This week, I spent some more time
in the Center for Sleep Medicine shadowing Dr. Ebben. The most exciting part is
meeting with new patients and conducting the standard questionnaire. Sometimes,
these resemble Encyclopedia Brown cases where the answer to one key question can
diagnose the problem. Other times, the underlying cause remains enigmatic,
warranting an overnight sleep study or additional follow-up.
One case that stands out involved a young
lawyer whose inability to sleep through the night began two years ago, the same
time she moved into a new apartment (which was purchased by her parents as a
real estate investment). She felt guilty knowing how nice/expensive the new
place was, yet she wasn’t feelin’ it from the very beginning. Was her problem
mostly psychological? An act of rebellion against her parents? Did she
coincidently develop a sleep disorder around the same time she moved? Dr. Ebben
was confident that her problem was environmental in nature. What was different
about this new place? Was it brighter? Noisier? The patient had accounted for
these and nothing helped. According to Dr. Ebben, the most likely culprit was
temperature. Her new place was on the top floor and lacked a thermostat with a
visible readout. High temperatures during the night may prevent the body from
efficiently offloading heat, a necessary process for avoiding sleep
fragmentation. The patient was excited to hear about another possible culprit
and left the appointment with a renewed sense of hope.
In practice, Sleep Medicine is mostly common
sense, heavily drawing on logic to solve people’s sleep problems. However,
there are many mysteries waiting to be solved, many of which will require
advancements in neurobiology. For example, why do some apnea patients still
feel chronically fatigued following positive airway pressure treatment, even if
the number of times they stop breathing per hour is reduced from ~100 to ~5? Why
is the duration of REM sleep correlated with depression? What the heck even
happens during REM sleep besides rapid eye movements, muscle atonia and
increased EEG activity? What is the relationship between synucleinopathies
(e.g. Parkinsons, dementia) and REM behavior disorder (RBD, loss of muscle
atonia during REM)? RBD is thought to involve degeneration of the brainstem, which
goes from posterior to anterior. Why is there a polarity in disease
progression? It will be exciting to
track how sleep science progresses in the upcoming years.
During the past week I also had the
opportunity to shadow in the ER with Dr. Ryan McGarry, who is also the director
of an award-winning documentary entitled “Code Black” which he filmed during
his residency at County Hospital in LA. The most interesting case involved a
patient with L4/L5 disc degeneration who, upon receiving an epidural injection
of contrast agent and lidocaine, suffered altered mental status within 60
seconds. I also observed my first
orthopedic surgery, coincidently an L4/L5 Transforaminal Lumbar Interbody
Fusion. A laminotomy was performed to decompress the spinal cord and all
removed bone was ground up (in what I called the Spinuccino machine) and saved
for later use in the interbody fusion. The procedure was guided by fluoroscopy
and so we needed to wear lead vests.
The weeks are flying by here and it is time
to buckle down on my project while checking off all of the items on my hospital
bucket list!
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