Sphygmomanometer Cuff Research Articles

Scintigraphic Imaging of Endothelium-Dependent Vasodilation in the Forearm A Preliminary Report

The diagnosis of endothelial dysfunction has been gaining clinical importance, but although endothelial function testing is available in the research setting, no technique yet exists that is simple, safe, reproducible and easily performed as a clinical screening method. The aim of this study was to design a new, scintigraphic method of imaging the flow-mediated dilation in the forearm, which represents the functional characteristic of endothelial dysfunction. The study group comprised 118 subjects in whom left forearm ischemia was induced by inflating a sphygmomanometer cuff to supra systolic pressure for 4.5 min. Later, dynamic acquisition (2 s frame/min) was initiated after the injection of technetium-99m methoxy-isobutyl isonitril into the dorsal pedal veins. Equivalent regions of interest were drawn on both arms to detect total activity counts during 1 min and the perfusion ratios (left arm/right arm) were calculated. The left arm counts (22,203.3+/-12,372.7) were significantly higher than the right arm counts (9,980.9+/-5,931.9) (p<0.001). A significant decrease in perfusion ratios was noted in the hypertension and hypercholesterolemia groups. An increase in the number of risk factors caused an insignificant decrease in perfusion ratio (p=0.346). Non-invasive evaluation of endothelium-dependent vasodilation by semiquantitative scintigraphic method using radioactive perfusion tracer provided promising results.

Rationalisation of First-Aid Measures for Elapid Snakebite

Summary The plasma of monkeys envenomated with tiger snake (Notechis scutatus) venom was monitored by radioimmunoassay for both crude venom and a neurotoxin. When the injected limb was immobilised and a pressure of 55 mm Hg applied to the injection site, only very low levels of circulating venom or neurotoxin were detectable. In practical terms, venom movement can be effectively delayed for long periods by the application of a firm crepe bandage to the length of the bitten limb combined with immobilisation by a splint. Pressure alone or immobilisation alone did not delay venom movement.

Effects of External Pressure on Arteries Distal to the Cuff During Sphygmomanometry

The aim of this study was to examine the effect on distal arteries of external pressure, applied by upper arm sphygmomanometer cuff. Photoplethysmographic (PPG) signals were measured on the index fingers of 44 healthy male subjects, during the slow decrease of cuff air pressure. For each pulse the ratio of PPG amplitude to its baseline (AM/BL) and its time delay (deltaTD) relative to the contralateral hand were determined as a function of cuff pressure. At cuff pressures equal to systolic blood pressure, pulses reappeared with the pulse time delay in the cuffed arm significantly greater than in the noncuffed arm, with (deltaTD) (mean +/- SD) 150 +/- 31 ms (p < 0.001). At cuff pressures equal to diastolic blood pressure (81 +/- 12 mmHg), deltaTD was 42 +/- 19 ms (p < 0.001), and at 50 mmHg, which is below diastolic blood pressure, (deltaTD) was still significantly positive at 6 +/- 9 ms (p < 0.001). AM/BL relative to its initial value rose at cuff pressures between systolic and diastolic blood pressure, then deceased to 0.6 +/- 0.41 (p < 0.001) at diastolic blood pressure and 0.54 +/- 0.24 (p < 0.001) at 50 mmHg. The changes in (deltaTD) and AM/BL can be interpreted as originating from changes in the compliance of conduit arteries and small arteries with cuff inflation and deflation.

Manual Sphygmomanometer Cuff: A Suitable Replacement To Pressure Bag

In few cases during perioperative period, the anesthesiologist has to transfuse fluid rapidly to restore the intravascular volume and save the patient from impending hypovolumic shock. Rapid infusion of fluid can ideally be achieved with either a pressure bag or manually squeezing the fluid bottle. But in situations where pressure bag is not available (or none functioning) and trained assistant is not there to squeeze the bottle manually, we used the manual sphygmomanometer cuff as a replacement to pressure bag.

