Biomedical subjects
Publications and source records attributed to D J Read.
A case of subacute sensory neuropathy associated with Hodgkin's disease improved as the tumour was treated. The poor prognosis usually associated with this neuropathy may be attributable to its more common association with untreatable tumours.
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Respiratory and cardiac monitoring was undertaken in the home for seven months in an infant at increased risk for cot-death (SIDS). The infant was a surviving non-identical twin of a SIDS sibling. In hospital, clinical and cardio-respiratory studies during sleep were normal. Analysis of eleven 24-hour tape-recordings showed that many of the alarms at home were the result of technical problems. Suspected apnoeas were identified initially from an oscilloscopic display of the original waveforms and from a compressed-record and histogram of the computed breath-to-breath intervals. Expanded pen-recordings confirmed some, but not all, of these suspected apnoeas (greater than 15s). The results indicate (i) the importance of verifying apnoeic episodes; (ii) the value of 24-h compressed recordings for identifying and timing the sleep cycles and their possible relationships to breathing defects; (iii) the need for improved instrumentation; (iv) the dangers of evaluating clinical prognosis or research from parental diaries.
Urodynamic assessment was performed in 52 patients with urinary symptoms positively diagnosed as suffering from multiple sclerosis. Fifty-one patients had unequivocal bladder instability on filling cystometry the exception had inappropriate relaxation of the urethral sphincter at a small bladder capacity and low bladder pressure. Results of sphincter electromyography and synchronous cineradiography of voiding in a number of our patients led to the conclusion that many of these patients also suffer detrusor sphincter dyssynergia. There was no correlation between any measurable urodynamic parameter and the severity of the physical disability.
Ventilatory and arousal responses to progressive, isocapnic hypoxia were assessed in five full-term calves, aged 1-8 d, during normo-glycaemia and insulin-induced hypoglycaemia; replicate tests were made during both quiet and active sleep. Hypoxia was produced by rebreathing 8-10% (W/V) oxygen; end-tidal PO2 and PCO2 confirmed the mask-seal, and the constancy of PCO2 achieved by a soda-lime CO2-absorber. Oxygen saturation was recorded continuously by aspirating aortic blood through a cuvette-oximeter. Airflow through a tightly fitting face-mask was digitized at 50 ms intervals to calculate breath-by-breath ventilation and rate. Sleep-state and arousal were characterized by EEG, electro-oculogram, nuchal electromyogram and behaviour. An intravenous dose of 2.5 units/kg of soluble insulin produced hypoglycaemia within 60 min (blood glucose less than 1 mmol/l). In the normoglycaemic control state, ventilation during quiet sleep increased linearly; typically the ventilation ratio to pre-hypoxic control was 1.5 at an arterial O2-saturation of 85-90%. In contrast, during active sleep, hypoxaemia progressed without any ventilatory response to a very low arterial O2-saturation of less than 70%. Severe hypoglycaemia did not alter these ventilatory responses during either quiet or active sleep. Thus, the relationship between ventilation ratio and arterial O2-saturation at a saturation of 75% did not differ significantly from control. In quiet sleep the mean ventilation ratio values at an arterial O2-saturation of 75% were 1.92 +/- 0.07 (SEM) and 1.62 +/- 0.07 (P greater than 0.05) for normoglycaemia and hypoglycaemia respectively; in active sleep these were 1.08 +/- 0.09 (SEM) and 1.06 +/- 0.04 (P greater than 0.20). The arterial O2-saturation at which reflex arousal occurred differed between sleep-states but was not altered by hypoglycaemia. In quiet sleep, values were 85.0 +/- 1.4 (SEM) and 84.4 +/- 2.5; in active sleep, 57.8 +/- 3.9 (SEM) and 60.4 +/- 1.4, for normoglycaemia and hypoglycaemia respectively.
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Eleven patients with static or slowly progressive multiple sclerosis were treated with continuous spinal cord stimulation via epidural electrodes for a minimum of two weeks. An extensive battery of objective tests was used to assess results. Significant improvement in urinary bladder function was seen in 2 of the patients with a lesser degree of improvement in 4 others and reduction of lower limb spasticity in 6 patients. Five additional patients selected for these disabilities were then treated with further evidence of improvement in bladder function in 4 and in lower limb spasticity in 2. It is suggested that benefit results from inhibition of excessive spinal reflex activity.
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Over an 18 month period, 19 patients were referred for assessment of excessive daytime sleepiness and/or loud snoring. Respiratory studies during sleep were performed in 14 of these patients with additional features such as disturbed sleep, observed apnoea during sleep, morning headache, mental and personality changes, hypertension and cardiac failure. Nocturnal respiratory studies undertaken for periods of 4-8 hours confirmed a diagnosis of the Sleep Apnoea Syndrome in eight patients. In these patients apnoeas, lasting from 30-144 seconds, occurred frequently during sleep (from 35-291 episodes per patient). In one severely affected patient, tracheostomy abolished all symptoms. The use of conservative therapy such as weight loss, protriptyline or a neck collar, highlighted the inadequacies of current medical treatment. Awareness of the symptom complex and potential complications of the Sleep Apnoea Syndrome is important because the diagnosis may easily be missed if the patient presents with one or two isolated complaints.
