IGRAINE IS A COMMON, chronic, multifactorial neurovascular disorder typically characterized by recurrent attacks of disabling headache and autonomic nervous system dysfunction (migraine without aura); up to one third of patients also have neurological aura symptoms (migraine with aura). 1,2 Migraine has been suggested to be an independent risk factor for stroke, but the evidence is conflicting and seems to be restricted to certain subpopulations (eg, women with migraine with aura who are younger than 45 years, particularly ones who smoke or use oral contraceptives [OCs]). 3-9 Case reports on patients with so-called migrainous infarction suggest that the posterior circulation territory (PCT) is most commonly affected. 8,9 However, data are lacking on prevalence of subclinical infarcts in a wide spectrum of migraine patients in the general population. Patients with migraine may also be at increased risk of more diffuse subclinical lesions in the deep white matter or periventricular areas that are only detected on neuroimaging. 10-12 Several clinic-based magnetic resonance imaging (MRI) studies have reported this,
Purpose To investigate whether the blood-brain barrier (BBB) leaks blood-circulating substances in patients with early forms of Alzheimer disease (AD), and if so, to examine the extent and pattern of leakage. Materials and Methods This study was approved by the local medical ethical committees of the Maastricht University Medical Center and Leiden University Medical Center, and written informed consent was obtained from all subjects. For this pilot study, 16 patients with early AD and 17 healthy age-matched control subjects underwent dynamic contrast material-enhanced magnetic resonance (MR) imaging sequence with dual time resolution for 25 minutes. The Patlak graphical approach was used to quantify the BBB leakage rate and local blood plasma volume. Subsequent histogram analysis was used to determine the volume fraction of the leaking brain tissue. Differences were assessed with linear regression analysis, adjusted for confounding variables. Results The BBB leakage rate was significantly higher in patients compared with that in control subjects in the total gray matter (P < .05) and cortex (P = .03). Patients had a significantly higher volume fraction of the leaking brain tissue in the gray matter (P = .004), normal-appearing white matter (P < .04), deep gray matter (P = .01), and cortex (P = .004). When all subjects were considered, scores on the Mini-Mental State Examination decreased significantly with increasing leakage in the deep gray matter (P = .007) and cortex (P < .05). Conclusion The results of this study showed global BBB leakage in patients with early AD that is associated with cognitive decline. A compromised BBB may be part of a cascade of pathologic events that eventually lead to cognitive decline and dementia. RSNA, 2016 Online supplemental material is available for this article.
EAD INJURY IS ONE OF THE most common injuries in the Western world with an estimated incidence of hospitaltreated patients with minor head injury of 100 to 300 per 100 000 population. 1 Minor head injury is commonly defined as blunt trauma to the head, after which the patient has lost consciousness for less than 15 minutes or has a short posttraumatic amnesia of less than 1 hour, or both, as well as a normal or minimally altered mental status on presentation (a Glasgow Coma Scale [GCS] score of 13-15). 2,3 Intracranial complications of minor head injury are infrequent (6%-21%) but potentially life-threatening and may require neurosurgical intervention in a minority of cases (0.4%-1.0%). 3-8 Neurocranial injury that does not require See also pp 1511 and 1551 and Patient Page.
We demonstrated a larger tissue volume with subtle BBB leakage in patients with cSVD than in controls. This was shown in the NAWM, WMH, and CGM, supporting the generalized nature of cSVD.
