6 results on '"Ramlackhansingh AF"'
Search Results
2. Africanised honey bee sting-induced ischaemic stroke.
- Author
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Ramlackhansingh AF and Seecheran N
- Subjects
- Aged, Animals, Aspirin therapeutic use, Histamine Antagonists therapeutic use, Humans, Insect Bites and Stings drug therapy, Ischemic Stroke diagnostic imaging, Male, Steroids therapeutic use, Bees, Insect Bites and Stings complications, Ischemic Stroke etiology
- Abstract
The Africanised honey bee, vernacularly known as the 'killer bee', is a hybrid of the western honey bee species. These bees tend to be more aggressive with a greater tendency for swarm formation. Their stings are frequently encountered with a broad spectrum of clinical manifestations, ranging from local to systemic effects, even with recorded fatalities. We report a case of an elderly man, who experienced a cerebrovascular event confirmed by neuroimaging within 24 hours after a multitude of Africanised honey bee stings., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2020. No commercial re-use. See rights and permissions. Published by BMJ.)
- Published
- 2020
- Full Text
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3. Clinical approach to the diagnosis and successful management of anti-NMDA receptor encephalitis when antibody testing is not possible.
- Author
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Ramlackhansingh AF, King AC, Maharaj S, and King DJ
- Subjects
- Adult, Diagnosis, Differential, Electroencephalography, Female, Humans, Magnetic Resonance Imaging, Tomography, X-Ray Computed, Young Adult, Anti-N-Methyl-D-Aspartate Receptor Encephalitis diagnosis, Anti-N-Methyl-D-Aspartate Receptor Encephalitis drug therapy, Ovarian Neoplasms diagnostic imaging, Ovarian Neoplasms therapy, Teratoma diagnostic imaging, Teratoma therapy
- Abstract
Anti-N-methyl-D-aspartate (NMDA) receptor encephalitis is a multistage illness that progresses from psychosis, memory deficits, seizures and language disintegration to a state of unresponsiveness with catatonic features often associated with abnormal movements, and autonomic and breathing instability. While the disorder predominantly affects children and young adults, and occurs with or without tumour association, the presence of a tumour (usually an ovarian teratoma) is dependent on the age, sex and ethnicity.Teratomas present more frequently in women older than 18 years, and are more predominant in black women than Caucasians. Here we present the case of a patient with probable anti-NMDA receptor encephalitis. She was subsequently found to have a mature teratoma of the ovary (dermoid cyst). Despite immune-modulated therapy, surgery was eventually performed to remove the cyst. This was met with a good clinical recovery., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2019. No commercial re-use. See rights and permissions. Published by BMJ.)
- Published
- 2019
- Full Text
- View/download PDF
4. Amyloid pathology and axonal injury after brain trauma.
- Author
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Scott G, Ramlackhansingh AF, Edison P, Hellyer P, Cole J, Veronese M, Leech R, Greenwood RJ, Turkheimer FE, Gentleman SM, Heckemann RA, Matthews PM, Brooks DJ, and Sharp DJ
- Subjects
- Adult, Amyloid Neuropathies metabolism, Biomarkers metabolism, Brain Injuries metabolism, Diffusion Tensor Imaging methods, Female, Humans, Longitudinal Studies, Male, Middle Aged, Multimodal Imaging methods, Positron-Emission Tomography methods, Reproducibility of Results, Sensitivity and Specificity, Tissue Distribution, Amyloid Neuropathies diagnosis, Amyloid Neuropathies etiology, Amyloid beta-Peptides metabolism, Axons pathology, Brain Injuries complications, Brain Injuries diagnosis
- Abstract
Objective: To image β-amyloid (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 disease (AD)., Methods: Patients 11 months to 17 years after moderate-severe TBI underwent (11)C-Pittsburgh compound B ((11)C-PiB)-PET, structural and diffusion MRI, and neuropsychological examination. Healthy aged controls and patients with AD underwent PET and structural MRI. Binding potential (BPND) images of (11)C-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, was estimated and correlated with (11)C-PiB BPND., Results: Twenty-eight participants (9 with TBI, 9 controls, 10 with AD) were assessed. Increased (11)C-PiB BPND was found in TBI vs controls in the posterior cingulate cortex and cerebellum. Binding in the posterior cingulate cortex increased with decreasing fractional anisotropy 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 neuropathologic features of dementia, which may relate to axonal damage produced by the injury., (© 2016 American Academy of Neurology.)
- Published
- 2016
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5. Thalamic inflammation after brain trauma is associated with thalamo-cortical white matter damage.
- Author
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Scott G, Hellyer PJ, Ramlackhansingh AF, Brooks DJ, Matthews PM, and Sharp DJ
- Subjects
- Adult, Brain Injuries diagnostic imaging, Cerebral Cortex diagnostic imaging, Female, Humans, Inflammation diagnostic imaging, Inflammation metabolism, Male, Middle Aged, Neural Pathways diagnostic imaging, Neural Pathways metabolism, Radionuclide Imaging, Thalamus diagnostic imaging, White Matter diagnostic imaging, Brain Injuries metabolism, Cerebral Cortex metabolism, Thalamus metabolism, White Matter metabolism
- Abstract
Background: Traumatic 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., Findings: Using [(11)C]-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., Conclusions: These findings support a link between axonal damage and persistent inflammation after brain injury.
- Published
- 2015
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6. Inflammation after trauma: microglial activation and traumatic brain injury.
- Author
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Ramlackhansingh AF, Brooks DJ, Greenwood RJ, Bose SK, Turkheimer FE, Kinnunen KM, Gentleman S, Heckemann RA, Gunanayagam K, Gelosa G, and Sharp DJ
- Subjects
- Adult, Amnesia etiology, Brain Injuries psychology, Cluster Analysis, Cognition Disorders pathology, Diffusion Tensor Imaging, Educational Status, Executive Function, Female, Glasgow Coma Scale, Humans, Image Processing, Computer-Assisted, Isoquinolines, Macrophage Activation, Magnetic Resonance Imaging, Male, Memory physiology, Middle Aged, Neuropsychological Tests, Positron-Emission Tomography, Thalamus pathology, Wechsler Scales, Brain Injuries pathology, Inflammation pathology, Microglia pathology
- Abstract
Objective: Patient outcome after traumatic brain injury (TBI) is highly variable. The underlying pathophysiology of this is poorly understood, but inflammation is potentially an important factor. Microglia orchestrate many aspects of this response. Their activation can be studied in vivo using the positron emission tomography (PET) ligand [11C](R)PK11195 (PK). In this study, we investigate whether an inflammatory response to TBI persists, and whether this response relates to structural brain abnormalities and cognitive function., Methods: Ten patients, studied at least 11 months after moderate to severe TBI, underwent PK PET and structural magnetic resonance imaging (including diffusion tensor imaging). PK binding potentials were calculated in and around the site of focal brain damage, and in selected distant and subcortical brain regions. Standardized neuropsychological tests were administered., Results: PK binding was significantly raised in the thalami, putamen, occipital cortices, and posterior limb of the internal capsules after TBI. There was no increase in PK binding at the original site of focal brain injury. High PK binding in the thalamus was associated with more severe cognitive impairment, although binding was not correlated with either the time since the injury or the extent of structural brain damage., Interpretation: We demonstrate that increased microglial activation can be present up to 17 years after TBI. This suggests that TBI triggers a chronic inflammatory response particularly in subcortical regions. This highlights the importance of considering the response to TBI as evolving over time and suggests interventions may be beneficial for longer intervals after trauma than previously assumed., (Copyright © 2011 American Neurological Association.)
- Published
- 2011
- Full Text
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