Summary:The rat subarachnoid haemorrhage (SAH) model was further studied to establish the precise time course of the globally reduced CBF that follows and to ascertain whether temporally related changes in cerebral perfusion pressure (CPP) and intracranial pressure (lCP) take place. Parallel ultrastructural studies were per formed upon cerebral arteries and their adjacent perivas cular subarachnoid spaces. SAH was induced by a single intracisternal injection of autologous arterial blood. Serial measurements of regional cortical CBF by hydrogen clearance revealed that experimental SAH resulted in an immediate 50% global reduction in cortical flows that per sisted for up to 3 h post SAH. At 24 h, flows were still significantly reduced at 85% of control values (p < 0.05), but by 48 h had regained normal values and were main tained up to 5 days post SAH. ICP rose acutely after haemorrhage to nearly 50 mm Hg with C-type pressure waves being present. ICP then fell slowly, only fully re turning to control levels at 72 h. Acute hydrocephalus was observed on autopsy examination of SAH animals but not in controls. Reductions in CPP occurred post SAH, but only in the order of 15%, which could not alone account for the fall in CBF that took place. At 48 and, to a lesser extent, 24 h post SAH, myonecrosis confined largely to smooth muscle cells of the immediately sub in-

Objectives: To assess in a prospective randomised study the association between motor block resulting from high and low dose epidural infusions of bupivacaine in labour and the incidence of long term backache after childbirth, and to compare the incidence of backache in women not receiving epidural analgesia. Design: Women requesting epidural analgesia in labour between October 1991 and March 1994 were randomised to receive infusions of either bupivacaine alone or low dose bupivacaine with opioid. Data were collected during labour and the immediate postpartum period from these women and from women recruited at random over the same time from those who had laboured without epidural analgesia. A postal questionnaire about symptoms was sent three months after childbirth to all women. Further data were collected one year after childbirth from those who had reported new backache at three months. Setting: St Thomas's Hospital, London. Subjects: 599 women were recruited, of whom 450 (75%) replied to a follow up questionnaire. Results: 152 women (33.8% of responders) reported backache lasting three months after delivery and, of these, 33 (7.3%) had not previously suffered with backache. There were no significant differences between the treatment groups in the incidence of postnatal backache overall or of new backache or any symptoms after childbirth. Among all demographic, obstetric, and epidural variables examined the only factors significantly associated with backache after childbirth were backache before and during pregnancy. Conclusions: The incidence of new long term backache was not significantly increased in women who received epidural analgesia in labour. Motor block resulting from epidural local anaesthetic administration was not a significant factor in the development of backache. Key messages About half of all women suffer backache during pregnancy, but many forget this when questioned retrospectively A prospective study showed that the incidence of new postpartum backache is 7.3 The use of epidural analgesia in labour had no effect on the incidence of postpartum backache In a randomised trial motor block in labour was not associated with an increase the incidence of backache

SUMMARYThe influence of the duration of ischemia on the pattern of cerebral blood flow in recirculation was studied in anesthetised rats. Severe incomplete cerebral ischemia (mean ischemic flow = 5.8 ± 0.4 ml/100 g/min) was produced by four-vessel occlusion and recirculation permitted after 15,30 or 60 minutes ischemia. All three groups showed an immediate hyperemia followed by hypoperfusion. Hyperemia was maximal following 15 minutes ischemia and least pronounced following 60 minutes ischemia (p = 0.0249). Hypoperfusion started most quickly following 15 minutes ischemia and was delayed following 60 minutes ischemia (p < 0.001). In established hypoperfusion there was no difference in flow between the three groups. The possible mechanisms of these changes in flow are discussed.Stroke Vol 17, No 3, 1986RECIRCULATION after cerebral ischemia is a common clinical event. It occurs after the spontaneous break-up of cerebral emboli and follows the removal of clips used for temporary hemostasis during surgery for aneurysm and arteriovenous malformation. Operations such as extracranial-intracranial by-pass are designed to increase circulation to chronically ischemic brain. The initial period of recirculation after ischemia is of paramount importance and two patterns of post-ischemic circulatory disturbance have been described, the 'no-reflow phenomenon' and 'hyperemia-hypoperfusion'. The no-reflow phenomenon was originally demonstrated as an absence of carbon black staining after 5-7 minutes global cerebral ischemia in rabbits 1 and has also been demonstrated in primates 2 and rats. 3 Noreflow can be reversed or prevented by recirculation at a satisfactory blood pressure, even if ischemia is prolonged. -3 Explanations for the no-reflow phenomenon have included blockage of the vascular lumen by platelets or red cell aggregates; 6 -7 change in blood viscosity; 8 local intravascular coagulation; 9 and direct capillary compression from edematous endothelial and glial cells. "12 The alternative pattern of post-ischemic circulatory disturbance is where an initial increase in cerebral blood flow, 'reactive hyperemia', is followed by a reduction in flow, 'delayed hypoperfusion'. This secondary hypoperfusion has been demonstrated in the isolated canine brain;13 following global cerebral ischemia in the cat, 14 dog, 15 monkey 16 and rat 17 and following focal cerebral ischemia in the cat. 18It has been difficult to reconcile these two postischemic circulatory changes. Recent work has suggested that the no-reflow phenomenon will follow complete cessation of cerebral blood flow and does not It is important to define the factors in ischemia that influence post-ischemic circulatory changes. In these studies, we have chosen to vary the duration of ischemia with a fixed ischemic flow in order to decide whether post-ischemic hyperemia and hypoperfusion are universal phenomena or whether the degree and duration of these events are influenced by the duration of the preceding ischemia. Methods Animal PreparationExperiments were performed in ...

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SUMMARY Regional cerebral blood flow (rCBF) and oedema following profound temporary ischaemia were studied in the gerbil. Ninety-four per cent of animals died within 24 hours of reperfusion; 50% by 4 hours. Regional differences in oedema (specific gravity method), Evans blue (EB) staining and rCBF (hydrogen clearance technique) occurred. Oedema developed during arterial occlusion, being inversely proportional to residual flow and was markedly exacerbated during reperfusion. Reperfusion hyperaemia was maximal in the parietal and hippocampal regions (ischaemic rCBF 4 ml 100 g-I min-'). Oedema was disappearing in all areas by 3 hours of reperfusion and autoregulation returned in the occipital region (mean ischaemia rCBF 8 ml 100 g-' min-'). EB staining and haemorrhage appeared in the thalamus (rCBF 10 ml 100 g-' min-') as oedema was decreasing. It is suggested that the amount of oedema and hyperaemia during reperfusion are dependent on the severity of the ischaemia. Areas of moderate ischaemia (8-10 ml 100 g-' min-') show little hyperaemia and greater oedema resolution during reperfusion as compared to areas of severe ischaemia (circa 4 ml 100 g-' min-') where there is marked hyperaemia with less oedema resolution. Early in the reperfusion period, oedema is not associated with EB staining and indicates a cytotoxic mechanism. The vasogenic component, with macroscopic haemorrhages and leakage of EB occurs later. In this model it is concluded that the early cytotoxic oedema formation and hyperaemia are phenomena with little bearing on mortality, which correlates better with later vasogenic changes.