Studies of electrically induced seizures are reported to show that cortical blood flow is increased by 300%, and cerebral metabolic rate of glucose and oxygen increases approximately 200% during seizure activity (49). Magnetic resonance imaging (MRI) studies have indicated that ECT induces a temporary functional breakdown of the blood–brain barrier, with increased vascular permeability (91). This marked cerebral hyperperfusion increases cerebral blood volume and puts persons with brain tumours who receive ECT at risk for brain herniation and possible death (92). Small or chronic SOLs pose minimal risk, unless associated with increased ICP or other mass effects (93,94), where risk may be substantial. Most successful prospectively treated SOL cases have involved asymptomatic meningiomas that are unlikely to cause obstruction of cerebrospinal fluid circulation and sudden elevations of ICP or peritumour edema. Although no controlled trials have been done, strategies to reduce the risk have been suggested, such as the use of hyperventilation and medication, including antihypertensives, diuretics, and steroids.

Brain Tumours. Several case reports have noted safe and successful ECT in the presence of intracranial tumours, particularly meningiomas (96,97). Recently, there was a first- published report of successful ECT administered to a patient with depression who had a brain tumour and increased intracranial pressure (98). In this case, ECT was used to treat severe, medication-resistant depression. Although no prospective trials exist, various investigators have successfully administered ECT to patients with brain tumours following pretreatment with steroids, particularly dexamethasone, to reduce edema (99). In addition, pretreatment with a beta blocker such as esmolol, a short acting selective beta-1 receptor blocker, has been shown to block seizure- induced increases in heart rate and blood pressure safely and effectively, without significantly effecting seizure duration (100). Along with dexamethasone and

esmolol, the authors used furosemide, a short-acting diuretic with antihypertensive effects, as well as hyperventilation with 100% oxygen to reduce ICP during ECT with brain tumour (101). Historically, ECT has been associated with poor outcome among patients with brain tumours who had CT or MRI evidence of increased ICP, focal neurological deficits, or a history of headaches (96,102).

In the past, few patients with brain tumours had received specific attention to reduce the ECT-associated risk. With increased clinical experience and development of newer pharmacologic agents, ECT may be used cautiously to treat profound depression, even in the presence of ICP. To optimize outcome and minimize post-ECT delirium, combined factors are important. These include unilateral placement of electrodes, lowering the stimulus dose, and spacing the treatments; using little or no anticholinergic medications, particularly those that cross the blood–brain barrier; and obtaining pre-ECT consultations with specialists in neurosurgery and ophthalmology. We require further studies to reevaluate the safety of ECT in such patients. Even though the risk remains high, it must be weighed carefully against the severity and persistence of the psychiatric manifestations in each case.

Intracranial Vascular Masses. Patients being considered for ECT who have intracranial vascular masses (IVMs) are at increased risk for serious morbidity and mortality. The concern is for the possibility of rupture, as well as for their mass effect. Cardiovascular side effects during ECT—including arterial hypertension, increased cerebral blood flow, and increased ICP—are of concern for such patients, as evidenced by case reports of catastrophic and fatal events (102). As of June 1995, however, cases of uncomplicated recovery have also been reported (102,103). There have been no reports of ECT-induced rupture of intracranial aneurysm, despite an estimated 4% prevalence in the adult population (104).