Excitability differences in lower‐limb motor axons during and after ischemia

Neuropathic diseases typically begin distally and spread proximally. Irrespective of the etiology, pathological investigations often indicate changes consistent with ischemia. In the present study, threshold tracking was used to investigate length-dependent differences in ischemic susceptibility of lower-limb axons in 6 healthy volunteers, with ischemia induced by a sphygmomanometer cuff inflated to 200 mm Hg and maintained for 13 minutes. Following stimulation of the peroneal nerve at the fibula neck, compound muscle action potentials were recorded proximally from tibialis anterior (TA) and distally from extensor digitorum brevis (EDB). During ischemia, excitability changes were consistent with nerve depolarization, with a greater reduction in threshold in EDB than TA. This reduction in threshold was associated with an increase in refractoriness, decrease in superexcitability, and prolongation of strength-duration time constant, consistent with axonal depolarization. With release of ischemia, reversal of these changes was associated with an increase in threshold, greater in EDB than TA, indicating axonal hyperpolarization. The rate of recovery of threshold was similar proximally and distally, arguing against a gradient in Na(+)/K(+) pump function along the peroneal nerve. The greater changes in threshold in EDB during and after ischemia suggest an increased susceptibility of more distal axons to ischemia and are likely to contribute to the length-dependent development of neuropathy.

Surface mechanomyogram amplitude is not attenuated by intramuscular pressure.

The electromyogram (EMG) and intramuscular pressure (IMP) increase linearly with force during voluntary static contractions, while the surface mechanomyogram (MMG) increases linearly only up to approximately 70% of the maximal voluntary contraction (MVC) and then levels off. The aim of this study was to investigate the possible influence of IMP on the non-linear MMG increase with force and hence on the signal generation process. Seven subjects performed static contractions of the elbow flexors during: (1) ramp contractions from 0 to 60% of the MVC, and (2) steps at 10, 20 and 40% of the MVC. An external pressure of 0 and 50 mmHg for the ramps or 0, 20, 40, 60, 80 and 100 mmHg for the steps was applied by means of a sphygmomanometer cuff in separate trials. The EMG and the MMG were detected in the biceps brachii by means of a pair of surface electrodes and an accelerometer. The IMP was measured using a Millar tipped pressure transducer, and the data was presented as the mean and standard deviation in each case. The IMP was strongly and linearly related to the external pressure and contraction force both during ramps and steps. The EMG(rms) and MMG(rms) were never reduced as a consequence of the IMP increments. In contrast, a steeper MMG(rms) versus %MVC relationship during ramps at 50 mmHg cuff pressure, and an influence of the cuff pressure at 40% of MVC on MMG(rms) were evident. We conclude that IMP per se does not attenuate the MMG generation process during voluntary contraction, suggesting that the previously described MMG(rms) decrease at near maximal static efforts must be attributed to other determinants, such as a fusion-like situation due to the high motor unit firing rate.

Management of ventral hernia after giant exomphalos with external pressure compression using helmet device

Purpose The aim of this study was to evaluate an alternative technique of reducing a ventral hernia that follows the primary conservative treatment of a giant omphalocoele. Methods The patient is a full-term male neonate with a giant exomphalos. Initially triple dye was applied as an eschar-inducing agent. This resulted in a ventral hernia after 1 month. It was decided to achieve expansion of the abdominal cavity based on the principle of external pressure compression using a sphygmomanometer cuff over the hernia. The cuff was worn continuously, and manual pressure was applied daily. Care was taken to avoid intraabdominal hypertension using the reading of the manometer that was attached. The external pressure was corroborated with observations of respiration and circulation. Results The child did not show any ill effects of raised intraabdominal pressure. Throughout the treatment, the child was on full oral feedings and did not require any ventilator support. Reduction of the ventral hernia was achieved in 9 months. Surgical repair of the residual hernia defect was carried out by double breasting of the fascia. Conclusions The application of controlled external pressure using a specially constructed device is a safe, noninvasive, and effective method of achieving reduction of a ventral hernia after primary conservative treatment of a giant omphalocoele.

Venous obstruction in healthy limbs: a model for chronic compartment syndrome?

