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-

We report a case of epidural haematoma following a steroid injection into the cervical epidural space. The complication occurred on the seventh such injection over a 2 year period for chronic spinal pain. Surgical decompression over the seventh cervical and the upper 3 thoracic vertebrae was required to alleviate the symptoms of paralysis and anaesthesia. The patient subsequently required skin grafting to the surgical site and two trans-urethral resections of the prostate gland during his 6 week hospital admission. He made a full recovery.

Transforming growth factor-beta1 (TGF-beta1) is a fibrogenic cytokine that is involved in postinjury repair and is implicated in the etiology of postsubarachnoid hemorrhage (SAH) chronic communicating hydrocephalus. TGF-beta1 was measured by enzyme-linked immunosorbant assay (ELISA) in sequential samples of cerebrospinal fluid (CSF) in 11 patients with hydrocephalus after SAH; levels were seen to be biphasically elevated and sources were investigated. TGF-beta1 levels were compared with albumin levels that estimated CSF blood content. Control samples from nonhemorrhagic hydrocephalics were tested similarly. Mean total TGF-beta1 levels were elevated to 4400+/-3435 (+/-SD) pg/mL greater than control levels of 97+/-42 at 1 to 2 days posthemorrhage. Thereafter, levels fell to 714+/-401 by 5 to 6 days posthemorrhage, then rose to a second peak of 1667+/-774 at 9 to 10 days posthemorrhage, remaining significantly increased until 19 days posthemorrhage (P = 0.007). The first peak probably derived from extravasated platelets and correlated with increased albumin levels in the CSF. The second TGF-beta1 peak rose greater than CSF albumin levels that had stabilized at this time, and thus was attributed to a tissue-specific response rather than a re-bleed. TGF-beta1 was detected in the choroid secretory epithelium from controls, but levels were greater in SAH patients at 10 to 12 days posthemorrhage. The authors conclude that the elevated levels of TGF-beta1 in CSF after SAH are derived initially from blood and later from endogenous sources such as the choroid plexus.

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Acutely measured levels of TGFbeta1/beta2 in the CSF of patients with subarachnoid haemorrhage are thus potential prognostic biomarkers for the subsequent development of chronic communicating hydrocephalus, indicating likely dependency on CSF shunting.