Ipsilateral Vocal Cord Paralysis After Acute Anterior Ischemic Stroke


Khalid Sawalha MD1; Ahmed Abd Elazim MD2; Omar Hussein MD2

Perm J 2020;25:20.104 [Full Citation]

E-pub: 12/02/2020


Introduction: The vocal cord is innervated by the recurrent laryngeal nerve and the superior laryngeal nerve, which are branches of the vagus nerve. The nucleus ambiguous is a motor nucleus of the vagus nerve and it is located in the medulla. It receives supratentorial upper motor regulatory fibers. Commonly, this regulation is bilaterally represented in the brain. Less commonly, it is contralaterally represented. This case describes a rare presentation.

Case Presentation: We present a female patient in her early sixties with a past medical history significant for hypertension who presented with acute right-sided weakness and expressive aphasia (National Institutes of Health Stroke Scale = 20). Computed tomography (CT)-head was unremarkable but she was outside the window for chemical thrombolytic therapy. CT-angiogram revealed occlusion of the left extracranial and intracranial internal carotid artery and, thus, she was deemed not a candidate for mechanical thrombectomy. CT-perfusion scans (Rapid software) showed a large penumbra within the respective vascular territory affected including the operculum and the insula. The core infarction was relatively small and located in the left basal ganglia. After inducing therapeutic hypertension, the patient’s aphasia improved. Surprisingly, this unmasked a moderate to severe hypophonic voice. The patient underwent flexible fiberoptic laryngoscopy which showed a paralyzed left vocal cord but without signs of inflammation.

Conclusion: Our case is a rare case of transient ipsilateral vocal cord paralysis associated with anterior unilateral cerebral ischemia. The paralysis resolved with improvement of the cerebral ischemic penumbra.


Phonation is the process of producing sound. It involves intrinsic and extrinsic laryngeal muscle interplay to adjust the position, orientation, length, and tension of the vocal cords (folds). Articulation is the process of making the sound into words. It involves adjusting the position and the movement of the tongue, jaw, lips, and others while voice is being produced. Vocalization is a more general term and represents the process of voice and speech formation (cortical function in Broca’s area mainly) and voice and speech production (the function of phonation and articulation; central and peripheral).1-3 Each of these is a highly complex process that involves upper and lower motor neuron coordination as well as interplaying brain stem sensorimotor reflexes and auditory feedback processes.3,4

Phonation is a delicately organized process that requires fine coordination and high precision between the laryngeal and respiratory muscle movements within a few milliseconds. Briefly, voice is produced when the vocal folds are at a midline position. Trans-glottic pressure during expiration makes airflow through the folds from inside outward, which consequently vibrate. Vibration of the vocal folds is a passive process. However, maintaining it in a midline position, as well as adjusting its position (higher or lower), orientation (3-dimensional process), length (shorter or longer), and tension during expiration are automated volitional processes that require training during growth.3 Needless to say, paralysis of one or both vocal cords has a significant effect on this sophisticated process of voice production.

Each vocal cord is innervated by the recurrent laryngeal nerve and the superior laryngeal nerve, which are branches of the vagus nerve. The nucleus ambiguous is a motor nucleus of the vagus nerve and is responsible, along with the periaqueductal gray and the nucleus retro-ambiguous, for providing the executive motor orders of the vocal cords for vibration and phonation. It is located in the medulla. It receives higher regulatory commands from the bilateral cerebral hemispheres, specifically from the larynx motor area of the primary motor (inferior vocalization region; LX) and premotor cortex in the frontal lobes, through the corticobulbar tracts.3-6

Each facial nerve and hypoglossal nerve contains fibers for speech articulation controlling the jaw, lips, and tongue. These fibers have higher control from the bilateral motor cortex for the jaw, lips, and tongues (smc). In addition, the diaphragm and the respiratory muscle have bilateral higher cortical control from an area in the primary motor cortex superior to the LX and smc (Figure 1 A, B, D, and E).3-6 Other locations that were seen to fire during phonation and articulation via functional magnetic resonance imaging (MRI) were the supplementary motor area, the cerebellum, and the superior anterior and posterior temporal lobes (Figure 1 A, B, and C).2-6

Figure 1

Figure 1. A sketch demonstrating the central control of speech by the locations involved in speech formation and production. (A) Sagittal left hemisphere (medial view) showing the supplementary motor area (SMA) (1), frontal operculum (8), and anterior medial temporal lobe (9). (B) Sagittal left hemisphere (lateral view) showing Broca’s area (2), laryngeal motor cortex (LX) (3), the motor cortex active for jaw, lips, and tongue (smc) (4), the motor cortex for the diaphragm and the chest wall (mc) (5), the temporal lobe area active audition (tc) (6), and the cerebellum (7). Speech production is bilaterally presented in all these locations; however, speech formation from the Broca’s area has a predominant left presentation. The frontal operculum and the anterior medial temporal lobe are involved in the narrative speech but not the whistle speech. (C) Coronal brain section showing where narrative speech is unilaterally presented. These are the left globus pallidum (10), the left posterior temporal gyrus (11), the right thalamus (12), and the right anterior cingulate. (D) Axial pontine section showing periaqueductal gray (gray color), which is involved in the narrative speech production. It also shows facial (VII) nucleus (brown star) and respective nerve that supplies the lips and jaws involved in articulation. (E) Axial medullary section showing the ambiguous nucleus (brown star) sending fibers through the vagus (X) nerve to supply laryngeal musculature and related muscles that are involved in phonation. It also shows the hypoglossal (XII) nucleus (brown cross) and its respective nerve supplying the tongue that is involved in articulation.

