Background: In postmortem analysis of late stage Parkinson's disease (PD) neuronal loss in the substantial nigra (SN) correlates with the antemortem severity of bradykinesia and rigidity, but not tremor. Objective: To investigate the relationship between midbrain nuclei volume as an in vivo biomarker for surviving neurons in mild-to-moderate patients using 7.0 Tesla MRI. Methods: We performed ultra-high resolution quantitative susceptibility mapping (QSM) on the midbrain in 32 PD participants with less than 10 years duration and 8 healthy controls. Following blinded manual segmentation, the individual volumes of the SN, subthalamic nucleus, and red nucleus were measured. We then determined the associations between the midbrain nuclei and clinical metrics (age, disease duration, MDS-UPDRS motor score, and subscores for bradykinesia/rigidity, tremor, and postural instability/gait difficulty). Results: We found that smaller SN correlated with longer disease duration (r =-0.49, p = 0.004), more severe MDS-UPDRS motor score (r =-0.42, p = 0.016), and more severe bradykinesia-rigidity subscore (r =-0.47, p = 0.007), but not tremor or postural instability/gait difficulty subscores. In a hemi-body analysis, bradykinesia-rigidity severity only correlated with SN contralateral to the less-affected hemi-body, and not contralateral to the more-affected hemi-body, possibly reflecting the greatest change in dopamine neuron loss early in disease. Multivariate generalized estimating equation model confirmed that bradykinesia-rigidity severity, age, and disease duration, but not tremor severity, predicted SN volume. Conclusions: In mild-to-moderate PD, SN volume relates to motor manifestations in a motor domain-specific and lateralitydependent manner. Non-invasive in vivo 7.0 Tesla QSM may serve as a biomarker in longitudinal studies of SN atrophy and in studies of people at risk for developing PD.

Background Although sensory feedback is a vital regulator of deglutition, it is not comprehensively considered in the standard dysphagia evaluation. Difficulty swallowing secondary to sensory loss may be termed “sensory dysphagia” and may account for cases receiving diagnoses of exclusion, like functional or idiopathic dysphagia. Methods and Results Three cases of idiopathic dysphagia were suspected to have sensory dysphagia. The patients had (1) effortful swallowing, (2) globus sensation, and (3) aspiration. Endoscopic sensory mapping revealed laryngopharyngeal sensory loss. Despite normal laryngeal motor function during voluntary maneuvers, laryngeal closure was incomplete during swallowing. The causes of sensory loss were identified: cranial neuropathy from Chiari malformation, immune‐mediated neuronopathy, and nerve damage from prior traumatic intubation. Conclusions Sensory loss may cause dysphagia without primary motor dysfunction. Sensory dysphagia should be classified as a distinct form of swallowing motility disorder to improve diagnosis. Increasing awareness and developing appropriate assessment tools may advance dysphagia care.

Objectives To determine if the internal branch of the superior laryngeal nerve (iSLN) provides direct motor innervation to the interarytenoid muscle, a laryngeal adductor critical for airway protection. We studied the iSLN‐evoked motor response in the interarytenoid and other laryngeal muscles. If the iSLN is purely sensory, there will be no detectable short latency motor response upon supramaximal stimulation, indicating the absence of a direct efferent conduction path. Study Design Intraoperative case series. Methods In seven anesthetized patients undergoing laryngectomy for unilateral laryngeal carcinoma, the iSLN of the unaffected side was electrically stimulated intraoperatively with 0.1‐ms pulses of progressive intensities until supramaximal stimulation was reached. Electromyographic responses were measured in the ipsilateral interarytenoid, thyroarytenoid, and cricothyroid muscles. Results None of the subjects exhibited short‐latency interarytenoid motor responses to iSLN stimulation. Supramaximal electrical stimulation of the intact iSLN evoked ipsilateral motor responses with long latencies: 18.7–38.5 ms in the interarytenoid (n = 6) and 17.8–24.9 ms in the thyroarytenoid (n = 5). Supramaximal stimulation of the recurrent laryngeal nerve evoked ipsilateral motor responses with short latencies: 1.6–3.9 ms in the interarytenoid (n = 6) and 1.6–2.7 ms in the thyroarytenoid (n = 6). Conclusion The iSLN provides no functional efferent motor innervation to the interarytenoid muscles. The iSLN exclusively evokes an interarytenoid motor response via afferent activation of central neural circuits that mediate the laryngeal reflex arc. These findings suggest that the role of the iSLN in vital laryngopharyngeal functions, such as normal swallowing and protection of the airway from aspiration, is purely sensory. Level of Evidence 4 Laryngoscope, 131:E207–E211, 2021