S261 S290
Case/Program Description:
A 59-year-old man developed leg
cramps immediately following a routine 6 mile jog which was
initially evaluated and attributed to lipid lowering agent myop-
athy. Symptoms progressed to include neck stiffness, hand
tingling/weakness, and subsequently leg weakness over the 4 days,
causing the patient to present to the ED. Other pertinent symp-
toms included constipation following several days of new onset
diarrhea and abdominal cramps. On physical examination the pa-
tient demonstrated severe strength deficits worse in distal versus
proximal upper and lower extremities. There was diffuse areflexia
noted in the upper and lower extremities. Sensation testing was
unremarkable.
Setting:
Acute Inpatient Rehabilitation Unit.
Results:
Further testing included lumbar puncture with elevated CSF
protein without elevated WBC’s. Serum testing had elevated titers of
Anti-GM1 antibodies. MRI of the Lumbar spine showed evidence of
increased enhancement of the nerve roots. EMG was consistent with
motor axonopathy with distal conduction block without signs of
demyelination or involvement of sensory nerves. The patient subse-
quently underwent plasmapheresis followed by an acute inpatient
rehabilitation course with gradual improvements.
Discussion:
A chief complaint of muscle cramps has a variety of po-
tential etiologies. Exercise associated muscle cramps are a common
condition with athletes and lipid lower agents can also be a culprit. We
present a case of muscle cramps in an athlete who ultimately was
diagnosed with AMAN. AMAN and AIDP are the two main variants of
GBS. Of GBS cases in Europe and the United states, AMAN is
<
10% while
AIDP is 90% of the cases.
Conclusions:
This report highlights a case of AMAN variant of GBS in
an athlete with a common initial presentation. Although AMAN is rare
in the United States, it is still important to consider in the evaluation
of more common musculoskeletal complaints, as it may rapidly prog-
ress and timely treatment is crucial.
Level of Evidence:
Level V
Poster 406:
Chronic Inflammatory Demyelinating Polyneuropathy
as the First Manifestation in a Patient with Human
Immunodeficiency Virus: A Case Report
David Q. Atkins, MD (San Juan VA Medical Center, Carolina, Puerto
Rico, Puerto Rico), Rafael Romeu, MD, Jean C. Gallardo, MD,
Keryl Motta-Valencia, MD
Disclosures:
David Atkins: I Have No Relevant Financial Relationships
To Disclose
Case/Program Description:
A 52-year-old man with history of right
cerebellar stroke and controlled diabetes mellitus type 2, who pre-
sented to the acute hospital with a 10-week history of progressive
generalized limb weakness, distal lower extremity numbness,
imbalance and multiple falls. Previous to symptom development he
was modified independent with activities of daily living (ADLs) and
ambulated with a rolling walker. Over the last month he became
dependent for manual wheelchair mobility and needed increased
assistance in ADL’s. Magnetic resonance imaging of the brain and
lumbo-sacral spine revealed no clear etiology for weakness. Patient
was admitted to an Acute Inpatient Rehab Facility (AIRF). Neurology
recommended a trial of intravenous immunoglobulin (IVIGs) for 5
days. Upon discharge patient achieved minimal assistance level for
ADLs and ambulating 60 feet with rolling walker and minimal
assistance.
Setting:
Acute Inpatient Rehab Facility (AIRF).
Results:
Electrodiagnostic Studies (EDX) was performed and it
revealed a peripheral neuropathy, most likely to a demyelinative
pathology in multiple nerves, possibly consistent with chronic inflam-
matory demyelinating polyneuropathy (CIDP). Lumbar puncture
revealed elevated CSF protein and cell count. Human immunodefi-
ciency virus (HIV) Elisa test was ordered and resulted positive with CD-
4 count
>
500 cells/mm
3
. Laboratory testing of Folic Acid, Vitamin B-
12, TSH and HgA1c are within normal limits.
Discussion:
As with our patient, symptoms seen with an acquired
demyelinating polyneuropathy may be the initial presentation of a
patient debuting with HIV and must be thought as part of the
differential diagnosis of CIDP. After IVIGs were provided, this
patient showed improvement in strength and performance in
therapies, translating into greater independence in ADLs and
ambulation.
Conclusions:
Human immunodeficiency virus infection should be
considered as a possible etiology of a patient presenting with chronic
inflammatory demyelinating polyneuropathy. Moreover, patients may
show improved outcomes from an admission to an acute inpatient
rehabilitation facility to improve functional outcomes.
Level of Evidence:
Level V
Poster 407:
3rd and 4th Finger “Drop”
e
An Ignored Sign of C8
Radiculopathy? Three Case Reports
April Ap. Pruski, MD (Rusk Inst of Rehab Med, New York, New York,
United States), Qiang Fang, MD, Ronald Shin, DO, Arpit Kaul, DO
Disclosures:
April Pruski: I Have No Relevant Financial Relationships
To Disclose
Case/Program Description:
Patient 1 had a history of chronic neck
pain and two prior negative EMG and he was referred for Posterior
Interosseous Neuropathy (PIN) with the finger extensor weakness.
Patient 2 was referred for ulnar neuropathy as his simultaneous
tingling of left medial forearm and ulnar hand was focused. Patient 3
had similar sensory complaint and severe bilateral foraminal stenosis
(left
>
right) reported in MRI and he was referred for ulnar neuropathy
vs. cervical radiculopathy.
Setting:
Outpatient.
Results:
EMG suggested left C8 radiculopathy in all the cases with
the abnormal spontaneous activities at left Extensor Digitorum
Communis (EDC), at least one C8/T1 muscle and lower cervical
paraspinals (Table 1). All three patients had left severe neuro-
foraminal stenosis at C7/T1 level confirmed with MRI. Patient 1
underwent left C6-7/C7-T1 foraminotomies and postop rehab. Pa-
tient 3 chose nonsurgical treatments including cervical posture
education and hand/neck strengthening. Both claimed return of
full strength. Patient 2 did home exercise and did not return for
follow-up.
Discussion:
C8/T1 radiculopathy often presents with radiated
neck pain, sensory complaint and hand intrinsic muscle weakness.
PIN shows finger extension weakness and often 2nd finger extensor
weaker. All three patients had no radiating neck pain and his/
her 3rd and 4th finger extensor strength was below 3/5 and
weaker than hand intrinsic muscles and other finger extensors.
Hand intrinsic muscles are innervated by both C8 and T1 roots.
EDC muscle is innervated by C8 mostly and C7. It may explain
why 3rd and 4th finger extensors were weaker in these C8
radiculopathy.
Conclusions:
3rd and 4th finger “drop” may be a clinical sign for C8
radiculopathy. These cases suggest the importance of cervical posture
and exercise for protecting root from neuroforaminal stenosis. It re-
mains to be explored why 3rd and 4th finger extensors were weaker
than 2nd and 5th finger extensor in this group.
Level of Evidence:
Level V
S261
Abstracts / PM R 9 (2017) S131-S290