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After an initialisation phase of 15 min supine, eachpostural challenge lasted up to15 min depending uponsubjects comfort in the position.

A two-channel NIRO 300 (Hamamatsu PhotonicsK.K. Japan) was used to record data on cerebraloxygenation at 2 Hz. The NIRO 300 produces infra-redlight via an emitting probe which directs the photonsperpendicular to the tissue surface. A receiving probedetects the incident and transmitted light intensitiesfrom the tissue. Inbuilt computational software utilisingalgorithms generated from the modified BeerLambert lawdisplay and record relative changes in the concentrationof oxygenated haemoglobin ([HbO2]), deoxygenatedhaemoglobin ([Hb]) and oxidised cytochrome oxidase([CtOx] ) over the period of study. Using the technique ofspatially resolved spectroscopy (SPS), a measure of absolutetissue oxygen saturation, the tissue oxygenation index (TOI)can be generated. TOI is the ratio of oxygenated ([HbO2])to total tissue haemoglobin concentrations ([HbT]) [17].

The multi-position chair used for testing had an adjustable

back- and leg-rest enabling any positionbetween lying supineand sitting with hips, knees and ankles at 90

. Position wascontrolled by the researcher through a hand-held electronicdevice.

The descriptive data collected for participants were: age,gender and the National Institute of Health Stroke Scale(NIHSS) [18].

The primary outcome was bihemispheric NIRS monitoredTOI (i.e. the ratio of oxygenated ([HbO2]) to totaltissue HbT.

The probability of serial dependency in 1-min sets of data,collected immediately before and after each posture change,was tested using the autocorrelation coefficient and Bartletts

test. All data sets were significantly autocorrelated-r>0.183,range 0.285 0.991. Statistical comparison of phases wastherefore invalid and data were plotted and then interpretedby visual inspection for trend and level.

Results

Seven people who met the study criteria were included.In summary, their mean age was 70.71 years (range5881 years); five were male and the median timefor measurement after stroke was 5 days (range 4 7).Subject characteristics are presented in Appendix 1 in thesupplementary data on the journals website. Two patients

(subjects 2 and 3) had their anti-hypertensive medicationcontinued after stroke onset and one patient (subject 2) hadocclusion of the ipsilateral internal carotid artery. One patient(subject 2) exhibited orthostatic hypotension (defined as adrop in systolic blood pressure 20 mmHg) on posturalchallenges. There were no changes noted in heart rate oroxygen saturations.

Visual inspection of the plotted data indicated that six ofthe seven patients (subjects 1, 2, 3, 5, 6, 7) demonstratedchanges in TOI between supine and sitting up positions. Inthese patients, the pattern displayed a maximum value of

TOI in the supine position and a reduction of TOI on sittingup in the affected middle cerebral artery territory (Figures 1and 2). There were also similar changes in TOI observed inthe contra-lateral lobe (subjects 1, 2, 3, 6, 7); but these were

less marked. In one patient (subject 5), TOI was maximal inthe upright position and reduced in the supine position inthe contra-lateral lobe only.

Discussion

This is the first study to examine changes in cerebraloxygenation in relation to positioning during the acute phaseof ischaemic stroke using NIRS, and has demonstrated thatchanges in body position in the first week after a MCAcortical ischaemic stroke might produce changes in cerebraloxygenation in the lesion site. An important observation wasthat cortical cerebral oxygenation in the infarcted territory, asmeasured by TOI, was consistently lowest during orthostaticpostural challenges and maximal in supine positions in themajority of subjects, although there was no difference in

