White matter hyper intensities evoke cortical atrophy but their influence on cognitive deterioration seem to be later event

2018 ◽  
Vol 07 ◽  
Author(s):  
Huwon Kim
Sexual Health ◽  
2018 ◽  
Vol 15 (4) ◽  
pp. 358 ◽  
Author(s):  
Harmanpreet Tiwana ◽  
Aiesha Ahmed

Background Common causes of temporal lobe hyper intensities are central nervous system infections like herpes simplex encephalitis, Lyme disease, limbic encephalitis and vascular pathology like Cerebral Autosomal Dominant Arteriopathy with Subcortical infarcts and Leukoencephalopathy. Methods: Personal assessment, laboratory data analysis and neuroimaging for the patient who was admitted to a central Pennsylvania tertiary care referral centre were conducted. Results: A 52-year-old male presented with a 1-year history of diffuse dysesthesia in upper and lower extremities with associated intermittent headaches and neck stiffness. Evaluation with lumbar puncture revealed increased nucleated cells (50 ul) with lymphocytic predominance (96%) and an elevated protein level of 109 mg/dl. Magnetic resonance imaging (MRI) of the brain showed T2/FLAIR hyper intensity in bilateral subcortical temporal white matter, left-greater-than-right and associated volume loss in cerebral parenchyma. Additional abnormal work up included reactive serum reactive plasma regain and Treponema pallidum antibody particle agglutination. Diagnosis of neurosyphilis was made and the patient was treated with intramuscular (IM) penicillin for 3 weeks. At the time of discharge, his headache and neck stiffness resolved and dysesthesias were decreased in intensity. Conclusions: The diagnosis of neurosyphilis is intricate, and no reference standard exists. Neuroimaging findings of neurosyphilis commonly are cerebral infarctions, leptomeningeal enhancement or non-specific white matter lesions. Less common features on fluid-attenuated inversion recovery (FLAIR) sequences are cortical atrophy and mesial temporal parenchymal signal changes. It is prudent to keep neurosyphilis in differential of mesial temporal lobe white matter changes, as early diagnosis and treatment results in better prognosis.


2017 ◽  
Vol 13 (7) ◽  
pp. P1499
Author(s):  
Daniel T. Ohm ◽  
Garam Kim ◽  
Tamar Gefen ◽  
Alfred Rademaker ◽  
Sandra Weintraub ◽  
...  

1994 ◽  
Vol 35 (2) ◽  
pp. 117-122 ◽  
Author(s):  
P. Christiansen ◽  
H. B. W. Larsson ◽  
C. Thomsen ◽  
S. B. Wieslander ