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Journal articleJamall O, Feeney C, Zaw-Linn J, et al., 2016,
Prevalence and correlates of vitamin D deficiency in adults after traumatic brain injury
, Clinical Endocrinology, Vol: 85, Pages: 636-644, ISSN: 1365-2265Objectives: Traumatic brain injury (TBI) is a major cause of long-term disability with variable recovery. Preclinicalstudies suggest that vitamin D status influences recovery after TBI. However, there is no publishedclinical data on links between vitamin D status and TBI outcomes. To determine the: (i) prevalence ofvitamin D deficiency/insufficiency, and associations of vitamin D status with (ii) demographic factors andTBI severity, and with (iii) cognitive function, symptoms and quality of life, in adults after TBI.Design: Retrospective audit of patients seen between July 2009 and March 2015. Serum vitamin D (25-hydroxy-cholecalciferol) was categorised as deficient (<40nmol/L), insufficient (40-70nmol/L) or replete(>70nmol/L).Patients: 353 adults seen in tertiary hospital clinic (75.4% lighter-skinned, 74.8% male, age median 35.1y,range 26.6-48.3y), 0.3-56.5 months after TBI (74.5% moderate-severe).Measurements: Serum vitamin D concentrations; Addenbrooke’s Cognitive Examination (ACE-R), BeckDepression Inventory II (BDI-II), SF-36 Quality of Life, Pittsburgh Sleep Quality Index.Results: 46.5% of patients after TBI had vitamin D deficiency and 80.2% insufficiency/deficiency. Patientswith vitamin D deficiency had lower ACE-R scores than those vitamin D replete (mean effect size ± SEM 4.5± 2.1, P=0.034), and higher BDI-II scores than those vitamin D insufficient (4.5 ± 1.6, P=0.003), correcting forage, gender, time since TBI, TBI severity. There was no association between vitamin D status and markers ofTBI severity, sleep or quality of life.Conclusion: Vitamin D deficiency is common in patients after TBI and associated with impaired cognitivefunction and more severe depressive symptoms.
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Conference paperUnderwood J, Cole JH, Sharp D, et al., 2016,
Brain MRI changes associated with poorer cognitive function despite suppressive antiretroviral therapy
, 22nd Annual Conference of the British HIV Association (BHIVA), Publisher: Wiley, Pages: 6-6, ISSN: 1464-2662 -
Journal articleScott GPT, Ramlackhansingh A, Edison P, et al., 2016,
Amyloid pathology and axonal injury after brain trauma
, Neurology, Vol: 86, Pages: 821-828, ISSN: 0028-3878Objective: To image amyloid-β (Aβ) plaque burden in long-term survivors of traumatic brain injury (TBI), test whether traumatic axonal injury and Aβ are correlated, and compare the spatial distribution of Aβ to Alzheimer’s disease.Methods: Patients 11 months to 17 years after moderate-severe TBI had 11C-Pittsburgh compound-B (PIB) PET, structural and diffusion MRI and neuropsychological examination. Healthy aged controls and AD patients had PET and structural MRI. Binding potential (BPND) images of 11C-PIB, which index Aβ plaque density, were computed using an automatic reference region extraction procedure. Voxelwise and regional differences in BPND were assessed. In TBI, a measure of white matter integrity, fractional anisotropy (FA), was estimated and correlated with 11C-PIB BPND.Results: 28 participants (9 TBI, 9 controls, 10 AD) were assessed. Increased 11C-PIB BPND was found in TBI versus controls in the posterior cingulate cortex (PCC) and cerebellum. Binding in the PCC increased with decreasing FA of associated white matter tracts, and increased with time since injury. Compared to AD, binding after TBI was lower in neocortical regions, but increased in the cerebellum. Conclusions: Increased Aβ burden was observed in TBI. The distribution overlaps with, but is distinct from, that of AD. This suggests a mechanistic link between TBI and the development of neuropathological features of dementia, which may relate to axonal damage produced by the injury.
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Journal articleLorenz R, Hampshire A, Leech R, 2016,
Neuroadaptive Bayesian Optimization and Hypothesis Testing
, TRENDS IN COGNITIVE SCIENCES, Vol: 21, Pages: 155-167, ISSN: 1364-6613 -
Journal articleOdlaug BL, Hampshire A, Chamberlain SR, et al., 2016,
Abnormal brain activation in excoriation (skin-picking) disorder: evidence from an executive planning fMRI study.
, Br J Psychiatry, Vol: 208, Pages: 168-174BACKGROUND: Excoriation (skin-picking) disorder (SPD) is a relatively common psychiatric condition whose neurobiological basis is unknown. AIMS: To probe the function of fronto-striatal circuitry in SPD. METHOD: Eighteen participants with SPD and 15 matched healthy controls undertook an executive planning task (Tower of London) during functional magnetic resonance imaging (fMRI). Activation during planning was compared between groups using region of interest and whole-brain permutation cluster approaches. RESULTS: The SPD group exhibited significant functional underactivation in a cluster encompassing bilateral dorsal striatum (maximal in right caudate), bilateral anterior cingulate and right medial frontal regions. These abnormalities were, for the most part, outside the dorsal planning network typically activated by executive planning tasks. CONCLUSIONS: Abnormalities of neural regions involved in habit formation, action monitoring and inhibition appear involved in the pathophysiology of SPD. Implications exist for understanding the basis of excessive grooming and the relationship of SPD with putative obsessive-compulsive spectrum disorders.
