This paper describes a series of patients with a petrous temporal bone cholesteatoma paying particular attention to the complications and their management. Sixteen patients who underwent surgery in our department were reviewed. Topographically, the petrous bone cholesteatomas were grouped into five categories according to the classification proposed by Sanna et al. There were five massive labyrinthine; five infralabyrinthine; one apical; four supralabyrinthine; and one infralabyrinthine-apical. Clinically, the presenting symptom of these lesions were facial nerve paralysis (10 patients) and unilateral deafness (13 patients). Total removal of the cholesteatomas was achieved in all patients using different surgical approaches according to their site and extent. Recurrences were observed in two patients after 8 months and 24 months, respectively. The facial nerve was infiltrated and compressed by the cholesteatoma in eight patients. Seven were managed with cable grafts using sural nerve. One of these patients was treated using a facial-hypoglossal anastomosis because of the failure of the graft. In the remaining patient, a baby-sitter procedure was employed. In the other two patients, the preoperative facial paralysis was due to compression by the cholesteatoma, and its removal allowed partial recovery of facial function. The rationale of the surgical management of petrous bone cholesteatoma is its radical and total removal. Our present policy is to prefer approaches which result in a closed cavity obliterating the eustachian tube and closing the auditory canal as a blind sac. Facial nerve function is the main complication of these lesions, Facial nerve involvement requires rapid management because the duration of the paralysis is directly related to poor recovery of facial function.

Delayed onset of facial palsy is possibly an underestimated but distressing complication of acoustic neuroma surgery. The incidence of this complication reported in the literature has varied from 11.7 to 41%. This study reviewed retrospectively 60 primary acoustic neuroma surgeries performed by a single neurotologist. The delayed onset of facial dysfunction was defined according to the guidelines described by of Lalwani Butt, Jackler, Pitts and Jingling in 1995. They considered either a deterioration of facial function from normal to abnormal or an increased severity of the degree of facial paralysis, which was grouped using the House-Brackmann scale system. Fifteen of the 60 patients (25%) were found to have a deterioration of facial function. The incidence of delayed facial palsy was not influenced by age, sex or tumor size. The majority of the patients had a favorable prognosis. Only three patients had a grade III-IV facial function at 1 year. It is possible that these latter cases might have benefited from intraoperative meatal facial nerve decompression, as advocated by Sargent, Kartush and Graham.

No abstract

We report the clinical observation of interferon beta-1a effectiveness in the treatment of skin lesions in a patient affected by multiple sclerosis (MS) and systemic sclerosis (SSc), 1 suggesting a common pathogenesis.A 51-year-old woman was admitted to the department of neurology of the ''Federico II'' University with a 5-day history of muscle weakness and sensory disturbance in her right leg preceded by optic neuritis. Diagnosis of MS, according to the McDonald 2 criteria was carried out; the Expanded Examination Rating Scale (EDSS) 3 was 3.5.A trial of intravenous methylprednisolone resulted in relief of the patient's symptoms. The neurological status improved to EDSS 1.0. After 30 days, the patient started the interferon (IFN) beta-1a treatment to prevent relapses. To date, the patient shows no relevant neurological alterations and is relapse-free.The patient has also been receiving care from the rheumatology department of the Second University of Naples for SSc since the age of 48 years. The clinical picture includes sclerodermatous skin involvement, symmetrical distal and proximal polyarthritis, lung fibrosis and Raynaud's phenomenon. Immunological tests showed both haemagglutinating antibodies for Scl-70 and anticentromere antibodies. For treatment of SSc, the patient receives methylprednisolone, 25 mg daily.The modified Rodnan skin method 4 5 was used to evaluate the skin thickness assessed in 17 body surface areas using a 0 (normal) to 3(severe) scale. At the time of diagnosis the Rodnan Skin Score was 32/51. The skin involvement was characterised by two painful ulcerations on the lateral aspect of the abdomen and on the left knee. The lesion found on the left knee covered a large area (15610 cm), was red in colour, necrotic and covered with scabs. The patient treated these ulcers with topical drugs with no effect.Fifteen days after starting MS treatment with IFN beta-1a, we documented healing of the skin lesions; the ulcerations had reverted to an atrophic stage and the Rodnan Skin Score had improved to 10/51 (fig 1). After 30 days, the patient interrupted the treatment because of side effects (flu-like symptoms) and the skin lesions reappeared after 10 days. Further administration of IFN beta-1a led to disappearance of the ulcers. The patient continued with the IFN treatment and, during a followup period of 12 months, did not develop new lesions. Unfortunately, other manifestations of SSc did not change with the administration of IFN beta-1a.The effectiveness of IFN beta-1a treatment for MS on the resolution of SSc skin lesions is an original observation. Its mode of action is still unclear, 6 but there is a large amount of evidence from in vitro studies that IFN beta directly modulates the function of immune cells. IFN beta treatment reduces cellular IFNc expression, 7 a cytokine which stimulates fibroblast glycosaminoglycan production 8 ; this ability as a fibroblast modulator and a glycosaminoglycan production inhibitor might explain the effect on cutaneous manifestation of SSc.Our observation suppo...