peripheral oxygen saturations. Orthostatic stress during theacute phase of stroke might impair the maintenance ofcortical oxygenation once cerebral autoregulation has beenbreached, placing the ischaemic penumbra at further risk.Reasons for a reduction in cerebral oxygenation duringorthostatic challenges might have included a reduction ofcerebral blood flowthrough hydrostatic changes;direct bloodpressure changes below the autoregulation range in patientswith occlusive carotid disease [12]; and increased oxygenextraction by the brain in an attempt to maintain oxygenationduring a period of hypoperfusionor redistribution of blood toother areas to support at risk tissue [19, 20]. The presenceof hypertension, use of anti-hypertensive medication andassociated carotid disease may also have contributed tosome of the changes observed; however, similar findingswere also observed in healthy elderly persons subjected topostural challenges in the absence of decreases in orthostaticBP [20]. Likewise, Panayiotou and colleagues demonstratedno significant differences in orthostatic BP levels acutelycomparing stroke patients on and off anti-hypertensivemedication [21]. Similar trends of TOI changes were alsoobserved in the contra-lateral hemispheres thus supportingage-related changes in the decline in cerebral oxygenationduring orthostatic postural challenges [20], although themagnitude of changes on visual inspection appeared less

marked.The study has its limitations. The numbers of case

studies are small and coupled with the heterogeneity of thecharacteristics of the stroke group may explain some of theinter-individual response variation. In addition, continuousblood pressure monitoring wasnot used and thereforebeat tobeat haemodynamic measures in association with TOI werenot calculated. NIRS can only measure cerebral oxygenationand cerebral blood flow indirectly at the cortical level andnot at the subcortical level where transcranial Doppler maybe more informative.

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A2 B1 B2 A1 A2 C1 C2 A1 A2 B1 B2 A1 A2 C1 C2 A1

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Figure 1. NIRS trace demonstrating value of TOI in supine and on sitting up in affected hemisphere and non affected hemisphere.

Index of phases: A2 = last minute of supine lying, B1 = first minute of 45

sitting with legs up, B2 = last minute of 45

sitting up

with legs up, A1 = first minute of supine lying, A2 = last minute of supine lying, C1 = first minute of 90 sitting with legs down,

C2 = last minute of 90

sitting with legs down, A1 = first minute of supine lying.

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Figure 2. NIRS trace demonstrating value of TOI in supine and on sitting up in affected hemisphere and non affected hemisphere.

Index of phases: A2 = last minute of supine lying, B1 = first minute of 45

sitting with legs up, B2 = last minute of 45

sitting up

with legs up, A1 = first minute of supine lying, A2 = last minute of supine lying, C1 = first minute of 90

sitting with legs down,

C2 = last minute of 90

sitting with legs down, A1 = first minute of supine lying.

Patients who suffer an ischaemic stroke form a heteroge-neous group. No single strategy regarding positioning in the

acute setting will applyto all. NIRS does offerthe opportunityto study individual patients response to orthostatic postural

sitting challenge in real time after acute stroke. This may lendsupport to understand the physiological changes that occuracutely after stroke and also how this changes with position-

ing. However, the observed changes in cerebral oxygenationafter passive postural challenges may not be transferable toactive postural challenges as part of an early mobilisation

strategy [22, 23]. Studies examining the relationship between

the effects of positioning on cerebral cortical oxygenationand outcome in a wider range of patients such as those withcarotid occlusion and different stroke subtypes are required.

Key points

NIRS offers measurement of cerebral oxygenation in realtime at the bedside post stroke.

Changes in cerebral oxygenation can occur betweensupine and upright positioning after stroke.

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Cerebral oxygenation as measured by TOI was lowest inthe upright position and highest in the supine position.

Future studies should address the effects of positioningon cerebral oxygenation and outcome after stroke.

Supplementary data

Supplementary data for this article are available at Age andAgeingonline.

DAVID HARGROVES,1 RAYMOND TALLIS,1 VALERIE POMEROY,1

AJAY BHALLA1,2

1Department of Geriatric Medicine, Centre for Rehabilitationand Ageing, 3rd Floor, Lanesbrough Wing, St Georges,

University of London, London, SW17 ORE, UK2Department of Geriatric Medicine, St Helier Hospital,

Wrythe Lane, Carshalton, Surrey, SM51AA, UKEmail: [email protected]

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3. Somerville ER. Orthostatic transient ischemic attacks: asymptom of large vessel occlusion. Stroke 1984; 15: 10667.

