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tone. Currently the patient is able to ambulate approx. 300 ft total
with rolling walker (RW) and bilateral Ankle-Foot Orthoses (AFOs)
which limits his ADLs, although he is functionally independent. He
relies on a scooter for distances. The patient was enrolled into a 5-
week (2 days per week) program to strengthen the lower extremities
using a powered exoskeleton orthosis system (PEOS). This system
permitted safe graduated mechanical assistance during gait training.
Setting:
Outpatient Rehabilitation Facility.
Results:
Initial 6 min walking test (6MWT) with RW and B/L AFOs was
120ft. The patient’s initial distance with exoskeleton was 328 ft in
17:07 min. At the 5-week mark the 6MWT was 150 ft with RW and B/L
AFOs, showing a 30-ft increase or approximately 20% improvement.
Discussion:
GBS is an acquired disease of autoimmune etiology char-
acterized by rapid onset of ascending paresthesia and weakness up to
total body paralysis, autonomic disturbances and respiratory failure.
Mortality is
<
5% and only approximately 10% of the patients have
pronounced residual disability. This case report provides evidence of
potential functional improvement in ambulation including endurance
and efficiency utilizing training with a PEOS, which are shown as a 20%
increase distance.
Conclusions:
PEOS should be considered and used for GBS patients
with limited ambulation to improve distance and endurance which
results in better ADLs and quality of life.
Level of Evidence:
Level V
Poster 354:
Progression of Progressive Multifocal Leukoencephalopathy
after Discontinuing Natalizumab Therapy: A Case Report
Vivek Sindhi, MD (Vidant Rehab Ctr/East Carolina Univ/Brod,
Greenville, NC, United States)
Disclosures:
Vivek Sindhi: I Have No Relevant Financial Relationships
To Disclose
Case/Program Description:
A 64-year-old woman with history of
multiple sclerosis treated with natalizumab was diagnosed with pro-
gressive multifocal leukoencephalopathy (PML) on routine brain im-
aging 6 months into starting treatment. Patient was discontinued from
therapy and was admitted for apheresis in March of 2015. Patient
presented in October 2016 with new-onset severe, throbbing head-
aches in the left fronto-temporal region. Throughout her hospital
course, headaches worsened and coincided with insidious onset of
right hemiparesis and expressive aphasia. Magnetic resonance imaging
(MRI) of the brain revealed worsening PML with more diffuse T2
hyperintensity white matter lesions. Lesions were significant for
increased spread from deep fronto-temporal white matter to subcor-
tical white matter compared to MRI of brain one year prior where only
deep lesions were present. Lumbar puncture was performed which
detected 10 copies of the John Cunningham (JC) virus in the cere-
brospinal fluid.
Setting:
Inpatient Rehabilitation at Tertiary Care Hospital.
Results:
Soon after transfer to inpatient rehabilitation, she experi-
enced 9 episodes of seizure activity associated with severe right-sided
facial grimacing and right gaze preference. She was given lorazepam
for seizure abortion. She was started on zonisamide for headaches and
seizure prevention. After 2 weeks, zonisamide dose was up-titrated to
100 mg twice daily and the patient’s headaches completely resolved.
She had no further seizure activity.
Discussion:
The progression of PML is a disabling and potentially fatal
process. Patients may progress with a myriad of neurological deficits
based on the location of their white matter lesions. Progression real-
ized on neuroimaging is quite impressive with more diffuse T2 hyper-
intensity white matter lesions spreading to the subcortical white
matter.
Conclusions:
Although patients who develop PML during natalizumab
therapy are discontinued from this therapy and receive apheresis
treatment to remove all circulating medication, they are still prone to
disabling disease progression.
Level of Evidence:
Level V
Poster 355:
Carbon Monoxide Poisoning and Peripheral Neuropathy:
A Case Report
Walter Gaudino, MD (Nassau Univ Med Ctr), Lincy Thadathil, DO,
Lyn D. Weiss, MD
Disclosures:
Walter Gaudino, MD: I Have No Relevant Financial Re-
lationships To Disclose
Case/Program Description:
We report two cases of an individuals with
carbon monoxide (CO) poisoning who developed peripheral neuropa-
thy. The first is a 53-year-old man who suffered anoxic encephalopathy
following CO poisoning while inside a car in 2007. As a result of the
traumatic brain injury, patient had cognitive deficits, lower extremity
weakness, impaired coordination and balance. He was using a walker
and attending physical and occupational therapy. The second is a 43-
year-old man who presented with bilateral lower extremity foot and
calf pain following CO poisoning in 2013 which also lead to cognitive
deficits including memory loss, chronic headaches, and lower ex-
tremity weakness. Patient complained of sharp stabbing pain in
bilateral lower extremities with decreased sensation, numbness and
intermittent localized edema. Patient is an independent ambulator
without assistive device and attending physical therapy.
Setting:
Outpatient Clinic.
Results:
In the second patient electromyography studies were normal.
Patient had tried Gabapentin and Nortriptyline with minimal relief.
Discussion:
Central nervous system pathology following CO poisoning
have been studied and well reported in literature. However, periph-
eral neuropathy in CO patients have rarely been reported or under-
stood. Patients may report symptoms of weakness, sensory
abnormalities, local edema, and tingling or neuropathic pain. Most
reported cases affect the lower extremity more than the upper ex-
tremity. Cases that have been previously reported show reversible
neuropathy with complete resolution of symptoms. EMG studies are
important in monitoring progression and or resolution of symptoms.
Damage to small unmyelinated or autonomic nerve fibers may have
been responsible for the symptoms in the patients described above.
Conclusions:
The two cases highlight the importance of clinicians to
recognize and diagnose symptoms of peripheral neuropathy in CO
poisoning. It is important to obtain a detailed history, physical, and
electrophysiological studies to monitor the course of the injury so that
patients can be treated appropriately.
Level of Evidence:
Level V
Poster 356:
Subarachnoid Hemorrhage Leading to Terson’s
Syndrome and Charles Bonnet Syndrome: A Case
Report
King S. Cachola, MD (Univ of TX-UT Houston, Houston, Texas, United
States), Michael J. Irvine, DO, Christopher M. Falco, MD
Disclosures:
King Cachola: I Have No Relevant Financial Relationships
To Disclose
Case/Program Description:
This is a case of a 54-year-old man who
was found unconscious for 40 minutes. Imaging revealed a large frontal
lobe hematoma measuring 6x3cm with intraventricular extension. A
cerebral angiogram found a ruptured ACOM aneurysm, which was then
embolized. He later required EVD placement due to worsening hy-
drocephalus and underwent craniotomy with partial hematoma evac-
uation. His hospital course was complicated by bilateral upper and left
lower extremity DVTs, for which he was started on Xarelto. He
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Abstracts / PM R 9 (2017) S131-S290