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vol. 6(1)
62-67
EN
Objective: Congenital cholesteatomas of the petrous apex are rare lesions that develop insidiously, which delays diagnosis and requires a high index of suspicion. A case report of supralabyrinthine congenital petrous bone cholesteatoma and review of recent literature are presented. Methods: A 27-year-old woman presented with progressive facial palsy. Otomicroscopy did not reveal any abnormalities, and hearing was normal. Although there were no complaints of vertigo or instability, vestibular examinations indicated a non-compensated peripheral vestibular lesion. Radiological examinations revealed a lesion in the petrous apex and epitympanum that had features of a cholesteatoma. Results: To preserve normal hearing, the middle fossa approach was chosen for surgery. A damaged part of the facial nerve was reconstructed with cable graft. Conclusion: Advances in radiological imaging facilitate surgical planning, and improvements in the techniques of lateral skull base surgery enable safe and radical removal of petrous bone cholesteatomas with minimal morbidity.
EN
Introduction: The most common mechanism of post-traumatic facial nerve palsy are road accidents and falls. Treatment schemes as well as proper timing of surgery are still controversial. Aim: The aim of the study was the evaluation of the effects of surgical treatment in patients with post-traumatic facial nerve palsy. Treatment results were correlated with epidemiological factors, mechanism of injury, level of nerve damage, time of surgery and its extent. Material and methods: 9 patients with facial nerve palsy after head trauma were analyzed. In all patients complete paresis of the VII nerve occurred immediately after the injury. In 5 patients the nerve was damaged in the course of the longitudinal fracture of the temporal bone, in 3 as a result of its transverse fracture while in one woman there was no evident fracture line. In all cases, surgical treatment was performed between 4 days and 13 weeks after the trauma. In all cases transmastoid approach was used. Edema lesions of the nerve dominated in 6 patients, in two cases a bone fragment was noted along its course, in one person nerve was disrupted but primary reconstruction was not possible – the man was excluded from further analysis. The results of treatment were assessed by House-Brackmann (HB) scale 12 months after the procedure. Results: Very good (HBI) or good (HBII) recovery of facial nerve function was achieved in 2 and 4 out of 8 patients respectively. Surgical timing, the extent of surgery, patient’s age, mechanism of injury and level of nerve damage had no effect on the final outcome. Conclusions: The management of post-traumatic facial nerve palsy should be individual. The commonly accepted recommendation on surgical treatment is to undertake it in patients with immediate-onset and complete paralysis. Patients who, due to their severe general condition, cannot undergo early facial nerve decompression may benefit from delayed treatment for up to 3 months after the injury.
EN
The facial nerve is the seventh, paired cranial nerve. The pathogenesis of the facial nerve disorders is strictly connected with the way it is placed. The peripheral or central paralysis of the nerve may occur at any age. The most common causes of the palsy are: idiopathic, post‑traumatic, post‑viral infectious paralysis, the transition of the inflammation from the middle ear to the VII nerve stem as well as neoplastic changes and vascular changes on the nerve. Melkersson‑Rosenthal syndrome is a rare cause of the recurrent facial nerve palsy. Though Melkersson‑Rosenthal syndrome develops most commonly between the age of 20 and 30, the early manifestation of the syndrome can start at any age. Melkersson‑Rosenthal syndrome is reported to occur also in young children. The main causes of this syndrome still have not been clearly established, however, the infectious, allergic, immunological and genetic factors are taken into consideration as the ones implicated in its aetiology. The syndrome is characterized by a triad of symptoms: recurrent facial nerve palsy, facial oedema and a fissured tongue. The full triad of symptoms occurs very rarely and thus is very uncommon. Most often the symptoms are oligosymptomatic. The paper presents a 10‑year‑old girl with the recurrent facial nerve palsy, fissured tongue and lip oedema. On the basis of the examination the girl was diagnosed to suffer from the Melkersson‑Rosenthal syndrome. The aggravation of the pathological symptoms was accompanied by the recurrent, caused by Herpes simplex virus infections.
PL
Nerw twarzowy jest siódmym, parzystym nerwem czaszkowym. Patogeneza schorzeń nerwu VII jest ściśle związana z jego przebiegiem. W każdej grupie wiekowej może wystąpić porażenie nerwu twarzowego – ośrodkowe lub obwodowe. Wśród najczęstszych przyczyn porażenia nerwu VII wymienia się: porażenie idiopatyczne, porażenie pourazowe, porażenie po infekcji wirusowej, przejście stanu zapalnego na pień nerwu VII ze struktur ucha środkowego, zmiany nowotworowe, a także naczyniowe na przebiegu samego nerwu. Zespół Melkerssona‑Rosenthala jest rzadką przyczyną nawracającego porażenia nerwu twarzowego i choć występuje zazwyczaj między 20. a 30. rokiem życia, to jego wczesne objawy mogą pojawić się w każdym wieku. Występowanie tego zespołu opisywane jest także w populacji pediatrycznej. W nieustalonej do końca etiologii zespołu bierze się pod uwagę między innymi czynniki infekcyjne, alergiczne, immunologiczne i genetyczne. W zespole Melkerssona‑Rosenthala występuje charakterystyczna triada objawów klinicznych: nawracający obrzęk tkanek miękkich twarzy, porażenie nerwu twarzowego i bruzdy (pofałdowania) na powierzchni języka (lingua plicata). Postać zespołu Melkerssona‑Rosenthala z pełną triadą wymienionych objawów występuje rzadko, najczęściej spotykane są postacie niepełne czy monosymptomatyczne. W pracy przedstawiono przypadek 10‑letniej dziewczynki z nawracającym porażeniem nerwu twarzowego, bruzdami na języku i obrzękiem wargi, u której na podstawie badania przedmiotowego i podmiotowego rozpoznano zespół Melkerssona‑Rosenthala. Zaostrzeniom choroby towarzyszyły nawracające zakażenia wirusem Herpes simplex.
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