S234 S290
neurologic disorders. This case consequently demonstrates a need to
closely monitor patients in the full scope of neurologic rehabilitation.
Level of Evidence:
Level V
Poster 321:
A Stiff Diagnosis: An Unusual Case of Low Back Pain
Komal G. Patel, DO (North Shore-LIJ Health System),
Fergie-Ross L. Montero-Cruz, DO, Surya M. Vishnubhakat, MD
Disclosures:
Komal Patel: I Have No Relevant Financial Relationships
To Disclose
Case/Program Description:
A 44-year-old man with a past medical
history of agoraphobia, depression, migraines, and hypertension who
presented with low back and hip pain, and impaired ambulation sec-
ondary to “legs locking up,” requiring the use of an assistive device.
Initially, he developed pressure like sensations in his lumbar spine,
later being diagnosed with Guillain-Barre´ syndrome (GBS) after
developing bilateral foot drop and muscular atrophy. GBS treatment
provided minimal improvement. Ten years later, a “sporting injury”
cascaded this current progressive symptomatology. Physical and mas-
sage therapy provided only a 30% improvement. Further investigation
raised suspicion for stiff person syndrome and anti-glutamic acid
decarboxylase (GAD) antibody was tested, revealing antibody levels
>
5,000 units/mL. The patient then received three 40mg/day intra-
venous immunoglobin (IVIG) treatments in addition to Baclofen, with
minimal generalized improvement. An additional 3 days of IVIG then
provided significant functional improvement, particularly with ambu-
lation. Follow-up anti-GAD antibody levels revealed a 66% decline. A
third round of IVIG treatment was planned in conjunction with physical
therapy and Baclofen to continue this improvement.
Setting:
Neurology clinic.
Results:
Decreasing levels of anti-GAD antibodies in a patient with
stiff person syndrome lead to marked functional improvements.
Discussion:
Stiff person syndrome, an uncommon disorder, is typified
by progressive truncal muscle stiffness, axial muscle spasms, gener-
alized rigidity, and wide based gait. These symptoms causing marked
functional decline. The primary pathophysiology is related to anti-GAD
antibodies. Increased antibody levels lead to increased muscle activity
secondary to decreased central nervous system (CNS) inhibition as a
result of decreased CNS gamma amino butyric acid. Reduction in
antibody level with IVIG treatment not only reduces presenting
symptoms but also allows patients to make marked functional
improvement in conjunction with Baclofen and physical therapy.
Conclusions:
Proper diagnosis and treatment of the debilitating stiff
person syndrome can lead to significant functional improvements.
Level of Evidence:
Level V
Poster 322:
Acute Non-Traumatic Intracranial Hemorrhage Due to
Thrombocytopenia from Radiation for Prostate Cancer:
A Case Report
Varun Patibanda (Rutgers New Jersey Medical School Physic, Harrison,
NJ, USA), Benjamin Seidel, DO
Disclosures:
Varun Patibanda: I Have No Relevant Financial Re-
lationships To Disclose
Case/Program Description:
The patient presented to a level II trauma
center having been found unresponsive in a park. Computed tomog-
raphy scan (CT) revealed a large right frontoparietal intraparenchymal
bleed with surrounding edema and compression of the right lateral
ventricle, mass effect and midline shift. Since admission laboratory
studies showed a platelet count of 65000, he received a total of 5 units
of platelets and underwent a craniotomy with partial evacuation and
drain placement. The etiology of his thrombocytopenia was worked up
with negative results. The patient had received radiation to the
prostate eight weeks prior to the hemorrhage. It was deduced that the
bleed was due to thrombocytopenia likely caused by radiation
therapy.
Setting:
Tertiary care hospital.
Results:
The patient was transferred to an acute rehabilitation fa-
cility where he participated in a comprehensive rehabilitation pro-
gram. At the time of discharge, he remained total assistance with all
mobility, but was able to achieve moderate assistance with eating and
grooming. He also required total assistance for dressing, bathing and
transfers. His oropharyngeal dysphagia improved such that he was able
to safely swallow pureed solids and nectar thickened liquids at the
time of discharge. Aside from significant dysarthria, his cognition
remained intact and without aphasia. Following acute rehabilitation,
the patient was transferred to sub-acute rehabilitation care to
continue his rehabilitative course.
Discussion:
To our knowledge, this is the first reported case of
intracranial hemorrhage thought to be from thrombocytopenia caused
by radiation to the prostate. Hypertension was an unlikely source of
bleeding since the patient had a record of excellent adherence to
home regimen and the imaging findings were uncharacteristic of hy-
pertensive bleeds.
Conclusions:
Radiation exposure should also be considered as an
etiology of intracranial hemorrhage in the setting of thrombocyto-
penia. Strict follow-up, along with continued and extensive monitoring
of hematologic studies, are warranted after radiation therapy.
Level of Evidence:
Level V
Poster 323:
Cefepime-Induced Myoclonus in a Brain Injury Patient:
A Case Report
Bonny Su Wong (Baylor College of Medicine), Viola Q. Hysa, MD
Disclosures:
Bonny Su Wong: I Have No Relevant Financial Relation-
ships To Disclose
Case/Program Description:
An 80-year-old man previously indepen-
dent presented with 3 weeks of progressive cognitive decline, falls,
and urinary incontinence. He was diagnosed with normal pressure
hydrocephalus (NPH), underwent a ventriculoperitoneal shunt (VPS)
placement, and was transferred to inpatient rehabilitation. His reha-
bilitation was complicated by
Pseudomonas aeruginosa
pyelonephritis
with bacteremia and was started on cefepime 1 gram every 8 hours. On
day 13 of antibiotic therapy, he had an acute decline in functional
status with worsening cognition, myoclonic jerks of his trunk and lower
extremities, and decrease in his ambulation distance from 117 feet to
46 feet with a rolling walker.
Setting:
Acute inpatient rehabilitation unit in an academic hospital.
Results:
Workup revealed no obvious etiology. Repeat brain imaging
and infectious workup were unremarkable. Neurosurgery had no con-
cerns for a VPS failure. On day 21, cefepime was discontinued. One
day after his last dose of cefepime, the patient’s mental status
returned to baseline and he was able to ambulate 160 feet with a
rolling walker.
Discussion:
Cefepime-induced neurotoxicity is an under-recognized
and a serious side effect mainly reported in patients with acute renal
failure. However, another potential risk factor stated in literature is
underlying central nervous system disease. Although our patient had
normal kidney function, his underlying brain injury likely caused him
to be more susceptible to the neurotoxic effects of cefepime. The
resolution of his symptoms after discontinuation suggests cefepime as
the causative agent.
Conclusions:
Cefepime-induced neurotoxicity should be considered in
the differential diagnosis in brain injury patients who develop an acute
decline in functional status.
Level of Evidence:
Level V
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Abstracts / PM R 9 (2017) S131-S290