Laryngeal manifestations of stroke via both direct and indirect mechanisms play a significant role in the morbidity and mortality of stroke (Videos 6.1 and 6.2). Airway protection, respiration, and phonation can be affected. Poststroke dysphagia and aspiration are topics of Chap. 11. Primary dysfunction of the larynx following stroke is often the result of an insult to the nucleus ambiguus and the nucleus solitarius. Insults to the cortical and subcortical pathways can result in loss of the laryngeal cough reflex [2]. Patients with hemispheric stroke show delayed laryngeal elevation and delayed laryngeal closure affecting the airway protection [3]. Stroke is an uncommon cause of vocal fold paralysis. In cases of stroke, an isolated vocal paralysis is uncommon [4]. In this setting, vocal fold paralysis is usually associated with a brainstem stroke, or lateral medullary syndrome (Wallenberg syndrome), which is characterized by severe pharyngeal dysphasia, palatal incompetence, vertigo, facial pain, and Horner syndrome [5]. Infarction of the nucleus ambiguus is usually related to occlusion of the posterior inferior cerebellar artery (PICA), which also results in lateral medullary infarction (Wallenberg syndrome). Infarction of the cortical and subcortical motor and sensory pathways may result in vocal fold incoordination rather than paresis or paralysis [6].

Laryngoscopy should be performed while the patient is at rest and during phonation. Dysphagia assessment is not presented here. The resting tone and position of the vocal folds should be noted. Involuntary motion of the vocal folds, including tremor, myoclonus, and spasm, should be identified. Laryngeal tremor is characterized by involuntary rhythmic movements of the vocal folds during rest and during phonation. In contrast to tremor, myoclonus is characterized by an abrupt, nonrhythmic nature of the movement, although slow (4–6 Hz) rhythmic movements may also be observed. Unilateral weakness of laryngeal mobility suggests a lower motor neuron lesion, whereas global weakness suggests upper motor neuron dysfunction. Motion-induced movement disorders (laryngeal dystonia) may also be observed. A supranuclear lesion may result in dysphonia without obvious vocal fold paralysis. In such a case, additional diagnostics are necessary for proper diagnosis. Although dysphonia must be differentiated from pure dysarthria, aphasia, or dyspraxia, phonatory dysfunction (frequently resulting from presbylarynx as many stroke patients are older than 60 years of age) is very common as a comorbid condition in patients with dysarthria [7].

Concerning prognosis, recovery from vascular insult to the motor innervation of the larynx is similar to that of other central nervous system motor deficits. The clinical consequences of vocal fold paralysis may range from none (asymptomatic) to airway obstruction that requires urgent tracheostomy [7].

Parkinson’s disease is the most common movement disorder in patients older than 55 years of age. The disease is characterized by progressive degeneration of the brainstem nuclei, particularly the substantia nigra. Dysphonia can be the first presenting sign. Characteristic tremors (arm, leg, pill-rolling), rigidity, festinating gate, and slow initiation of movement are common. About 70–90% of the patients have voice difficulties. In about a third of these patients, the voice disorder is the most disabling part of the disease. Patients present with a typically soft, breathy, monotone voice. The voice is perceived by the patient to be of normal loudness. Additional components of Parkinson’s dysphonia include voice tremor, poor articulation, variable rate, stuttering-like quality, difficulty initiating speech, and a “flat” effect [8].

Laryngoscopy and stroboscopy show that vocal fold bowing, midfold opening of the glottis on phonation, and slowed vibration are common characteristics. Glottal incompetence has been one of the most consistent findings described. Nowadays, if vocal fold immobility is present (in <5–10% of patients [9]), it is often considered a sign of a Parkinson’s plus syndrome. Parkinson’s plus syndromes include multisystem atrophy (see next Sect. 4), basal ganglia degeneration, and progressive supranuclear palsy. These disorders show rapidly progressive deterioration of motor function, with significantly worse speech deficits. Laryngeal electromyography findings demonstrate a decreased firing rate and increased variability of the interspike interval of single laryngeal motor units in older males only. This is a possible contributing factor to the pathophysiology of Parkinson’s dysphonia.

Standard Parkinson’s treatment with L-dopa has had mixed results in dysphonia. Sanabria et al. showed decreased jitter and increased fundamental frequency in a mildly affected population, but other investigators have shown no statistical improvement [10]. Deep brain stimulation has shown limited improvement in voice and speech function despite significant changes in limb movements [11]. Despite the many therapies tried, only behavioral therapy has shown a sustained beneficial effect on the voice and speech function of patients with Parkinson’s disease [9].

Multiple system atrophy (MSA) is a degenerative neurological disorder with a typical age of onset in the late 50s to early 60s [12]. The cause is unknown. The main symptoms of MSA are movement and balance disturbances. Often autonomic functions such as bladder control or blood pressure regulation are affected. MSA often presents with some of the same symptoms as Parkinson’s disease (see above Sect. 3), but MSA does not show a significant response to dopamine medication. MSA is characterized by a slowness of the initiation of movements (like in Parkinson’s disease), i.e., in the larynx by slowness of vocal cord movement (mimicking a vocal cord palsy). Like in Parkinson’s disease, the patients can also show signs of muscle rigidity, tremor, and/or ataxia. Additionally, MSA patients present with symptoms of autonomic dysfunction (p.e. dysregulation of body temperature due to sweating deficiency, dry mouth and skin). In the past, the term Shy–Drager syndrome was sometimes used when autonomic dysfunction predominated. This term should not be used anymore, given terminology changes. In rare cases, the patients have a vocal cord paralysis. Even bilateral vocal ford paralysis has been recognized in patients with MSA [13]. Other typical otorhinolaryngological symptoms are loud snoring, sleep apnea, abnormal breathing, or inspiratory stridor during sleep. Therefore, work-up should also include polysomnography [13].