Parkinson’s disease

Published on 02/04/2015 by admin

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Last modified 02/04/2015

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45 Parkinson’s disease

Instruction

Examine this patient.

Salient features

History

• Tremor: usually unilateral at onset; usually starts in upper limbs. Also seen in the legs and jaws

• Rigidity: ask about history of falls, poor balance, pain and muscle stiffness

• Poverty of movement: ask about drooling of saliva, difficulty in writing (micrographia), difficulty in turning in bed and change in voice (softness of voice)

• Family history of disease (susceptibility genes include α-synuclein, leucine rich repeat kinase 2 and glucocerebrosidase)

• History of encephalitis

• History of smoking (never smokers are twice as likely to develop disease) and caffeine intake (those who take no or very low quantities of daily caffeine, are at increased risk, ~25%) (Lancet 2009;373;2055–66)

• History of exposure to managanese dust, carbon disulfide or carbon monoxide

• Use of 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) for recreational purposes

• Elicit a drug history, particularly regarding neuroleptics (reserpine, metoclopramide)

• History of herbal medications, particularly Pacific sedative kava kava and Indian snake root Rauwolfia serpentina

• History of severe head injury, encephalitis, hypertension or cerebrovascular disease.

Examination

• Usually florid cases are seen in the examination and the striking abnormalities (Fig. 45.1) are:

• an expressionless or ‘mask-like’ face (fixed stare, infrequent blinking and ironed-out wrinkles)
• drooling of saliva
• resting or pill-rolling movement (most common in the distal extremities).
image

Fig. 45.1 Parkinson’s disease. (A) The slightly anxious frozen face and characteristic flexed posture. (B) Development of anterocollis. (C) Typical facial expression of a patient with progressive supranuclear palsy, illustrating worried or surprised appearance, with furrowed brow and fixed expression of lower face.

Proceed as follows:

• Comment on the expressionless face, pill-rolling movement and drooling of saliva so that the examiner knows that you have observed these abnormalities. Elicit bradykinesia by asking the patient to touch her thumb with each finger in turn.

• Examine the tone, in particular at the wrist for cog-wheel rigidity.

• Proceed to do the glabellar tap (tap the forehead just above the bridge of the nose repeatedly (about twice per second): in normal subjects, the blinking will stop whereas the patient with Parkinson’s disease continues to blink: referred to as Myerson’s sign. (It must be remembered that this sign is unreliable.)

• Ask the patient to walk and comment on the paucity of movement including the absence of arm swing and festinating gait (the patient walks with a stooped posture as if trying to catch up with her centre of gravity). The feet may scrape the floor in taking steps so the patient trips easily (be prepared to prevent the patient from falling when examining the gait).

• Tell the examiner that you would like to:

• ask the patient a few questions with a view to assessing her speech
• assess handwriting (tremulous and small, micrographia).

• Tell the examiner that you would like to look for:

• postural hypotension (Shy–Drager syndrome, levodopa treatment)
• impaired vertical gaze (Steele–Richardson–Olzewski syndrome)
• check for anosmia (an early sign)
• seborrhoea.

Note: The diagnosis of Parkinson’s disease is entirely clinical but the results of certain investigations may help in recognizing alternative causes for parkinsonism.

Diagnosis

This patient has features of Parkinson’s disease (lesion) that are caused by long-standing use of phenothiazines (aetiology). The patient is severely disabled by the bradykinesia (functional status).

Questions

What comprises Parkinson’s disease?

• Upper body dyskinesia must be present; it is a symptom complex containing many of the following features:

• Slowness of movement (bradykinesia)
• Poverty of movement (mask-like facies, diminished arm swing)
• Difficulty in initiating movement
• Diminished amplitude of repetitive alternative movement
• Inordinate difficulty in accomplishing some simultaneous or sequential motor acts.

• Rigidity is usually but not always present:

• Lead-pipe rigidity is where the increase in tone is equal in flexors and extensors of all four limbs but slightly more in flexors, resulting in a part flexed ‘simian’ posture
• Cog-wheel rigidity is caused by superimposed or underlying tremor.

• Postural instability is usually a late feature

• Tremor:

• Absent in about one-third of patients with Parkinson’s disease at presentation and throughout its course in some
• Resting, 3–5 Hz pill, pronation and supination rolling tremor of the upper limb
• Intermittent (can usually be brought about by getting the subject to count backwards with the eyes closed and hands dangling over the armrests of the seat)
• Intensified by emotion or stress and disappearing during sleep
• May affect legs, head and jaw as well; jaw tremor is rare but is most distressing as the teeth may pound together until they become unbearably painful.

Advanced-level questions

What are the pathological changes in Parkinson’s disease?

The most typical pathological hallmarks of Parkinson’s disease are:

• neuronal loss with depigmentation of the substantia nigra

• Lewy bodies, which are eosinophilic cytoplasmic inclusions in neurons consisting of α-synuclein.

The following associations have been made with clinical features and pathological changes:

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Clinical deficit Pathology
Motor symptoms Degeneration of dopaminergic nigrostriatal pathway

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