Thus, according to this simplified explanation, unilateral cerebral lesions above the level of nucleus ambiguous are unlikely to cause paralysis of either of the vocal cords. However, to make things more complicated, recent studies have demonstrated that there are differences between narrative voiced speech and whispered speech. Using positron emission tomography, the periaqueductal gray along with the bilateral ventral frontal operculum, the bilateral anterior medial temporal gyrus, the left globus pallidum, the left posterior medial temporal gyrus, the right thalamus, and the right anterior cingulate were activated during narrative speech as compared to whispered speech. This indicates that parts of the narrative speech production can be ipsilaterally or contralaterally controlled (Figure 1, C and D); however, whispered speech seems to be less complicated.6-8

On the other hand, speech formation from the Broca’s area has a predominant left cortical control (Figure 1B).6,9 It does this through planning the chain of articular movements coming from the motor cortex and is needed to pronounce a word and/or a speech. A lesion in the Broca’s area produces Broca’s (motor – expressive) aphasia. However, lesions in areas surrounding the Broca’s area also can cause the same aphasia due to presence of multiple interconnected circuits involved in this process. These areas are Brodmann areas 6, 8, 9, 10, and 26, as well as the insula.9


We present a right-handed female patient in her early seventh decade of life with a past medical history significant for hypertension who presented with acute right-sided weakness and expressive aphasia. Her presenting National Institutes of Health Stroke Scale (NIHSS) was 20. Computed tomography (CT)-head was unremarkable but she was outside the window for thrombolytic therapy. CT-angiogram of the head and neck showed complete extracranial and intracranial left internal carotid artery occlusion and thus was not a candidate for mechanical thrombectomy. CT-perfusion scans (Rapid software) showed large penumbra including the cortex, subcortex, operculum, and the insula within the left internal carotid artery territory. The core infarction was located in the left basal ganglia (Figure 2). MRI-brain diffusion scans showed partial middle cerebral artery ischemic stroke matching with the core infarction but mismatching with the rest of the perfusion deficit (Figure 3). Because of this large penumbra (salvageable ischemic tissue if treated) and the relatively small core infarction (relatively lesser risk of bleeding), the treating team decided to treat the patient using induced therapeutic hypertension to improve brain perfusion and save the penumbra. Systolic blood pressure was maintained between 180 and 220 mm Hg using norepinephrine infusion. The patient’s expressive aphasia partially but steadily improved. This was evident clinically, as the patient started to produce some meaningful words. It was also evident radiologically, as seen on the repeat perfusion scans in the form of cortical penumbra improvement at the Broca’s area location. However, the patient’s voice was surprisingly whispery and hypophonic despite never being intubated.

Figure 2

Figure 2. Cerebral perfusion study using RAPID software showing (A) T max > 6 seconds on presentation showing increased transient time at almost the entire middle cerebral artery (MCA) territory. (B) Cerebral blood flow (CBF) volume on presentation showing deficits at the areas of the left insula, basal ganglia, and the subcortex with sparing the rest of the MCA territories. (C) T max > 6 seconds after 2 weeks (following receipt of hypertensive therapy) showing improvement of the penumbra.

Figure 3

Figure 3. Magnetic resonance imaging (MRI) showing (A) apparent diffusion coefficient (ADC) sequence on presentation showing restricted diffusion at the area of the insula, basal ganglia, and subcortex. (B) Fluid attenuated inversion recovery (FLAIR) sequence after 2 weeks showing almost stable stroke size without evidence of significant expansion.

The patient underwent flexible fiberoptic laryngoscopy by the ENT (ear, nose, and throat) team, which showed a paralyzed left vocal cord with no signs of inflammation that might be expected with a viral infection of the cords.

The patient’s induced hypertensive therapy lasted for 2 weeks, during which time the patient’s hypophonia steadily improved. Although slightly improved, the patient’s right hemiparesis persisted (likely due to the involvement of the left basal ganglia). In a 2-month outpatient follow-up visit, a repeat flexible fiberoptic laryngoscopy showed resolution of the vocal cord paralysis.


