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Biomedical subjects

J M Bamford

Publications and source records attributed to J M Bamford.

At least 19 recordsLinked to original sources

Change in stroke incidence, mortality, case-fatality, severity, and risk factors in Oxfordshire, UK from 1981 to 2004 (Oxford Vascular Study).

BACKGROUND: The incidence of stroke is predicted to rise because of the rapidly ageing population. However, over the past two decades, findings of randomised trials have identified several interventions that are effective in prevention of stroke. Reliable data on time-trends in stroke incidence, major risk factors, and use of preventive treatments in an ageing population are required to ascertain whether implementation of preventive strategies can offset the predicted rise in stroke incidence. We aimed to obtain these data. METHODS: We ascertained changes in incidence of transient ischaemic attack and stroke, risk factors, and premorbid use of preventive treatments from 1981-84 (Oxford Community Stroke Project; OCSP) to 2002-04 (Oxford Vascular Study; OXVASC). FINDINGS: Of 476 patients with transient ischaemic attacks or strokes in OXVASC, 262 strokes and 93 transient ischaemic attacks were incident events. Despite more complete case-ascertainment than in OCSP, age-adjusted and sex-adjusted incidence of first-ever stroke fell by 29% (relative incidence 0.71, 95% CI 0.61-0.83, p=0.0002). Incidence declined by more than 50% for primary intracerebral haemorrhage (0.47, 0.27-0.83, p=0.01) but was unchanged for subarachnoid haemorrhage (0.83, 0.44-1.57, p=0.57). Thus, although 28% more incident strokes (366 vs 286) were expected in OXVASC due to demographic change alone (33% increase in those aged 75 or older), the observed number fell (262 vs 286). Major reductions were recorded in mortality rates for incident stroke (0.63, 0.44-0.90, p=0.02) and in incidence of disabling or fatal stroke (0.60, 0.50-0.73, p<0.0001), but no change was seen in case-fatality due to incident stroke (17.2% vs 17.8%; age and sex adjusted relative risk 0.85, 95% CI 0.57-1.28, p=0.45). Comparison of premorbid risk factors revealed substantial reductions in the proportion of smokers, mean total cholesterol, and mean systolic and diastolic blood pressures and major increases in premorbid treatment with antiplatelet, lipid-lowering, and blood pressure lowering drugs (all p<0.0001). INTERPRETATION: The age-specific incidence of major stroke in Oxfordshire has fallen by 40% over the past 20 years in association with increased use of preventive treatments and major reductions in premorbid risk factors.

Adult↗

Stroke after internal jugular venous cannulation.

OBJECTIVE: To alert clinicians to the stroke risk associated with carotid artery injury secondary to attempted internal jugular venous (IJV) cannulation. METHODS: Case reports and review of the literature. RESULTS: Four patients developed a stroke following carotid artery (CA) injury during attempted IJV cannulation using the landmark technique. In all cases the arterial puncture was detected immediately and firm pressure applied for several minutes. In three cases there was evidence of intimal injury and thrombus formation. Two strokes were delayed by more than 24 h. One patient died. A review of studies describing 4487 IJV line insertion attempts using the landmark technique reveals that 5.9% of attempts are associated with CA injury. CONCLUSION: Cannulation of the IJV using visible and palpable landmarks is associated with a risk of stroke. Arterial injury and stroke should be mentioned when consent is obtained for cannulation. Consideration should be given to a reduction of the arterial injury risk by using ultrasound guidance during line insertion.

Adult↗

Angiotensin converting enzyme insertion/deletion genotype is associated with leukoaraiosis in lacunar syndromes.

