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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