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Background: The working alliance between therapist and patient has been investigated frequently, but much less is known about the working alliance in specific patient groups in specific settings., Aim: To obtain insight into the characteristics of the working alliance in intensive inpatient psychotherapy involving patients with severe personality disorders, and to pay special attention to patient characteristics such as diagnosis and attachment., Method: At the end of the first phase of treatment we collected, on the basis of questionnaires, information about the working alliance and attachment of 60 patients with a severe personality disorders who had received inpatient psychotherapy., Results: Working alliances with therapist and team were found to be weaker than in outpatient populations; working alliances with the therapist proved to be stronger than working alliances with the treatment team. Cluster C patients developed a better working alliance with the treatment team than did cluster B patients, particularly in the domain of treatment goals. Patients in this study turned out to be attached more anxiously and 'avoidantly' than patients in general outpatient populations; no correlation was found between patients' attachment and the strength of the working alliance. However, when a distinction was made between patients with extreme scores and patients with average scores, results showed that the more anxiously patients felt attached, the higher were their scores for their working alliance with the treatment team., Conclusion: It is more difficult to establish a working alliance with patients who have a severe personality disorder than with patients suffering from a less severe personality disorder. Patients with a severe personality disorder seemed to show a higher degree of anxious attachment and to have a more critical attitude to the working alliance.

Neurofibromatosis type 1 (NF1) is an autosomal dominant disease characterised by café-au-lait spots, freckling in the axillary or inguinal region, dermal and plexiform neurofibromas and Lisch nodules. Complications are severe in one third of patients, and the clinical variability is pronounced, even within families. The NF1 gene has been localised to chromosome 17q11.2 and encodes the protein neurofibromin. The gene is proposed to be a tumour suppressor gene. Inactivation of neurofibromin leads to a disruption in cell growth regulation. Mutation analysis is possible but laborious, and therefore NF1 is generally a clinical diagnosis based on diagnostic criteria.