Background: The results of recent studies on cognitive disability after traumatic brain injury-associated diffuse axonal injury (DAI) are inconsistent. In these studies, the diagnosis of DAI relied on cranial computed tomography. Objective: To further clarify the extent and severity of a possibly DAI-associated cognitive impairment by the use of magnetic resonance imaging (MRI) and detailed neuropsychological testing. Design and Participants: From a databank of 299 patients with traumatic brain injury, 18 patients (age range, 17-50 years; median initial Glasgow Coma Scale score, 5) who showed an MRI lesion pattern compatible with pure DAI were identified. All of the patients had undergone MRI on a 3-T system. Pure DAI was defined by the findings of traumatic microbleeds on T2*-weighted gradient-echo images in the absence of otherwise traumatic or nontraumatic MRI abnormalities. Main Outcome Measures: Neuropsychological performance in the categories of attention and psychomo-tor speed, executive functions, spans, learning and memory, and intelligence 4 to 55 months (median, 9 months) after traumatic brain injury. Results: All of the patients showed impairments of 1 or more cognitive subfunctions, and no cognitive domain was fundamentally spared. Memory and executive dysfunctions were most frequent, the former reaching a moderate to severe degree in half of the patients. In comparison, deficits of attention, executive functions, and short-term memory were mostly mild. Correlations between the amount of traumatic microbleeds and specific or global cognitive performance were absent. Conclusions: An MRI lesion pattern compatible with isolated DAI is associated with persistent cognitive impairment. The traumatic microbleed load is no sufficient parameter for the assessment of DAI severity or functional outcome.

Comprehending language in context requires inferencing, particularly for the establishment of local coherence. In the neurolinguistic literature, an inference deficit after right hemisphere brain damage has been postulated, but clinical observation and imaging data suggest that left-frontal lesions might also result in inference deficits. In the present experiment, 25 nonaphasic patients performed a coherence judgment task requiring them to indicate a pragmatic connection between 2 successively presented sentences. Patients with left-temporal or right-frontal lesions performed the task well. In contrast, patients with left-and bifrontal lesions exhibited the most severe deficit. Both error rates and response times were elevated for coherent trials as compared with incoherent trials. These results confirm that the leftfrontal lobe contributes to inference processes.

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Small-vessel disease or cerebral microangiopathy (CMA) is a common finding in elderly people. It is related to a variety of vascular risk factors and may finally lead to subcortical ischemic vascular dementia. Because vessel stiffness is increased, we hypothesized that slow spontaneous oscillations are reduced in cerebral hemodynamics. Accordingly, we examined spontaneous oscillations in the visual cortex of 13 patients suffering from CMA, and compared them with 14 agematched controls. As an imaging method we applied functional near-infrared spectroscopy, because it is particularly sensitive to the microvasculature. Spontaneous low-frequency oscillations (LFOs) (0.07 to 0.12 Hz) were specifically impaired in CMA in contrast to spontaneous very-lowfrequency oscillations (0.01 to 0.05 Hz), which remained unaltered. Vascular reagibility was reduced during visual stimulation. Interestingly, changes were tightly related to neuropsychological deficits, namely executive dysfunction. Vascular alterations had to be attributed mainly to the vascular risk factor arterial hypertension. Further, results suggest that the impairments might be, at least partly, reversed by medical treatment such as angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers. Results indicate that functional near-infrared spectroscopy may detect changes in the microvasculature due to CMA, namely an impairment of spontaneous LFOs, and of vascular reagibility. Hence, CMA accelerates microvascular changes due to aging, leading to impairments of autoregulation.

Cortical thickness was identified as the most sensitive parameter to characterize CMA. A strong correlation was found of morphometric parameters to the severity of CMA based on a score derived from T2-weighted MRI. The degree of cortical atrophy was directly related to the degree of neuropsychological impairment. Our findings suggest that the cortical thickness is a valid marker in the structural and clinical characterization of CMA.