Ally Ferber, MD
Resident Physician
JFK Johnson Rehabilitation Institute
Edison, New Jersey, United States
Anastasia Ireland, MS CCC-SLP
Speech Language Pathologist
JFK Johnson Rehabilitation Institute
Wall, New Jersey, United States
Kristen A. Harris, MD
Attending Physician
JFK Johnson Rehabilitation Institute
Edison, New Jersey, United States
A 27 year old female was admitted to rehabilitation after hypoxic ischemic brain injury secondary to cardiac arrest in the setting of drug overdose. CTH and MRI brain showed signs of global hypoxic injury with hypoattenuation of bilateral frontal lobes, frontoparietal region, and posterior limbs of bilateral internal capsules. She required a tracheostomy with decannulation achieved after several months. Throughout her recovery, she demonstrated intact auditory comprehension with impaired attention but with severely limited verbal expression. Aphonia persisted during automatic functions (coughing, crying, laughing, throat clear). A laryngoscopy revealed no active vocal fold movement, however reflexive adduction with tactile stimulation. No functional improvement in her aphonia occurred despite extensive therapies.
Discussions:
Phonation occurs with proper functioning of the thyroarytenoid and cricothyroid larynx muscles to place the vocal folds in correct positioning. Laryngeal adductor reflexes are well documented and essential for airway protection, with sensory motor reflexes possibly influencing speech. The scarce literature describes 2 cases of voice recovery with therapy in patients with aphonia of unclear etiology after TBI, both of which had injury to the frontal lobes. Postulated explanations include psychogenic, apraxia, and true paralysis, all of which are unlikely in our patient given the lack of movement in automatic functions but intact reflexive movement. A disruption to the frontal lobe, limbic system, and interconnection may present with impairments in the drive for phonation from frontal lobe damage. EMG of laryngeal muscles may provide additional information, however is difficult to obtain.
Conclusions:
Persistent complete aphonia after acquired brain injury is rare. A comprehensive evaluation is necessary to understand aspects of pathophysiology. A more thorough understanding is necessary to determine etiology and multimodal rehabilitation approaches to achieve independence and communication.