Chronic exertional compartment syndrome (CECS) in the anterior tibial (AT) compartment is generally believed to be the result of reduced venous blood flow caused by restrictive compartments and increased intramuscular pressures. If this is so, then restricting venous flow in the muscles of healthy subjects during exercise should mimic CECS. This hypothesis was tested in 10 control subjects (aged 19-41 yr, five males) with and without external venous occlusion induced by a sphygmomanometer cuff fitted just below the knee and inflated to 80 mm Hg. Twenty CECS patients (20-39 yr, 16 males) were studied without external occlusion. Subjects performed intermittent, isometric maximal voluntary contractions (MVC) of the AT for 20 min (1.6-s contractions, 0.5 duty cycle). MVC, tetanic force (2 s at 50 Hz), muscle thickness (ultrasound imaging), and pain were measured during exercise and 10 min of recovery. Venous occlusion in the controls induced greater pain, fatigue, and increase in muscle thickness (P < 0.01). Initially the patients fatigued more slowly than the occluded controls, but at the end of exercise, the fatigue and pain were similar in these two groups. The controls showed a greater increase in muscle size (P = 0.01). Recovery was similar in all three groups, although the size of the patients' muscles recovered rather more slowly. External venous occlusion of the AT muscles in control subjects induces changes very similar to those of CECS patients, although the different time courses indicate that different processes are involved. The AT compartment of CECS patients is capable of distension.

Emergency room retrograde transbrachial arteriography for the management of axillosubclavian vascular injuries.

Our purpose was to determine the accuracy of single-injection, retrograde transbrachial arteriography (RTBA), performed in the emergency room, for suspected axillosubclavian injuries. Thirty-three patients were prospectively assigned for RTBA. Clinical indications for RTBA included high-risk mechanism of injury, decreased (n = 19) or absent (n = 5) brachial pulse, neurologic deficits (n = 11), external or intrathoracic bleeding (n = 4), and bruit (n = 2). Brachial artery was cannulated with an 18-gauge catheter. A sphygmomanometer cuff was placed at the forearm and inflated to 250 mm Hg. Twenty milliliters of nonionic contrast media was injected countercurrent and a single anteroposterior chest radiograph was obtained. Small intimal flaps were followed by serial ultrasound. Surgical findings were used to establish RTBA accuracy. RTBA was successfully performed in all cases. Arterial lesions were detected in 28 (84.8%) patients, including thrombosis (n = 8), arteriovenous fistula (n = 8), and false aneurysm (n = 7) as the most frequent lesions. A sensitivity of 96.5%, a specificity of 100%, a positive predictive value of 100%, and a negative predictive value of 80% were observed with RTBA. We conclude that RTBA is a safe and accurate technique to be used in the emergency room for the rapid detection of axillosubclavian arterial injuries.

Simultaneous pO2and HbO2measurement to determine absolute HbO2concentration forin vivonear infrared spectroscopy

Purpose: Near infrared spectroscopy (NIRS) monitors absolute changes in concentration of chromophores from an unquantified baseline. A change in oxygenation is required to obtain information. Clinically, knowing initial chromophore concentration is desirable. We sought absolute initial concentrations by combining NIRS measurements with simultaneous Eppendorf histograph measurement (absolute values of tissue partial pressure of oxygen (pO2)).Methods: There were 22 trials on 9 occasions in 2 adult volunteers. Following local anaesthetic, the histograph probe was inserted into the forearm muscle and NIRS optodes applied. A sphygmomanometer cuff was inflated over the upper arm to produce ischaemia and hypoxia. Change in pO2was determined as a percentage of the initial pO2. Change in HbO2was measured, and the initial HbO2calculated by assuming the percentage change in HbO2equaled the percentage change in pO2.Results: Mean percentage change in pO2was 20.7 ± 9.6. Mean change in HbO2was 22.4 ± 3.4µmol/l(tissue). Calculated initial HbO2was 146.4 ± 108.7µmol/l(tissue), range 51 to 508µmol/l(tissue). Correlation (r2) between pO2and HbO2was 0.97 ± 0.03.Conclusion: Although changes in pO2and HbO2were highly correlated, calculation of initial absolute concentration of HbO2was not achieved by this method. A reliable method of obtaining absolute concentrations of HbO2in vivoremains to be found.

Conduction block during and after ischaemia in chronic inflammatory demyelinating polyneuropathy.

