2008 AAN Fall Conference Takes Place October 10–12 in New Orleans

Background: Previous studies have yielded evidence of an enhanced risk of cardiovascular disease, especially stroke, among patients with migraine. Our understanding of the underlying mechanisms is far from complete. The aims of the present study were to investigate the potential association between migraine and atherosclerosis and to assess the risk of venous thromboembolism as a clinical surrogate for a procoagulant state in patients with migraine.Methods: The examination was part of the population-based Bruneck Study. During the 2005 evaluation, 574 participants aged 55-94 years underwent neurologic and laboratory examinations involving a standardized headache interview and scanning of the carotid and femoral arteries to evaluate presence, severity, and progression (2000-2005) of atherosclerosis.Results: A large number of well-founded and putative cardiovascular risk factors have emerged as being unrelated to migraine status. Prevalence, severity, and 5-year progression of carotid and femoral atherosclerosis did not differ significantly between migraineurs with and without aura and nonmigraineurs. In fact, there was even a tendency for atherosclerosis to be less pronounced among patients with migraine, and for the intima-media thickness to be lower (p = 0.029). As a novel finding migraineurs faced a significantly enhanced risk of venous thromboembolism (18.9% vs 7.6% in nonmigraineurs, age/sex-adjusted p = 0.031).Conclusion: This study is the first to compare the burden of atherosclerosis as quantified by high-resolution duplex ultrasound between migraineurs and nonmigraineurs in the general community, and provides solid evidence against the view that migraine predisposes to atherosclerosis. The higher risk for venous thromboembolism among migraineurs (prothrombotic state) awaits confirmation and elaboration in future research.GLOSSARY: CCA = common carotid arteries; CVD = cardiovascular disease; ICA = internal carotid arteries; IMT = intima-media thickness; MMSE = Mini-Mental State Examination; VTE = venous thromboembolism.(C)2008AAN Enterprises, Inc.

Background: Older adults get lost, in many cases because of recognized or incipient Alzheimer disease (AD). In either case, getting lost can be a threat to individual and public safety, as well as to personal autonomy and quality of life. Here we compare our previously described real-world navigation test with a virtual reality (VR) version simulating the same navigational environment.Methods: Quantifying real-world navigational performance is difficult and time-consuming. VR testing is a promising alternative, but it has not been compared with closely corresponding real-world testing in aging and AD. We have studied navigation using both real-world and virtual environments in the same subjects: young normal controls (YNCs, n = 35), older normal controls (ONCs, n = 26), patients with mild cognitive impairment (MCI, n = 12), and patients with early AD (EAD, n = 14).Results: We found close correlations between real-world and virtual navigational deficits that increased across groups from YNC to ONC, to MCI, and to EAD. Analyses of subtest performance showed similar profiles of impairment in real-world and virtual testing in all four subject groups. The ONC, MCI, and EAD subjects all showed greatest difficulty in self-orientation and scene localization tests. MCI and EAD patients also showed impaired verbal recall about both test environments.Conclusions: Virtual environment testing provides a valid assessment of navigational skills. Aging and Alzheimer disease (AD) share the same patterns of difficulty in associating visual scenes and locations, which is complicated in AD by the accompanying loss of verbally mediated navigational capacities. We conclude that virtual navigation testing reveals deficits in aging and AD that are associated with potentially grave risks to our patients and the community.(C)2008AAN Enterprises, Inc.

Imaging for headaches is one of the most frequent and at times challenging decisions a neurologist has to make in the clinical practice of neurology and is complicated by today's medical-legal milieu and overseeing regulatory organizations. Although the final decision should always be made by the treating physician, the American Academy of Neurology has developed practice parameters for the imaging of headaches. One strong criticism of the overzealous use of neuroimaging in patients with headache is the frequency of incidental findings, which may in turn increase a patient's anxiety and potentially cause an exacerbation of symptoms. This may subsequently lead to unnecessary testing as well as neurosurgical intervention. The clinical interpretation of incidental findings and headaches is best made by a neurologist who is able to correlate the imaging findings with the patient's symptoms and examination. One of the principal precepts in medicine, "primum nil nocere" or "first, do no harm" to patients, should be considered in the interpretation of these so-called abnormalities. The development of programs to certify competence in physicians who have completed accredited training programs in neuroimaging as well as headache medicine by the United Council for Neurologic Subspecialties is an important advancement that allows clinicians the opportunity to enhance quality of patient care.(C) 2008 American Academy of Neurology

Structural brain imaging with CT or MRI should be performed in any patient with progressive cognitive impairment to rule out a reversible cause, such as a benign brain tumor, a subdural hematoma, or hydrocephalus. But imaging can also help separate the various types of degenerative dementia and facilitates the prognosis of these disorders. Medial temporal atrophy is an early finding in Alzheimer disease (AD). Early in AD, metabolism is decreased in the parietotemporal association cortex and retrosplenial region. When these imaging findings are present in mild cognitive impairment, it is more likely to evolve to AD. Amyloid deposition in AD and Lewy body dementia can now be imaged, differentiating these disorders from dementias without amyloid deposition, such as frontotemporal dementia and corticobasal degeneration. Atrophy or the decrease in brain metabolic activity associated with the dementias could be used as surrogate markers of response to new therapies in clinical trials.(C) 2008 American Academy of Neurology