Intracerebral hemorrhage due to cerebral amyloid angiopathy after head injury: Report of a case and review of the literature.

Cerebral amyloid angiopathy (CAA) is an important cause of spontaneous intracerebral hemorrhage in the elderly. A few case reports of CAA-related intracerebral hemorrhage after head injury, usually following a fall, have been published. More rarely, it may occur in the setting of a traffic accident, with only four cases having been reported. We describe a case of CAA-related intracerebral hemorrhage in an 88-year-old man injured in a road traffic accident. The patient died 14 h after the accident. Autopsy examination revealed a left frontoparietal hematoma and CAA of most of the small leptomeningeal and cortical arteries, as well as several capillaries, predominantly in the parietal and occipital lobes. Except for bruises in the frontal and zygomatic regions, elbow and forearm, to the left, there were no skull fractures or traumatic lesions in other parts of the body. We review the literature on CAA-related intracerebral hemorrhage associated with head injury. CAA-related intracerebral hemorrhage after head injury may occur due to a minor trauma, minor and severe falls, or in the setting of a traffic accident. However, even in this last condition, it seems to happen mostly in patients who had a mild to moderate head injury. These facts show that replacement of the contractile components of the arterial tunica media by amyloid renders the affected cerebral blood vessels more vulnerable to head injury associated with acceleration and deceleration, independently of the severity of the dynamic loading acting on the head.

Diffuse vascular injury in fatal road traffic accident victims: its relationship to diffuse axonal injury.

The authors have reported a macro- and microscopic study of brain lesions in 120 victims of fatal road traffic accidents, independent of the survival time. Diffuse vascular injury (DVI) was found in 14 patients (11.7%). All patients with DVI died within 24 h after the accident. The 14 patients with DVI also showed severe (Grade 2 or 3) diffuse axonal injury (DAI). Since DVI is restricted to road traffic accidents and incompatible with life, the high frequency observed in our series could be explained by the fact that all 120 patients were victims of road traffic accidents, and 69.2% had died within 24 h after the accident. The association between DVI and severe DAI (Grades 2 and 3) suggests that both lesions depend on the same mechanism, with the degree of axonal and vascular damage being determined by the intensity of the head acceleration. Our results show a relationship between DVI and DAI that suggest there may be a spectrum or at least a continuum between these entities as distinct from DVI being a separate entity.

Chronic ethanol intake and ageing effects on cortical and basal forebrain cholinergic parameters: morphometric and biochemical studies.

Abstract Twenty-eight Wistar rats treated orally with 20% ethanol solution, were divided into two groups: adult group (n = 19) and aged group (n = 9) consisting of animals aged 4 and 12 months, respectively, at the beginning of the treatment. Neurons from the basal nucleus region were counted and the percentage of choline acetyltransferase-immunoreactive cholinergic neurons was determined in adjacent sections. Acetylcholine release and choline-acetyltransferase activity in the cerebral cortex were assessed in the same animals. Nutritional parameters of the ethanol treated animals were monitored and found to be normal. Chronic exposure to ethanol did not result in global neuronal loss or loss of cholinergic neurons in the basal nucleus region. However, a greater expression of ChAT-immunoreactivity in the basal nucleus region and a tendency toward increased ChAT activity in the cerebral cortex of the control and treated aged animals, compared respectively to adult ones, were observed. These findings suggest adaptive changes of the aged rats in response to the possible cholinergic hypofunction, manifested as a decreased release of acetylcholine under stimulated conditions.