S255 S290
Poster 386:
Lesion Localization and Rehabilitation of Apraxia of Speech:
A Case Report
Timothy K. Calvert, MD (Temple University Hospital/Moss Rehab,
Philadelphia, PA, United States), Riddhi Patira, MD, Lauren Ciniglia,
MS, CCC-SLP, Eric Altschuler, MD, PhD
Disclosures:
Timothy Calvert: I Have No Relevant Financial Relation-
ships To Disclose
Case/Program Description:
Isolated neurologic deficits with circum-
scribed brain lesions can be most helpful in localizing the neurophys-
iologic substrate for the ability/deficit and guiding rehabilitation
treatment. We have localized the brain area responsible for speech
motor coordination/apraxia of speech (AoS). A 68-year-old right-
handed man presented with acute onset of left arm weakness and
slurred speech. MRI showed an acute infarct in the superolateral
premotor cortex of the left frontal lobe. On admission to acute inpa-
tient rehabilitation (IPR) strength was 5/5 in the right leg, shoulder
abduction, elbow flexion/extension. Right wrist extension/flexion,
finger extension were 0/5, supination, finger flexion 1+/5. Light touch
and speech comprehension for basic tasks and information were
normal. Initially, speech output was severely limited and garbled. The
patient did not have limb or oral apraxia. He did have AoS.
Setting:
Tertiary Care Hospital.
Results:
Our patient had a circumscribed acute lesion involving the
superolateral premotor cortex just anterior, and distinct, from the
hand premotor area implicating this region as the speech motor co-
ordination area.
Discussion:
Using clinical and radiographic findings thus to guide
treatment after 2 weeks of acute inpatient rehabilitation the
patient reached a functional level of supervision for ADLs, speech
improved markedly with use of melodic intonation therapy (MIT)
and rhythmic pacing (tapping) with a hierarchical approach. At
discharge from IPR, though with speech errors consistent with
AOS, the patient could count 1-10, repeat, and slowly and halt-
ingly, but fully and extensively described the “cookie theft”
picture.
Conclusions:
We have localized the area for AoS. Better under-
standing of cortical representation of speech and motor control will
contribute to improved lesion localization and rehabilitation
protocols.
Level of Evidence:
Level V
Poster 387:
Safe and Effective Use of Neuro-Muscular Electrical
Stimulation (NMES) in Rehabilitation of Mononeuritis
Multiplex from Eosinophilic Granulomatosis with
Polyangiitis (EGPA): A Case Report
Vincent Y. Ma, MD (VA Greater LA Hlth Care Sys/UCLA, Los Angeles,
CA, United States), Juewon Khwarg, MD, Michael D. Scott, MD,
Ziyad A. Ayyoub, MD
Disclosures:
Vincent Ma: I Have No Relevant Financial Relationships
To Disclose
Case/Program Description:
A 51-year-old woman presented with
distal weakness and right wrist-drop, diagnosed as EGPA (Churg-
Strauss). Workup including EMG/NCS consistent with mononeuritis
multiplex with both motor and sensory axonopathy. She was
treated with IV solumedrol followed by Rituxan infusions. She was
prescribed gabapentin for neuropathic pain in the hands, but up-
titration was limited by her complaints of cold extremities. Her
rehabilitation regimen included a trial of NMES to the right wrist
extensors and finger flexors. She tolerated up to 45 minutes of
treatment per day by the fifth day without complications. On the
6th day she reported a new sensation of firmness and stiffness in
the forearm without accompanying pain, numbness, or new
weakness. NMES was held for the remaining 2 days of her hospital
stay.
Setting:
Acute rehabilitation hospital.
Results:
EMG/NCS repeated prior to discharge showed newly detect-
able right radial CMAPs in an axonopathic pattern. On exam, she
demonstrated improved wrist extension and grip strength and could
perform all self-care and ADLs with no more than minimal contact
assistance. When prompted, she endorsed persistent firmness of the
forearm that did not interfere with activity.
Discussion:
Incorporation of NMES into a rehabilitation regimen for a
rare condition is often limited by a paucity of evidence to support or
oppose its use. Basic lab data suggests that it may promote angio-
genesis to reverse neuropathy related to vasculitis-mediated hypoxia,
making it an attractive option for EGPA. Furthermore, NMES is well
studied for neuropathic pain management and may be useful in cases
such as this in which pharmacological interventions are poorly
tolerated.
Conclusions:
NMES is a well-tolerated and promising adjuvant therapy
in the rehabilitation of peripheral neuropathy due to EGPA. The
vasculopathic etiology may render EPGA especially amenable to NMES
for both symptomatic relief of neuropathic pain and functional
strengthening.
Level of Evidence:
Level V
Poster 388:
Motor Recovery Following Treatment with Zolpidem
in Osmotic Demyelination Syndrome
Cameron J. Collier (University of Texas Southwestern)
Disclosures:
Cameron Collier: I Have No Relevant Financial Relation-
ships To Disclose
Case/Program Description:
A 26-year-old man presented to inpatient
rehabilitation with tetraparesis, cerebellar ataxia, severe dysarthria
and dysphagia following correction of serum sodium from 105 mg/dL to
121 mg/dL in 24 hours. Imaging was consistent with Osmotic Demye-
lination Syndrome (ODS), involving the central pons, basal ganglia, and
bilateral thalami. He was completely dependent for self-care,
grooming, and mobility. Following the addition of zolpidem 5 mg, the
patient was found to have significant improvement in neurologic
symptoms.
Setting:
Inpatient Rehabilitation, Outpatient Clinic.
Results:
The patient made slow progress initially, with a motor FIM
of 35 on day 21, a 15 point change since admission. On day 22
zolpidem 5 mg at night was added. The following day his motor FIM
had improved to 53, an 18 point change. On day 30, a 48-hour
washout period resulted in worsening of his neurologic deficits.
Zolpidem was resumed at 10 mg with improvement in symptoms, and
continued at home following discharge. At follow-up 4 weeks after
discharge, the patient was independent in all functional measures,
however experienced increasing weakness later in the evenings. His
regimen was adjusted to 5 mg twice daily to extend any beneficial
effect.
Discussion:
In addition to our patient, there is one case study
reporting improvement in neurologic symptoms of ODS following
treatment with zolpidem. Improvement in neurologic symptoms have
been reported in Parkinson disease and spinocerebellar ataxia with
zolpidem. The mechanism in which zolpidem relieves neurologic
symptoms is unknown, but may involve a transient reversal of a dia-
schisis phenomenon within these structures leading to improved
neurologic function. Previous research has demonstrated relatively
higher densities of BZ-1 receptors in the thalamus, basal ganglia, and
pons, structures primarily affected in ODS.
Conclusions:
Zolpidem, a benzodiazepine-1 receptor agonist, may
improve neurologic symptoms in Osmotic Demyelination Syndrome.
Level of Evidence:
Level V
S255
Abstracts / PM R 9 (2017) S131-S290