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Contains fulltext : 167803.pdf (Publisher’s version ) (Open Access) Background High fear of cancer recurrence (FCR) is an understudied topic in prostate cancer (PCa) survivors. This study aimed to detect the prevalence, consequences and characteristics associated with high FCR in PCa survivors. Material and methods This cross-sectional study included patients diagnosed with localized PCa and treated with curative radical prostatectomy between 1992 and 2012. We administered the Cancer Worry Scale (CWS) to assess FCR severity (primary outcome measure). Secondary outcomes included distress, quality of life (QOL), post-traumatic symptoms, and multidimensional aspects of FCR. chi(2)-tests, t-tests and Pearson's correlations examined the relationship between FCR and medical/demographic characteristics. MANOVA analyses and chi2-tests identified differences between PCa survivors with high and low FCR. Results Two hundred eighty-three PCa survivors (median age of 70.0 years) completed the questionnaires a median time of 7.1 years after surgery. About a third (36%) of all PCa survivors experienced high FCR. High FCR was associated with lower QOL, more physical problems, higher distress and more post-traumatic stress symptoms. PCa survivors with high FCR reported disease-related triggers (especially medical examinations), felt helpless and experienced problems in social relationships. High FCR was associated with a younger age and having received adjuvant radiotherapy. Conclusions Results illustrate that FCR is a significant problem in PCa survivors. Younger men and those treated with adjuvant radiotherapy are especially at risk. Those with high FCR experience worse QOL and higher symptom burden. Health care providers should pay specific attention to this problem and provide appropriate psychosocial care when needed.

Experimental research during the past decade has greatly increased our understanding of the pathophysiology of traumatic brain injury (TBI) and allowed us to develop neuroprotective pharmacological therapies. Encouraging results of experimental pharmacological interventions, however, have not been translated into successful clinical trials, to date. Traumatic brain injury is now believed to be a progressive degenerative disease characterized by cell loss. The limited capacity for self-repair of the brain suggests that functional recovery following TBI is likely to require cellular transplantation of exogenous cells to replace those lost to trauma. Recent advances in central nervous system transplantation techniques involve technical and experimental refinements and the analysis of the feasibility and efficacy of transplantation of a range of stem cells, progenitor cells and postmitotic cells. Cellular transplantation has begun to be evaluated in several models of experimental TBI, with promising results. The following is a compendium of these new and exciting studies, including a critical discussion of the rationale and caveats associated with cellular transplantation techniques in experimental TBI research. Further refinements in future research are likely to improve results from transplantation-based treatments for TBI.

Background: Cerebral ischemia is considered a key factor in the development of secondary damage after Traumatic Brain Injury (TBI). Studies on Cerebral Blood Flow (CBF) have documented decreased flow in over 50% of patients with TBI, studied in the acute phase. Transcranial Doppler (TCD) sonography is a non-invasive technique, permitting frequent or continuous measurements of blood flow velocity in the basal cerebral arteries. Objectives: To investigate the potential of TCD to detect decreased blood flow velocity in the early phase after TBI; To investigate whether flow velocity differs between hemispheres in patients with focal lesions versus those with more diffuse injuries; To investigate if decreased blood flow velocity is indicative of cerebral ischemia, as evidenced by measurements of brain tissue pO2. Methods: TCD examinations were performed in 57 patients with severe TBI (GCS≤8) daily over a period of 10 days, with particular attention focused on the first 72 hours, during which period examinations were performed more frequently. A low flow velocity state (LFVS) was defined as a flow velocity≤35 cm/sec in one or both MCA's within 72 hours after trauma. PbrO2 was measured in 33 patients with an intraparenchymal Clark type electrode (Licox). Patients were differentiated into those with primarily unilateral pathology on the admission CT scan versus those with primarily more diffuse or bilateral pathology. Outcome was evaluated at six months after injury, according to the Glasgow Outcome Scale (GOS). Results: A low flow velocity state was observed in 63% of patients studied. Decreased flow was most pronounced during the first eight hours after injury and was accompanied by high pulsatility indices, especially at the side of the lesion. Flow velocity increased significantly after this time period. Initial Vmca values had a strong correlation with ipsilateral measured PbrO2 values (R=0.73). The occurrence of a LFVS was associated with poorer outcome (odds ratio 3.9). Conclusions: TCD studies show reduction of cerebral blood flow velocity in the acute phase after traumatic brain injury. Decreased flow velocity is most pronounced ipsilateral to focal pathology. A low flow velocity state is probably due to high peripheral resistance, and is indicative of ischemia, as demonstrated by the association with decreased PbrO2. A low flow velocity state is of prognostic value and identifies patients at increased risk for ischemia. Early TCD studies are recommended in TBI.

The intensity of experimental and clinical research to identify a neuroprotective drug for the treatment of traumatic brain injury is motivated by the devastating morbidity and mortality of this condition. Encouraging experimental work has led so far to disappointing clinical trials and the identification of new potential therapeutic targets is critically dependent on a better understanding of the chronic pathophysiology triggered by the initial insult. Future advances in the pharmacological treatment of traumatic brain injury are likely to include the evaluation of sequentially timed therapies combining multiple and targeted agents, and manipulation of the newly discovered neurogenic potential of the adult brain together with the refinement of traditional interventions to block specific cytotoxic cascades.