Spontaneous upper limb monoplegia secondary to probable cerebral amyloid angiopathy.

Cerebral amyloid angiopathy is a clinicopathological disorder characterised by vascular amyloid deposition initially in leptomeningeal and neocortical vessels, and later affecting cortical and subcortical regions. The presence of amyloid within the walls of these vessels leads to a propensity for primary intracerebral haemorrhage. We report the unusual case of a 77-year-old female who presented to our emergency department with sudden onset isolated hypoaesthesia and right upper limb monoplegia. A CT scan demonstrated a peripheral acute haematoma involving the left perirolandic cortices. Subsequent magnetic resonance imaging demonstrated previous superficial haemorrhagic events. One week following discharge the patient re-attended with multiple short-lived episodes of aphasia and jerking of the right upper limb. Further imaging demonstrated oedematous changes around the previous haemorrhagic insult. Cerebral amyloid angiopathy is an overlooked cause of intracerebral haemorrhage; the isolated nature of the neurological deficit in this case illustrates the many guises in which it can present.

Adrenergic agents modify cerebral edema and microvessel ultrastructure in porcine sepsis.

OBJECTIVE: To investigate the effects of adrenergic agents on the cerebral response to sepsis. DESIGN: Prospective, randomized, controlled, experimental animal study. SETTING: Medical school research laboratories. SUBJECTS: Twenty-eight middle white pigs (25-30 kg). INTERVENTIONS: Pigs were anesthetized, mechanically ventilated, and randomly assigned to one of the following groups: cecal peritonitis (n = 5), cecal peritonitis with dopexamine (n = 5), cecal peritonitis with dopexamine and the beta2-adrenergic receptor antagonist ICI 118,551 (n = 4), cecal peritonitis with methoxamine (n = 5), cecal peritonitis with dopexamine and methoxamine (n = 4), and sham-operated (n = 5). Sham-operated pigs were killed after laparotomy, and pigs with cecal peritonitis were killed 8 hrs after its induction. Samples of frontal cerebral cortex were taken immediately after death, processed for light and electron microscopy, and then subjected to morphometric analysis. MEASUREMENTS AND MAIN RESULTS: There was significantly more (p <.0005) cerebral perimicrovessel edema in pigs with cecal peritonitis (80.2 microm2 +/- 5.3 sem) than in sham-operated pigs (26.2 microm2 +/- 2.7 sem) and significantly less (p <.0005) perimicrovessel edema in dopexamine-treated pigs with cecal peritonitis (39.8 microm2 +/- 5.5 sem) than in pigs with cecal peritonitis alone (80.2 microm2 +/- 5.3 sem). There was no significant difference between the amount of perimicrovessel edema in pigs with cecal peritonitis treated with dopexamine plus ICI118,551 and pigs with cecal peritonitis alone. The mean cerebral microvessel endothelial cell cross-sectional area in methoxamine-treated pigs with cecal peritonitis (26.3 microm2 +/- 2.6 sem) was significantly greater than that in pigs with cecal peritonitis alone (16.3 microm2 +/- 2.1 sem, p =.008) or in sham-operated pigs (12.3 microm2 +/- 1.3 sem, p =.0005). CONCLUSIONS: Dopexamine protects against cerebral edema formation in sepsis by stimulation of beta2-adrenergic receptors, whereas the alpha1 adrenoceptor agonist methoxamine induces cerebral microvessel endothelial cell swelling.