Parkinson’s disease misdiagnosed as stroke

Abstract

Parkinson’s disease (PD) is a neurodegenerative disease, the clinical features of which are usually asymmetrical at presentation. This can lead to difficulty in differentiating it from other asymmetric neurological disorders. We present two cases where idiopathic PD was initially misdiagnosed as stroke, leading to a delay in appropriate symptomatic therapy. Physicians involved in diagnosis and treatment of people with strokes should consider PD when formulating their differential diagnosis.

BACKGROUND

Parkinson’s disease (PD) is a progressive neurodegenerative condition characterised by tremor, bradykinesia, rigidity, and postural instability. It is usually asymmetrical at presentation and of gradual onset. Indeed, onset can be so gradual that patients are unaware of symptoms until they are brought to their attention by other events, such as trauma or intercurrent illness. This can lead to problems in differentiation of PD from asymmetrical neurological disorders of acute onset. We present two cases where PD was initially misdiagnosed as a stroke.

CASE PRESENTATION

Case 1

A 57-year-old woman was seen at the PD clinic. Three years previously she had noticed increasing difficulty in using her right hand for fine movement, stiffness in her right shoulder while dancing, and shuffling of her right foot while walking. She also complained of a tremor in her right arm. She had mild untreated hypercholesterolaemia but no other vascular risk factors and was a lifelong non-smoker. At that time, her general practitioner referred her to the neurovascular clinic where a stroke physician felt she had a mild right hemiparesis. A computed tomography (CT) scan carried out there showed a little white matter ischaemic change but no focal lesion. She was diagnosed with a mild stroke and started on aspirin and simvastatin for secondary prevention.

Since then she had had progressive impairment of her balance, general slowness, and difficulty turning in bed. The tremor now affected her right arm and leg and was present on action as well as at rest. She was limited in her daily activities and had given up her job.

On examination, she had bilateral rigidity and bradykinesia of her arms and legs with the right more severely affected than the left. She had a moderate rest tremor in her right arm and leg. There was no evidence of weakness or hyperreflexia, and her plantar responses were down going bilaterally.

She was diagnosed with a PD and, as part of a research study, underwent an FP-CIT single photon emission computed tomography (SPECT) scan, which was consistent with this diagnosis. A magnetic resonance imaging (MRI) scan of her brain showed diffuse ischaemic white matter change, but no focal infarct to support a previous right hemiparesis. She was started on pergolide resulting in a notable improvement in symptoms.

Case 2

A 71-year-old woman was seen at the PD research clinic having responded to a screening questionnaire.¹ She had been admitted to hospital with a perforated duodenal ulcer 4 years previously and had undergone an emergency laparotomy. She was an ex-smoker and was being treated for hypertension. Soon after this she attended a rheumatology clinic with cervical spondylosis. There, it was noted that her left side was “weak”. She was told that she may have had a small stroke at the time of her operation and started on aspirin for secondary prevention, although no investigations were carried out to support the diagnosis. Over the next few years she became increasingly aware of slowing of her movements, deterioration in her walking, and problems with her balance. She did not complain of a tremor. On examination, she had monotonous speech and reduced facial expression. No tremor was seen, but she did have asymmetrical rigidity and bradykinesia of upper limbs, the left more than the right, and symmetrical bradykinesia of her lower limbs. She had equivocal plantar responses but no other upper motor neurone features. She was diagnosed with PD and, after an unsuccessful trial of ropinirole, was started on co-careldopa (Sinemet) with good effect.

DISCUSSION

The large variability in the initial presentation of stroke, along with the fact that routine brain imaging has insufficient sensitivity and specificity to diagnose an ischaemic stroke reliably, mean that it is often misdiagnosed in patients with other neurological and non-neurological conditions.² Given that PD is usually unilateral at onset,³ it is possible to misdiagnose it as a mild stroke, with bradykinesia misinterpreted as weakness and rigidity as spasticity. This is a particular problem if the typical rest tremor of PD is absent, as is the case in as many as 30% of people with PD.³ Unlike PD, stroke is characteristically of acute onset but, as discussed above, the onset of PD may be so insidious that people with it may describe a sudden onset around the time of another event. This was the case in our second patient who was assumed to have a sudden onset of her symptoms at the time of her anaesthetic.

Incorrect diagnosis has important consequences both in terms of individual patients and of health service provision. We cannot be certain that the delay in diagnosis in our two patients adversely affected their quality of life. It may well be that even if they had been diagnosed earlier, they would not have required treatment of their PD at that time (though among some clinicians there is a move to start treatment for PD earlier in the disease).⁴ However, informed discussion of the correct treatment cannot begin until the correct diagnosis has been made. Moreover, the second patient was only detected by screening for PD as part of a research project, without which her initial misdiagnosis may never have been detected. The most significant problem experienced by our patients was a lengthy delay in the instigation of dopaminergic treatment and in referral to specialist care. Both responded quickly when the correct treatment was initiated. Misdiagnosis may also lead to inappropriate administration of medication. In our patients, aspirin and statins were needlessly prescribed for the secondary prevention of vascular disease. While neither of our patients was adversely affected by these, people should not be prescribed medication they do not need.

Differentiation of PD and stroke is not always straightforward, particularly where the history of onset is unclear. Careful questioning regarding the timing of symptom onset, with a supportive history from family members where possible, is essential. The presence of a tremor should raise the possibility of PD, and it is important to differentiate weakness and spasticity from bradykinesia and rigidity with a thorough examination. Physicians involved in diagnosis and treatment of people with strokes should consider PD when formulating their differential diagnosis.

LEARNING POINTS

• Parkinson’s disease can be mistaken for a subacute presentation of stroke.

• This can lead to significant delay in referral to specialist care and consideration of appropriate therapy.

• This delay can be avoided through careful clinical examination and a high index of suspicion.

• Unilateral neurological symptoms and signs do not necessarily equal stroke