Although it is known that processing speed deficits are one of the primary cognitive impairments in multiple sclerosis (MS), the underlying neural mechanisms responsible for impaired processing speed remain undetermined. Using BOLD functional magnetic resonance imaging, the current study compared the brain activity of 16 individuals with MS to 17 healthy controls (HCs) during performance of a processing speed task, a modified version of the Symbol Digit Modalities Task. Although there were no differences in performance accuracy, the MS group was significantly slower than HCs. Although both groups showed similar activation involving the precentral gyrus and occipital cortex, the MS showed significantly less cerebral activity than HCs in bilateral frontal and parietal regions, similar to what has been reported in aging samples during speeded tasks. In the HC group, processing speed was mediated by frontal and parietal regions, as well as the cerebellum and thalamus. In the MS group, processing speed was mediated by insula, thalamus and anterior cingulate. It therefore appears that neural networks involved in processing speed differ between MS and HCs, and our findings are similar to what has been reported in aging, where damage to both white and gray matter is linked to processing speed impairments.

Context/Objective: Cognitive deficits can impact as many as 60% of individuals with spinal cord injury (SCI). In an effort to identify the nature of cognitive deficits in SCI, we examined neuropsychological test performance in individuals with SCI, age matched healthy controls and older healthy controls. Design: Participants completed a motor-free neuropsychological test battery assessing attention, working memory, information processing speed, new learning /memory and executive control. Setting: Outpatient rehabilitation research facility. Participants: Participants included 60 individuals with chronic spinal cord injury [SCI; 32 with paraplegia (T2-T12) and 28 with tetraplegia (C3-T1)], 30 age-matched healthy controls (AMHC; 30-40 years old) and 20 older healthy controls (OHC; 50-60 years old). Outcome Measures: Wechsler Intelligence Scale-3 rd edition (WAIS-III) Digit Span and Letter-Number Sequencing; Symbol Digit Modalities Test (SDMT)oral version; California Verbal Learning Test-II; Paced Auditory Serial Addition Test (PASAT); Wechsler Abbreviated Scale of Intelligence (WASI); Delis-Kaplan Executive Function System; Verbal Fluency subtest. Results: Significant differences were noted between the SCI and AMHC groups on measures of information processing speed, new learning and memory, and verbal fluency. No significant differences were noted between the groups on tests of attention or working memory. Conclusion: The current study documented differences in specific realms of cognitive functioning between a chronic SCI sample and AMHC. Implications for cognitive rehabilitation and overall quality of life are discussed. Additional research is needed utilizing a more comprehensive battery of motor-free neuropsychological tests that avoid the confound of upper limb motor limitations on cognitive performance.

Our results support the notion that executive deficits in MS may be explained by slow PS. These findings highlight the role of slowed PS as a primary impairment underlying other cognitive functions. Disentangling the relative contribution of PS to executive function is an important step toward the development of appropriate rehabilitation strategies for persons with MS.

Background Working memory deficits are common in multiple sclerosis (MS). The modified Story Memory Technique (mSMT) has been shown to improve new learning and memory in MS, but its effects on working memory (WM) are currently unknown. Objective The present study presents a secondary analysis of data from a larger double-blind, placebo-controlled, randomized clinical trial and examines changes in cerebral activation on a WM task following mSMT treatment. Methods Sixteen participants with clinically definite MS were randomly assigned to treatment (n = 7) or placebo-control groups (n = 9) matched for gender, age and education. Baseline and immediate follow-up functional Magnetic Resonance Imaging (fMRI) was obtained for all subjects. During fMRI participants completed an N-back task, consisting of 0-, 1- and 2-back conditions. Results Significant increases in cerebral activation were noted in the dorsolateral prefrontal cortex, supplementary motor area and inferior parietal lobule at follow-up in the treatment group. No significant changes were noted in the placebo control group. Conclusion Due to the small sample size, results of the current study should be interpreted as preliminary. However, the observed pattern of activation of the frontoparietal network involved in WM found in the treatment group, suggests that mSMT training increases recruitment of attention- and WM-related neural networks. We conclude that mSMT treatment leads to changes in WM-related cerebral activation.

Patients with multiple sclerosis (MS) demonstrate worse cognition on warmer days. Here, we examine the neurophysiology underlying this temperature-cognition relationship. The association between task-related BOLD fMRI activation and outdoor temperature was investigated in 28 MS patients who demonstrated worse cognitive function on warmer days. In MS patients, warmer outdoor temperature was associated with greater BOLD activation during performance of a simple sustained attention task. The brain areas that showed greater activation on warmer days (p = .01) were regions that have been shown to be more activated by MS patients during task performance: frontal, dorsolateral prefrontal, and parietal cortex. The relationship between outdoor temperature and cerebral activation was absent in healthy controls. The purpose of this study was to identify the neurophysiological basis for worse cognition among MS patients on warmer days. We show here that MS patients activate task-related brain regions more on warmer days. Increased brain activation required by MS patients on warmer days to perform a simple task may signify neural inefficiency.

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Mild traumatic brain injury (TBI) is common and associated with a spectrum of symptoms, which usually resolve within 3 months. But 5%–15% of patients are left with chronic disabling symptoms which challenge the current construct of mTBI. Increasingly mTBI has been a common subject of legal cases where neu- rologists have been ensnared.The main reason for such legal challenges is the lack of clarity in mTBI definition and prognosis. The current mTBI construct is heavily dependent on the Mayo classification of Brain Injury Assessment, where Post-traumatic amnesia (PTA) is often taken as the principal index of severity, without attention to other relevant phenomena. Unfortunately, PTA is an unreliable indicator for the whole spectrum of brain injury and there is an urgent need for a better diagnostic construct, specifically utilizing the recent advances in TBI-pathophysiology (neurovascular cascade and cone of vulnerability).We propose 1) evaluation for all brain injuries using multimodal imaging (MRI/fNIRS) protocol to capture the dynamic neurovascular changes seen in the entire spectrum of TBI severity. 2)Explore the relation between neuroimaging changes to the clinical symptoms occurring in various TBI stages by correlat- ing the comprehensive imaging data to the structured clinical assessments. 3) We will develop a novel clinical scoring system of injury severity across the spectrum of TBI by integrating the clinical outcome data with radiological (microvascular & macroscopic) and molecular biomarkers (Salivary RNA) for use in routine clinical practice.

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