Wednesday 3 August 2016

My Encounter with Parkinsonism

I had the pleasure of meeting Mrs B, who has been suffering from Parkinson disease for over 15 years. At the time of the home visit, she had no obvious difficulty moving about and getting on with her daily activities. She did not exhibit any resting tremor, akinesia/freezing, or any signs that could be indicative of her moderately advanced stage of Parkinson’s disease. On questioning, she admitted having just taken Levodopa medication which explained the lack of hypokinetic symptoms.

Levodopa is a precursor to dopamine. Unlike dopamine, L-dopa is able to pass through the blood brain barrier and gets converted to dopamine to replenish the lack of dopamine in the substantia nigra pars compacta of the midbrain. This relieves motor symptoms of PD

As we spoke about her medications, she described how her motor symptoms would decline before the next dose, presenting a phenomenon of ‘end-dose deterioration’. I had the opportunity of doing a PNS (peripheral nervous system) examination on her. On closer inspection, it was clear that she was suffering from ‘peak-dose’ dyskinesia. As opposed to hypokinetic movements, she presented with hyperkinetic; almost choreic (dance-like movements). Athetosis of her arms was prominent but disappeared during voluntary movements. These chorea-like movements seem to be a component of levodopa-induced dyskinesia. While she did not present with classical ‘lead-pipe’ or ‘cog-wheel’ rigidity, I found that her left arm showed a greater tone especially on rapid supination of her forearm and rapid extension of her elbow.  This rigidity was less prominent on the right arm. Such clinical finding is in line with the asymmetrical nature of Parkinson’s motor symptoms. Her power and reflexes were normal and unremarkable.

Mrs B also suffers from chronic pain that radiates down her arms and back pain. It is understood that her PD is preventing her from getting adequate control. For instance, there is great technical difficulty in administering analgaesic injections due to her inability to keep still.

There is evidently a social component to this case. Mrs B complained of having no one whom she could speak to, and whom she could rely on. Her parkinsonism is accompanied by features of postural instability which makes it unsafe for her to go out on her own. While PD has certainly contributed to her low mood, it is undeniable that she was becoming mildly depressed due to the lack of social support network.

She requested for befriending services or regular help from social workers but her social circumstances (presence of family members/ carers) put her at a low priority for social services. Given the circumstances, I feel that it would be appropriate to seek cooperation and help from her family members to provide more support to Mrs B.

This case reiterates the importance of ‘No Health without Mental Health’. Besides, it serves as a reminder of the need to consider the social impact of the disease. EPC certainly has provided me with a good grounding as I progress to the clinical year. From my experiences in EPC, I learn to appreciate the importance providing a holistic treatment and the need to treat patients (and not just the disease).

Parkinson’s disease at a glance



Parkinson’s disease is a neurodegenerative disorder, characterised by death of nigrostriatal dopaminergic neurones located at the substantia nigra pars compacta. Motor symptoms such as rigidity, bradykinesia, resting pill-rolling tremor and loss of postural reflexes are well-known cardinal signs seen in PD patients. In addition, there are non-motor symptoms such as anosmia, dementia, hallucination, cognitive decline, depression and autonomic dysfunction.





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