K W Delank1, G Fechner. 1. Klinik und Poliklinik für Hals-Nasen-Ohrenheilkunde der WWU Münster.
Abstract
BACKGROUND: Head injury is one of the most common causes of olfactory disturbances. The incidence of posttraumatic anosmia depending from the severity of the injury lies between 5% and over 80%. METHODS: Clinical assessments were performed in 26 cases with posttraumatic anosmia using subjective olfactometric tests. Additionally, morphological studies were performed in 26 other patients, who died between 36 hours and six weeks after head injuries. RESULTS: Frontal basal injuries as well as minor occipital blows are capable of causing complete olfactory loss. About one-third of all patients were not aware of their chemosensory deficits, especially when associated neurological deficits occurred. Moreover, the studies show that: 1: The vulnerability of the fila olfactoria varies extremely and depends on unknown, highly individual parameters. 2: Trauma can induce local hemorrhage within the olfactory tracts and bulbs without any other intracranial lesions. 3: An intracerebral contusion is often misunderstood as the direct substrate of a posttraumatic anosmia. However, in a number of cases it is merely the sign of a strong injuring force, potentially capable of injuring the fila or the olfactory bulbus. CONCLUSIONS: The findings indicate that the pathophysiology and biomechanics of posttraumatic anosmia should be the subject of critical discussion.
BACKGROUND:Head injury is one of the most common causes of olfactory disturbances. The incidence of posttraumatic anosmia depending from the severity of the injury lies between 5% and over 80%. METHODS: Clinical assessments were performed in 26 cases with posttraumatic anosmia using subjective olfactometric tests. Additionally, morphological studies were performed in 26 other patients, who died between 36 hours and six weeks after head injuries. RESULTS:Frontal basal injuries as well as minor occipital blows are capable of causing complete olfactory loss. About one-third of all patients were not aware of their chemosensory deficits, especially when associated neurological deficits occurred. Moreover, the studies show that: 1: The vulnerability of the fila olfactoria varies extremely and depends on unknown, highly individual parameters. 2: Trauma can induce local hemorrhage within the olfactory tracts and bulbs without any other intracranial lesions. 3: An intracerebral contusion is often misunderstood as the direct substrate of a posttraumatic anosmia. However, in a number of cases it is merely the sign of a strong injuring force, potentially capable of injuring the fila or the olfactory bulbus. CONCLUSIONS: The findings indicate that the pathophysiology and biomechanics of posttraumatic anosmia should be the subject of critical discussion.
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