Cancer patients exhibit an elevated stroke risk (1)(2)(3)(4)(5). In a case-control study examining the epidemiology of cancer in stroke patients and their clinical course, we identified 72 active cancer and 72 control patients from the 1493 stroke admissions to Princess Margaret Hospital, Hong Kong in 2009. The prevalence of cancer among stroke patients was 4·8% (Table 1), and stroke was the first symptom of their cancer in nine patients. The proportions of ischemic stroke (IS) (79·2%) and haemorrhagic stroke (HS) (20·8%) in cancer group were comparable with noncancer group, and vascular risk factors (hypertension, diabetes mellitus, and hyperlipidemia) were less prevalent. The cancers we identified followed the local cancer epidemiology, with lung and colorectal cancer being the two most common types. In HS, both groups had similar proportions of deep parenchymal and lobar haemorrhages, but multiple haemorrhages were only seen in the three cancer patients. Except for the two acute promyelocytic leukaemia patients who bled, the distributions of other cancers among HS patients were similar to those with IS. Among IS, the proportions of patients in the four Oxfordshire-classified syndromes were comparable in the two groups. The etiology of IS was undetermined in half of the cancer patients compared with only 28·3% of the noncancer patients. There was no difference in the severity of neurological impairment [National Institutes of Health Stroke Scale (NIHSS) 10·7 (cancer) and 11·8 (noncancer)], but cancer patients had a higher hospital-acquired pneumonia (11·1% vs. 4·2%) and hospital mortality (31·9% vs. 12·5%) rates. At three-months poststroke, cancer remained the most important independent predictor of mortality [odds ratio 12·4 (3·0-51·4)], and more cancer patients were disabled. We concluded that stroke and cancer, when coinciding, carried a high morbidity and mortality rate. Often, the occurrence of stroke in cancer patients could not be sufficiently explained by conventional etiology, implicating the role of cancer-related factors in their stroke pathophysiology.

m.3243A>G MT-TL1 mutation is the most common mitochondrial DNA mutation that results in a wide spectrum of disorders in a maternally inherited pedigree. In adult patients, many present with symptoms and signs indistinguishable from acquired diseases and the correct diagnosis is often delayed after many years. Nevertheless, clues suggesting m.3243A>G usually exist early in the disease course but are only realized late. These hints, from the evolution of symptoms and signs, family background, investigation results, or a combination of these, enable the physician to make the correct diagnosis early, which is important for appropriate treatment and better patient care. As with other inheritable diseases, genetic counselling should be offered regarding the disease management, inheritance mode, recurrence risk, usefulness and limitations of genetic testing and reproductive options.

SummaryA 42‐year‐old patient with epilepsy was admitted to the hospital for fever and generalized skin rash. He has known allergy to phenytoin. Valproate was started in 2012, but failed to control his seizure despite gradual increase in dosage. Phenobarbitone was added 16 days before admission and was stopped on admission. He was treated with beta‐lactam antibiotics. The rash subsided gradually after the cessation of phenobarbitone. Lacosamide was subsequently added for seizure control. Unfortunately, he developed drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome soon after introduction of lacosamide that required the use of systemic steroid for acute hepatitis. A cross‐reactivity with lacosamide was suspected in view of the rapid onset of DRESS syndrome after the initial rash resolution and soon after the introduction of lacosamide. We postulated that the rapid onset of DRESS syndrome may be related to the aromatic ring that is in common among phenytoin, phenobarbitone, and lacosamide.