Parkinson’s Disease

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Parkinsons Disease (PD)

Chronic progressive CNS syndrome of extrapyramidal system due to continuous degeneration of dopaminergic cells in the substantia nigra and depletion of dopamine in the corpus striatum  develop 3 cardinal features - bradykinesia, rigidity and resting tremor. Prevalence of 1.5-2/1000; affects 1% > age 50 yrs. 8% develop before age 40 – most commonly develops around 60 years. M=F (or slightly more males). First described in 1817 by James Parkinson.

Unknown. Genetic factors been identified in familial cases. Suggestion that there may be environmental neurotoxin – methyl-phenyl-tetrahydropyridine (MPTP) has been shown to cause Parkinsonism in drug abusers and can be induced in primates by inducing nigral cell death.

Main process is degeneration and loss of melanin containing dopaminergic neurones of substantia nigra in basal ganglia (need to loose 80% before clinical features apparent). Reduced output of dopamine  reduced inhibitory effects on subthalamic nucleus  neurones become more active from unopposed excitatory influence of acetylcholine  bradykinesia.

Clinical Features:
Onset is insidious – initial symptoms are variable and often missed, but can include apathetic facial expression, softening of voice, muscular weakness and cramps, tremor, foot dystonia

4 major neurological signs:
• Tremor – more evident at rest – “pill rolling”; unilateral tremor at rest of one limb is most common presenting complaint; frequency of 4 to 6 Hz; usually resolves on activity; up to 30% do not have tremor initially
• Rigidity – best seen in wrist and elbow – jerky rigidity to motion when examined – ‘cogwheel rigidity’; may complain of muscle soreness and general aches; can be unilateral or bilateral
• Akinesia – difficulty in initiating movement
• Bradykinesia – slowness of movement (combined with akinesia  responsible for most of disability seen in Parkinson’s disease).

At time of initial diagnosis, symptoms may have been present for up to a year but help not necessarily sought (eg difficulty buttoning shirts, difficulty cutting food, handwriting changes, feeling of stiffness, difficulty in tying shoelaces).

Other clinical features:
• Pain (deep cramping sensation in limbs – may be secondary to levadopa; may also have a burning superficial dysaesthesia)
• mask life fascial expression; hypokinetic speech (decrease in volume, increase in rate, mumbling); decreased blinking; drooling
• micrographia – small handwriting is common
• seborrhoea
• mental state alterations (anxiety, depression, dementia, confusion, hallucinations)
• autonomic abnormalities - postural hypotension; impotence; constipation; sweating abnormalities
• postural instability, stumbling and falls

Parkinson’s disease has major effects of quality of life – there are difficulty with reading, writing, driving a car, loss of employment and eventually a loss of autonomy.

Gait :
Slow to start walking; stride length reduced; festination (rapid short accelerating steps); problems in stopping an changing sequential movements; less arm swing; poor balance when turning; difficulty crossing obstacles; less toe elevation at heel strike; increase in stance phase and double support phase duration; increased variability of gait; more difficulty walking when performing simultaneous motor or cognitive tasks. Gait abnormalities increase risk for falling.
Gait analysis has been used to demonstrate the effectiveness of drug treatment of Parkinson’s . Those on active treatment versus placebo had a greater stride length and a decrease in double support time. Force plate analysis has shown the second peak to be significantly reduced in size with asymmetry in duration of the stance phase

Involvement of foot:
Foot dystonia (sustained muscle contraction  twisting, repetitive patterned movement or an abnormal posture) triggered by walking and relieved by rest can occur in up to a third of those with PD. Stewart (1898) first described a dystonia in which the lessor toes of the foot flexed and the great toe hyperextends while walking in the early stages of some patients with PD. After standing still for a few minutes, it resolves. Dystonia of the lower limb is the presenting feature in up to 1-3% of those with PD – most of these involve the foot ; usually brought on with walking – may also get cramp like pains in arch. If not treated early  usually an equinovarus posture with an extended great toe (not to be confused with Babinski’s sign). In all patients who developed levodopa induced dystonia’s, the first site of initial involvement was the foot on the opposite side to which the Parkinsonism first developed. Dystonia’s seen in the ‘off’ period of levadopa dose cycle are usually painful and start in the foot, usually on side with initial or most severe forms of Parkinson's . Plantar pressure changes have been described – mean heel force at contact reduced, increased loading in midfoot, decreased force during propulsion . Significant changes in plantar pressure patterns are also seen in those in mild to moderate disease, with a tendency to higher forefoot loading and a medial shift in the load, which may be related to strategies to reduce unsteadiness of gait .

Parkinsonism has been reported as appearing in one of the lower limbs in 30% as the initially presenting feature, either concurrently or preceding the upper limb features – which contradicts the common belief that most start in the upper limb. May present with unilateral onset of resting tremor or ‘dragging’ of one leg during walking. Younger patients may present with involuntary internal rotation of the foot when walking. They may be ignored in the lower limb as upper limb problems are easier to detect . Movements of the foot are more ‘simple’ than the hand, so subtle impairments in the foot/lower limb may not be detected.

A pseudo-rheumatoid type deformity of the feet (and hands) resembling Jaccoud’s arthropathy has been described in cases of Parkinsonism . Other typical features seen in the feet include clawing and flexion of the toes, inverted position of the foot during the festinating gait – assumed to due to rigidity of muscles.

Those with PD will have difficulty in foot self care due to tremors and other motor disturbances.

Two approaches to drug management:
1) Decrease cholinergic activity by anticholinergic/antimuscarinic drugs
2) Increase dopaminergic activity by dopaminergic drugs

The decision to use which drug when is not well supported by many well designed trials.

Levadopa – improves most features of Parkinsons; first line drug; may cause nausea; postural hypotension; dyskinesia’s
Dopamine agonists (bromocriptine, pergolide, ropinirole) – less effective than levadopa, but less likely to cause dyskinesia; may cause nausea, hypotension
Anticholinergics (eg benzhexol) – second line drug for tremor but not rest of Parkinsons (symptoms can substantially worsen if drug is rapidly withdrawn)
COMT inhibitors (eg entacapone, talcapone) - second line drug
amantadine – has mid anti-parkinsonism effects

Surgical – ablative procedures (pallidotomy to disrupt outflow of basal ganglia); thalamactomy for tremor; deep brain electrical stimulation; foetal tissue implants
Physiotherapy – for rigidity and posture maintenance; gait retraining
Speech therapy – for communication disorders of dysarthria and dysphonia
Nutrition – well balanced diet

Gait retraining:
• gait can be improved by guidance of a visible pattern on the ground
• visual clues on the ground have been shown to improve gait parameters . The cues consisted of yellow coloured rods with a height of 2cm, 45cm apart.

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