Ipsilateral Vocal Cord Paralysis after Acute
Anterior Ischemic Stroke

Omar Hussein MD; Khalid Swalha MD; Ahmed Abd Elazim MD; Omar Hussein MD; Michel
Torbey MD
The Ohio State University Wexner Medical Center – Department of Neurology – Division of Neurovascular
Disease and Neurocritical Care

Introduction
Vocal cords are innervated by the recurrent laryngeal nerve and superior laryngeal nerve which are branches of the vagus nerve. The
nucleus ambiguous is the motor nucleus of the vagus nerve and it is located in the medulla. It receives stimuli from the bilateral
hemispheres through the corticobulbar tracts. Thus, unilateral cerebral lesions above the level of nucleus ambiguous is unlikely to cause
paralysis of the vocal cord.

Case

Discussion

We present a sixty-two-year-old female patient with past history significant for
hypertension who presented with acute right-sided weakness and aphasia. CT-head was
unremarkable but she was outside the window for thrombolytic-therapy. MRI-brain
diffusion scan showed partial middle cerebral artery ischemic stroke while the CTangiogram of the head and neck showed complete extracranial and intracranial left
internal carotid artery occlusion. CT-perfusion showed large penumbra. The patient
partially improved after induced hypertensive therapy. She was able to pronounce few
words; however, her voice was hypophonic. The otolaryngology team was consulted for
vocal-cords evaluation.

In literature, there is a reported case of
unilateral stroke, in the operculum and insula
with bilateral vocal cord paralysis. There is
another report of cerebral ICH and transient
ipsilateral vocal cord paralysis. Regarding the
first case, there is no clear anatomical
explanation of how unilateral brain lesion
cause bilateral vocal cord paralysis unless
this is a coincidental finding and likely related
to viral infection. As for the second case, it
was reported that the patient's dysphonia has
completely resolved in one week thus it was
attributed to resolved brain edema around the
hematoma at the area of the operculum and
insula. We believe that this explanation is
likely incorrect because of the less likelihood
of the edema to resolve by itself without
treatment in that early stage and the authors
didn’t provide evidence of antiedematous
treatment given or any imaging proving the
resolution of the edema. Unlike these two
cases, our case provides a clear resolution of
the cerebral ischemia after aggressive
induced hypertensive therapy. We also
provided an imaging evidence of resolution of
such ischemia correlating with patient’s
induced ischemia.

MRI - DWI

Results
Pre induced hypertension CTP
showed left cerebral hemisphere
large penumbra with significant size
core
infarction.
The
patient
underwent
flexible
fiberoptic
laryngoscopy which showed a
paralyzed left vocal cord.
The post induced hypertension CTP
showed remarkable resolution of
the ischemia. 2 months outpatient
follow
up
flexible
fiberoptic
laryngoscopy showed improved
vocal cord paralysis.

CT Perfusion – Pre and Post Treatment

Conclusion
Our case is a rare case of transient unilateral
vocal cord paralysis associated with
ipsilateral cerebral ischemia. The paralysis
resolved with resolution of ischemia.
Our case highlights the possible different
anatomical variants in cortical control of the
vocal cords. Of these, the most common is
bilateral control of each vocal cords. Less
commonly, contralateral control has been
described in the literature.
Our case represents evidence of ipsilateral
control that is considered extremely rare.

References
1- Nasrat T et al. Bilateral Vocal Cord
Paralysis with Acute Ischemic Stroke.
2- Park O et al. Transient Vocal Cord
Paralysis after a Supratentorial Intracerebral
Hemorrhage.
3Toutounchi SJ, Eydi M, Golzari SE,
Ghaffari MR, Parvizian N. Vocal cord
paralysis and its etiologies.