Objectives: Intermittent hypoxia resulting in endothelial dysfunction in microvascular circulation constitutes one of the mechanisms underlying complications of obstructive sleep apnea syndrome (OSAS), such as hypertension and atherosclerosis. The role of intermittent hypoxia on peripheral nerves, however, is still debated. Here, we designed a study in patients with OSAS to investigate different levels of the central and peripheral nervous systems, in order to delineate what kind of pathologic substrate was present, if any, and at which level of the neuromuscular pathway. Methods: A total of 20 patients with OSAS and 18 sex- and age-matched healthy controls were enrolled in our study. All participants underwent nerve conduction studies (NCSs) to analyze peripheral nerves, evoked potentials for somatosensory, visual evoked potential (VEP) and brainstem auditory pathways, blink reflex studies to analyze brainstem and subcortical structures, and transcranial magnetic stimulation to analyze the motor cortex and corticospinal pathway. Results: A comparison of NCSs between the two groups showed that the motor amplitudes of the ulnar nerve (P = 0.015) and sensory amplitudes of the sural nerve (P = 0.026) were significantly smaller in the OSAS group than those in the control group. The mean P100 amplitudes of VEP responses were 7.11 ± 2.73 μV in the OSAS group and 9.75 ± 3.52 μV in the control group (P = 0.022). In correlation analysis, the amplitude of P100 responses was positively correlated with the lowest oxygen saturation (P = 0.026). Conclusion: Our results confirmed the presence of generalized axonal involvement in the peripheral nervous system in OSAS, probably secondary to chronic intermittent hypoxemia.

Narcolepsy is one among the disorders of central hypersomnolence characterized by excessive daytime sleepiness not related to disturbances in nocturnal sleep or misalignment in circadian rhythms. The cardinal symptom of this group of disorders is disabling daytime sleepiness, characterized by the repeated episodes of irresistible daytime sleepiness or lapses into sleep in monotonous situations, but also under unusual conditions such as eating. Narcolepsy is defined as type 1 and type 2 on the basis of the presence of cataplexy. The most pathognomonic feature of narcolepsy type 1 is cataplexy, which is characterized by sudden episodes of brief loss of muscle tone-sparing consciousness, usually triggered by strong emotions. Other nonspecific symptoms associated with rapid eye movement sleep dissociation include fragmentation of nocturnal sleep, hypnagogic or hypnopompic hallucinations, and sleep paralysis. The pathophysiology of narcolepsy type 1 is well established as the deficiency of hypocretin (orexin) signaling in the lateral hypothalamus. In narcolepsy type 2, on the other hand, hypocretin levels are not decreased, and it has been suggested that there is probably a partial deficiency in hypocretin signaling system to cause excessive daytime sleepiness but not severe enough to cause cataplexy. Instead of types 1 and 2, primary (idiopathic) narcolepsy, familial narcolepsy, secondary (symptomatic) narcolepsy, and narcolepsy plus (hereditary forms with additional neurological symptoms) forms were suggested to better classify the clinical entities. In this paper, the diagnosis of symptomatic or secondary narcolepsy is reviewed and classified based on the underlying pathophysiologic mechanisms.

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