OBJECTIVES: Pathological and clinical data suggest that patients presenting with ischaemic lacunar syndromes may be a heterogenous group. Those with isolated lacunar infarction are thought to have localised atherosclerosis whereas in those with coexisting leukoaraiois a distinct diffuse small vessel vasculopathy may be the predominant underlying pathology. The ACE insertion/deletion (I/D) polymorphism is an important candidate gene in ischaemic cerebrovascular disease but, where lacunar stroke specifically has been examined, there have been discrepant reports concerning a possible association. It was hypothesised that the influence of the ACE gene may be different among the two subgroups of ischaemic lacunar stroke reflecting the heterogeneity of the small vessel disease phenotype. METHODS: Eighty four consecutive patients presenting with classic lacunar syndromes were studied. All had acute cranial CT to exclude primary intracerebral haemorrhage and these were subsequently assessed for the presence and extent of leukoaraiosis. All patients were genotyped for the ACE insertion/deletion polymorphism. RESULTS: There was a significant difference in the distribution of ACE genotype with the DD genotype occurring more often in patients with leukoaraiosis and the II and ID genotypes occurring more often among those in whom this was absent (chi(2)=9.06, p=0.01). In a logistic regression model the ACE DD genotype remained as an independent predictor for the presence of leukoaraiosis (p=0.02) in patients presenting with classic lacunar syndromes. CONCLUSION: This study supports the hypothesis that there may be different types of small vessel disease in patients with classic lacunar syndromes and that the influence of the ACE DD genotype may be relevant in mediating the diffuse form of vessel injury.

Aged↗

Prevalence of permanent childhood hearing impairment in the United Kingdom and implications for universal neonatal hearing screening: questionnaire based ascertainment study.

OBJECTIVE: To estimate the prevalence of confirmed permanent childhood hearing impairment and its profile across age and degree of impairment in the United Kingdom. DESIGN: Retrospective total ascertainment through sources in the health and education sectors by postal questionnaire. SETTING: Hospital based otology and audiology departments, community health clinics, education services for hearing impaired children. PARTICIPANTS: Children born from 1980 to 1995, resident in United Kingdom in 1998, with severe permanent childhood hearing impairment (hearing level in the better ear >40 dB averaged over 0.5, 1, 2, and 4 kHz). MAIN OUTCOME MEASURES: Numbers of cases with date of birth and severity of impairment converted to prevalences for each annual birth cohort (cases/1000 live births) and adjusted for under ascertainment. RESULTS: 26 000 notifications ascertained 17 160 individual children. Prevalence rose from 0.91 (95% confidence interval 0.85 to 0.98) for 3 year olds to 1.65 (1.62 to 1.68) for children aged 9-16 years. Adjustment for under ascertainment increased estimates to 1.07 (1.03 to 1.12) and 2.05 (2.02 to 2.08). Comparison with previous studies showed that prevalence increases with age, rather than declining with year of birth. CONCLUSIONS: Prevalence of confirmed permanent childhood hearing impairment increases until the age of 9 years to a level higher than previously estimated. Relative to current yields of universal neonatal hearing screening in the United Kingdom, which are close to 1/1000 live births, 50-90% more children are diagnosed with permanent childhood hearing impairment by the age of 9 years. Paediatric audiology services must have the capacity to achieve early identification and confirmation of these additional cases.

Adolescent↗

Universal neonatal hearing screening: past, present, and future.

After a brief review of the history of newborn hearing screening including the Downs behavioral testing procedure, the Crib-o-gram and similar devices, and the use of auropalpebral reflex and otoacoustic emissions, there is a discussion of key issues that need to be resolved before universal hearing screening is introduced. Included are questions regarding the target population(s) of screening programs, well baby versus NICU screening, dealing with false-positives and the effects on parent-child relationships, and finally, the availability of resources for screening and follow-up. The results of a recent study in the United Kingdom that assessed the current state of audiology services and found there is a difference between existing standards and what is actually being done in practice, are presented and considered in terms of current trends in the United States to move ahead with universal screening without a solid database of information regarding the preparedness of clinical centers to deal with the need for services that will result from the initiation of universal programs. Caution is urged.

Follow-Up Studies↗

Primary diffuse leptomeningeal gliomatosis predominantly affecting the spinal cord: case report and review of the literature.

