Parkinson's disease and parkinsonism Flashcards Preview

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Flashcards in Parkinson's disease and parkinsonism Deck (33):

Movement disorders - where is the problem in 'pyramidal' or 'upper motor neurone' disorder? what does this result in?

Problems with corticospinal/pyramidal tract

Pyramidal weakness



Movement disorders - where is the problem in hyperkinetic movement disorder?

problem in the basal ganglia







movement disorders - where is the problem in hypokinetic movement disorder?

-lack of dopamine in the basal ganglia


ataxia - where is the problem?



What is the aetiology of parkinson's disease?

sections through brainstem reveals loss of the normally dark pigment in the substantia nigra and locus coeruleus

pigment loss correlates with dopaminergic cell loss

neurohistological landmark of PD are Lewy bodies

usually an asymmetric disorder


Describe the tremor in parkinson's disease
-what is it like?
-what does it affect?
-when is it present?

Involuntary, repetitive, rhythmic sinusoidal movement usually affecting one or more limbs

Primarily affects hands, may involve upper/lower limbs, less frequently jaw and lips, never head or neck

Pill-rolling in the hands, or finger flexion-extension or abduction/adduction

Present at rest, exacerbated by anxiety or stress

Improves/disappears on action

Typically reappears after few sec when arms held outstretched

Tremor frequency in low to mid range (3-6hz) with varying amplitude

Can observe tremor while patient is focused on a particular mental task e.g. counting backward


Describe the rigidity in parkinson's disease
-what is it like?
-what is cogwheel rigidity?
-how can rigidity be accentuated?

Increase in muscle tone in parkinson’s disease is relatively constant throughout the range of movement: lead pipe rigidity

No increase with higher mobilising speed (distinguishing it from spasticity)

Cogwheel rigidity is a consequence of the tremor of parkinsons disease being superimposed on background of lead-pipe rigidity

Rigidity in one arm can be accentuated by asking the patient to lift and lower the contralateral arm repeatedly at the same time

Positive froments manouvre


Describe the bradykinesia found in parkinson's disease
-what is it like?
-what is micrographia
-how can lack of spontaneous movement manifest?

Slowness of movement with progressive loss of amplitude or speed during attempted rapid alternating movement of body segments

Assessed by foot tapping/opening and closing hand, quickly and widely as poss.

Particular difficulty with complex motor tasks (micrographia)

Smaller hand writing

Lack of spontaneous movement nay manifest:

Poverty facial expression/mask-like face and eye-blinking - hypomimia

Difficulty changing position

Quiet/monotonous speech - hypophonia

Abnormal gait and stance


Describe the gait seen in parkinson's disease
-what is particularly difficult?
-what are steps like?

Flexed or stooped posture

In some cases extreme anterior truncal flexion - camptocormia

Unable to maintain a normal stance in response to pressure

Initiation of walking may be difficult – freezing

Turning may be difficult

Patients may use trick such as deliberately stepping over a walking stick to change direction

Steps are small and shuffling

Normal arm swing on walking is lost

Festination – very fast succession of steps and difficulty stoppping


Other motor symptoms in parkinsons disease:
-what kind of gaze is difficult?
-what is difficult to do in the GI system?
-is there any MSK manifestations?
-is muscle power/reflexes/sensations/plantar response affected?

Mild impairment of upgaze, eyelid tremor

Difficulty swallowing, including saliva

Many patients have a frozen shoulder

Muscle power/reflexes/sensations/plantar response is normal


What are the non-motor symptoms found in parkinson's disease? 7

Depression – chemical depression

Visual hallucinations – esp. at night

Psychosis – worsening hallucinations and delusions may escalate

Dementia – common feature of advanced parkinsons, >80% of pt.s after 20years


Autonomic symptoms – greasy skin, constipation, bladder disturbance, erectile dysfunction



Parkinson's disease epidemiology:
-is it common?
-male to female?
-what increases the probability of a genetic cause?

Second most common neurodegenerative disorder after AD

!- 2% over 60- 65’s affected

0.3% population

male to female 3:2

annual incidence rates 8.6-19 per 1000

due to ageing population, prevalence and socioeconomic burder expected to rise exponentially

early onset (below 40years) increases probability of genetic cause


What are the risk factors for parkinson's disease?

old age = strongest risk factor

28 distinct chromosomal regions have been linked to PD

6 of these contain genes that conclusively cause monogenetic PD

monogenetic PD accounts for 30% familial and 3-5% sporadic cases

pesticide exposure and +ve FH are other risk factors

possible protective role of NSAIDs and high uric acid levels

smoking has a protective affect

therefore etiology is genetically heterogeneous and multifactorial – genes, modifying effects by susceptible alleles and environmental factors


Should you see sensory/pyramidal/cerebellar signs in parkinson's disease?



What are the investigations for parkinsons disease?

To rule out treatable conditions of asthenia: hypothyroid, anaemia

Structural brain imaging

Possibly dopamine functional imaging

PET with fluoro-dopa (limited avail. And high cost)


These are unable to distinguish PD from other causes of parkinsonism, but should be normal in essential tremor, dystonic tremor, psychogenic parkinsonism

Positive levodopa challenge (or s.c. apomorphine)

Genetic testing if appropriate


What are common causes of parkinsonism? 6

-drug-induced/iatrogenic parkinsonism (prochloperazine, metoclopramide, antipsychotics, severe calcium channel blockers, amiodarone, chloroquine)

-progressive supranuclear palsy

-multi system atrophy – parkinsonism

-dementia with lewy bodies

-diffuse white matter ischaemia/vascular parkinsonism

-lower half parkinsonism with marked gait apraxia


Describe drug induced parkinsonism

Any drug that bocks action of dopamine esp. neuroleptic drugs


coarse postural tremor

presence of other drug induced disorders

orolingual dyskinesias, tardive dystonia, akathisia

series of events important: emergence of symptoms after drug exposure

improvement/resolutions within a few mths of complete withdrawal of drug


what is progressive supranuclear palsy?