Isocapnic progressive hypoxia was produced by rebreathing 8-10% oxygen in replicate tests during quiet and active sleep, in five full-term calves aged 1-8 days. Airflow through a tightly fitting mask was digitized at 50-ms intervals to calculate breath-by-breath ventilation and rate. Using a cuvette oximeter, arterial O2 saturation (SaO2) was recorded continuously. A mass-spectrometer record of end-tidal PO2 and PCO2 confirmed the mask seal and the constancy of PCO2. Sleep state was characterized by EEG, EOG, neck EMG, and behavior. In quiet sleep the ratio of ventilation to its normoxic control (VR) increased linearly as SaO2 fell; reflex arousal occurred at SaO2 84.9 +/- 4.3% (SD) with VR 1.4 +/- 0.39 (SD). In contrast, during active sleep, hypoxemia progressed without any ventilatory response to a very low SaO2; a reflex arousal occurred at SaO2 59.2 +/- 11.0%, often with a ventilatory response developing abruptly just prior to arousal. The slope of the VR/SaO2 regression lines for the overlapping range of SaO2 differed significantly with state in each animal (P < 0.001); the pooled VR values at SaO2 75% were 1.73 +/- 0.15 (SD) and 0.91 +/- 0.18 for quiet and active sleep respectively. The depression of the ventilatory response to hypoxia in active sleep differs from previous reports on adult dogs. The basis for this difference needs to be evaluated in relation to species and age, in particular in relation to both the mechanics of breathing and to chemoreceptor reflexes.
This study investigated the production of lung petechiae by 4 modes of death in anaesthetized rabbits: (i) apnoeic asphyxia from rapid intravenous overdose of pentobarbitone; (ii) obstructive asphyxia from 3 episodes of tracheal occluson (2 min, 2 min, 4 min); (iii) hypotensive insult from intra-cardiac electrocution, producing hypotension and death in 30-80 s; (iv) hypertensive insult from rapid intravenous noradrenaline, terminating in fatal cardiac arrhythmia (1.2-6.8 min). A single fatal episode of apnoeic asphyxia did not produce any petechiae. In contrast, many lung petechiae resulted from the repeated obstructive apnoeic episodes. These results confirmed previous work. However, petechiae were not confined to these asphyxial forms of death. They also occurred in hypotensive or hypertensive circulatory deaths, with or without gasping.. The peak level of systemic hyprtension, in the obstructive asphyxia and hpertensive experiments, did not correlate with the numbers of lung petechiae. Pulmonary oedema, confirmed microscopically, occurred in most animals except those in the apnoeic asphyxial group. The number of lung petechiae increased significantly (P < 0.025) with the severity of pulmonary oedema, defined by the index % lung/body weight. In future research, the aetiology of petechiae needs to be evaluated in terms of circulatory pressures as well as of respiratory factors.
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The effects of raising body temperature on the visual (VEP) and somatosensory (SEP) evoked potentials were observed in normal subjects and in patients with multiple sclerosis. The amplitude of the VEP was significantly reduced to the same degree after heating in normal subjects and in patients with multiple sclerosis but there was no effect on the latency of the potential. Changes in amplitude could not be related to reduction in acuity. In contrast, the cervical SEP was greatly disorganised after heating in many patients with multiple sclerosis while the only effect in normal subjects was to reduce the latency by increasing peripheral conduction velocity. These results suggest that heat caused conduction block in demyelinated axons in the sensory pathways of the cervical spinal cord.
In a previous study of newborn infants we observed overall rib cage collapse during active sleep and postulated that the lungs also could be deflated, leading to reduced oxygen stores and circumstances favoring the rapid development of hypoxemia during apnea. In this study, thoracic gas volume (TGV) has been measured directly by occlusion plethysmography in six normal babies during behavioral quiet and active sleep and related to the different movements of the rib cage and abdomen-diaphragm that occur during each sleep state. TGV was significantly reduced in each baby during active sleep and was associated with rib cage deflation and increased abdomen-diaphragm excursions. The average reduction of TGV was 31% when compared with the volume in quiet sleep and did not depend on the order in which the sleep states were tested. The reduced lung volume in active sleep could have implications for the regulation of breathing in that state. A reduction of lung oxygen stores in active sleep suggests an age-related vulnerability of the young infant to hypoxemia.
Ventilatory responses to rapidly developing hypoxaemia during N2-rebreathing were compared for active and quite sleep in three newborn lambs and four puppies. In lambs, active sleep was associated with: (i) development of ribcage deflation during inspiration, which persisted during progressive hypoxaemia; (ii) depressed ventilatory response to hypoxaemia despite increments of respiratory rate; (iii) delayed arousal. In the puppies, inspiratory collapse of the ribcage did not occur in active sleep and the ventilatory responses during hypoxaemia were similar to those in quite sleep. While apparently defective when related to adults, these responses to hypoxaemia in the lamb are normal. This study illustrates the importance of considering behavioural state and species differences when studying the regulation of breathing, particularly during development.
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Three patients with peripheral neuropathy and an associated benign IgG paraproteinaemia are described. No direct immunological evidence for an aetiological role of the paraprotein was found, and the implications of this are discussed.