ANSWER 95
There is evidence in the history and examination of tremor, rigidity and bradykinesia. Her
writing shows micrographia secondary to the rigidity and slowness of movement. Her hyper-
tension is well controlled on the beta-blocker. Beta-blockers can cause tiredness and slowness
but not to the extent seen in this woman. This woman has Parkinson’s diseasepresenting with
the classic triad of tremor, rigidity and hypokinesia. Tremor is usually an early symptom and
may be unilateral. The combination of tremor with rigidity leads to the cogwheel form of rigid-
ity. The patient often goes on to have a blank mask-like facies. There is difficulty starting to
walk (freezing) and the patient uses small steps and has difficulty stopping (festination). There
is generally normal intellectual function, but there is often depression. Sleep is often disturbed
contributing to daytime tiredness. The characteristic pathological abnormality is degeneration
of dopamine-secreting neurones in the nigrostriatal pathway of the basal ganglia.
Parkinsonian features (parkinsonism) may occur in a variety of diseases:
- Parkinson’s disease
- postencephalitic parkinsonism
- neuroleptic drug-induced Parkinson’s disease
- parkinsonism in association with Alzheimer’s/multi-infarct dementia.
- Rest tremor: the tremor is worse at rest and is typical of parkinsonism.
- Postural tremor: this is characteristic of benign essential tremor, physiological
tremor and exaggerated physiological tremor caused by anxiety, alcohol and
thyrotoxicosis. Benign essential tremor is not present at rest, but appears on
holding the arms outstretched but is not worse on movement (finger–nose testing).
Tests of co-ordination are normal and walking is unaffected. There is usually a
family history of tremor and the tremor is helped by alcohol and beta-blockers. - Intention tremor: the tremor is worse on movement and is most obvious in
finger–nose testing. It is usually caused by brainstem or cerebellar disease caused by
such diseases as multiple sclerosis, localized tumours or spinocerebellar degeneration.
! Classification of tremor
A variety of drugs are available to treat this woman’s Parkinson’s disease. Selegiline, an
inhibitor of monoamine oxidase B may delay the need to start levodopa and may slow the
rate of progression of the disease, but has significant side-effects. Levodopa is usually used
in combination with a selective dopa decarboxylase inhibitor which does not cross the
blood–brain barrier and reduces peripheral adverse effects. The commonest side-effects
are nausea, vomiting, dizziness, postural hypotension and neuropsychiatric problems. After
many years of treatment the effects tend to diminish and the patient may develop rapid
oscillations in control – the ‘on–off ’ effect. When these develop, a sustained release for-
mulation of levodopa or a dopamine agonist, e.g. bromocriptine, may produce improve-
ment. Because of the loss of effect with time, treatment should not be started too early.
This requires careful discussion with the individual patient. She should be assessed by a
physiotherapist and occupational therapist and provided with advice and aids. With time
her house may need to be altered to aid her mobility.
- Parkinson’s disease is characterized by tremor, rigidity and hypokinesia.
- Patient management is long term and multidisciplinary.
- Benefits of levodopa treatment in Parkinson’s disease may lessen with time.