4. Sedal L, Heywood J. Focal cerebral ischaemia induced bypostural change. Clin Exp Neurol 1989; 26: 22935.

5. HayashidaK, HiroseY, Kaminaga T et al. Detection of posturalcerebral hypoperfusion with technetium-99m-hmpao brain

spect in patients with cerebrovascular disease. J Nucl Med1993; 34: 1931 5.

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7. Carr JH, Kenny F. A Motor Relearning Programme for Stroke.London: William Heinemann Medical Books, 1982.

8. Carter P, Edwards S. General principles of treatment. In:Edwards S (ed.) Neurological Physiotherapy: A ProblemSolving Approach. Edinburgh: Churchill Livingstone, 199515562.

9. Chatterton HJ, Pomeroy VM, Gratton J. Positioning for strokepatients: a survey of physiotherapists aims and practices.Disabil Rehabil 2001; 23: 41321.

10. Lincoln NB, Willis D, Philips SA et al. Comparison of

rehabilitation practice on hospital wards for stroke patients.Stroke 1996; 27: 18 23.

11. Rosner MJ, Rosner SD, Johnson AH. Cerebral perfusionpressure: Management protocol and clinical results.

J Neurosurg 1995; 83: 949 62.12. Ouchi Y, Nobezawa S, Yoshikawa E et al. Postural effects

on brain hemodynamics in unilateral cerebral artery occlusivedisease: a positron emission tomography study. J Cereb BloodFlow Metab 2001; 21: 105866.

13. Casellas D, Bouriquet N, Moore LC. Branching patterns andautoregulatory responses of juxtamedullary afferent arterioles.

Am J Physiol 1997; 272: F416 21.

14. Schwarz S, Georgiadis D, Aschoff A et al. Effects of bodyposition on intracranial pressure and cerebral perfusion inpatients with large hemispheric stroke. Stroke 2002; 33:497501.

15. Wojner AW, El-Mitwalli A, Alexandrov AV. Effect of headpositioning on intracranial blood flow velocities in acuteischemic stroke: a pilot study. Crit Care Nurs Q 2002; 24:5766.

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19. Passant U, Warkentin S, Minthon L et al. Cortical blood flowduring head up postural changes in subjects with orthostatichypotension. Clin Auton Res 1993; 3: 3118.

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Cerebral oxygenation declines in health elderly subjects inresponse to assuming the upright position. Stroke 2000; 31:161520.

21. Panayiotou B, Reid J, Fotherby M et al. Orthostatichaemodynamic responses in acute stroke. Postgrad Med J1999; 75: 2138.

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doi:10.1093/ageing/afn143

Positional vertigo in a falls service

SIR Dizziness is one of the commonest symptomsdescribed by older people [1] and is associated with balancedisorders, functional decline, reduction in quality of life andfalls [2 4]. At least 50% of older people with dizzinesscomplain of two different dizzy symptoms; the mostcommon being a gait disorder (a feeling of disequilibrium onwalking) [5], and the other arising from the cardiovascularand peripheral vestibular systems [6]. Dizziness and balance

disorders in older people are common presenting symptomsat Falls clinics.

Positional vertigo (brief episodes of vertigo withnystagmus provoked by changes in head position) is oneof the most common symptoms [7] presented to an ear, noseand throat (ENT) service. Benign paroxysmal positionalvertigo (BPPV) accounts for the great majority of these casesand is caused by peripheral vestibular rather than centralpathology [8]. Posterior canal benign paroxysmal positionalvertigo (p-BPPV) is the commonest type of positional vertigoseen and is treatable [9].

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posisi okesigenasi age ageing 2008 hargroves 581 5

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