Discerning a smile - The intricacies of analysis of post-neck dissection asymmetry.

INTRODUCTION: Iatrogenic facial nerve palsy is distressing to the patient and clinician. The deformity is aesthetically displeasing, and can be functionality problematic for oral competence, dental lip trauma and speech. Furthermore such injuries have litigation implications. Marginal mandibular nerve (MMN) palsy causes an obvious asymmetrical smile. MMN is at particular risk during procedures such as rhytidoplasties, mandibular fracture, tumour resection and neck dissections. Cited causes for the high incidence are large anatomical variations, unreliable landmarks, an exposed neural course and tumour grade or nodal involvement dictating requisite nerve sacrifice. An alternative cause for post-operative asymmetry is damage to the cervical branch of the facial nerve or platysmal dysfunction due to its division. The later tends to have a transient course and recovers. Distinction between MMN palsy and palsy of the cervical branch of the facial nerve or platysma division should therefore be made. In 1979 Ellenbogen differentiated between MMN palsy and "Pseudo-paralysis of the mandibular branch of the facial nerve". Despite this, there is paucity in the literature & confusion amongst clinicians in distinguishing between these palsies, and there is little regarding these post-operative sequelae and neck dissections. METHOD: This article reflects on the surgical anatomy of the MMN and cervical nerve in relation to danger zones during lymphadenectomy. The authors review the anatomy of the smile. Finally, case studies are utilised to evaluate the differences between MMN palsy and its pseudo-palsy to allow clinical differentiation. CONCLUSION: Here we present a simple method for clinical differentiation between these two prognostically different injuries, allowing appropriate reassurance, ongoing therapy & management.

Phase II study of pegylated liposomal doxorubicin (Caelyx) as induction chemotherapy for patients with squamous cell cancer of the head and neck.

A phase II trial of pegylated liposomal doxorubicin (Caelyx) as induction chemotherapy was conducted in 20 patients with treatment-naïve squamous cell cancer of the head and neck (SCCHN). 10 patients received two cycles of Caelyx (40 mg/m(2)) every 3 weeks before starting radical radiotherapy (RT). Subsequently, consecutive groups of 3 patients received a third escalating dose of Caelyx (10, 15 and 20 mg/m(2)) 3 days before RT. 9 of 18 (50%, 95% confidence intervals (CI): 26-74%) evaluable patients responded to Caelyx, with 11 responses in 26 (42%, 95% CI: 24-62%) evaluable sites (three complete responses (12%), eight partial responses (31%)). There was no grade 3/4 haematological, mucosal or cardiac toxicity. Nausea and vomiting were minimal. There were no drug-related RT delays. Local RT-induced toxicity was not increased. Caelyx has significant activity against SCCHN and warrants further investigation in this disease. In view of its tumour targeting properties and activity at moderate doses, it may be useful in concomitant chemoradiotherapy strategies for SCCHN.

Randomised phase II trial of pegylated liposomal doxorubicin (DOXIL/CAELYX) versus doxorubicin in the treatment of advanced or metastatic soft tissue sarcoma: a study by the EORTC Soft Tissue and Bone Sarcoma Group.

CAELYX/DOXIL, pegylated liposomal doxorubicin, has shown antitumour activity and reduced toxicity compared with standard doxorubicin in other tumour types. In this prospective randomised trial, 94 eligible patients with advanced soft-tissue sarcoma (STS) were treated, 50 with CAELYX (50 mg/m(2) by a 1 h intravenous (i.v.) infusion every 4 weeks) and 44 with doxorubicin (75 mg/m(2) by an i.v. bolus every 3 weeks). Histological subtypes were evenly matched, 33% were leiomyosarcoma (CAELYX: 18; doxorubicin: 13). Primary disease sites were well matched. CAELYX was significantly less myelosuppressive, only 3 (6%) patients had grade 3 and 4 neutropenia, versus 33 (77%) on doxorubicin; febrile neutropenia occurred in 7 (16%) patients given doxorubicin, but only 1 (2%) given CAELYX. 37 (86%) patients on doxorubicin had grade 2-3 alopecia, but only 3 (6%) on CAELYX, and the major toxicity with CAELYX was to the skin. Palmar-plantar erythrodysesthesia with CAELYX was grade 1: 4 (8%) patients, grade 2: 11 (22%) patients, grade 3: 9 (18%) patients and grade 4: 1 (2%) patient. Other non-haematological grade 3 and 4 toxicities were rare. Confirmed responses were observed with both agents: CAELYX: complete response (CR) 1 (uterine), partial response (PR) 4 (response rate (RR) 10%); and doxorubicin: CR 1, PR 3 (RR of 9%); with the best response being stable disease (NC) in 16 and 18 patients, respectively. The reason for the low response rate is unknown, but it may be due partly to a high proportion of gastrointestinal stromal tumours. In conclusion, CAELYX has equivalent activity to doxorubicin in STS with an improved toxicity profile and should be considered for further investigation in combination with other agents such as ifosfamide.

Granuloma formation in patients receiving BCG immunotherapy.

