S257 S290
Poster 393:
Transient Visual Anosognosia with Hypoxic Encephalopathy:
A Case Report
Roger Luo (NJ Med Schl/Rutgers), Neil Jasey, MD, Stephen
Hampton, MD
Disclosures:
Roger Luo: I Have No Relevant Financial Relationships To
Disclose
Case/Program Description:
The patient was undergoing an elective
cervical foraminotomy at an ambulatory surgical center. While
sedated and in the prone position, he began vomiting and desa-
turating 90 minutes into the procedure; ultimately, he was resus-
citated for 30 minutes then transferred to a tertiary care medical
center. He presented with slurred speech, confusion, bilateral
blindness, dyskinetic movements of his jaw, and choreiform
movements involving his entire left upper extremity. His move-
ments precluded magnetic resonance imaging, but workup with
computed tomography and an electroencephalogram were sug-
gestive of hypoxic encephalopathy likely secondary to intra-
operative hypoxia and hypercapnea. A trial of steroids failed to
improve his symptoms. After transfer to an acute rehabilitation
hospital, he demonstrated persistent denial of his blindness with
confabulation of responses.
Setting:
An acute rehabilitation hospital.
Results:
The patient’s medications were adjusted to minimize
sedating agents to improve arousal and participation in therapy. His
movements significantly subsided with benztropine, which was
adjusted to avoid oversedation. He slowly began to display insight into
his deficits and experienced gradual improvement with light percep-
tion, tracking, and naming colors. Neuro-ophthalmologic evaluation 3
weeks after admission revealed decreased peripheral fields bilaterally
with intact pursuit. His improved dyskinesia makes further imaging
possible.
Discussion:
This case adds to a limited body of literature on Anton’s
syndrome, a rare form of cortical blindness with compromised visual
association centers and resulting anosognosia. While various etiol-
ogies have been published, the most common cause involves bilat-
eral occipital lobe infarction. Though Anton’s original description
emphasized anosognosia without global cognitive impairment, this
patient’s presentation was congruent with previously reported cases
despite some cognitive impairment. Further workup with MRI, which
may clarify the extent of injury to his occipital lobes, will be ob-
tained and discussed.
Conclusions:
We report a transient case of Anton’s syndrome in a
patient after a complicated foraminotomy procedure.
Level of Evidence:
Level V
Poster 394:
Movement Disorder in an Anoxic Brain Injured Patient:
A Case Report
Ryan A. Menard, DO (Temple Univ Hosp, Philadelphia, PA, United
States), Brandon Barndt, OMS-II, Ernesto Cruz, MD, Katie Hatt, DO
Disclosures:
Ryan Menard: I Have No Relevant Financial Relationships
To Disclose
Case/Program Description:
A 50-year-old previously healthy man
presented with acute change in mental status after being found down
for unknown period of time. Workups were negative, including imaging
studies. After being intubated, he had a prolonged ICU course
complicated by sepsis secondary to pneumonia, ventilator-dependent
respiratory failure s/p tracheostomy, dysphagia s/p PEG tube. He was
intubated for 4 weeks. Following extubation, he continued to have
poor mental status, along with weakness in four extremities. On day 8
post-extubation, he began displaying purposeless, athetoid-like
movements of his upper extremity group of muscles, R
>
L. Abnormal
movement only occurred while awake and worsened with voluntary
movement. Physical exam was also notable for decreased arousal,
aphasia, coarse tremors of head, antigravity movement of four ex-
tremities. Myoclonic-type movement worsened over the subsequent 7
days with improvement in strength of four limbs.
Setting:
Tertiary care hospital.
Results:
Further workup included MRI of brain, which revealed thin
posterior right temporoparietal subdural hematoma. EEG revealed
prolonged background slowing. Remainder of workup was negative.
Discussion:
Myoclonus is defined as brief, abrupt, involuntary move-
ments. There are several conditions that may lead to myoclonic-type
movement, which can be classified according to clinical presentation/
etiology, examination, or pathophysiology. In the above case, the
patient began displaying rhythmic jerking movement 8 days following
extubation. The remainder of his examination was consistent with
injury to the basal ganglia. The basal ganglia are primarily supplied by
the lenticulostriate branches of the anterior and middle cerebral ar-
teries. These vessels are terminal arteries without anastomoses,
making them the most susceptible to ischemia. Our presumptive
mechanism for this myoclonic-type movement is hypoxic brain injury
to the basal ganglia.
Conclusions:
Myoclonic-type movement disorder should be consid-
ered as one of the serious complications of hypoxic injury to deep
subcortical structures of the brain.
Level of Evidence:
Level V
Poster 395:
An Unusual Presentation and Rehabilitation Course of
a Young Adult Woman Diagnosed with Neuromyelitis
Optica Spectrum Disorder: A Case Report
Salman Hirani, MD (Icahn School of Medicine at Mount Sinai, New
York, NY, United States), Andrew McCoy, Medical Student,
Avniel Shetreat-Klein, MD, PhD
Disclosures:
Salman Hirani: I Have No Relevant Financial Relationships
To Disclose
Case/Program Description:
A 25-year-old patient w/history of
Streptococcal pharyngitis treated w/amoxicillin 1 week prior to pre-
sentation, presented w/refractory nausea and vomiting, uncontrolled
hiccups, right-sided sharp neck pain and hemiparesis with dysesthesia,
loss of appetite and progressive weakness that developed over the
period of 1 week. She denied change in vision or pain behind the eyes.
Initial MRI Brain notable for expansive T2-FLAIR hyperintense right-
sided lesion in the medulla and posterior pons w/inferior involvement
of upper cervical cord. MRI/MRA brain showed no significant stenosis or
occlusions. Follow-up MRI demonstrated lesion extending to C6 level.
Differential included ADEM vs NMO. Laboratory work-up was negative
for Anti-Aquaporin 4 IgG, also known as NMO-antibody. However, given
presentation, age, and Asian background, she was diagnosed with
NMO-SD. She was treated w/intravenous steroids with taper, seven
courses of plasmapheresis, and started on rituximab therapy. Hospital
course complicated by pneumonia and acute respiratory failure
requiring intubation. Prior to this, she was independent in ADLs.
Rehab admission exam notable for hoarseness, right-sided weakness
w/dysmetria and ataxia more pronounced in the right upper and lower
extremities. Impairments included dysphagia, right leg weakness,
right sided dysesthesia, and pain.
Setting:
Acute Rehab.
Results:
After 2 weeks of inpatient rehabilitation, patient made sig-
nificant improvements in strength, transfers, and ADLs, which is
unique for this diagnosis.
Discussion:
Previously, NMO-SD was thought to be a variant of MS,
however, recent studies point to a humoral-mediated demyelinating
disorder with distinct autoantibodies, most notably, Anti-Aquaporin 4
IgG. This is the first reported case, to our knowledge, of an initial
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Abstracts / PM R 9 (2017) S131-S290