Anosmia, the loss or alteration of the sense of smell, is a condition with multifactorial causes and consequences for patient safety, nutrition, and mental health. This review explores the neurophysiological mechanisms underlying anosmia, focusing on both peripheral and central components of olfactory dysfunction. In traumatic brain injury, anosmia occurs due to direct mechanical damage to the olfactory nerve fibers or olfactory bulb, with experimental models revealing sustained inflammation, microglial activation, and oxidative stress that disrupt olfactory signaling. Chronic rhinosinusitis-induced anosmia, attributed to mechanical obstruction, and inflammatory changes within the olfactory mucosa that impair neurogenesis and sensory function. COVID-19-related anosmia is prevalent and involves multiple mechanisms: local epithelial inflammation due to angiotensin-converting enzyme 2 receptor-mediated viral entry, damage to sustentacular cells, disruption of olfactory cilia, cytokine release, and olfactory bulb. These diverse etiologies share overlapping pathological features including neuroinflammation, impaired neuronal regeneration, and altered olfactory processing. Anosmia is not only a symptom but may also serve as an early biomarker of neurological decline, particularly in neurodegenerative disorders. Accurate diagnosis requires objective olfactory testing, and management may include pharmacological, rehabilitative, and supportive strategies. Understanding the shared neurophysiological underpinnings of anosmia can enhance early detection of systemic disease and guide targeted therapeutic interventions.
Reiza Ventura (Sun,) studied this question.
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