Recent advances in novel cancer therapies have resulted in a growing number of survivors of cancer. Nevertheless, it is increasingly clear from the results of a childhood cancer survivor study that the therapies that cured theirprimary malignancies place them at increased, life-long risk for cardiovascular complications. In this manuscript,we briefly reviewed the essence of existing clinical guidelines and related studies on cardiomyopathy surveillancefor survivors of childhood cancer, including the topics of 1) the timeline of evolution on Cardio-Oncology, 2) abackground of needs on Cardio-Oncology, 3) a concept of cancer therapy-related cardiac dysfunction (CTRCD),4) diagnostic tools for CTRCD, 5) recent key studies on Cardio-Oncology, and 6) a new clinical trial of cardiomyopathy surveillance for survivors of childhood cancer, underscoring the clinical importance of this new interdisciplinary field.

Spinal muscular atrophy (SMA) is a lower motor neuron disease that causes muscle atrophy and progressivemuscle weakness due to degeneration and loss of spinal cord anterior horn cells. SMA was first described in 1891,and the survival motor neuron1 gene was identified as the cause in 1995. The prevalence of SMA is 1–2/100,000,and the carrier frequency is 1/40–60.The onset of the disease ranges from prenatal to adulthood and is classified into 5 groups (types 0–IV) based onage of disease onset and archived motor functions. Type I onset in infancy is characterized by decreased muscletone, loss of tendon reflexes, and decreased voluntary movements of the proximal limbs and trunk from approximately 1 to 3 months of age. Sitting posture is not acquired throughout life. As muscle weakness progresses,respiratory function declines, and ventilatory management is introduced at an average age of 6 months. Withoutventilatory management, 90% of children die by the age of 2 years due to respiratory infections. There is no treatment other than symptomatic treatment, such as tracheostomy and ventilatory management at home, and it hasbeen considered one of the most serious diseases in the field of pediatric neurology.Recently, international clinical trials have resulted in the development of nusinersen, a nucleic acid drug, onasemnogene abeparvovec, a gene therapy drug, and risdiplam, a small molecule drug. These new therapies havedramatically changed SMA practice. They have halted the progression of symptoms and have the potential to improve not only life expectancy but also neurological prognosis. It is also now possible to prevent the onset of thedisease itself by administering the drug before onset. It is becoming more important to diagnose the disease at anearlier stage and to detect and treat the disease before it develops through newborn mass screening.

A 73-year-old man with putaminal hemorrhage was diagnosed with obstructive sleep apnea syndrome two yearsafter he suffered putaminal hemorrhage, which was well treated by continuous positive airway pressure (CPAP).Although his apnea hypopnea index (AHI), indicating the number of apnea or hypopnea episodes divided by thenumber of hours of sleep, had been < 5 for several years, it had gradually increased, and he complained aboutdaytime sleepiness despite adjustments of CPAP levels. When his AHI reached 19, chest X-ray showed cardiomegaly. Although polysomnography was not possible due to his condition after apoplexy, we assumed that theapnea would change from obstructive to central according to his age, pulmonary congestion, and/or brain damagefollowing apoplexy. We switched from CPAP to adaptive servo-ventilation, which can control not only obstructive but also central sleep apnea. The AHI again became well controlled (AHI 3.8), and his daytime sleepinessimproved. From this case, we learned that the characteristics of apnea might change and could be again controlledwith symptoms by careful medical observation and treatment.

We report a case of enforced superficial temporal artery-middle cerebral artery (STA-MCA) bypass for ICA stenosis with a contralateral ICA occlusion associated with crescendo transient ischemic attack (TIA). A 52-year-oldman suffered from weakness of right lower limb. MRI showed cerebral infarction of the bilateral watershed areaat frontal lobe and right ICA occlusion. DSA and perfusion-weighted imaging using arterial spin labeling revealedright ICA occlusion, left ICA terminal stenosis, and hypoperfusion in the left side. Medical treatment with dualanti-platelet therapy and Edaravone was performed, however, lower limb motor weakness had been a frequentoccurrence. After STA-MCA bypass, the symptom disappeared. STA-MCA bypass for crescendo TIA due to intracranial artery stenosis with a contralateral internal carotid artery occlusion was effective.

We experienced a case of rhabdomyosarcoma originating in the mastoid and infiltrating the intracranial posterior fossa in an adolescent patient. The first sign was hearing impairment, followed by posterior cervical pain andabducens nerve palsy. Preoperatively, we diagnosed an epidural abscess in the posterior fossa caused by mastoiditis with osseous destruction in the petromastoid portion of the temporal bone. Rhabdomyosarcoma originatingin the mastoid may be difficult to distinguish from infectious mastoiditis due to similar imaging features. Neuroimaging findings of infectious mastoiditis may indicate rhabdomyosarcoma of the mastoid, especially in patientswith symptoms atypical of infectious mastoiditis, such as cranial nerve palsy.

We herein show a case of symptomatic common carotid artery occlusion that underwent bonnet bypass (contralateral superficial temporal artery (STA) -saphenous vein (SV) - cortical segment (M4) of the middle cerebralartery (MCA) bypass) using an SV graft. STA-MCA bypass surgery has been established for the prevention ofsecondary cerebral infarction of symptomatic internal carotid artery occlusion. On the other hand, there has beenno standard surgical treatment for symptomatic common carotid artery occlusion. It has been reported that bonnetbypass using donor grafts is effective for these pathological conditions. We herein performed bonnet bypass surgery using an SV graft as a donor graft. The vascular reserve was improved in quantitative single photon emissioncomputed tomography, the bypass patency was also spared, and the postoperative course was uneventful.