A previous study suggested that axonal hyperpolariza tion produced by maximal voluntary contraction could accentuate conduction block in symptomatic patients with chronic inflammatory demyelinating polyneuropathy (CIDP). If this is so, conduction block should occur with hyperpolarization due to other causes such as the release of ischaemia. The effects of ischaemia on axonal excitability and on impulse conduction were therefore studied in 12 healthy control subjects and seven patients with symptomatic CIDP. The compound muscle action potential (CMAP) of abductor pollicis brevis was recorded in response to supramaximal stimuli to the median nerve at the wrist alternating with measurements of axonal excitability before, during and after ischaemia for 10 min produced by inflation of a sphygmomanometer cuff around the arm. During ischaemia, the amplitude/area of the maximal CMAP was reduced in the patients by 10% and, after release of ischaemia, it was attenuated by 19%. There were only slight changes in the CMAPs in the healthy controls. The attenuation of the CMAP during ischaemia presumably results from depolarization-induced inactivation of Na(+) channels in axons critically dependent on the number of functioning Na(+) channels for action potential generation. The attenuation of the CMAP after release of ischaemia paralleled the post-ischaemic hyperpolarization and was probably precipitated by it. This study provides suggestive evidence that axonal depolarization can produce conduction block in CIDP, in addition to providing confirmation that axonal hyperpolarization can also do so. In patients with chronic demyelinating disorders, conduction block can probably result from a wider range of physiological stresses than previously appreciated, such as natural activity, ischaemia or recovery from transient ischaemia--all of which could produce fluctuations in symptoms.

TIP OF THE ISSUE.

Dear Editor, Sometimes as in cases of burns, during mastectomy or any other procedure on the arm, only other arm of the patient is available for various activities like IV infusion, recording blood pressure, pulse oximetry etc. Recording blood pressure and running intravenous line on the same arm then is tricky. Back flow of the fluid and sometimes blood occurs when the cuff of sphygmomanometer is inflated. This can be easily avoided by passing the intravenous line tubing between the layers of the sphygmomanometer cuff. Inflating the cuff will kink the line and block the back flow. The flow of the fluid will restart on deflating the cuff (Fig. 1). Fig. 1

PREOPERATIVE BLEEDING TIME AND CLOTTING TIME TESTS :USEFUL OR WASTEFUL?

Dear Editor, Preoperative Bleeding Time (BT) and Clotting Time (CT) tests are expected to detect occult haemostatic disorders. Conversely it is assumed that normal BT-CT results exclude haemostatic disorders. This presumption is the basis of selecting BT-CT as the screening tests. In our hospital, in two years, 1662 BT and 1713 CT preoperative tests were performed. BT test was performed by modified method and CT by capillary method [1], No patient had history or clinical findings suggestive of haemostatic disorders. None of the patients suffered from excessive intra or postoperative blood loss that could be attributed to haemostatic disorders. We did not find any abnormal BT or CT result that could indicate haemostatic disorder in these patients. On the contrary, in established cases of haemostatic disorders, BT- CT results were abnormal only when the disorder assumed severe form. Are we justified in relying on BT - CT as preoperative screening tests for haemostatic disorders? Bleeding time test should be performed by Standard Template Method or Ivy's method. Standardization is very important as even minor deviation like a change in the size of sphygmomanometer cuff can alter the results. The modified method commonly used in service hospitals [1] is too crude and unreliable for any valuable information. There is no correlation between a skin template bleeding time, certain visceral bleeding times, preoperative BT results and surgical blood loss or transfusion requirements [2, 3]. Trauma to vascular system, not haemostatic disorders, causes most of the perioperative blood loss. Whole blood clotting time measures the time required for formation of the first traces of thrombin sufficient to produce a visible clot. The CT is abnormal only with severe coagulation factors deficiency (as low as 10-15%). It is a poor screening test that seldom provides information not obtained by other more reliable tests. The CT test by capillary method as practised in service hospitals, is highly unreliable [1]. These investigations (BT-CT) are not sensitive screening tests to detect haemostatic disorders [1]. Their role in preoperative screening is questionable [4, 5, 6]. Despite thousands of these tests not a single case of haemostatic disorder was detected in our hospital in preoperative workout. Informal discussions with surgeons, anaesthesiologists and pathologists revealed that in their cumulative experience of over 100 practicing years not a single asymptomatic case of haemostatic disorder was detected by BT-CT tests. More often than not, these tests are carried out as an empirical legacy, perhaps for completion of medical documents. Our experience and review of literature reveal that BT-CT tests do not fulfill the criteria required for screening tests. Haemostatic disorders can be easily suspected by history and clinical examination, the first step to diagnosis. A guestimate at the number of BT-CT tests performed in all service hospitals would be mind-boggling. Are we justified in such colossal waste of time, resources and effort in performing these non-contributory tests? The surgeons, anaesthesiologists and pathologists need to ponder over it. The BT-CT tests as routine blind preoperative screening, should be dispensed with. This would require change of perception and attitude. The Senior Advisers perhaps can issue suitable instructions to streamline preoperative investigations. The time and resources thus saved can be redirected to more fruitful work.