Abstract-Aortic stiffness predicts an excess risk of stroke, supposedly via cerebral small-vessel disease. White matter hyperintensities, silent lacunar infarcts, and brain microbleeds, manifestations of cerebral small-vessel disease on neuroimaging, may precede overt cerebrovascular disease. Therefore, we assessed whether aortic stiffness is also related to such lesions. In 167 hypertensive patients (85 men) without a history of cardiovascular or cerebrovascular disease, a mean age of 51.8Ϯ13.1 years, and untreated office blood pressure levels of 169Ϯ25/104Ϯ12 mm Hg, we determined aortic pulse wave velocity and office and ambulatory 24-hour pulse pressure (off medication), as well as the volume of white matter hyperintensities and the presence of lacunar infarcts and microbleeds using brain MRI. Linear and logistic regression analyses were performed to assess the relationships between the arterial stiffness measures and brain lesions. Aortic stiffness and pulse pressure were significantly related to each of the brain lesions in univariate analyses (PϽ0.05). Multivariate analyses, adjusted for age, sex, brain volume, mean arterial pressure, and heart rate, showed that a higher pulse wave velocity was significantly associated with a greater volume of white matter hyperintensities (unstandardized regression coefficient: 0. Key Words: aortic stiffness Ⅲ pulse wave velocity Ⅲ pulse pressure Ⅲ cerebral small-vessel disease Ⅲ brain Ⅲ hypertension T he arterial system gradually stiffens because of the shared effects of ageing, high blood pressure (BP), and other vascular risk factors. 1 Arterial stiffness can be assessed by noninvasive pulse wave velocity (PWV) measurements. 2 In particular, the velocity of the carotidfemoral or aortic pulse wave appears to be of prognostic importance and is considered to be the "gold standard" for arterial stiffness. 3 Several studies, in both population-and patient-based cohorts, have demonstrated a strong association between increased aortic PWV and excess risk of cardiovascular complications, including stroke. 4 -6 Whether the risk of stroke is mediated by large-and/or small-vessel disease is not clear, but the previously reported increased risk of stroke in the presence of preclinical cerebral microvascular disease, ie, white matter hyperintensities (WMHs), silent lacunar infarcts (LACs), and/or brain microbleeds (BMBs), suggests small-vessel disease involvement. 7,8 O'Rourke and Safar 9 hypothesized that cerebral microvascular disease results from the damaging forces of abnormal flow pulsations extending into small cerebral arteries as a consequence of arterial stiffening. However, the relationship between arterial stiffness and manifestations of cerebral small-vessel disease has not been investigated in great detail, and studies have yielded conflicting results. 10 -12 The present study was undertaken to assess the associations between aortic PWV and WMHs, LACs, and BMBs as manifestations of silent cerebral small-vessel disease on MRI of the brain in a cohort of hypertensiv...
Context A previous cross-sectional study showed an association of migraine with a higher prevalence of magnetic resonance imaging (MRI)–measured ischemic lesions in the brain. Objective To determine whether women or men with migraine (with and without aura) have a higher incidence of brain lesions 9 years after initial MRI, whether migraine frequency was associated with progression of brain lesions, and whether progression of brain lesions was associated with cognitive decline. Design, Setting, and Participants In a follow-up of the 2000 Cerebral Abnormalities in Migraine, an Epidemiological Risk Analysis cohort, a prospective populationbased observational study of Dutch participants with migraine and an age- and sexmatched control group, 203 of the 295 baseline participants in the migraine group and 83 of 140 in the control group underwent MRI scan in 2009 to identify progression of MRI-measured brain lesions. Comparisons were adjusted for age, sex, hypertension, diabetes, and educational level. The participants in the migraine group were a mean 57 years (range, 43–72 years), and 71% were women. Those in the control group were a mean 55 years (range, 44–71 years), and 69% were women. Main Outcome Measures Progression of MRI-measured cerebral deep white matter hyperintensities, infratentorial hyperintensities, and posterior circulation territory infarctlike lesions. Change in cognition was also measured. Results Of the 145 women in the migraine group, 112 (77%) vs 33 of 55 women (60%) in the control group had progression of deep white matter hyperintensities (adjusted odds ratio [OR], 2.1; 95%CI, 1.0–4.1; P=.04). There were no significant associations of migraine with progression of infratentorial hyperintensities: 21 participants (15%) in themigraine group and 1 of 57 participants (2%) in the control group showed progression (adjusted OR, 7.7; 95% CI, 1.0–59.5; P=.05) or new posterior circulation territory infarctlike lesions: 10 of 203 participants (5%) in the migraine group but none of 83 in the control group (P=.07). There was no association of number or frequency of migraine headaches with progression of lesions. There was no significant association of high vs nonhigh deep white matter hyperintensity load with change in cognitive scores ( 3.7 in the migraine group vs 1.4 in the control group; 95% CI, 4.4 to 0.2; adjusted P=.07). Conclusions In a community-based cohort followed up after 9 years, women with migraine had a higher incidence of deep white matter hyperintensities but did not have significantly higher progression of other MRI-measured brain changes. There was no association of migraine with progression of any MRI-measured brain lesions in men.
The abnormal, strong functional connectivity in PNES patients provides a neurophysiological correlate for the underlying psychoform and somatoform dissociation mechanism where emotion can influence executive control, resulting in altered motor function (eg, seizure-like episodes).
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