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An 82-year-old gentleman has been referred with a tremor and some slowness of movement (bradykinesia) by his GP who would like advice on starting medications. His wife has been encouaging him to see the GP for several years. He has been very reluctant and only now is seekign help. You see the patient and he complains of slowing up over the past 2 years and people have commented on his "shake". He is now embarrassed going out and the shake worsens when he is anxious. He is frustrated at not being able to walk to the corner shop now as it takes him so much time and he almost fell.
You see him and there is a more flexed gait and posture and tremor over a year. When you get him to walk there is an absence of arm swing. You ask him to do up his shirt buttons which he finds very difficult. He seems to find it very difficult to turn over in bed at night. There is a dry scaly rash on his face. He is not on any medications other than PRN paracetamol. Other than that he has no sleep disturbance. he has noticed that he needs to take laxatives more often now. His wife feels that he is depressed.
What do you suspect is the diagnosis
This looks and sounds very much like Idiopathic Parkinson's disease which is a progressive movement disorder with both motor and non-motor effects. It sounds like it is fairly advanced now which makes the diagnosis easier.
What are the usual clinical findings?
Bradykinesia: slowness of movement
Rigidity and what is called cogwheel rigidity (increased tone + tremor)
Tremor which is looks as if he is rolling a pill
Mask like expressionless face.
Postural instability which usually comes later
Micrographia, increased risk of seborrheic dermatitis
Flexed posture on walking, loss of normal arm swing
Impaired sense of smell is seen early but non-specific
Sialorrhoea “dribbling” as rate of swallowing diminishes. There is progression over time.
Where is the cause in the brain
There is a loss of the pigmented dopamine-secreting neurones of the substantia nigra in the midbrain. There is no clear understanding of why this occurs. This forms part of the extrapyramidal system which affects the smoothness and control of motor systems.
What is the spectrum of movement disorder?
One can simplistically think of Parkinson's disease as one end of a spectrum of too little movement (too little dopamine) and Chorea “dance” (Excess Dopamine) as the other end of the spectrum. Drugs that treat PD may cause dyskinesias and extra movements, drugs for chorea induce parkinsonism.
Is imaging useful
Generally, no. The diagnosis is largely based on a clinical presentation in an older patient with a steady progression of the clinical signs and no obvious secondary cause. In a younger patient or one with the atypical disease, one might consider a DaTscan which is useful in the following questions which is usually is a tremor due to Parkinson's disease or essential or dystonic tremor or functional.
Responsiveness to medical therapy cannot be predicted from a scan. A Normal DATscan is comma-shaped: What we are seeing is the highlighted putamen and caudate and B PD is a full stop or period: reduced activity in caudate
What is the current treatment?
Treatment aim is simply to try and re-establish normal dopamine levels in the required pathways in the CNS. This is done by giving L-Dopa which becomes Dopamine. Preventing its metabolism.
Amantadine an antiviral can help some patients often used in mild disease
In early disease when symptoms are mild consider MAOI B which can boost dopamine levels. They can be used alone or with co-beneldopa or co-careldopa for 'end-of-dose fluctuations.
Rasagiline: Rasagiline 1 mg OD
Selegiline 5-10 mg immediate-release once daily in the morning.
L-Dopamine + Decarboxylase inhibitor: start when disabling symptoms interfering with life. Low dose Madopar or Sinemet TDS. The L-Dopa is metabolised to Dopamine. Giving Peripheral decarboxylase inhibitor ensures that this happens centrally. L-Dopa crosses the blood-brain barrier and into the CNS. By inhibiting that peripherally it reduces the toxicity of it and increases the amount crossing the Blood-brain barrier.
Dopamine agonists can be used along with or instead of L-Dopa but these do not have the same effectiveness and fewer side effects. Preferred in younger patients or these may be added to L-Dopa.
Anticholinergics were used but their negative effect on cognition means that they are generally avoided especially in those over 60
What are the side effects of treatment with L-Dopa
Hypotension, Nausea, Confusion, Dyskinesias are troubling and are extra non-voluntary uncontrolled movements that may even be painful
How do you manage Nausea related to L-Dopa
Domperidone is usually recommended
He is having on / off phenomenon - what is this and how may it be treated
He is seen by a specialist who considers a COMT (catechol-O-methyl transferase) inhibitor. This again prevents Dopamine breakdown and helps to regulate levels and so may be added on to therapies.
In PD are there any surgical options
Surgery: this is an option for some patients where medications are not controlling symptoms adequately. It involves Deep brain stimulation (DBS) surgery in which electrodes are inserted into a targeted area of the brain, using MRI (magnetic resonance imaging) and recordings of brain cell activity during the procedure. A second procedure is performed to implant an IPG, impulse generator battery (like a pacemaker) under the collarbone or in the abdomen. The IPG provides an electrical impulse to a part of the brain involved in motor function. Those who undergo DBS surgery are given a controller to turn the device on or off. There is a small risk of infection, stroke, bleeding or seizures. DBS surgery may be associated with reduced clarity of speech. A small number of people with PD have experienced a cognitive decline after DBS surgery.
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