In vivo release of tissue-type plasminogen activator antigen from the human brachial artery

The rate of secretion of t-PA from vascular endothelial cells has been proposed as a good marker of endothelial function. Our aim was to measure the rate of in vivo t-PA antigen release from the human brachial artery and not from the combined vascular pool of the upper extremity. In 10 healthy male volunteers, we have occluded the forearm by a sphygmomanometer cuff for 5–7 min in order to reduce the blood flow in the brachial artery. Arterial blood samples were taken from the cubital artery above the occlusion and from the contralateral artery that served as the control. The arterial t-PA antigen concentrations were significantly higher after forearm occlusion than in the non-occluded contralateral arteries: median 3.3 (range between first and third quartile 2.1–3.6) vs. 2.5 (2.0–3.2) ng/ml, p=0.03. The PAI-1 antigen concentrations did not change significantly: 6.9 (2.3–18.6) ng/ml in the contralateral artery vs. 5.4 (1.8–8.0) ng/ml after occlusion, p=0.09. The average forward blood flow in the distal 15 cm of the brachial artery that was measured by duplex ultrasound decreased from 107 (97–118) ml/min at baseline to 25 ml/min (19–33) ml/min during occlusion. The release rate of circulating t-PA antigen was calculated as the product of the increment in arterial t-PA concentration and the average plasma flow in the arterial segment of interest with a volume of 2 ml. The median release rate of t-PA antigen under conditions of reduced blood flow in the brachial artery was 3.3 (1.1–11.5) ng/min. We conclude that the secretion of t-PA antigen from arterial endothelium of healthy subjects is substantial, whereas the arterial wall is not an important source of PAI-1 in vivo.

Vascular factors in carpal tunnel syndrome

An increase in hand and forearm volume was induced without hand movement in ten subjects who had carpal tunnel syndrome (CTS). A tester, unaware of sides affected by CTS, performed the Volume Provocation Test (VPT) by inflating a sphygmomanometer cuff around the upper arm to 15 mm Hg less than diastolic pressure for four minutes. Pre- and post-test volumes, intensity of discomfort, and quality and distribution of produced symptoms were recorded. The VPT induced significant increases of segment volumes bilaterally (p1 tailed<0.05), but not more on the side of strongest symptoms compared to the less affected, or asymptomatic side (p1 tailed=0.07). Mean discomfort on the side of strongest symptoms (5.4/10) was significantly higher (p1 tailed<0.01) than on the contralateral side (2.4/10). In 44% of the affected arms, some or all of the subjects' nocturnal symptoms were reproduced after volume increase, suggesting that CTS is a vascular phenomenon in these patients. J HAND THER. 2002;15:22-30.

Delayed onset muscle soreness: effect of an ischaemic block upon mechanical allodynia in humans

The current study, for which ethical approval was obtained, was designed to assess the extent to which the tenderness or mechanical allodynia observed in delayed onset muscle soreness (DOMS) might be mediated by large diameter myelinated nerve fibres. Healthy human volunteers were recruited and randomly allocated to one of three groups: Normal-Control, Ischaemic-Control, and Test-DOMS (total n=21; n=7 in each group). In the Normal-Control group, subjects attended on a single occasion for assessment of mechanical pain threshold (MPT) at standardized sites over the biceps brachii using a pressure algometer for a period of 20 min. In both remaining groups, ischaemia was induced in subjects' non-dominant upper limbs by elevation of the limb, followed by application of a sphygmomanometer cuff at a pressure of 250 mmHg. Throughout the period of the block (20–40 min), sharp/blunt sensation was assessed at regular intervals. MPT was assessed upon inflation of the cuff and reassessed at 10 min intervals until deflation. In the two ischaemic block groups, current level of pain was also monitored using a computerized visual analogue scale (VAS) at the beginning and end of the procedure. Subjects in the Test-DOMS group attended 48 h prior to ischaemic block for induction of DOMS using a standardized regime of eccentric exercise, but thereafter were treated in exactly the same manner as the Ischaemic-Control group. Results showed a significant ( P<0.05; ANOVA) increase in MPT in the Test-DOMS group by the 20 min point, corresponding to a ‘normalization’ of MPT; loss of the ability to distinguish between sharp/blunt sensation accompanied such changes. Parallel increases in reported pain were seen in both groups undergoing ischaemic block, indicating that the procedure did not alter nociception. While not definitive, these results suggest that altered processing of activity in large diameter (myelinated) afferents might underlie the mechanical allodynia observed in DOMS; thus, this is an area which warrants further investigation.

