Carbamazepine-responsive paroxysmal nausea and vomiting in a patient with meningeal carcinomatosis

In neurology, paroxysmal syndromes are well-known, eg, as manifestations of multiple sclerosis. We report a patient with meningeal carcinomatosis, who presented with therapyrefractory nausea and vomiting. The clinical suspicion of a paroxysmal syndrome prompted a trial of carbamazepine, which resulted in complete cessation of the symptoms. In cancer patients with central nervous system (CNS) involvement and therapy-refractory symptoms with sudden onset, carbamazepine treatment should be considered

Choosing wisely at the end of life: the crucial role of medical indication.

At the end of life, several treatments are administered routinely that lack medical indication and may cause significant harm to patients. Examples include artificial hydration and oxygen therapy in the dying phase, as well as enteral nutrition in advanced dementia. Medical indication is defined as the appropriateness of a therapeutic or diagnostic measure in the patient's concrete clinical situation, in light of the best available evidence. The decision about the absence or presence of a medical indication is a core competence of physicians. They have no obligation to perform or even mention measures that are not indicated. The decision about medical indication is a clinical compound decision, composed of both a factual, evidence-based judgement and a value judgement, which should always be patient-centred. Acknowledging the crucial role of medical indication in clinical decision making in medicine generally and at the end of life specifically opens up ways of enhancing patient-physician communication by clarifying roles, responsibilities and competencies. This may facilitate preventing overtreatment, improving patient wellbeing, and realising the patients' goals of care

Involvement of ras p2I in Neurotrophin-induced Response of Sensory, but Not Sympathetic Neurons

Little is known about the signal transduction mechanisms involved in the response to neurotrophins and other neurotrophic factors in neurons, beyond the activation of the tyrosine kinase activity of the neurotrophin receptors belonging to the trk family. We have previously shown that the introduction of the oncogene product ras p21 into the cytoplasm of chick embryonic neurons can reproduce the survival and neurite-outgrowth promoting effects of the neurotrophins nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), and of ciliary neurotrophic factor (CNTF). To assess the potential signal- transducing role of endogenous ras p21, we introduced function-blocking anti-ras antibodies or their Fab fragments into cultured chick embryonic neurons. The BDNF-induced neurite outgrowth in E12 nodose ganglion neurons was reduced to below control levels, and the NGF- induced survival of E9 dorsal root ganglion (DRG) neurons was inhibited in a specific and dose-dependent fashion. Both effects could be reversed by saturating the epitope-binding sites with biologically inactive ras p21 before microinjection. Surprisingly, ras p21 did not promote the survival of NGF-dependent E12 chick sympathetic neurons, and the NGF-induced survival in these cells was not inhibited by the Fab-fragments. The survival effect of CNTF on ras-responsive ciliary neurons could not be blocked by anti-ras Fab fragments. These results indicate an involvement of ras p21 in the signal transduction of neurotrophic factors in sensory, but not sympathetic or ciliary neurons, pointing to the existence of different signaling pathways not only in CNTF-responsive, but also in neurotrophin-responsive neuronal populations