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A growing body of research examining neurological aspects of clinically “silent” cerebrovascular disease suggests that neurological signs indicative of generalised organic brain damage may occur in the absence of completed stroke.1 These soft signs include primitive reflexes (frontal release signs), representing an anatomical and functional deafferentation of cortical from subcortical structures. Primitive reflexes are known to occur in a wide variety of dementias, including Alzheimer's disease2 and vascular dementia.3 It is likely that the presence of undetected cerebrovascular disease accompanying peripheral vascular disease is underestimated, as peripheral vascular disease is known to be a risk factor for transient ischaemic attacks. A study assessing 373 older patients with peripheral vascular disease found that 72 of the 144 patients who had not experienced a transient ischaemic attack or stroke were found to have a degree of carotid stenosis of between 60% and 99%.4
In the present study, the prevalence of primitive reflexes was examined in older people with peripheral vascular disease and a non-vascular control group. Independent predictors of these reflexes were also examined in peripheral vascular disease. Both groups were drawn from the same geographical area. All were interviewed and examined outside hospital by myself. Interviewees were community residents from the catchment area of an inner city London teaching hospital.
Twenty five consecutive non-amputees on the waiting list for femoropopliteal bypass operation were compared with 25 postoperative patients who had undergone elective hip or knee replacement and a period of inpatient rehabilitation. All participants were aged 65 and over at the time of interview. Patients with peripheral vascular disease all had clinical and Doppler proved evidence of peripheral ischaemia. Controls were interviewed between 6 months and 1 year after their operation. Both groups had no history of stroke or transient ischaemic attack.
A more detailed description of instruments is provided elsewhere.1 All subjects were examined using a rating scale for the examination of frontal release signs (FRSS), with nine operationally defined items, each on a seven point semiquantitative scale. The nine reflexes were paratonia and palmomental, hand grasp, foot grasp, glabellar, rooting, snout, and visual/tactile sucking reflexes. Neuropsychological measures included the assessment of frontal lobe function (trailmaking tests A and B, behavioural dyscontrol scale, and the controlled word association test) and generalised cognitive impairment (CAMCOG). Depression was assessed using the Hamilton rating scale for depression, 15 item geriatric depression scale, and diagnostic criteria for DSM IV major depressive disorder. Family history of depression, wish to die, and suicidal ideation within the past year were also recorded, as were blood pressure and a checklist for chronic physical illness.
Total FRSS scores and scores on FRSS subscales were compared between groups using the Mann-Whitney U test for independent samples. In the peripheral vascular disease group, a correlation matrix for total FRSS score against DSMIV depression, CAMCOG score, behavioural dyscontrol scale score, verbal fluency score (total number of words beginning with F, A, and S) and trailmaking test times was examined using the Spearman correlation coefficient, controlling for age, sex, blood pressure, and chronic physical illness. Behavioural dyscontrol scale scores, trailmaking A/B test times, and verbal fluency scores were first converted into binary variables according to whether they were at/above or below the median value for the group. CAMCOG score was divided into subjects scoring 69 or above or less than 69. Those associations with a two tailed significance of 0.1 or less were then entered into a linear regression equation using the stepwise method.
Patients with peripheral vascular disease had a higher mean score on the frontal release signs scale than controls (5.8 (SD 4.6)v 1.7 (SD 1.9)) (Mann-WhitneyU=144.500, Z=−3.33, two tailedp=001), as well as on glabellar and rooting reflexes (table). Only one variable (trailmaking B test time) was entered into the equation; this accounted for 23% of the variance in FRSS score (B=4.6, 95% confidence interval (95% CI) (B) 1.3–8.0, p=0.01).
In peripheral vascular disease, there is limited information available concerning the intellectual and neurological sequelae of coexisting cerebrovascular disease. Phillips et alfound greater impairment in psychomotor speed and abstract reasoning in patients with peripheral vascular disease than age/sex matched controls, with less significant differences between the groups in verbal fluency, concentration, abstract thought, perception, and constructional skills.5 Another study by the same group found poorer performance in patients with peripheral vascular disease than controls on visual memory, trailmaking B test, and visuospatial skills. Patients with peripheral vascular disease were also equally impaired in these areas compared with a matched group of stroke patients.6
Small numbers of patients, which may also have obscured other significant findings between the two groups, limit the present study. However, there is some evidence that clinically relevant cerebrovascular disease may accompany peripheral vascular disease and that concomitant disruption of frontal/subcortical brain function may not present with hard neurological signs. As it is possible that silent brain infarction was present in patients with peripheral vascular disease, further studies incorporating brain imaging are required before there can be a clearer understanding of the relation between peripheral and central vascular pathology.
I thank Dr Robert Howard for supervision of this study and Professor Stephen Jackson and Mr Paul Baskerville for allowing me to interview patients under their care. The study was carried out as part of a University of London MD thesis.
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