The cutaneous vasoconstrictor response to venous stasis is normal in subjects with primary Raynaud's disease.

In control subjects and in subjects with primary Raynaud's disease, sudden sound or a mild cool stimulus evokes the pattern of alerting response that includes cutaneous vasoconstriction but vasodilatation in forearm muscle. In control subjects, response habituates on repetition of these stimuli both within experimental sessions and over successive days. However, in subjects with primary Raynaud's disease, the cutaneous vasoconstriction and the muscle vasodilatation persist. We have now tested whether a similar disparity exists for the cutaneous vasoconstriction evoked by venous stasis, a response considered to be a veno-arteriolar reflex mediated by sympathetic fibers, but not requiring transmission through the spinal cord. In 10 subjects with primary Raynaud's disease and in 10 matched controls, a sphygmomanometer cuff on the left arm was inflated to 40 mm Hg for 2 minutes, five times on each of three experimental sessions on days 1, 3, and 5. Cutaneous red cell flux (RCF) was recorded from the pulp and dorsum of the left index finger by using a laser Doppler meter; digital vascular conductance (DCVC) was computed as RCF divided by arterial pressure. The first venous stasis, in session 1, evoked a decrease in pulp and dorsum DCVC in the control and primary Raynaud's subjects. There were no differences between the groups in the magnitudes or durations of these responses. Within session 1, the magnitude of the decrease in DCVC diminished on repetition of venous stasis in the dorsum in controls and in the pulp in primary Raynaud's subjects. We propose these effects reflected the similar reductions in baseline DCVC over time; there was no change in the duration of the responses. Repetition of venous stasis had similar effects in both groups of subjects within sessions 2 and 3. Further, judging from the mean of the responses evoked in each Session the decreases evoked in pulp and dorsum DCVC by venous stasis were fully consistent in magnitude and duration over the three sessions in both groups. These results indicate that the direct constrictor influence of sympathetic fibers upon cutaneous blood vessels is similar in magnitude and similarly reproducible in controls and subjects with primary Raynaud's disease. This reinforces our view that the lack of habituation of the cutaneous vasoconstrictor component of the alerting response in subjects with primary Raynaud's disease reflects impairment of the central neural process of habituation, rather than a peripheral phenomenon, and that this lack of habituation predisposes these subjects to vasospasm.

Sphygmomanometer-induced increases in forearm and hand volume

Swelling, or increased volume, secondary to venous congestion is thought to be a factor in some upper limb conditions. This study aimed to establish a safe, easily applied method of inducing a transitory increase in forearm and hand volume that could be used as a symptom provocation test for upper limb conditions. Using the principles of venous occlusion plethysmography, movement of blood volume into the forearm and hand of asymptomatic subjects was measured after occlusion with three different sphygmomanometer cuff pressures over four minutes. Increases of between 37 and 62 ml (2.5% and 4.1%) were achieved at pressures between diastolic pressure minus 30 mm Hg and diastolic pressure plus 5 mm Hg, with minimal reported side effects. These data demonstrate that a sphygmomanometer can be used to induce transitory fluid congestion of the forearm and hand.

Can stroke patients use visual analogue scales?

Visual analogue scales (VAS) have been used for the subjective measurement of mood, pain, and health status after stroke. In this study we investigated how stroke-related impairments could alter the ability of subjects to answer accurately. Consent was obtained from 96 subjects with a clinical stroke (mean age, 72.5 years; 50 men) and 48 control subjects without cerebrovascular disease (mean age, 71.5 years; 29 men). Patients with reduced conscious level or severe dysphasia were excluded. Subjects were asked to rate the tightness that they could feel on the (unaffected) upper arm after 3 low-pressure inflations with a standard sphygmomanometer cuff, which followed a predetermined sequence (20 mm Hg, 40 mm Hg, 0 mm Hg). Immediately after each change, they rated the perceived tightness on 5 scales presented in a random order: 4-point rating scale (none, mild, moderate, severe), 0 to 10 numerical rating scale, mechanical VAS, horizontal VAS, and vertical VAS. Standard tests recorded deficits in language, cognition, and visuospatial awareness. Inability to complete scales with the correct pattern was associated with any stroke (P<0.001). There was a significant association between success using scales and milder clinical stroke subtype (P<0.01). Within the stroke group, logistic regression analysis identified significant associations (P<0.05) between impairments (cognitive and visuospatial) and inability to complete individual scales correctly. Many patients after a stroke are unable to successfully complete self-report measurement scales, including VAS.

