cognitive performance

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CONCLUSION!

REVIEW AND

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PARKINSONISM

CASE 1 Mr Poudel, 65 years old

man Difficulty in walking and

speaking , tremor in left hand and leg

Sleep disturbances

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Rx: Levodopa 250 mg+ carbidopa 25mg

Medication reduced his symptoms but did not stop the disease from getting worst.

His loss of mobility and speech impairment limited his social interactions.

He and his wife also have had to give up many of their retirement travel plans.

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ALZHEIMER’S

Case2

Mrs Ellis Grey, 76 years old woman

Anomic and paraphasic speech

Cognitive domain was below average

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On neurological examination Unable to focus on the nurse’s questions. Knew her own identity, unsure of her exact

location and current date Mild cognitive impairment Mild anomic aphasia

No thyroid disease & vitamin deficiencies MRI

Diffuse & posteriorly predominant hippocampal and cortical atrophy

RX :Tab DonepezilMental excercises

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Alzheimer’s Disease

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