Primary leptomeningeal gliomatosis is a rare, fatal neoplastic syndrome. A 71 year old man is reported on, who after a 2 month history of back stiffness, epigastric pain, and weight loss developed visual blurring. Cranial CT and MRI studies showed no leptomeningeal enhancement. Examination of CSF 10 weeks premortem showed an increase in protein and decrease in glucose but no malignant cells. He became increasingly confused and repeated CSF examination showed inflammation and a few suspicious cells but no definitive evidence of neoplasia. He died 7 months after onset of his initial symptoms. At postmortem meningeal whitening was seen at the base of the brain and over the spinal cord. Histology disclosed diffuse leptomeningeal gliomatosis (GFAP positive, cytokeratin negative) over the brain, optic nerves, and spinal cord without parenchymal involvement. No tumour was found in internal organs. The diagnosis of primary leptomeningeal gliomatosis was not evident after cranial CT and MRI and CSF examination premortem. Suspected cases need MRI scanning of the entire neuraxis and meningeal biopsy.

Aged↗

Quantifying associated reactions in the paretic arm in stroke and their relationship to spasticity.

OBJECTIVES: (1) To present a measurement protocol for assessing associated reactions (AR) in the paretic arm and (2) to use it to investigate the pattern of AR and its association with spasticity. SETTING: Inpatient rehabilitation unit. DESIGN: Associated reactions in 49 adults with stroke were measured in terms of force generated, electrical muscle activity and wrist movement in the paretic arm using hand dynamometry, surface electromyography and electrogoniometry respectively. Simultaneous recording of the effort used to elicit the associated reaction was made using a second hand dynamometer. The magnitude and persistence of AR was compared with the clinical assessment of spasticity (using the modified Ashworth Scale, MAS). RESULTS: There was poor correlation between peak AR and MAS, suggesting that AR are not confined to patients with severe spasticity. Co-activation of forearm flexors and extensors was evident during the AR. AR fluctuated during a single period of effort in some patients. Only 12 out of 31 patients who maintained uniform effort over the measurement period produced a uniform AR. AR often persisted for some time after effort had ceased. Eight were classified as minimal (median AR 0.23 N), 25 as mild (median AR 2.7 N), 11 as moderate (median AR 6.4 N) and 3 as severe (median AR 11.0 N). AR tended to persist in patients with higher MAS although this result was not statistically significant. CONCLUSION: The magnitude, profile and persistence of AR varied considerably between individuals. Associated reactions were present in people with minimal spasticity. As this technique allows the magnitude of AR to be quantified in relation to effort it has the potential to be a useful outcome measure in clinical trials evaluating the treatments (e.g. physiotherapy) directed at reducing associated reactions.

Activities of Daily Living↗

Apolipoprotein E polymorphism in cerebrovascular disease.

OBJECTIVES: The aim of this study was to investigate the relationship between the apo E genotype with acute cerebral infarction and primary intracerebral haemorrhage and to examine the relationship of the apo E genotype with mortality following acute stroke. MATERIALS AND METHODS: We studied 592 cases of acute stroke and 289 healthy control subjects clinically free of cerebrovascular disease. Pathological type of stroke was determined by cranial computed tomography and the subtype of cerebral infarction classified according to the Oxfordshire Community Stroke Project Classification (OCSP). Apo E genotype was determined using polymerase chain reaction. RESULTS: There was no difference in apo E genotype frequency between cases and controls (chi2 = 3.58, 5 d.f., P = 0.60). Apo E genotypes were not related to the pathological type of stroke (cerebral infarction, CI, n = 532 and primary intracranial haemorrhage, PICH, n = 60, (chi2 =3.738, 4 d.f., P=0.44) nor with the Oxfordshire Community Stroke Project Classification subtypes of cerebral infarction, lacunar infarction, LACI (n = 169), total anterior circulation infarction, TACI (n = 117), partial anterior circulation infarction, PACI (n = 173), posterior circulation infarction, POCS (n = 54) and including those cerebral infarcts which could not be classified (n= 19), chi2 =31.1, 20 d.f., P=0.153). At the time of the analysis, 243 cases (41.0%) had died. The median follow-up (including death) was 851 days. There was no relationship between time to death and apo E genotype in cases of either CI or PICH. CONCLUSION: In this population, there was no relationship between the apolipoprotein E polymorphism and the pathogenesis of cerebral infarction or primary intracerebral haemorrhage. Apo E genotype was not related to all-cause mortality following stroke.

Aged↗

Impact of botulinum toxin type A on disability and carer burden due to arm spasticity after stroke: a randomised double blind placebo controlled trial.

