Plaque Components in Symptomatic Moderately Stenosed Carotid Arteries Related to Cerebral Infarcts The Plaque At RISK Study

Background and Purpose-Carotid plaque composition is a major determinant of cerebrovascular events. In the present analysis, we evaluated the relationship between intraplaque hemorrhage (IPH) and a thin/ruptured fibrous cap (TRFC) in moderately stenosed carotid arteries and cerebral infarcts on MRI in the ipsilateral hemisphere. Methods-A total of 101 patients with a symptomatic 30% to 69% carotid artery stenosis underwent MRI of the carotid arteries and the brain, within a median time of 45 days from onset of symptoms. The presence of ipsilateral infarcts in patients with and without IPH and TRFC was evaluated. Results-IPH was seen in 40 of 101 plaques. TRFC was seen in 49 of 86 plaques (postcontrast series were not obtained in 15 patients). In total, 51 infarcts in the flow territory of the symptomatic carotid artery were found in 47 patients. Twenty nine of these infarcts, found in 24 patients, were cortical infarcts. No significant relationship was found between IPH or TRFC and the presence of ipsilateral infarcts. Conclusions-MRI detected IPH and TRFC are not related to the presence of old and recent cortical and subcortical infarcts ipsilateral to a symptomatic carotid artery stenosis of 30% to 69%

Recovery from mild traumatic brain injury: a focus on fatigue.

Contains fulltext : 50465.pdf (publisher's version ) (Closed access)BACKGROUND: Fatigue is one of the most frequently reported symptoms after Mild Traumatic Brain Injury (MTBI). To date, systematic and comparative studies on fatigue after MTBI are scarce, and knowledge on causal mechanisms is lacking. OBJECTIVES: To determine the severity of fatigue six months after MTBI and its relation to outcome. Furthermore, to test whether injury indices, such as Glasgow Coma Scale scores, are related to higher levels of fatigue. METHODS: Postal questionnaires were sent to a consecutive group of patients with an MTBI and a minor-injury control group, aged 18-60, six months after injury. Fatigue severity was measured with the Checklist Individual Strength. Postconcussional symptoms and limitations in daily functioning were assessed using the Rivermead Post Concussion Questionnaire and the SF-36. RESULTS: A total of 299 out of 618 eligible (response rate 52%) MTBI patients and 287 out of 482 eligible (response rate 60%) minor-injury patients returned the questionnaire. Ninety-five MTBI patients (32%) and 35 control patients (12%) were severely fatigued. Severe fatigue was highly associated with the experience of other symptoms, limitations in physical and social functioning, and fatigue related problems like reduced activity. Of various trauma severity indices, nausea and headache experienced on the ED were significantly related to higher levels of fatigue at six months. CONCLUSIONS: In conclusion, one third of a large sample of MTBI patients experiences severe fatigue six months after injury, and this experience is associated with limitations in daily functioning. Our finding that acute symptoms and mechanism of injury rather than injury severity indices appear to be related to higher levels of fatigue warrants further investigation

Plasma endothelin-1 as screening marker for cerebral vasospasm after subarachnoid hemorrhage

Cerebral vasospasm complicating subarachnoid hemorrhage causes ischemic stroke and worsens the neurological outcome. The potential role of endothelin-1 in vasospasm pathogenesis may provide therapeutic opportunities. A recent meta-analysis however, did not support the use of endothelin antagonists. Apart from clinical assessment, transcranial Doppler and interval angiography, there are no sensitive screening markers for evolving vasospasm. We investigate the ability of serial measurement of endothelin-1 to predict the development of vasospasm following subarachnoid hemorrhage

Biochemical and neurochemical sequelae following mild traumatic brain injury: summary of experimental data and clinical implications.

Although numerous studies have been carried out to investigate the pathophysiology of mild traumatic brain injury (mTBI), there are still no standard criteria for the diagnosis and treatment of this peculiar condition. The dominant theory that diffuse axonal injury is the main neuropathological process behind mTBI is being revealed as weak at best or inconclusive, given the current literature and the fact that neuronal injury inherent to mTBI improves, with few lasting clinical sequelae in the vast majority of patients. Clinical and experimental evidence suggests that such a course, rather than being due to cell death, is based on temporal neuronal dysfunction, the inevitable consequence of complex biochemical and neurochemical cascade mechanisms directly and immediately triggered by the traumatic insult. This report is an attempt to summarize data from a long series of experiments conducted in the authors' laboratories and published during the past 12 years, together with an extensive analysis of the available literature, focused on understanding the biochemical damage produced by an mTBI. The overall clinical implications, as well as the metabolic nature of the post-mTBI brain vulnerability, are discussed. Finally, the application of proton MR spectroscopy as a possible tool to monitor the full recovery of brain metabolic functions is emphasize