Orofacial neuralgia associated with a middle cerebral artery aneurysm

Chronic orofacial pain of neuropathic origin can present diagnostic and management dilemmas to dental practitioners and also affects the patient's quality of life. Intracranial aneurysms are a potential cause of stroke (e.g. sub‐arachnoid haemorrhage) that is usually associated with, high rates of mortality and morbidity. A patient who had been previously managed for symptoms of temporomandibular joint disorder (TMD) presented with sharp, shooting pain of moderate intensity. It was precipitated by swallowing, and radiated to the right throat, posterior border of the mandible, ear and temporomandibular joint. Clinical and radiological investigations ruled out odontogenic pain, TMD and other more common types of facial pain. Magnetic resonance imaging revealed a 7 × 6 mm aneurysm in the right middle cerebral artery (MCA) which was subsequently surgically clipped. Interestingly, the facial pain resolved after this procedure. Compression of the insular region of the brain innervated by the trigeminal, glossopharyngeal and vagus nerves provides a plausible explanation for the pain reported. To our knowledge, this is the first case of facial neuralgia associated with an aneurysm in the MCA which emphasizes the importance of a multidisciplinary approach in the diagnosis and management of unusual cases of chronic orofacial pain.     

CARBAMAZEPINE USE IN AGGRESSIVE BEHAVIOUR ASSOCIATED WITH SENILE DEMENTIA

In a randomized placebo crossover controlled study, six patients meeting DSM-III-R criteria for Alzheimer's disease and exhibiting significantly aggressive behaviour were administered carbamazepine (in doses up to 600 mg daily) and placebo, with each treatment period lasting 8 weeks. Levels of aggression as measured by the RAGE scale were significantly reduced compared with placebo (p<0.05). The results suggest that carbamazepine is an effective anti-aggressive agent in patients with dementia. Recommendations for further studies are made.     

Studies on the mechanism of experimental proteinuria

When renin is administered intramuscularly to the rat, massive proteinuria occurs without a significant elevation of mean arterial blood pressure. The intravenous administration of renin to normal rats results in a great increase in urinary protein excretion. This response to renin is abolished by bilateral adrenalectomy. While the adrenalectomized rat fails to respond to intravenous renin with increased proteinuria, it does exhibit a normal elevation in mean arterial blood pressure. It is concluded that in the rat, the proteinuric property of renin is not related to the ability of this compound to elevate arterial blood pressure. The passage of plasma proteins has been followed through the kidney and into the urine by attaching them to the dye T-1824 (Evan's blue). The intra-peritoneal injection of renin causes a massive, transient proteinuria in the rat. From a study of frozen sections of the kidney of rats whose plasma proteins are labelled with T-1824, it is concluded that the preponderant basis for renin proteinuria is an increase in glomerular permeability.