Parkinson’s
disease affects millions over the world and is not a pleasant experience for
the patients and their families. Parkinson’s disease (PD) is one of the most
debilitating neuro-degenerative disorders which occur because of gradual death
of dopamine generating cells in substantia niagra (an area of the mid brain
responsible in formation of dopamine neurotransmitter).
Initially,
PD presents itself with some obvious, movement related deficits which include muscle
rigidity, shaking and trembling, slowness in movement and drooping eyelids. Later
on, as the disease progresses, it causes cognitive deficits (problems related
to thinking, memory, judgement). Dementia is a dangerous psychiatric by-product
of PD whereas Depression is one of the most common co-morbidities which is
obviously related to the debilitation and loss of dopamine.
Neuro-cognitive
deficits can be seen in early phases of PD which relate to difficulties in
making judgment, slurred speech, strange thoughts and impaired mood. Patients
often experience apathy and an inability to experience normal range of
emotions. As the disease progresses, one can also not the visuo-spatial
difficulties, memory impairments, impulse control disorders, hypersexuality and
psychotic symptoms.
Medicines
for PD include Levodopamine, the aim of which is to replace the lost dopamine
in the brain. Co-adjunct treatment alongside Dopamine agonists are
antidepressants and Pacitane. However, Pacitane in some cases is known to
trigger delirium. An anti-depressant is also started alongside.
However,
despite these medications, as PD advances, an individual may become more
vulnerable to environmental stressors and these stressors combined with dopamine
deficiency may cause psychotic reactions.
One
of my patients with old ischemic heart disease was admitted for Angiography
when I saw him. He maintained a good conversation despite the obviously visible
tremors and mild hyperexcitability. Since he was already 82, I thought it was a
normal reaction to hospitalization. The medical chart hadn’t mentioned anything
about him being on Levodopamine or Pacitane.
He
inquired about the procedure of angiography as any other patient would.
However, after the angiography, his reaction changed markedly. He started
showing irritability, became extra-sensitive to bodily symptoms and showed
increased drowsiness. I still treated it as a normal, transient psychiatric
reaction to hospitalization and the pain in the radial area to angiography.
However,
on the third day, he developed severe psychosis. He started experiencing visual
hallucinations and began responding to them. He saw his friends and people who
weren’t present in the room inquiring after his health and started answering
them.
Since
he was in the ICU, I was left with no other option but to communicate with his
grandson. The young boy then told me that his grandfather had been diagnosed
with PD about one and a half months back but hadn’t adhered to medication which
is the reason why the tremors still persisted.
I
could suddenly see the block fitting in and the clouds suddenly started to
disappear giving way to light. I could see that the old man’s psychotism was
directly related to PD. He was shifted to the general ward from the ICU as he
became haemodynamically more stable. The foley’s catheter, IV cannula and the
monitor leads were removed. He felt much better and the presentation of
psychoticism gradually decreased but not to the desired level.
His
newly acquired psychiatric reaction was a matter of concern for his family
members too. The only plan I, along with the admitting cardiologist could
devise was to restart him on PD medications and revisit his neurophysician.
The possible prognosis is that we can
expect the tremors, gait and psychiatric reactions to improve once the patient
restarts on PD medications. The only way to know about his current state of
well-being is nto wait until his next follow-up.
