Neuromuscular taping reduces blood pressure in systemic arterial hypertension.

Systemic arterial hypertension, a well-known cause of morbidity, is associated with dysfunction of the autonomic nervous system. Neuromuscular taping (also known as kinesio taping, medical taping and Vendje neuromuscular) allows movement and muscle activity to treat pain, muscle disorders and lymphoedema, in which its mode of action may involve muscular stimulation leading to increased local blood circulation or stimulating dermatological, muscular and fascial structures with a form of passive massage. We hypothesised that neuromuscular taping may reduce blood pressure in systemic arterial hypertension. This hypothesis was tested by carrying out the first pilot study of its kind to determine whether the non-invasive technique of neuromuscular taping can reduce blood pressure in patients suffering from systemic arterial hypertension. Neuromuscular taping was symmetrically applied to the back, between C1 and T2, of seven hypertensive patients for 5-7 days. Cardiovascular autonomic parameters were assessed at baseline and at the end of the study. Taping was associated with falls in mean arterial blood pressure (p = .001), mean systolic blood pressure (p < .01), mean diastolic pressure (p < .01) and cardiac vagal tone at rest (p = .063). The beneficial effects on blood pressure appeared to last for at least five days post-neuromuscular taping. There is an indication, given the reduction in cardiac vagal tone at rest, that the mechanism of action of this intervention involves modulation of the brainstem parasympathetic system during cardiovascular control. Further studies are indicated to replicate the present findings, further investigate the effects of taping on autonomic functioning, and establish the optimum time-period and taping positioning.

Carbon dioxide therapy in hypocapnic respiratory failure.

Oxygen therapy, usually administered by a facemask or nasal cannulae, is the current default treatment of respiratory failure. Since respiration entails intake of oxygen and release of carbon dioxide from tissues as waste product, the notion of administering carbon dioxide in respiratory failure appears counter-intuitive. However, carbon dioxide stimulates the chemosensitive area of the medulla, known as the central respiratory chemoreceptor, which activates the respiratory groups of neurones in the brainstem and stimulates inspiration thereby initiating oxygen intake during normal breathing. This vital initiation of normal breathing is via a reduction in the pH of the cerebrospinal fluid and the medullary interstitial fluid. We hypothesise that in cases of type I respiratory failure in which the PaCO2 is low, administration of carbon dioxide by inhalation would stimulate the respiratory groups of brainstem neurones and facilitate breathing, which would be of therapeutic value. Preliminary clinical evidence in favour of this hypothesis is presented and we recommend that a formal randomised study be carried out.

Non-invasive real-time measurements of cardiac vagal tone in dogs with cardiac disease.

In dogs with spontaneous heart disease, an electronically generated measurement of cardiac vagal tone, the cardiac index of parasympathetic activity, was a sensitive, simple and inexpensive measure of the severity of heart failure. Dogs with cardiac disease and an index score less than 3 were at 15.8 (95 per cent confidence interval 2.9 to 87.2) times the risk of dying within a year than those with a score of 3 and over. The measurement of the index provided an objective and reliable beat-by-beat measurement of cardiac vagal tone, which was prognostically useful in dogs with heart disease.

Cardiovascular regulation in the period preceding vasovagal syncope in conscious humans.

To study cardiovascular control in the period leading to vasovagal syncope we monitored beat-to-beat blood pressure, heart rate (HR) and forearm blood flow in 14 patients with posturally related syncope, from supine through to tilt-induced pre-syncope. Signals of arterial blood pressure (BP) from a Finapres photoplethysmograph and an electrocardiograph (ECG) were fed into a NeuroScope system for continuous analysis. Non-invasive indices of cardiac vagal tone (CVT) and cardiac sensitivity to baroreflex (CSB) were derived on a beat-to-beat basis from these data. Brachial vascular resistance (VR) was assessed intermittently from brachial blood flow velocity (Doppler ultrasound) divided by mean arterial pressure (MAP). Patients underwent a progressive orthostatic stress test, which continued to pre-syncope and consisted of 20 min head-up tilt (HUT) at 60 deg, 10 min combined HUT and lower body suction (LBNP) at -20 mmHg followed by LBNP at -40 mmHg. Pre-syncope was defined as a fall in BP to below 80 mmHg systolic accompanied by symptoms. Baseline supine values were: MAP (means +/- S.E.M.) 84.9 +/- 3.2 mmHg; HR, 63.9 +/- 3.2 beats min-1; CVT, 10.8 +/- 2.6 (arbitrary units) and CSB, 8.2 +/- 1.6 ms mmHg-1. HUT alone provoked pre-syncope in 30 % of the patients whilst the remaining 70 % required LBNP. The cardiovascular responses leading to pre-syncope can be described in four phases. Phase 1, full compensation: where VR increased by 70.9 +/- 0.9 %, MAP was 89.2 +/- 3.8 mmHg and HR was 74.8 +/- 3.2 beats min-1 but CVT decreased to 3.5 +/- 0.5 units and CSB to 2.7 +/- 0.4 ms mmHg-1. Phase 2, tachycardia: a progressive increase in heart rate peaking at 104.2 +/- 5.1 beats min-1. Phase 3, instability: characterised by oscillations in BP and also often in HR; CVT and CSB also decreased to their lowest levels. Phase 4, pre-syncope: characterised by sudden decreases in arterial blood pressure and heart rate associated with intensification of the symptoms of pre-syncope. This study has given a clearer picture of the cardiovascular events leading up to pre-syncope. However, the mechanisms behind what causes a fully compensated system suddenly to become unstable remain unknown.

A clinical neurological, neurophysiological, and neuropsychological study of sheep farmers and dippers exposed to organophosphate pesticides.

OBJECTIVES: To classify clinical diseases of the subjects with abnormal indices of peripheral neuropathy identified in field studies of sheep farmers and dippers exposed to organophosphate pesticides. To explore what neuropsychological profiles, if any, may be associated with neurophysiological damage in these subjects. METHODS: A case-control study (79 subjects) nested within the cross sectional study (685 subjects) of sheep farmers from the field study. Three groups with no, possible, and probable or definite neuropathy according to field studies were recruited. Investigations comprised symptoms of neuropathy, neurologial signs, motor and sensory nerve conduction, electromyography, quantitative sensory testing, and neuropsychological tests. RESULTS: The incidence of clinical neuropathy increased from 7% in the no neuropathy group to 52% in the probable or definite neuropathy group based on nerve conduction measurements or presence of neurological signs. Sensory abnormalities were found more often than motor deficits. Small diameter nerve fibres were also affected more than large fibres. CONCLUSIONS: The neuropathy is predominantly sensory and is characteristic of distal, chronic neuropathy with no acute features. Small fibre populations are affected more than large fibre populations. Increasing severity of neuropathy was associated with anxiety and depression as measured in the neuropsychological tests.