OBJECTIVES: After stroke, abnormal arm posture due to spasticity in a functionally useless arm may interfere with self care tasks. In these patients botulinum toxin treatment presents an opportunity to reduce disability. The purpose was to investigate whether reduction in spasticity after botulinum toxin treatment translates into reduction in disability and carer burden. METHODS: Forty patients with stroke with spasticity in a functionally useless arm (median duration 3.1 years) were randomised to receive intramuscular botulinum toxin type A (BT-A; Dysport) (n=20) or placebo (n=20) in a total dose of 1000 MU divided between elbow, wrist, and finger flexors. Spasticity (using the modified Ashworth scale), muscle power, joint movement, and pain were assessed. Disability and carer burden were measured using an eight item and a four item scale respectively. Two baseline and three post-treatment assessments (weeks 2, 6, and 12) were made. Concurrent treatments as far as possible remained unchanged and not optimised. RESULTS: Disability improved at week 6 with BT-A compared with placebo. This effect, present at week 2, wore off by week 12. Reduction in carer burden was seen at week 6 with BT-A and continued for at least 12 weeks. Forearm flexor spasticity was reduced with BT-A up to 12 weeks after treatment. Although significant improvement in elbow flexor spasticity was seen at week 2 with BT-A compared with placebo, this effect was not evident at weeks 6 and 12. Arm pain was not improved after BT-A. Grip strength was reduced with BT-A. No serious BT-A related adverse effects were reported. CONCLUSION: BT-A is useful for treating patients with stroke who have self care difficulties due to arm spasticity. The decision to treat should also include relief of carer burden. As muscle weakness may occur, its potential impact on functional activities must be assessed before intervention.

Adolescent↗

Evaluation of the use of a questionnaire to detect hearing loss in babies in China.

A questionnaire was used to screen hearing of 1020 babies 6-8 months in China. All babies failing the questionnaire and 10% of those who passed were tested using auditory brainstem audiometry (ABR). Babies with unilateral or bilateral hearing thresholds 30 dBnHL or more were investigated to determine the cause of the hearing impairment. Sixty-seven failing the questionnaire were tested and 23 were confirmed to have a hearing loss, 20 with bilateral hearing impairment. The causes were: 13 otitis media with effusion (OME), one hypoxia, one genetic and five unknown. One child with an OME related hearing loss passed the screen. The sensitivity of the questionnaire was estimated to be 70%, specificity 96%.

Acoustic Impedance Tests↗

Association of the platelet glycoprotein IIb HPA-3 polymorphism with survival after acute ischemic stroke.

BACKGROUND AND PURPOSE: The role of polymorphisms of the platelet glycoprotein (GP) IIb/IIIa receptor in the development of cardiovascular disease has been the subject of intensive research. The aim of this study was to determine the association of the HPA-3 polymorphism of platelet GPIIb with ischemic stroke and subsequent survival and to identify possible interactions of HPA-3 with classic risk factors. METHODS: HPA-3 genotype was determined by restriction fragment length polymorphism in 515 patients with ischemic stroke and 423 healthy, age-matched control subjects. RESULTS: There was no significant difference in the genotype distribution of patients and controls, nor was there any difference when patients were subclassified into small- and large-vessel disease. The genotype distribution of the 231 patients subsequently dying during 2.8 years of follow-up (aa=45.0%, ab=46.8%, bb=8.2%) was significantly different from that of those still alive (aa=37.0%, ab=48.2%, bb=14. 8%) (P=0.03). In a Cox regression model, the relative risks for poststroke mortality in patients of aa and ab genotype compared with those of bb genotype were 2.42 (95% CI, 1.24 to 4.71) and 2.13 (95% CI, 1.09 to 4.17), respectively, after we accounted for confounding factors. In addition, significant interactions of HPA-3 with the Pl(A) polymorphism of GPIIIa (P=0.002) and with fibrinogen (P=0.01) were identified in relation to mortality. CONCLUSIONS: HPA-3 is related to poststroke mortality, and the significant interaction of HPA-3 with Pl(A) and fibrinogen suggests that it may in some way influence the interaction of GPIIb/IIIa with fibrinogen, particularly in the presence of high fibrinogen.

Aged↗