parkinson's disease dr. kleyn department of geriatric medicine svcmc

Parkinson's DiseaseParkinson's Disease

Dr. Kleyn

Department of Geriatric Medicine

SVCMC

HistoryHistory

James Parkinson

1817, England

Shaking palsy

Paralysis agitans

“Involuntary tremulous motion, with lessened muscular power, in parts not in action and even when supported; with a propensity to bend the trunk forward, and to pass from a walking to a running pace, the senses and intellects being uninjured.”

IntroductionIntroduction

Parkinson’s disease is a chronic neurodegenerative movement disorder affecting voluntary and emotional movements and most commonly seen in the elderly, but is also found in the young and inexorably progresses leading to significant disability.

EpidemiologyEpidemiology

Primarily a disease of the elderlyMean age 55, Range 20 - 80 yearsJuvenile parkinsonism- Less than 20 yearsM/F = 3:2Prevalence increases with age

Aging and Parkinson’s diseaseAging and Parkinson’s disease

Exponential fall Linear fall

Anatomy-Basal GangliaAnatomy-Basal Ganglia

Caudate Nucleus

Internal capsule

Globus pallidus

Putamen

PATHOPHYSIOLOGYPATHOPHYSIOLOGY

PATHOPHYSIOLOGYPATHOPHYSIOLOGY

STRIATUMCAUDATE, PUTAMEN

SUBSTANTIA NIGRAGLOBUS, PARS RETICULATA

GABA

DA

ACH

Chemical Balance in Corpus StriatumChemical Balance in Corpus Striatum

Excitatory Cholinergic pathway

Inhibitory Dopaminergic pathway

BALANCE

Chemical Balance in Corpus StriatumChemical Balance in Corpus Striatum

Excitatory Cholinergic pathway

Inhibitory Dopaminergic pathway

Imbalance

Parkinson’s disease - PathophysiologyParkinson’s disease - Pathophysiology

Pathology - Lewy BodiesPathology - Lewy Bodies

Eosinophilic hyaline inclusion bodies

Spherical dense hyaline core with a clear halo

Mechanism of formation unknown

PathologyPathology

Lewy body dementia Parkinson’s disease

Pathology-Parkinson’s diseasePathology-Parkinson’s disease

MIDBRAIN

Classification and EtiologyClassification and EtiologyIdiopathic Parkinson’s diseaseParkinson-like syndromes Drug induced parkinsonism Hypoxia Tumor Trauma Vascular:Multiinfarct Toxin:Mn, CO, MPTP and cyanide Post-encephalitic parkinsonism (von Economo’s

encephalitis) Normal pressure hydrocephalus Wilson’s disease, Hutington’s disease

Classification and EtiologyClassification and Etiology

Medications that can cause parkinsonian symptoms, but not PD itself, include the following:o Metoclopramide o Domperidone o Reserpine-containing antihypertensives o Neuroleptics

Some evidence also indicates that certain environmental factors (including smoking and coffee drinking) may actually have protective associations.

Clinical features of Idiopatic Parkinson’s Clinical features of Idiopatic Parkinson’s disease.disease.

Major features Resting tremor in hands,

arms, legs, jaw, and face Bradykinesia Rigidity- cogwheel or

lead-pipe

Minor features Bradyphrenia Speech abnormalities Depression Dysautonomia Dystonia Constipation Hallucinations Dysphagia

Parkinson’s disease SymptomatologyParkinson’s disease Symptomatology

Parkinson’s disease -SymptomatologyParkinson’s disease -SymptomatologyTremor: Rest Fixed frequency 3-6 Hz Not a feature of old age Pill-rolling Usually starts in one limb, and then to

other limbs Rarely starts in lower limbs Intermittent for many years They usually disappear briefly during

movement and do not occur during sleep.

Tremors can also eventually occur in the head, lips, tongue, and feet. In younger patients tremor is usually predominant and often suggests a less aggressive form of the disease.

Tremor dominant

Parkinson’s disease-SymptomatologyParkinson’s disease-Symptomatology

Rigidity Striatal hand: Ulnar deviation, MCP

flexion, IP extension

Striatal toe: Big toe dorsiflexion

Sitting en bloc: Collapses into a chair on attempting to sit down


Posture Kyphosis Flexed elbows, knees

and hips Hands held in front of

body Trunk bent forward Head bowed


Bradykinesia Slowness of motion (bradykinesia) is one of the classic

symptoms of Parkinson's disease. Hypomimia- “masked facies”,expressionless face, blinking Speech abnormalities- Hypophonia: soft voice Aprosody of speech: monotonous and lack of inflection Tachyphemia: do not separate syllables together, running

words together Patients may eventually develop a stooped posture and a slow,

shuffling walk. The gait can be erratic and unsteady.

