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Malignant diseases lead to adecline in physical performance in alarge number of patients. This includes areduction of the musculoskeletal system, restrictions in cardiovascular fitness and psychogenically influenced syndromes such as fatigue and asthenia. It is not yet clear to what extent physical training can counteract these limitations or undesirable side effects and how this training needs to be designed in the individual situation.

The aim of this article is to find out whether physical training can be performed in cancer patients, how this training should be designed and which physical disorders can be influenced favorably.

In this review, the currently available work on this topic was evaluated and classified with regard to its feasibility and effects in cancer patients.

Physical training can be performed without complications in most patients even under treatment for the underlying malignant disease. It has apositive effect on physical performance, cardiovascular function, the perception of one's own cancer and overall well-being. Ideally, physical training for cancer patients should include amixture of strength and endurance training. It should be carried out regularly and its intensity should be slowly increased. The type of physical activity should be adapted to the individual needs of the patient, take into account the particularities of the malignant disease and exclude any risk to the patient.

In summary, aphysical training program to accompany cancer therapy should be offered to virtually all patients with malignant disease.

In summary, a physical training program to accompany cancer therapy should be offered to virtually all patients with malignant disease.In recent decades, major advances in the treatment of malignant diseases have significantly improved long-term survival. However, this has increased the spectrum of side effects of these treatment methods, particularly for the cardiovascular system. Cardiotoxicity can be acute and chronic, including hypertension, heart failure, arrhythmias, acute myocardial infarction, venous thromboembolism, stroke, and valvular heart disease. While the occurrence of cardiotoxicity is known for many older cancer therapies, it needs to be largely evaluated for newer forms of therapy. Diagnosing possible cardiotoxic side effects is essential for optimal treatment, but remains a challenge. Troponin and the natriuretic peptides play an essential role as cardiac biomarkers in the diagnosis of conventional heart diseases. However, they also appear to play an important role in the detection of cardiotoxicity, as well as in the treatment of cardio-oncology patients. Elevated troponin or B-type natriuretic peptide (BNP)/N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels are associated with increased overall mortality and were associated with the development of heart failure in selected cohorts. Troponin can also be used to identify myocarditis associated with immune checkpoint inhibitor therapy. This overview summarizes the current knowledge about biomarkers for the detection of cardiotoxicity due to tumor therapy. Possible clinical recommendations for the detection of cardiotoxic effects using biomarkers are also outlined.This article provides an overview of current prevention and treatment options for typical cardiovascular side effects of oncological therapies as well as cardiovascular complications of malignant disease. Focus is put on the prevention and treatment of heart failure under potentially cardiotoxic cancer therapies. In addition, current options for the treatment of common venous thromboembolism in cancer patients will be discussed.Early identification of cardiogenic vertigo (CV) is necessary to prevent serious complications of cardiovascular diseases. learn more However, the literature is limited to case reports without detailed clinical features or diagnostic criteria. The aim of this study was to define characteristics of CV and propose diagnostic criteria. This study included patients with CV diagnosed at Pusan National University and Keimyung University Hospitals. Demographic, clinical, laboratory, and treatment data were analyzed. Of 72 patients with clinically suspicious CV, 27 were finally included. The age ranged from 63 to 88 years (75.1 ± 7.2 years). Recurrent vertigo occurred without syncopal attacks in 52% [95% CI, 32-71], while it preceded (37% [19-58]) or followed (11% [2-29]) syncope. The patients with recurrent isolated vertigo had suffered from symptoms from 15 days to 5 years until final diagnosis (median 122 days). The vertigo lasted only for a few seconds (93% [76-99]) or a few minutes (7% [1-24]). Fourteen patients presented with spinning vertigo, and one of them showed spontaneous downbeat nystagmus during the attack. Accompanying symptoms including chest discomfort, palpitation, headache, arm twitching, and lightheadedness were found in 70% [50-86]. Between patients with and without syncope, there was no difference in clinical parameters and results of cardiac function tests. The most common cardiac abnormality during the attacks of vertigo was bradyarrhythmia (89% [71-98]). Cardiovascular diseases can develop recurrent isolated vertigo without or preceding syncope. Onset age, duration of vertigo, accompanying symptoms, and underlying cardiac diseases can aid in differentiation from other vestibular disorders. Early identification of CV would reduce morbidity and mortality associated with cardiac syncope.

Clinicians have questioned whether any disorder involving seizures and neural antibodies should be called "(auto)immune epilepsy." The concept of "acute symptomatic seizures" may be more applicable in cases with antibodies against neural cell surface antigens. We aimed at determining the probability of achieving seizure-freedom, the use of anti-seizure medication (ASM), and immunotherapy in patients with either constellation. As a potential pathophysiological correlate, we analyzed antibody titer courses.

Retrospective cohort study of 39 patients with seizures and neural antibodies, follow-up ≥ 3years.

Patients had surface antibodies against the N-methyl-D-aspartate receptor (NMDAR, n = 6), leucine-rich glioma inactivated protein 1 (LGI1, n = 11), contactin-associated protein-2 (CASPR2, n = 8), or antibodies against the intracellular antigens glutamic acid decarboxylase 65kDa (GAD65, n = 13) or Ma2 (n = 1). Patients with surface antibodies reached first seizure-freedom (88% vs. 7%, P < 0.001) and terminal seizure-freedom (80% vs.