Anti-high mobility group box 1 antibody suppresses local inflammatory reaction and facilitates olfactory nerve recovery following injury.

BACKGROUND: Refractory olfactory dysfunction is a common finding in head trauma due to olfactory nerve injury. Anti-inflammatory treatment using steroids is known to contribute to functional recovery of the central and peripheral nervous systems in injury models, while there is a concern that steroids can induce side effects. The present study examines if the inhibition of proinflammatory cytokine, high mobility group box 1 (HMGB1), can facilitate olfactory functional recovery following injury. METHODS: Olfactory nerve transection (NTx) was performed in OMP-tau-lacZ mice to establish injury models. We measured HMGB1 gene expression in the olfactory bulb using semi-quantitative polymerase chain reaction (PCR) assays and examined HMGB1 protein localization in the olfactory bulb using immunohistochemical staining. Anti-HMGB1 antibody was intraperitoneally injected immediately after the NTx and histological assessment of recovery within the olfactory bulb was performed at 5, 14, 42, and 100 days after the drug injection. X-gal staining labeled OMP in the degenerating and regenerating olfactory nerve fibers, and immunohistochemical staining detected the presence of reactive astrocytes and macrophages/microglia. Olfactory function was assessed using both an olfactory avoidance behavioral test and evoked potential recording. RESULTS: HMGB1 gene and protein were significantly expressed in the olfactory bulb 12 h after NTx. Anti-HMGB1 antibody-injected mice showed significantly smaller areas of injury-associated tissue, fewer astrocytes and macrophages/microglia and an increase in regenerating nerve fibers. Both an olfactory avoidance behavioral test and evoked potential recordings showed improved functional recovery in the anti-HMGB1 antibody-injected mice. CONCLUSIONS: These findings suggest that inhibition of HMGB1 could provide a new therapeutic strategy for the treatment of olfactory dysfunction following head injuries.

Posttraumatic olfactory dysfunction.

Impairment of smell may occur following injury to any portion of the olfactory tract, from nasal cavity to brain. A thorough understanding of the anatomy and pathophysiology combined with comprehensively obtained history, physical exam, olfactory testing, and neuroimaging may help to identify the mechanism of dysfunction and suggest possible treatments. Although most olfactory deficits are neuronal mediated and therefore currently unable to be corrected, promising technology may provide novel treatment options for those most affected. Until that day, patient counseling with compensatory strategies and reassurance is essential for the maintenance of safety and QoL in this unique and challenging patient population.

Resfriado-gripe: pérdida grave del olfato a largo plazo / Long term serious olfactory loss in colds and/or flu

Introducción: Las personas afectadas por pérdida olfativa total y de por vida se sitúan entre el 2 y el 3% de la población. Dos de las causas más frecuentes son los resfriados comunes y las gripes. El objetivo de este trabajo es mostrar el grado de afectación de las alteraciones olfativas sufridas, a largo plazo, a causa de un resfriado o una gripe. Métodos: Este estudio se ha basado en la asistencia a 240 pacientes, aquejados de pérdida olfativa por resfriado o gripe. Fueron excluidos todos aquellos que padecían otras enfermedades intercurrentes (66 pacientes), el resto (n = 174) estaba formado por 51 hombres (29,3%) y 123 mujeres (70,7%). Fueron sometidos a estudio olfatométrico ( I y V par craneal) y tomografía axial computarizada nasosinusal, y resonancia magnètica del sistema nervioso central (RM-SNC) comparándose el resultado con un grupo control (n = 120). Resultados: Se confirmó que la pérdida olfativa tanto para el nervio olfativo (p < 0,00001) como la alteración del nervio trigémino (p < 0,0001) eran muy significativas. Conclusiones: La pérdida del olfato, pasados más de 6 meses desde su inicio supone una reducción grave de las capacidades olfativas de las personas afectadas (AU)

Introduction: In the general population, we can find 2%–3% of lifelong olfactory disorders (from hyposmia to anosmia). Two of the most frequent aetiologies are the common cold and flu. The aim of this study was to show the degree of long-term olfactory dysfunction caused by a cold or flu. Methods: This study was based on 240 patients, with olfactory loss caused only by flu or a cold. We excluded all patients with concomitant illness (66 patients), the rest of patients (n = 174) consisted of 51 men (29.3%) and 123 women (70.7%). They all underwent olfactometry study ( I and V cranial nerve) and a nasal sinus computed tomography scan, as well as magnetic resonance imaging of the brain. Results were compared with a control group (n = 120). Results: Very significant differences in levels of olfactory impairment for the olfactory nerve (P<0.00001) and trigeminal nerve (P<0.0001) were confirmed. Conclusions: People who suffer olfactory dysfunction for more than 6 months, from flu or a cold, present serious impairment of olfactory abilities (AU)

Lesões olfatórias pós-traumáticas / Post traumatic olfactory lesions

OBJETIVO: Documentar a incidência de lesões traumáticas do nervo olfatório, assim como a etiologia traumática; correlacionar as lesões do nervo olfatório com achados radiológicos (lesões cranianas e intracranianas) e estudar lesões múltiplas de nervos cranianos. MÉTODOS: Vinte e quatro pacientes admitidos no Serviço de Emergência da Santa Casa de Misericórdia de São Paulo com lesão traumática do nervo olfatório foram incluídos. Os pacientes foram divididos em três grupos, de acordo com o escore da escala de coma de Glasgow (ECG): trauma leve (ECG de 13 a 15), moderado (ECG de 9 a 12) e grave (ECG de 3 a 8), assim como em diferentes graus de lesão do olfatório, como hiposmia, anosmia e parosmia, distribuição quanto a gênero, presença de fraturas, lesões intracranianas, fístulas liquóricas e mecanismo de trauma. RESULTADOS: Dos 24 casos, 15 lesões ocorreram em conjunto com outros nervos cranianos e em nove casos houve lesão exclusiva do nervo olfatório. O atropelamento foi a causa mais comum de lesão do nervo olfatório de forma isolada, assim como nas lesões de múltiplos nervos. Hematomas extradurais foram as lesões intracranianas mais frequentes e a ausência de fraturas predominou nos indivíduos estudados. CONCLUSÃO: Neuropatia traumática do olfatório deve ser pesquisada na admissão do paciente (quando possível), sobretudo quando houver evidência de traumas frontais ou occipitais.

OBJECTIVE: To register the incidence of the traumatic lesions to the cranial nerves and its etiology; to correlate the lesions to the radiological ndings (cranial and intracranial) and study multiple cranial nerve lesions. METHODS: Fifty-four patients admitted to the Emergency Service of Santa Casa de Misericórdia de São Paulo Hospital have been studied and lesions to the different cranial nerves were described. All patients were submitted do radiographic exams, computed tomography, and, when necessary, magnetic resonance imaging. The patients were divided into 3 groups according to the Glasgow Coma Scale (GCS) in: mild trauma (GCS: 13 to 15), moderate (GCS: 9 to 12) and severe (GCS: 3 to 8). RESULTS: Posttraumatic single nerve lesion was more frequent seen on olfactory, facial and oculomotor nerves.Running over was the main cause of these lesions (single nerve and multiple nerves). Contusions and extradural hematomas were the most frequent intracranial lesions. CONCLUSION: Traumatic cranial neuropathy occurs frequently and must be searched on the patient admission, because it can surgical decompression may necessary, such as decompression of the optic or facial nerves.