Symmetric akinetic-rigid syndrome with predominantly axial involvement

Gait and balance impairment (early falls)

Tremor is infrequently seen in these patients

Vertical gaze supranuclear palsy

Pseudobulbar symptoms


Continuous activity of the frontalis muscle with eyes wide open (staring)

Frontal-subcortical cognitive deficits

No response to levo-dopa

Some patients may also present with parkinsonism (PSP-parkinsonism)


what is multi system atrophy?

Common cause of degenerative parkinsonism

Age of onset 6th/7th decade

Core triad: dysautonomia (atonic bladder/postural hypotension), cerebellar features and parkinsonism

Jerky postural tremor, pyramidal signs (generalised hyperreflexia and extensor plantar responses)

Sub-optimal and short-lived levodopa response in 1/3 pts.

Other suggestive features:

Severe dysarthria or dysphonia

Marked antecollis

Inspiratory sighing

Orofacial dystonia

MRI may show cerebellar and pontine atrophy (hot cross bun sign or hypertense rim surrounding theputamen in T2-weighted sequences


What is dementia with lewy bodies?

Dementia is predominant feature

Daily fluctuations in alertness and cognition

Visual hallucinations (colourful, often involving human figures)

Extreme sensitivity to neuroleptic medication


Controversial as to whether this is a separate disease entity


What is vascular parkinsonism?

affects predominantly lower limbs

rest tremor uncommon

other signs of brain vascular lesions might be present – spasticity/hemiparesis/pseudobulbar palsy

poor levodopa response

structural brain imaging guides diagnosis


Describe an essential tremor:
-what does it respond to?

symmetrical, postural or kinetic tremor with higher frequency (up to 12Hz)

infrequently observed at rest

often autosomal dominant inheritance with mean onset 15yrs

alcohol responsiveness

head tremor – if present – mild


What is SWEDDs?

(scans without evidence of dopaminergic deficit)

Often rest and asymmetrical tremor but no true bradykinesia

Clinical and electrophysiological characteristics of dystonia


Describe the principles of treatment of parkinson's disease?

Delay treatment until onset of disabling features and then initiate treatment.

Initial maintenance dose of levodopa should start with 50mg TDS and not exceed 600mg/day

All other agents for the treatment of motor symptoms can be combined with levodopa to reduce end of dose deterioration and the on-off syndrome


Why is levodopa used with a decarboxylase inhibitor?
-side effects of levodopa?

usually combined with a decarboxylase inhibitor (e.g. carbidopa or benserazide) to prevent peripheral metabolism of levodopa to dopamine

reduced effectiveness with time (usually by 2 years)

unwanted effects: dyskinesia (involuntary writhing movements), 'on-off' effect, dry mouth, anorexia, palpitations, postural hypotension, psychosis, drowsiness

no use in neuroleptic induced parkinsonism


What are dyskinesias/'wearing off' and on-off effects in relation to levodopa?

Dyskinesia are involuntary movements occurring in association with drug treatment, e.g. twisting/turning movements when dopamine levels are high (peak-dose dyskinesia)

Wearing off is when individual doses only produce short lived affects

On-off is where the patient switches from symptomatic benefit of medication (on) to an akinetic-rigid state often without any predictable relationship to the timing of drug doses


What other drugs exist for the treatment of motor symptoms in parkinson's disease?

Dopamine agonists:
-Ergot derivatives: bromocriptine, pergolide, di-hydroergocryptine
-Non-ergot derivatives: ropinirole, pramipexole, rotigotine, apomorphine

Catechol-O-methyltransferase inhibitor (entacapone, tolcapone)


MAO-B inhibitors



What are ergot derivative dopamine agonists assoc. with? what does this mean for initiation of this treatment?

ergot-derived dopamine receptor agonists (bromocriptine, cabergoline, pergolide*) have been associated with pulmonary, retroperitoneal and cardiac fibrosis. The Committee on Safety of Medicines advice that an echocardiogram, ESR, creatinine and chest x-ray should be obtained prior to treatment and patients should be closely monitored


What side effects are assoc. with all dopamine agonists?

patients should be warned about the potential for dopamine receptor agonists to cause impulse control disorders and excessive daytime somnolence

more likely than levodopa to cause hallucinations in older patients. Nasal congestion and postural hypotension are also seen in some patient


What is the role of COMT inhibitors in parkinson's disease?

e.g. Entacapone, tolcapone
COMT is an enzyme involved in the breakdown of dopamine, and hence may be used as an adjunct to levodopa therapy
used in conjunction with levodopa in patients with established PD


What is the role of amantadine in parkinsons disease?

mechanism is not fully understood, probably increases dopamine release and inhibits its uptake at dopaminergic synapses
side-effects include ataxia, slurred speech, confusion, dizziness and livedo reticularis


How do MAOB inhibitors help treat parkinson's disease?

e.g. Selegiline
inhibits the breakdown of dopamine secreted by the dopaminergic neurons


When are anti-muscarinics used to treat parkinsonism?

block cholinergic receptors

now used more to treat drug-induced parkinsonism rather than idiopathic Parkinson's disease
help tremor and rigidity
e.g. procyclidine,

benzotropine, trihexyphenidyl (benzhexol)