S256 S290
Poster 390:
Pathologic Femoral and Lumbar Fractures During
Rehabilitation for a Traumatic Spinal Cord Injury in
Osteogenesis Imperfecta: A Case Report
Brendon S. Ross, DO (McGaw MC of NW Univ NW Med Schl/RIC,
Chicago, IL, United States), Leslie K. Rydberg, MD
Disclosures:
Brendon Ross: I Have No Relevant Financial Relationships
To Disclose
Case/Program Description:
A 51-year-old woman with Type I
Osteogenesis Imperfecta (OI) was involved in a high-speed motor
vehicle accident leading to a lumbar burst fracture resulting in
paraplegia. Her inpatient rehabilitation course was complicated by
pathologic fractures of the femur and lumbar spine during partici-
pation in a model system spinal cord injury (SCI) rehabilitation
program.
Setting:
Acute Inpatient Rehabilitation Hospital.
Results:
The pathologic fractures this patient experienced during
the functional postures and mobility strategies which are normally
taught to SCI patients obligated the team to evaluate each adaptive
strategy to prevent fracture and ensure patient safety. These
fractures significantly altered her inpatient functional goals and
increased the required assistance upon discharge which will be
discussed.
Discussion:
OI coupled with SCI creates a difficult combination for
the rehabilitation team. This is the first case report to our knowl-
edge discussing the complexity of designing an appropriate reha-
bilitation program and the associated functional outcomes in this
unique clinical presentation. The combined forces of high-fracture
risk, poor bone health, and her high body mass index challenged her
possibilities for future independence normally achieved by many
paraplegics.
Conclusions:
This report highlights the importance of rehabilitation
teams understanding the fracture-risk boundaries when managing OI
with SCI and appropriate risk analysis of functional goals with the
rehabilitation team is necessary to prevent additional injury. In
spite of these challenges, it is possible to create an appropriate
rehabilitation plan for individuals with the combination of OI and
SCI.
Level of Evidence:
Level V
Poster 391:
Wernicke’s Encephalopathy in a Nonalcoholic Patient:
A Case Report
Mayya Gorbal, MD (Albert Einstein Col of Med), Gary N. Inwald, DO
Disclosures:
Mayya Gorbal: I Have No Relevant Financial Relationships
To Disclose
Case/Program Description:
This is a 64-year-old woman without sig-
nificant history of alcohol use who presented with progressive weak-
ness, mental status changes and gait ataxia for one month in the
setting of poor nutritional intake. Physical examination was notable
for horizontal nystagmus and fluctuating weakness in the bilateral
upper and lower extremities. A urine toxicology screen and infectious
workup were negative. Serum salicylate, acetaminophen and ethanol
levels were within normal limits. TSH, vitamin B12, magnesium,
phosphorus, HIV, syphilis testing and brain CT and MRI yielded normal
results. She was started on IV thiamine per neurology recommenda-
tions, with significant improvement in her nystagmus and mental
status. The patient was diagnosed with Wernicke’s encephalopathy
based on her clinical presentation and improvement after thiamine
administration. She was then discharged to acute inpatient rehabili-
tation for functional optimization.
Setting:
Acute Inpatient Rehabilitation Facility.
Results:
On admission to rehabilitation, the patient continued to
complain of weakness and pain in the bilateral legs. MRI of the lumbar
spine showed only minimal degenerative changes. Electromyography
was consistent with a predominantly axonal sensory-motor poly-
neuropathy, worse in the lower than the upper extremities. The pa-
tient was continued on thiamine repletion and started on gabapentin
with notable improvement in pain and muscle strength prior to
discharge home.
Discussion:
Wernicke’s encephalopathy is an acute neuropsychiatric
condition due to thiamine deficiency that presents with the classic
triad of nystagmus, gait ataxia and mental status changes and is most
commonly associated with alcohol misuse. However, it can also pre-
sent in patients with unbalanced nutrition, various systemic diseases
and genetically predisposed individuals. Although this patient showed
the classic clinical findings of Wernicke’s encephalopathy, the etiology
was likely malnutrition rather than alcoholism.
Conclusions:
This case demonstrates a classic presentation of Wer-
nicke’s encephalopathy in a patient with poor nutritional status who
showed clinical improvement after treatment with thiamine and a
comprehensive rehabilitation regimen.
Level of Evidence:
Level V
Poster 392:
Myeloneuropathy of the Conus Medullaris and
Lumbosacral Nerve Roots Caused by Copper Deficiency:
A Case Report
Benjamin Ingraham, DO (McGaw MC of NW Univ NW Med Schl/RIC),
Alan S. Anschel, MD
Disclosures:
Benjamin Ingraham: I Have No Relevant Financial Re-
lationships To Disclose
Case/Program Description:
A 59-year-old man was admitted to an
acute inpatient rehabilitation hospital after developing copper defi-
ciency myeloneuropathy. He initially presented with 2 weeks of
buttock and bilateral hip pain, progressive lower extremity weakness,
and urinary retention. Magnetic resonance imaging (MRI) of his lumbar
spine initially showed increased T2 signal from the L1 level to the
conus. Lumbar puncture showed elevated protein and IgG index sug-
gesting potential inflammatory etiology. He was treated with a full
course of plasma exchange therapy without improvement and subse-
quently treated with high dose steroids and IV immunoglobulin again
without improvement. On subsequent imaging, signal abnormalities
extended to the T10-11 level with enhancement of the lumbosacral
nerve roots. Late in his hospital course he was found to have a low
serum copper level of 40 micrograms/dL and low ceruloplasmin of 11
micrograms/dL. Intravenous then oral copper supplementation was
initiated, and he was subsequently transferred to acute inpatient
rehabilitation.
Setting:
Academic inpatient rehabilitation hospital.
Results:
After combined treatment with copper supplementation and
intensive inpatient rehabilitation, his reflexes and proximal lower
extremity strength improved, but he continued to have significant
lower extremity distal weakness and neurogenic bowel and bladder
problems. He progressed to moderate assistance for sit to stand
transfers and ambulated 32 feet in the 6 minute walk test.
Discussion:
This case presents a patient with a rare presentation of
idiopathic copper deficiency myeloneuropathy involving the conus
medullaris and lumbosacral nerve roots, leading to cauda equina
syndrome. This is the first case report to describe cauda equina syn-
drome as a result of copper deficiency myeloneuropathy.
Conclusions:
Although rare, copper deficiency myeloneuropathy can
present cauda equina syndrome. Copper deficiency should be included
early in the differential diagnosis for myeloneuropathy involving the
conus medullaris and lumbosacral nerve roots.
Level of Evidence:
Level V
S256
Abstracts / PM R 9 (2017) S131-S290