Eleven patients with acute myeloblastic leukaemia have received repeated intravenous injections of BCG containing 4-9 X 10(6) live organisms per millilitre. Non-caseating epithelioid granulomas, sometimes with giant-cell formation, have been demonstrated in eight bone marrow aspirates. Seven patients had granulomas in the liver, three in the lung, one in the spleen, one in lymph nodes, and one in a skin biopsy. One patient had a raised serum alkaline phosphatase, but none of the patients had any illness which could be related to the presence of granulomas. Granuloma formation appeared more extensive in four patients who were probably anergic before BCG treatment. Until the significance of this finding becomes clear great care should be taken when giving BCG by the intratumour of intravenous routes to potentially immunoincompetent patients.

The effect of non-ionic surfactant vesicle (niosome) entrapment on the absorption and distribution of methotrexate in mice.

Non-ionic surfactant vesicles (niosomes) prepared from a non-ionic surfactant, cholesterol and dicetyl phosphate and containing methotrexate (MTX) have been administered to mice. Given intravenously the niosomes prolong the levels of MTX in the blood, large amounts of the drug being taken up by the liver. There was also an increased uptake of MTX into the brain, perhaps due to an effect of the niosome components on the permeability of the blood brain barrier. Absorption of the drug from the gastrointestinal tract following oral ingestion, appeared to be increased at some doses; most of the entrapped MTX was taken up by the liver, but uptake of MTX into the brain was also increased. The metabolic profile of the drug is altered by the niosomes which appear to prevent the rapid formation of 7-hydroxy methotrexate.

The histologic evaluation of the implant interface with heterograft and allograft materials--an eight-month autopsy report, Part II.

This paper presents post mortem histologic specimens of the implant/osseous tissue interface from a patient who had had simultaneous bilateral maxillary sinus augmentation and root-form implant placement eight months prior. Two implants were observed: One implant was totally submerged in bone and graft material (2E), and other implant (3E) was devoid of bone at the apex. Microscopic examination revealed that a bony interface existed around implant 2E but that implant 3E had minimal bony interface. It is suggested that the minimal bony interface was the result of minor implant movement induced by variations in barometric pressure on the apex of implant 3E, and that eight months would not have been enough healing time prior to loading for this patient.

Suspension mechanism of subperiosteal implants in baboons.

It has been noted that overloading of an implant can lead to the premature loss of implants (Jones et al., 1979; Travis and Jones, 1986). An understanding of the mechanism by which subperiosteal implants support masticatory loads could lead to appropriate design changes for best utilization of this mechanism and thus increase the predictability of subperiosteal implants (James, 1983). This study attempts to analyze the suspension mechanism in implants recovered from a baboon after 10 years' use.

The management of bone loss in revision total knee replacement.

The management of bone loss in revision replacement of the knee remains a challenge despite an array of options available to the surgeon. Bone loss may occur as a result of the original disease, the design of the prosthesis, the mechanism of failure or technical error at initial surgery. The aim of revision surgery is to relieve pain and improve function while addressing the mechanism of failure in order to reconstruct a stable platform with transfer of load to the host bone. Methods of reconstruction include the use of cement, modular metal augmentation of prostheses, custom-made, tumour-type or hinged implants and bone grafting. The published results of the surgical techniques are summarised and a guide for the management of bone defects in revision surgery of the knee is presented.

The effect of niosomes and polysorbate 80 on the metabolism and excretion of methotrexate in the mouse.

The effect of non-ionic surfactant vesicle (niosome) encapsulation on the metabolism and urinary and faecal excretion of methotrexate (MTX) in mice has been studied following oral and intravenous administration, and compared with the effects of co-administration of free drug and polysorbate 80, which does not form vesicles. Niosome entrapment reduces the excretion of MTX into urine and bile whereas polysorbate 80 increases its excretion. Monitoring of the levels of MTX and its 7-hydroxy metabolite indicates that entrapped MTX is protected from rapid metabolism in vivo, particularly in niosomes but to a small degree in the micellar systems formed by polysorbate.

Survival of male patients with incontinentia pigmenti carrying a lethal mutation can be explained by somatic mosaicism or Klinefelter syndrome.

Incontinentia pigmenti (IP), or "Bloch-Sulzberger syndrome," is an X-linked dominant disorder characterized by abnormalities of skin, teeth, hair, and eyes; skewed X-inactivation; and recurrent miscarriages of male fetuses. IP results from mutations in the gene for NF-kappaB essential modulator (NEMO), with deletion of exons 4-10 of NEMO accounting for >80% of new mutations. Male fetuses inheriting this mutation and other "null" mutations of NEMO usually die in utero. Less deleterious mutations can result in survival of males subjects, but with ectodermal dysplasia and immunodeficiency. Male patients with skin, dental, and ocular abnormalities typical of those seen in female patients with IP (without immunodeficiency) are rare. We investigated four male patients with clinical hallmarks of IP. All four were found to carry the deletion normally associated with male lethality in utero. Survival in one patient is explained by a 47,XXY karyotype and skewed X inactivation. Three other patients possess a normal 46,XY karyotype. We demonstrate that these patients have both wild-type and deleted copies of the NEMO gene and are therefore mosaic for the common mutation. Therefore, the repeat-mediated rearrangement leading to the common deletion does not require meiotic division. Hypomorphic alleles, a 47,XXY karyotype, and somatic mosaicism therefore represent three mechanisms for survival of males carrying a NEMO mutation.