S251 S290
Poster 374:
Unusual Etiology of Neck Mass: Cervical Spine
Heterotopic Ossification after Brain Injury: A Case
Report
Araj Sidki, DO (SUNY At Stony Brook), Jun Zhang, MD
Disclosures:
Araj Sidki: I Have No Relevant Financial Relationships To
Disclose
Case/Program Description:
A 40-year-old man with no past medical
history was admitted to an acute care hospital after a near pool
drowning, post phencyclidine ingestion. Patient was intubated for
airway safety, extubated, medically stabilized and transferred to
acute inpatient rehabilitation. On admission, he responded well to
external stimuli and spoke single words. On physical exam, he was
confused and had difficulty following commands. Although he was able
to move all extremities, he demonstrated weakness throughout. He
fell as he attempted to walk without assistance, and was placed on
restraints for safety. He was noted to have a painful neck mass, which
increased in size, limiting cervical range of motion. X-ray, CT and MRI
showed heterotopic ossification (HO) of the cervical spine, but no
protrusion into the spinal canal. His only complaint was neck pain, but
he didn’t experience any neurologic deficits. He underwent inpatient
physical, occupational and speech therapy and his strength, speech,
and comprehension greatly improved. The patient also experienced a
decrease in size and pain of the neck mass.
Setting:
Community Rehabilitation Hospital.
Results:
Ongoing physical and occupational therapy, range of motion
exercises and mobilization techniques provided relief and diminished
the neck mass size.
Discussion:
HO is the formation of mature lamellar bone in soft tissue.
It may develop in patients with traumatic brain injury (TBI), spinal
cord injury, or those with severe neurologic disorders. Patients
demonstrate swelling, warmth, progressive loss of range of motion,
and elevated alkaline phosphatase. Triple phase bone scan is the
definitive diagnostic test for early HO diagnosis. Pharmaceutical
treatment includes bisphosphonates. As TBI patients usually develop
HO in hip joints, this patient’s cervical spine HO describes an atypical
location.
Conclusions:
Surgery, radiation, and conservative treatments pro-
vided by physical therapy or occupational therapy have been shown to
lower the incidence of HO in patients with severe TBI.
Level of Evidence:
Level V
Poster 375:
The Funny Looking Stroke: Cortical Laminar Necrosis:
A Case Report
Mark A. Rouff, MD (Vidant Rehab Ctr/East Carolina Univ/Brod)
Disclosures:
Mark Rouff: I Have No Relevant Financial Relationships To
Disclose
Case/Program Description:
A 52-year-old Filipino woman with past
medical history of poorly controlled diabetes mellitus and essential
hypertension presented with acute altered mental status, left-
sided weakness and generalized, clonic seizure activity for the past
24 hours. MRI brain on admission was initially read as right hemi-
spheric stroke, although encephalitis could not be ruled out. Upon
review by neurology and neurosurgery teams, there was concern
that the diffuse nature of the MRI may be more consistent with
encephalitis or possible malignancy. Given the uncertain appear-
ance of the MRI brain and ongoing altered mental status, patient
underwent extensive workup including cerebral arteriogram to rule
out vasculitis and multiple lumbar punctures with extensive CSF
analysis to rule out infectious and paraneoplastic etiology. After
experiencing breakthrough seizure, patient was taken by neuro-
surgery for temporal lobe biopsy, which confirmed the diagnosis of
cortical laminar necrosis. Patient was eventually stabilized on
seizure prophylaxis and had improved glycemic control. She
regained functional independence after 3-week inpatient rehabili-
tation admission.
Setting:
Academic medical center.
Results:
CSF negative for paraneoplastic and infectious etiology. Ce-
rebral angiogram was negative for signs of vasculitis or thrombus.
Surgical pathology confirmed cortical laminar necrosis, most likely
secondary to poor glycemic control.
Discussion:
Cortical laminar necrosis results when metabolically
active and vulnerable layers of cortical laminae are deprived of nu-
trients, as is the case in anoxia, hypoglycemia, or severe anemia. As
individual cortical laminae can be effected, there can be unique
radiographic findings, which may lead to a wide differential diagnosis.
Conclusions:
Patient’s diagnosis of cortical laminar necrosis was
confirmed by surgical biopsy. It was likely that her poor glycemic
control resulted in decreased metabolic supply to vulnerable cortical
laminae. The unique imaging of such an infarct resulted in a significant
workup to rule out other treatable pathologies.
Level of Evidence:
Level V
Poster 376:
Post Meningioma Resection Complicated by Intracranial
Hemorrhage in a Neurosyphilis Patient: A Case Report
Kirill Alekseyev, MD, EMBA (Kingsbrook Jewish Med Cntr, Brooklyn,
NY, United States), Malcolm Lakdawala, MD, Marc K. Ross, MD,
Thao Doan, MD
Disclosures:
Kirill Alekseyev: I Have No Relevant Financial Relation-
ships To Disclose
Case/Program Description:
A 48-year-old woman with a medical
history of uncontrolled hypertension, GERD, asthma, neurosyphilis
and status post meningioma resection presented to the emergency
room with complaint of headaches and lethargy for 2 days. The pa-
tient had a remarkable past surgical history of 30 days post-operative
sphenoid meningioma resection with bilateral craniotomy and on-
going treatment of neurosyphilis with penicillin. Head CT performed
secondary to altered mental status demonstrated right frontal
intracranial hemorrhage and the patient underwent emergent
craniotomy with hematoma evacuation without noted complication
during surgery. CT angiography of the neck and brain was negative
for intracerebral aneurysm and arteriovenous malformation. Coagul-
opathy studies were negative. On the seventh day post-operative
from the first hematoma evacuation the patient reported progressive
bilateral vision loss. A CT was performed and demonstrated a left
frontal intracranial hemorrhage. A second emergent craniotomy and
hematoma evacuation was performed without complications. The
patient was noted to have had poor vision deteriorating at baseline
from optic atrophy secondary to the intracranial hemorrhage.
Ophthalmology was consulted and noted optic atrophy as well as Adie
syndrome of the eye. Her new functional state declined with severe
cognitive deficits of memory, language, and attention with periods of
agitation, confusion, and hallucinations.
Setting:
Traumatic brain injury unit of an inpatient rehabilitation
facility.
Results:
The patient was admitted to the traumatic brain injury
rehabilitation unit for functional deficits in mobility, transfers, ADL,
and iADL.
Discussion:
Neurosyphilis has several complications one being
meningo-encephalopathic syndrome which can cause severe cerebro-
vascular or myelovascular issues. There are very few cases discussing
the causation of intracranial hemorrhage by neurosyphilis. Patient was
tested positive with FTA-ABS and was treated for the reoccurrence of
syphillis.
Conclusions:
It is essential to understand the complications that arise
from neurosyphilis and how to manage a patient with appropriate
rehabilitation of new onset vision loss.
Level of Evidence:
Level III
S251
Abstracts / PM R 9 (2017) S131-S290