Parkinson’s disease-SymptomatologyParkinson’s disease-SymptomatologyMotor fluctuations Freezing phenomenon- Sudden, transient inability to

perform active movements, lasting no more than a few seconds

Start hesitation Turn hesitation Target hesitation Palilalia (speaking) Apraxia of eyelid opening Writing Kinesia paradoxica-Despite severe rigidity and

bradykinesia, they may rise suddenly and move normally


“Today is a sunny day in Toronto"

Loop drawing: Amplitude Interloop distance

“Micrographia”


Festinating gait Drooling of saliva Dysphagia Constipation Dementia Depression Orthostatic

hypotension

Low resting blood pressure

HTN Normotensive Sweating

abnormalities-excessive perspiration

Blepharospasm/ keratitis

Movement DisordersMovement Disorders

Parkinson’s disease Hutington’s disease Multiple system atrophy Motor neuron disease Cortical basal ganglionic

degeneration Patients with PD may develop

a stooped posture and a slow, shuffling walk. The gait can be erratic and unsteady.


“Off”phase


“On” phase

DiagnosisDiagnosis

There are currently no blood or laboratory tests that have been proven to help in diagnosing PD. Therefore the diagnosis is based on medical history and a neurological examination. The disease can be difficult to diagnose accurately.

Doctors may sometimes request imaging studies (i.e. MRI’s or brain scans) or laboratory tests in order to rule out other diseases.

Differential diagnosis of Parkinson’s diseases.Differential diagnosis of Parkinson’s diseases.

Neurologic disorder Features Multiple system atrophy Prominent dysautonomia

Cerebellar dysphanction orperiph. neuropathy.

Essential tremor Kinetic tremor plus instability.Family history.

Huntington’s diseases Younger patient,family Hx,no tremor.

Toxin-inducedparkinsonism

Exposure to CO, cyanide, Mn,MPTP, methanol or lacquerthiner.

Drug-inducedparkinsonism

Antidopaminergic exposureBilateral onset. Reversibility.

Cortical basal ganglionicdegeneration

Alien limb,dystonia,myoclonus,parietal sensory loss .

Parkinson’s disease - ManagementParkinson’s disease - Management

Nonpharmacologic ManagementNonpharmacologic Management

O ccu p a tio n a l co u n se lling(e a rly d ise a se )

L e g a l/f in a n c ia l co u n se lling

P ro fe ss io n a l co u n se lling

G ro u p su p p o rt(d ise a se sta g e a pp ro p ria te

P e e r su p p o rt

A ssess em o tio n al n eeds

Patient Fam ily

S uppo rt


E ducation

Assess exercise capacity and lim itations

AerobicStrenghtheningStretchingNon weight bearing

T raining

R egular,focussed exercise

E xercise


O bta in d ie ta ry h is to ry

E d u c a te a b o u t ba la n c e d d iet

N u t r it io n a l c o un s e ll ing

N u t r it ion

Drugs for Parkinson’s diseaseDrugs for Parkinson’s disease

Amantadine Well tolerated, possible ankleedema or livedo reticularis

Anticholinergics Good for tremorAvoid in patients age 65 and older

Carbidopa/Levadopa Side effects include dyskinesia,chorea, dystonia

Selegiline Controversial neuroprotectiveagent. Minimal symptom. benefit

Bromocriptine Helpful with superimposedrestless legs syndrome

Selective COMTinhibitor

Adjunctive therapy; increasesbioavailability of levadopa; sideeffects include diarrhea,dyskinesia

The Management of Parkinson’s diseaseThe Management of Parkinson’s disease

E du c a t ion

S u ppo rt

E x e rc ise

N u t r it ion

N o n P h a rm a c o lo g ic

? A n t ic h o lin e rg ic s

? A m a nta d ine

Do pa m in e A g o n is ts L e vodo pa

S u rg ic a l th e rapy if un a c c e pta b le c o n t ro l

w ith me d ic a l t h e ra py

+/-

C O M T in h ib it o r

C o m b in e d the ra py

Do pa m ine a go n is t

+

L e vodo pa

Y e s N O

F u n c t ion a l im pa irm e nt

N e uro p ro te c t ion

? S e le g il in e

P h a rm ac o lo g ic

P a rk in s o n's d is e a se

Dose Dose

Surgical Therapy- Deep brain stimulationSurgical Therapy- Deep brain stimulation

When symptoms are uncontrollable with medical therapy

None ablative method is used

Transpalntation of fetal nigral cells

Thalamotomy

Parkinson’s disease - ImagingParkinson’s disease - Imaging

Predicted developmentsPredicted developments

Research into the causes of Parkinson’s diseases are likely to show that multiple genetic and environmental factors are involved

Disease of early onset is more likely to be genetic New drugs acting on both dopaminergic and non-

dopaminergic transmitter systems will become available over the next 10 years

Clinical trials of new drugs with neuroprotective and neurorescue properties are in progress

ResearchResearch

At no time in the past have the basic and clinical sciences applied to Parkinson’s disease been so active.

Future progress in understanding the causation and pathogenesis of the disorder will permit the development of new treatments that will slow, halt, or even reverse the currently progressive course of Parkinson’s disease.

parkinson's disease dr. kleyn department of geriatric medicine svcmc

Documents

hutingtons disease slide

age slide

tremor dominant slide

palsy paralysis agitans

chemical balance

years juvenile parkinsonism

major features resting

younger patients tremor