To assess the frequency and natural history of swallowing problems following an acute stroke, 121 consecutive patients admitted within 24 hours of the onset of their stroke were studied prospectively. The ability to swallow was assessed repeatedly by a physician, a speech and language therapist, and by videofluoroscopy. Clinically 51% (61/121) of patients were assessed as being at risk of aspiration on admission. Many swallowing problems resolved over the first 7 days, through 28/110 (27%) were still considered at risk by the physician. Over a 6-month period, most problems had resolved, but some patients had persistent difficulties (6, 8%), and a few (2, 3% at 6 months) had developed swallowing problems. Ninety-five patients underwent videofluoroscopic examination within a median time of 2 days; 21 (22%) were aspirating. At 1 month a repeat examination showed that 12 (15%) were aspirating. Only 4 of these were persistent; the remaining 8 had not been previously identified. This study has confirmed that swallowing problems following acute stroke are common, and it has been documented that the dysphagia may persist, recur in some patients, or develop in others later in the history of their stroke.
SummaryBackgroundStents are an alternative treatment to carotid endarterectomy for symptomatic carotid stenosis, but previous trials have not established equivalent safety and efficacy. We compared the safety of carotid artery stenting with that of carotid endarterectomy.MethodsThe International Carotid Stenting Study (ICSS) is a multicentre, international, randomised controlled trial with blinded adjudication of outcomes. Patients with recently symptomatic carotid artery stenosis were randomly assigned in a 1:1 ratio to receive carotid artery stenting or carotid endarterectomy. Randomisation was by telephone call or fax to a central computerised service and was stratified by centre with minimisation for sex, age, contralateral occlusion, and side of the randomised artery. Patients and investigators were not masked to treatment assignment. Patients were followed up by independent clinicians not directly involved in delivering the randomised treatment. The primary outcome measure of the trial is the 3-year rate of fatal or disabling stroke in any territory, which has not been analysed yet. The main outcome measure for the interim safety analysis was the 120-day rate of stroke, death, or procedural myocardial infarction. Analysis was by intention to treat (ITT). This study is registered, number ISRCTN25337470.FindingsThe trial enrolled 1713 patients (stenting group, n=855; endarterectomy group, n=858). Two patients in the stenting group and one in the endarterectomy group withdrew immediately after randomisation, and were not included in the ITT analysis. Between randomisation and 120 days, there were 34 (Kaplan-Meier estimate 4·0%) events of disabling stroke or death in the stenting group compared with 27 (3·2%) events in the endarterectomy group (hazard ratio [HR] 1·28, 95% CI 0·77–2·11). The incidence of stroke, death, or procedural myocardial infarction was 8·5% in the stenting group compared with 5·2% in the endarterectomy group (72 vs 44 events; HR 1·69, 1·16–2·45, p=0·006). Risks of any stroke (65 vs 35 events; HR 1·92, 1·27–2·89) and all-cause death (19 vs seven events; HR 2·76, 1·16–6·56) were higher in the stenting group than in the endarterectomy group. Three procedural myocardial infarctions were recorded in the stenting group, all of which were fatal, compared with four, all non-fatal, in the endarterectomy group. There was one event of cranial nerve palsy in the stenting group compared with 45 in the endarterectomy group. There were also fewer haematomas of any severity in the stenting group than in the endarterectomy group (31 vs 50 events; p=0·0197).InterpretationCompletion of long-term follow-up is needed to establish the efficacy of carotid artery stenting compared with endarterectomy. In the meantime, carotid endarterectomy should remain the treatment of choice for patients suitable for surgery.FundingMedical Research Council, the Stroke Association, Sanofi-Synthélabo, European Union.
Bedside assessment of swallowing lacks the necessary sensitivity to be used as a screening instrument in acute stroke, but there are concerns about the use of videofluoroscopy as a gold standard. The relative importance of aspiration and bedside assessment in predicting complications and outcome needs to be studied.
screening by saturation assessments detects 86% of aspirators/penetrators and should be followed immediately by bedside swallowing assessment, as the combination of the two assessments gives the best positive predictive value. For patients with acute stroke, we advocate a 10 ml water-swallow screening test with simultaneous pulse oximetry by suitably trained medical and nursing staff. Use of this screening test would improve dysphagia detection whilst minimizing unnecessary restriction of oral intake in stroke patients.
SummaryThe inner ear and the epibranchial ganglia constitute much of the sensory system in the caudal vertebrate head. The inner ear consists of mechanosensory hair cells, their neurons, and structures necessary for sound and balance sensation. The epibranchial ganglia are knots of neurons that innervate and relay sensory signals from several visceral organs and the taste buds. Their development was once thought to be independent, in line with their independent functions. However, recent studies indicate that both systems arise from a morphologically distinct common precursor domain: the posterior placodal area. This review summarises recent studies into the induction, morphogenesis and innervation of these systems and discusses lineage restriction and cell specification in the context of their common origin. Key words: Epibranchial, Inner ear, Neurogenesis, Placode, Signalling IntroductionCranial placodes, found in all vertebrates, are transient thickenings of ectoderm that contribute extensively to the sensory component of the cephalic peripheral nervous system (see Box 1 and Glossary, Box 2). Individual placodes give rise to characteristic cell types, although the diversity of placodal derivatives varies (Box 1). Some placodes, such as the olfactory, otic and lateral line placodes, can form the receptive cell that responds to a stimulus, as well as the sensory neurons that transmit this information (Box 1). Others, such as the epibranchial and trigeminal placodes, only give rise to sensory neurons. The lens and adenohypophyseal placodes generate no sensory derivatives (Baker and Bronner-Fraser, 2001;Webb and Noden, 1993;Begbie and Graham, 2001b). In this review, we focus on the inner ear (or otic) placode and the epibranchial series of placodes and discuss their origins from a common progenitor domain: the posterior placodal area (PPA) (Fig. 1).The otic placode forms the complex inner ear structure that detects sound and balance, as well as the neurons that convey this information to the auditory hindbrain. The otic placodes form distinctive paired depressions adjacent to the caudal hindbrain and progressively deepen to form otocysts (see Glossary, Box 2). Transcriptional networks, influenced by extrinsic signals, drive the regional differentiation of the otic placode to generate mechanosensory hair cells, supporting cells and neurons (see Box 1 and Glossary, Box 2). This progressive differentiation results in a remarkable convolution of the simple spherical otocyst into an intricate structure that is dedicated to receiving information on balance, angular velocity and sound. These later morphogenetic events have been well reviewed (Bok et al., 2007;Fritzsch et al., 2006;Torres and Giráldez, 1998) and will not be covered here.The epibranchial placodes give rise to the geniculate, petrosal and nodose ganglia, which contribute sensory neurons to cranial nerves VII (facial), IX (glossopharyngeal) and X (vagus), in that order (see Box 1 and Glossary, Box 2; Fig. 1). Epibranchial placodes are located ventral to the...
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