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Journal articleSu T, Caan MWA, Wit FWNM, et al., 2016,
White matter structure alterations in HIV-1-infected men with sustained suppression of viraemia on treatment
, AIDS, Vol: 30, Pages: 311-322, ISSN: 0269-9370Objective: Cognitive impairment is highly prevalent in HIV-1-infected (HIV+) patients, despite adequate suppression of viral replication by combination antiretroviral therapy (cART). Cerebral white matter structure alterations are often associated with cognitive impairment and have commonly been reported in the natural course of HIV infection. However, the existence of these alterations in adequately treated HIV+ patients remains unknown, as well as its possible association with cognitive impairment.Design: We used diffusion tensor imaging (DTI) to investigate whether white matter structure alterations exist in HIV+ patients with sustained suppressed viral replication on cART, and if such alterations are related to HIV-associated cognitive deficits.Methods: We compared 100 aviraemic HIV+ men on cART with 70 HIV-uninfected, otherwise comparable men. Clinical and neuropsychological assessments were performed. From DTI data, white matter fractional anisotropy and mean diffusion were calculated. Subsequently, tract-based spatial statistics (TBSS) was performed, with and without masking out white matter lesions.Results: HIV+ patients showed diffuse white matter structure alterations as compared with HIV-uninfected controls, observed as widespread decreased fractional anisotropy and an increased mean diffusion. These white matter structure alterations were associated with the number of years spent with a CD4+ cell count below 500 cells/µl, but not with HIV-associated cognitive deficits.Conclusion: Cerebral white matter structure alterations are found in middle-aged HIV+ men with sustained suppression of viraemia on cART, and may result from periods with immune deficiency when viral toxicity and host-inflammatory responses were at their peak. These white matter structure alterations were not associated with the observed subtle HIV-associated cognitive deficits.
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Conference paperLorenz R, Monti RP, Hampshire A, et al., 2016,
Towards tailoring non-invasive brain stimulation using real-time fMRI and Bayesian optimization
, 6th International Workshop on Pattern Recognition in Neuroimaging (PRNI), Publisher: IEEE, Pages: 49-52, ISSN: 2330-9989- Author Web Link
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- Citations: 1
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Journal articleHampshire A, Hellyer PJ, Parkin B, et al., 2015,
Network mechanisms of intentional learning
, Neuroimage, Vol: 127, Pages: 123-134, ISSN: 1095-9572The ability to learn new tasks rapidly is a prominent characteristic of human behaviour. Thisability relies on flexible cognitive systems that adapt in order to encode temporary programs forprocessing non-automated tasks. Previous functional imaging studies have revealed distinctroles for the lateral frontal cortices (LFCs) and the ventral striatum in intentional learningprocesses. However, the human LFCs are complex; they house multiple distinct sub-regions,each of which co-activates with a different functional network. It remains unclear how these LFCnetworks differ in their functions and how they coordinate with each other, and the ventralstriatum, to support intentional learning. Here, we apply a suite of fMRI connectivity methods todetermine how LFC networks activate and interact at different stages of two novel tasks, inwhich arbitrary stimulus-response rules are learnt either from explicit instruction or by trialand-error.We report that the networks activate en masse and in synchrony when novel rules arebeing learnt from instruction. However, these networks are not homogeneous in their functions;instead, the directed connectivities between them vary asymmetrically across the learningtimecourse and they disengage from the task sequentially along a rostro-caudal axis.Furthermore, when negative feedback indicates the need to switch to alternative stimulusresponserules, there is additional input to the LFC networks from the ventral striatum. Theseresults support the hypotheses that LFC networks interact as a hierarchical system duringintentional learning and that signals from the ventral striatum have a driving influence on thissystem when the internal program for processing the task is updated.
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Journal articleScott G, Hellyer PJ, Ramlackhansingh AF, et al., 2015,
Thalamic inflammation after brain trauma is associated with thalamo-cortical white matter damage
, Journal of Neuroinflammation, Vol: 12, ISSN: 1742-2094BackgroundTraumatic brain injury can trigger chronic neuroinflammation, which may predispose to neurodegeneration. Animal models and human pathological studies demonstrate persistent inflammation in the thalamus associated with axonal injury, but this relationship has never been shown in vivo.FindingsUsing [11C]-PK11195 positron emission tomography, a marker of microglial activation, we previously demonstrated thalamic inflammation up to 17 years after traumatic brain injury. Here, we use diffusion MRI to estimate axonal injury and show that thalamic inflammation is correlated with thalamo-cortical tract damage.ConclusionsThese findings support a link between axonal damage and persistent inflammation after brain injury.
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Journal articleHampshire A, Sharp D, 2015,
Inferior PFC Subregions Have Broad Cognitive Roles
, TRENDS IN COGNITIVE SCIENCES, Vol: 19, Pages: 712-713, ISSN: 1364-6613- Author Web Link
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- Citations: 8
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