Objective: Post-stroke cognitive impairment is common, but mechanisms and risk factors are poorly understood. Frailty may be an important risk factor for cognitive impairment after stroke. We investigated the association between pre-stroke frailty and acute post-stoke cognition. Methods: We studied consecutively admitted acute stroke patients in a single urban teaching hospital during three recruitment waves between May 2016 and December 2017. Cognition was assessed using the Mini-Montreal Cognitive Assessment (min=0; max=12). A Frailty Index was used to generate frailty scores for each patient (min=0; max=100). Clinical and demographic information were collected, including pre-stroke cognition, delirium, and stroke-severity. We conducted univariate and multiple-linear regression analyses with covariates forced in (covariates included were: age, sex, stroke severity, stroke-type, pre-stroke cognitive impairment, delirium, previous stroke/transient ischemic attack) to investigate the association between pre-stroke frailty and post-stroke cognition. Results: Complete data were available for 154 stroke patients. Mean age was 68 years (SD=11; range=32–97); 93 (60%) were male. Median mini-Montreal Cognitive Assessment score was 8 (IQR=4–12). Mean Frailty Index score was 18 (SD=11). Pre-stroke cognitive impairment was apparent in 13/154 (8%) patients. Pre-stroke frailty was significantly associated with lower post-stroke cognition (Standardized-Beta=−0.40; p<0.001) and this association was independent of covariates (Unstandardized-Beta=−0.05; p=0.005). Additional significant variables in the multiple regression model were age (Unstandardized-Beta=−0.05; p=0.002), delirium (Unstandardized-Beta=−2.81; p<0.001), pre-stroke cognitive impairment (Unstandardized-Beta=−2.28; p=0.001), and stroke-severity (Unstandardized-Beta=−0.20; p<0.001). Conclusions: Pre-stroke frailty may be a moderator of post-stroke cognition, independent of other well-established post-stroke cognitive impairment risk factors. (JINS, 2019, 25, 501–506)

‘Cerebral small vessel disease’ is common in older adults and is an important cause of morbidity, functional impairment and cognitive decline. Small vessel disease is a collective term used to describe a number of underlying pathological processes and neuroimaging findings, such as lacunar infarcts, white matter lesions and microhaemorrhages.

With readily available neuroimaging, diagnostic accuracy has improved; however, the management of small vessel disease and prevention of cognitive decline remains uncertain. Treatment of conventional vascular risk factors may be appropriate, but future research is required to provide definitive answers. We have conducted a comprehensive literature review of cerebral small vessel disease in older adults. This highlights the clinical sequelae and underlying pathological processes, whilst discussing novel diagnostic neuroimaging and therapeutic strategies.

Over recent years, small-vessel cerebrovascular disease has become increasingly recognized as an important contributor to cognitive and functional decline in elderly people.

Investigations of culling and particularly involuntary culling (“functional” longevity) have often used different criteria on herds of varying size in different regions and with divergent average milk outputs (Young, Waddington, Sales, Bradley and Spooner, 1983; Esslemont and Kossaibati, 1997; Forbes, Gayton and McGeogh, 1999; Whitaker Kelly and Smith, 2000; Figure 1). Thus the evidence of increasing or decreasing culling for any particular entity is uncertain.

Cerebral multi-infarct states (MIS) have a very variable clinical presentation (Table 1). Dementia is often stressed as the primary feature, however, many patients have relative preservation of cognitive abilities and personality, although their mobility may be severely affected, with a small-stepped shuffling gait, poor balance and frequent falls associated with bilateral (often asymmetrical) pyramidal tract signs. Urinary incontinence is common, dysphagia and dysarthria may occur, and some patients develop emotionalism and/or depression. In the later stages, patients may become immobile, requiring 24-hour nursing care.

Ischaemia of the deep subcortical white matter in the brain may be a common contributor to disability and cognitive impairment in old age. There is tremendous potential for preventing, or at least slowing, some of this damage. However, progress both in research and in clinical practice has been hampered by the confused nosology, with various diagnostic and descriptive labels applied to appearances on neuroimaging, to the underlying pathology and to clinical states (Table 1).

The clinical significance of low serum vitamin B12 levels in elderly people is controversial. We aimed to document the prevalence of a low serum vitamin B12 (<175pmol/l) in patients referred to a geriatric medical unit, and to determine whether haemopoiesis is commonly affected in elderly patients with low serum vitamin B12. We studied prospectively 472 consecutive referrals to a geriatric medical unit; fifty-six (13%) had a low serum vitamin B12 level, of whom nineteen (34%) of the fifty-six also had evidence of Fe deficiency (serum ferritin<45ng/ml). Low vitamin B12 was associated with a raised mean erythrocyte volume (MCV; mean 96·0 (SD 6·7) fl), compared with a control group (91·7 (SD 6·0) fl; P=0·001). However, only thirteen (23%) of the fifty-six patients with a low vitamin Blz had an MCV≥100 fl. Mean haemoglobin (Hb) levels were not significantly reduced in those with a low vitamin B12. In a subsequent study the haematological response to intramuscular hydroxocobalamin was examined in thirty-four patients with a low serum vitamin B12. Treatment resulted in a significant fall in MCV and rise in Hb; these effects could be detected both in those patients with an initially normal full blood count (change in MCV -1·2 (SD 1·2); Hb + 0·5 (SD 0·6); P<0·01) and in those with macrocytosis and/or anaemia (-9·1 (SD 11·8); + 0·8 (SD 1·2); P<0·05). A low serum vitamin B12 is common in geriatric medical patients. This is usually associated with an upset in erythropoiesis, although the abnormalities are often subtle and may not be apparent on inspection of the full blood count. Elderly patients with serum vitamin B12<175pmol/l should be assumed to have vitamin deficiency even if their full blood count is normal.