In literature, unilateral vocal cord paralysis due to acute cerebral ischemia is rare but is not unheard of. Most reports were attributed to contralateral lesions. In contrast, unilateral vocal cord paralysis secondary to an ipsilateral cortical lesion is very rare. In literature, there is a reported case of unilateral stroke, in the operculum and insula with bilateral vocal cord paralysis. In this case, there was no clear anatomic explanation of how a unilateral brain lesion can cause bilateral vocal cord paralysis unless this is a coincidental finding and likely related to viral infection.10 There is another report of cerebral intracerebral hemorrhage associated with transient ipsilateral vocal cord paralysis. It was reported that the patient's dysphonia has completely resolved in 1 week. Thus, it was attributed to resolved brain edema around the hematoma at the area of the operculum and insula, although no imaging proof of such resolution was provided.11 Unlike these 2 cases, our case provides clear imaging (serial CT-perfusion) evidence of improvement of the cerebral ischemia involving the frontal followed by the temporal cortex after aggressive induced hypertensive therapy that correlates with the clinical improvement of her aphasia followed by improvement of her hypophonia. The transient unilateral vocal cord paralysis was confirmed via a flexible laryngoscopy performed by the ENT team. According to the anatomic theory of central vocal cord control, the initial resolution of aphasia was likely secondary to the resolution of the penumbra at the Broca’s area. This was followed by the unmasking of the hypophonia/whispering speech with consequent discovery of left vocal cord paralysis. This could have 1 of 2 explanations. This could be secondary to the involvement of 1 of the ipsilateral (left) areas contributing to the narrative speech production (Figure 1C). According to the serial CT-perfusion scans, the posterior temporal lobe is likely the area involved. In line with this hypothesis, when the penumbra in the posterior temporal lobe improved (Figure 2), hypophonia also improved. However, it is undetermined in literature if a lesion in the posterior temporal lobe can cause an ipsilateral vocal cord paralysis or not. The second explanation is the vocal cord paralysis is secondary to ischemia in the larynx motor area of the primary motor region (inferior vocalization region; LX), which has an unusual and rare ipsilateral cortical presentation rather than bilateral presentation.

Our case highlights the possible different anatomic variants of cortical control on the nucleus ambiguous and the periaqueductal gray matter responsible for vocalization. Of these, the most common are the bilateral control of each vocal cord.12 Less commonly, contralateral control has been described in the literature.13 Our case provides evidence of ipsilateral control that is considered extremely rare. However, the rationale behind these presentations can be made after understanding the voice and speech formation and production processes.


The patient’s quality of voice was evaluated perceptually by the family and the treating physician. This provided 2 evaluators, 1 familiar with the patient’s voice and pitch, and the other was not. Both agreed that the voice was initially severely hypophonic, which gradually improved over time. Unfortunately, other subjective methods to evaluate voice like the voice handicap index is inappropriate for her case, as it was originally developed to quantify chronic conditions like Parkinson-related dystonia. Most of the questionnaire is inapplicable to her case, especially in a patient recovering from large acute stroke with aphasia. An example is “I tend to avoid groups of people because of my voice,” “I speak with friends, neighbors, or relatives less often because of my voice, “My voice difficulties restrict my personal and social life,” and “My voice problem causes me to lose income.”14,15 In addition, objective methods to evaluate and quantify voice quality like acoustic and aerodynamic measurements of voice 16 were not available at the time.


Voice and speech formation and production are important neurological processes that involve several pathways and cerebral centers. Localizing the lesions to those pathways might be as important as any other clinical stroke localization. Hypophonia or whispered speech can coexist with aphasia in patients suffering from unilateral large vessel occlusion strokes; however, it can be clinically masked by the aphasia. Depending on the resolution of the salvageable ischemic tissues, hypophonia and/or whispered speech can be unmasked if aphasia resolved and can be improved or resolved if its central control region’s ischemia improved. Thus, it can be used as a clinical marker or sign for stroke recovery. Voice and speech production have bilateral central control in general. However, certain parts of this process seem to be unilaterally presented. If injured, it might be responsible for ipsilateral or contralateral deficits in the vocal cord functionality. Nonetheless, variation from the common bilateral presentation is also possible. Clinicians should be aware of such uncommon presentations.

Disclosure Statement

The author(s) have no conflicts of interest to disclose.


The content has not been submitted elsewhere and all authors have contributed significantly. All authors are in agreement with the content of the manuscript.

Author Affiliations

1Department of Internal Medicine, University of Massachusetts Medical School-Baystate, Springfield, MA

2Department of Neurology, The New Mexico University Health Sciences Center, Albuquerque, NM

Corresponding Author

Omar Hussein, MD (oyhussein@yahoo.com; ohussein@salud.unm.edu)

Informed Consent

Informed consent has been granted from patient to publish the case report. No identifying data were included in our submission. The paper is institutional review board exempted because it is describing 1 case.

Author Contributions

Khalid Sawalha, MD: Participated in study design and manuscript preparation, writing, and submission. Ahmed Abd Elazim, MD: Contributed to methods and data collection. Also participated in literature review. Omar Hussein, MD: Conceptualized the study, designed and executed the study, performed thorough literature review, drafted and revised manuscript.


All authors has no financial disclosures.

How to Cite this Article

Sawalha K, Abd Elazim A, Hussein O. Ipsilateral vocal cord paralysis after acute anterior ischemic stroke. Perm J 2020;25:20.104. DOI: 10.7812/TPP/20.104


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Keywords: hypophonia, ipsilateral, ischemic stroke, vocal cord paralysis


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