Neurology. 70(22, Parts 1 and 2): May 27, 2008

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Wermer, Marieke J.H. ; Koffijberg, Hendrik ; van der Schaaf, Irene C.
Effectiveness and costs of screening for aneurysms every 5 years after subarachnoid hemorrhage
p. 2053-2062
Abstract
Background: Patients who survive after subarachnoid hemorrhage (SAH) are at risk for a recurrence despite successful treatment of the ruptured aneurysm and may therefore benefit from screening for new aneurysms.Methods: We screened 610 patients with SAH with CT angiography 2-18 years after clipping of the aneurysms. Results of screening were used as input for a Markov decision model. We compared the expected number of recurrent hemorrhages, life expectancy, quality-adjusted life-years (QALYs), and costs associated with the strategies "screening every 5 years" and "no screening."Results: Screening individuals with previous SAH prevented almost half of the recurrences, slightly increased life expectancy (from 21.06 to 21.08 years), but reduced QALYs (from 12.18 to 12.04) and increased costs (from $2,750 to $4,165 per patient). Screening was cost-saving without increasing QALYs in patients with a more than twofold risk above baseline of both aneurysm formation and rupture and it was cost-saving while increasing QALYs if both risks were at least 4.5 times higher. In patients with reduced quality of life because of fear for a recurrence, screening increased QALYs at a maximum cost of $17,422 per QALY.Conclusions: In general, screening patients with previous subarachnoid hemorrhage (SAH) cannot be recommended. Screening can save costs and increase quality-adjusted life-years (QALYs) in patients with a relatively high risk of both aneurysm formation and rupture, and increases QALYs at acceptable costs in patients with fear for a recurrence. More data are needed on risk factors for aneurysm formation and rupture in patients with previous SAH and on management of fear for a recurrence to identify patients who can benefit from screening.

Kipps, C M. ; Nestor, P J. ; Dawson, C E. ; Mitchell, J ; Hodges, J R.
Measuring progression in frontotemporal dementia: Implications for therapeutic interventions.
p. 2046-2052
Abstract
Background: There is a need for instruments which can measure progression of disease in frontotemporal dementia (FTD), particularly with respect to the assessment of potential therapeutic agents.Methods: The Cambridge Early Onset Dementia Clinic database was reviewed for all prospectively enrolled cases of FTD with documented scores on the Mini-Mental State Examination (MMSE) or Addenbrooke's Cognitive Examination (ACE) on at least two occasions. We identified 50 cases fulfilling these criteria: pathologic confirmation was present in 11 of 16 patients who had died, 12 of the remainder had imaging abnormalities on their initial scans, and 22 had structural scans no different from controls. We compared these groups to a cohort with early AD (n = 25) and healthy controls (n = 10).Results: There was clear cognitive decline (measured by the MMSE and ACE) in patients who had died, and those with documented atrophy on initial MRI scan. In contrast, patients with FTD with normal scans showed no change in cognitive scores over a much longer interval, and serial ACE measurements paralleled those of controls. Power calculations showed that the inclusion of these patients with FTD would significantly increase the number of cases needed in any therapeutic trial.Conclusion: Addenbrooke's Cognitive Examination is a simple monitoring tool which can detect progression of disease in frontotemporal dementia over a 1- to 2-year interval without the need for serial imaging. We estimated that a clinical trial that enrolled subjects with abnormal MR scans would require 135 subjects per group to detect a small effect, and 35 for a medium effect.

Kwee, R M.; van Oostenbrugge, R J. , PhD; Hofstra, L ; Teule, G J. ; van Engelshoven, J et al Identifying vulnerable carotid plaques by noninvasive imaging
p. 2401-2409, June 10, 2008.
Abstract
Stroke results in considerable morbidity and mortality. Prevention is therefore of particular importance. On the basis of large clinical trials, carotid endarterectomy (CEA) is performed in selected patient groups to prevent stroke. Patient symptomatology and degree of carotid stenosis are the main clinical grounds to perform CEA. However, many individual patients undergo surgery with its attendant risks without taking advantage of it, whereas in others CEA is probably incorrectly withheld. There is therefore an urgent need for new adjuncts to identify high-risk subgroups of patients who particularly benefit from potentially hazardous interventions. Multiple noninvasive imaging modalities have shown their potential to differentiate high-risk, vulnerable carotid plaques from stable plaques. The ultimate goal is to implement one or a combination of these imaging modalities in daily clinical practice. This review gives an up-to-date overview of the clinical potential of these imaging modalities in identifying patients with carotid atherosclerosis who are at high risk for developing stroke. Advantages and limitations of each imaging technique are outlined. Additionally, recommendations for future research are presented.GLOSSARY: CEA = carotid endarterectomy; CCA = common carotid artery; GSM = gray-scale medium; ICA = internal carotid artery; IJV = internal jugular vein; MDCT = multidetector-row CT; MES = microembolic signal; RR = relative risk; TCD = transcranial Doppler; TFE = turbo field echo; TSE = turbo spin echo; USPIO = ultrasmall particles of iron oxide.

Kang, Suk Y. ; Kim, Jong S.
Anterior cerebral artery infarction: Stroke mechanism and clinical-imaging study in 100 patients.
p. 2386-2393, June 10, 2008.
Abstract
Background: Stroke mechanisms and clinical features of anterior cerebral artery (ACA) territory infarction have rarely been investigated using MRI.Objectives: To verify stroke mechanisms and to make clinical imaging correlation.Methods: Clinical, MRI, and angiographic findings of 100 consecutive patients with ACA infarction were studied.Results: Motor dysfunction (n = 91) was the most common symptom, and severe motor dysfunction was related to supplementary motor area/paracentral lobule involvement (p = 0.016). Hypobulia/apathy (n = 43) was related to involvement of fontal pole (p = 0.002), corpus callosum/cingulate gyrus (p = 0.003), and superior frontal gyrus (p < n =" 30)" n =" 25)" p =" 0.035)." n =" 20)," n =" 20)," n =" 12)," n =" 9)." p =" 0.077)" p =" 0.016)">