Parents’ Paradoxicality and Adolescents’ Self-Engendering Fantasy

In this paper, I discuss psychotherapy sessions that I undertook with a female adolescent patient. As a psychoanalyst specialized in couple and family psychoanalysis, I was primed to focus on her representation of her parents’ and family's dysfunctional dynamics. She felt locked in perverse narcissistic relationships and vampirized by her internal ‘objects’, her attachments causing her to experience libidinal haemorrhage. Her links to her internal ‘objects’ seemed like chains that impeded her individuation. In my analysis, I build on Racamier's concepts of pregenital ‘incestual’ functioning, primal mourning, paradoxicality, and self-engendering fantasy. However, while Racamier noted that the self-engendering fantasy is part of an ‘incestual’ picture, which serves the death drive, I interpret this fantasy as a constructive effort to achieve psychic reorganization; it helped my patient disengage from her internalized incestual family dynamics and the violence of an incestuous primal scene. Through this fantasy, she seemed to end the narcissistic depletion that threatened to overwhelm the boundaries of her weak ego. The self-engendering fantasy serves the life drive, albeit paradoxically, using this logic. With this thesis in mind, I accompanied my patient in her process of separation and individuation and interpreted transference and countertransference dynamics.     

‘That’s okay for me.’ ‘But it’s not okay for me.’ Tension and balance between patient’s will and surgeon’s motivation

This Reflective Practice describes the potential tension between the patient's will and surgeon's motivation. I, as the care given surgeon, learned a couple of intensive lessons trough the presented case, which I would like to share with colleagues to let them also reflect in similar situations about patient's will and their ambition to help and heal.The patient's will is inviolable, even if physicians sometimes wish differently. We have to respect patients’ wishes and support them in their decisions.Do not be ashamed to admit that you suffer in your role as physician, for example if you might lose a patient to complications. Regular conversations with the caregiver team are essential.Talking to others, or writing a reflection piece such as this, might be one of my coping strategies. We don’t know everything: medicine is sometimes unpredictable, even for experienced physicians.     

Modifying one’s hand’s trajectory when a moving target’s orientation changes

The path that the hand takes to intercept an elongated moving target depends on the target’s orientation. How quickly do people respond to changes in the moving target’s orientation? In the present study, participants were asked to intercept moving targets that sometimes abruptly changed orientation shortly after they started moving. It took the participants slightly more than 150 ms to adjust their hands’ paths to a change in target orientation. This is about 50 ms longer than it took them to respond to a 5-mm jump in the moving target’s position. It is only slightly shorter than it took them to initiate the movement. We propose that responses to changes in visually perceived orientation are not exceptionally fast, because there is no relationship between target orientation and direction of hand movement that is sufficiently general in everyday life for one to risk making an inappropriate response in order to respond faster.     

Felty’s Syndrome

Felty's syndrome is a complication of rheumatoid arthritis whereby patients develop neutropenia of varying severity. Although the main clinical concern is the development of serious infections, often patients remain asymptomatic or continue with clinical problems related to the rheumatoid arthritis and not to the neutropenia. There is now considerable clinical experience with the use of the recombinant human haemopoietic growth factors granulocyte and granulocyte-macrophage colony-stimulating factors (G-CSF and GM-CSF) in the treatment of patients with Felty's syndrome. The only indication for the use of either growth factor for Felty's syndrome is the onset of infectious complications, which may be recurrent and serious. In general, when this occurs, the neutropenia is severe (<10(8) cells/L). The mechanism(s) underlying development of the neutropenia in Felty's syndrome is similar to that in other forms of immune-mediated neutropenia, and in general is associated with a terminal defect in neutrophil maturation. It is likely that the maturational defect is a consequence of ;immune based' inhibition, although we lack detailed understanding of this inhibitory process. Growth factor therapy does not relieve the defect in terminal maturation, but in general may induce a significant improvement in the peripheral white cell count. Instances where growth factor therapy does not work appear to be due to an inability to overcome the maturational defect. Thus, the level of granulopoietic inhibition mediated by the rheumatoid process varies in severity among patients. To date, treatment options for Felty's syndrome have included disease-modifying antirheumatic drugs, corticosteroids and splenectomy. The addition of growth factor therapy is a welcome addition to these less than optimal treatment options. However, all of the above therapies fail on occasion. Moreover, the dosage and frequency of growth factors must be titrated to keep the white blood cell count <5 x 10(9) cells/L, since overshoot may result in complications, the most common being exacerbation of the rheumatoid arthritis. Another mechanism by which these drugs may exacerbate rheumatoid arthritis is through activation of neutrophils. The addition of disease-modifying drugs may relieve the maturational defect, improve the peripheral white cell count and minimise disease exacerbation by limiting neutrophil exposure to the administered haemopoietic growth factor. However, long term monotherapy with G-CSF has been successfully employed without requiring disease-modifying therapy.     

Non-Hodgkin’s Lymphoma

Non-Hodgkin's lymphomas (NHL) represent a heterogenous group of diseases including low, intermediate and high grade histological subtypes. Most entities are sensitive to chemotherapy and radiotherapy. However, most relapsed patients are incurable with conventional treatment. The major reason for unsatisfactory long-term results in NHL is tumour cells that persist after standard treatment. New sensitive techniques have been developed to detect occult lymphoma cells. These cells might be eradicated by new immunotherapeutic agents with different modes of action, such as cytokines or antibody-based agents. In NHL, most experience has been accumulated with interferon-alpha, which seems to be effective against minimal residual disease (MRD). The experience with interleukin-2 and interleukin-3 is less convincing. Monoclonal antibodies have been used in their native form, or conjugated with radioisotopes or toxins to selectively destroy lymphoma cells. Such immunotoxins and radioisotope-coupled antibodies have shown promising results in early clinical trials, and are now being evaluated in patients with smaller tumour burdens.     

Acrel’s ganglion

No data exists in the extant literature regarding the distal swelling of the posterior interosseous nerve (Acrel’s ganglion). To further elucidate this ganglion, ten adult cadavers (20 sides) underwent dissection and histological examination of this structure. No inflammatory response was noted in these histologically normal peripheral nerve structures. No neuronal cell bodies were identified. Although the etiology of such swellings is unclear, the term “ganglia” should not be applied to these enlargements of the distal posterior interosseous nerve.