Clinical implications of soluble intercellular adhesion molecule-1 levels in systemic sclerosis.

S sclerosis (SSc) is characterized by vascular endothelial stress test. sICAM-1 levels increased significantly following VO in SSc patients compared to abnormalities such as Raynaud’s phenomenon, telangiectasia, and thickening/fibrosis of the skin and visceral controls, and this change correlated inversely with skin score (Fig. 1). Levels of sE-selectin were not signifiorgans [1]. SSc may also be associated with peripheral large vessel arterial occlusion [2]. The mechanisms of cantly different in SSc patients compared to controls before or after VO. vascular damage are unclear, but may include endothelial cell (EC) dysfunction. Raised levels of factor VIII SSc is associated with abnormalities of small and large blood vessels [3]. ICAM-1 is an important molecvon Willebrand factor antigen (vWF ) are found in SSc patients, indicating possible EC damage/activation [3]. ule for WBC–EC interaction, an initiating event in the development of inflammation. ICAM-1 is expressed White blood cell ( WBC) activation is also found in SSc [4], suggesting that WBC–EC interaction may be constitutively on EC; however, expression may be induced on a variety of cells by cytokines, nitric oxide an important mechanism of damage. Soluble cell adhesion molecule (sCAM) levels have been measured in and other molecules. A previous study examining sCAM levels in SSc longitudinally over 28–72 months inflammatory diseases including SSc [5] and soluble intercellular adhesion molecule 1 (sICAM-1) levels showed that sE-selectin and sVCAM-1 may act as potential surrogate markers of disease progression [5]. may predict myocardial events in apparently healthy individuals [6 ]. sCAM levels were measured at one In another report, low levels of sCAM were associated with histological evidence of skin sclerosis, but this time point in these studies, although measures were repeated longitudinally in one study. Venous occlusion study did not examine clinical skin score [10]. While CAMs may be raised in a variety of vasculopathies [5, (VO) induces hypoxaemia, which in experimental models increases EC CAM expression in postcapillary 6 ], the function and kinetics of the soluble form are not fully understood; however, single measurements venules probably via cytokine and pro-inflammatory molecule production [7]. We report sCAM levels preare unlikely to reflect disease activity accurately. VO is a hypoxic stress proven to increase CAM expression and post-VO, as a dynamic measure of EC reactivity, in relation to clinical skin score in SSc. on EC in experimental conditions. This is the first time a ‘stress test’ has been SSc patients (ARA classification [8]) and healthy volunteer subjects, matched for age and sex, attended employed in vivo to examine sCAM in a controlled study of SSc patients and normal subjects revealing under standardized conditions. Patients underwent a full assessment with history and clinical examination, an inverse correlation of sICAM-1 change with clinical skin score. This may suggest maximal expresincluding skin score [9]. Briefly, a score of 0 (normal )–3 (thickened, unable to pinch) is assigned sion and shedding of ICAM-1 by activated EC, although other cells do express this CAM in inflamat 17 sites over the trunk, face and limbs to calculate a cumulative score (maximum= 51). Pre-VO blood matory disease. Higher levels of sICAM-1 post-VO was obtained from the antecubital fossa vein without a tourniquet. A sphygmomanometer cuff was inflated to 90 mmHg, on the opposite arm, for 10 min and post-VO blood was sampled prior to releasing the cuff. Serum was prepared and stored at −70°C until sCAM (ng/ml ) was measured in serum (ELISA kits, R&D Systems, UK ). Statistical analysis included the Mann–Whitney U and Spearman rank correlation tests. This study examined the change in sCAM levels (sICAM-1 and sE-selectin) in SSc patients, before and after a hypoxic stimulus (VO), providing a dynamic