7 a.m.,
11/8/2023. Nature called, but I took my unmerry old time to respond. No matter
how hard I tried, I couldn’t get out of bed. Nirmala, half-asleep beside me,
advised, quite reasonably, that I should do a few leg exercises first to wake
up my rigid limbs. Lying flat on my back, I bicycled the air for a while; soon
I felt like Kafka’s Gregor Samsa, as I observed my lower limbs struggling to no
avail. I eventually got up, and made it—just in time!
And, oh! the
fatigue.
Waking up
tired; after a nap, tired; early to bed, exhausted; waking up, tired, etc.
Falling
down in the park and unable to get up; falling out of bed and unable to get up;
breakfast- lunch- and dinner-time, unable to rise from the chair. Way too much
time spent on getting dressed; way too little time spent on moving. You get the
idea.
Of the four
major criteria used in diagnosing Parkinson’s, I have all four: bradykinesia, slow
movement; tremors; mobility issues including balance problems and, muscle
stiffness.
As mentioned before, the cause of Parkinson’s is
multifactorial; In most cases, it remains unknown. On average, 60% of the
dopamine-generating cells in the substancia nigra area of the brain are
already dead at the time of diagnosis. The health of the substancia nigra is
what is revealed by the DaTscan, a test which I underwent on October 8, 2123 (see
my previous blog entry, Parkinson’s Disease: Episode Four).
Not an
especially sanguine person, I expected the results of the scan to show devastation
of the substancia nigra and of the basal ganglia. I was surprised:
“There is visualization of the bilateral caudate nuclei and the putamen, (which, along with the globus pallidus--my note—compose the basal ganglia, which receive dopamine from the substancia nigra), although the putamen is slightly decreased. The findings are less likely to support a diagnosis of presynaptic Parkinson’s Disease." Italics mine.
The results
are of a basically normal scan. I was indeed surprised. What was causing my
symptoms then? (Including all those minor symptoms as well: flat affect,
buildup of saliva, rather severe illegibly small handwriting called
micrographia, etc.) When I told my physical therapist, she was surprised as
well and informed me that my Parkinson’s symptoms were more advanced than her
average client’s. (Usually, she tells me, clinicians start a patient on medication, based on clinical symptoms alone, and then refer to a neurologist.) The neurologist at the Physical Therapy center says that she knows of many cases like mine/ The clinical presentation is what's important, and mine is that of PD.
One possibility
is a medication I had been prescribed for depression years ago, a low dosage of
bupropion, Wellbutrin. I had to
discontinue this medication for eight days prior to the scan. There is a case I
read online (Google To Be or Not Bupropion—Conclusion: “Despite the
widely known benefits of bupropion…rare cases of tremor, Parkinsonism and
dystonia have been reported.” It took the seventy year old man in question a
month to recover from his symptoms; I haven’t taken bupropion since the first
week of October. I have seen some minor improvements since then; very minor
indeed.
Since the
diagnosis of PD is primarily clinical, I asked my neurologist if he would
agree to a trial of Sinemet, the carbi/levodopa combination that is the
standard in treating PD. He agreed. I am to take ½ tablet three times daily for
two weeks, followed by three tablets daily after that. So far, I have tolerated
the medicine well and have seen definite improvement of symptoms. (I can get up
from chairs better, and no longer have a lot of difficulty getting out of the
car.)
Hope the
future will bring more improvements; I have a long way to go.
This is me, sandwiched between Nirmala in the background and the shadow of Philip taking the picture. The Alpine walking sticks, which I have dubbed as les cannes jumelles d'un vieux, have helped my mobility a lot by transferring some of the work to my hands and arms.
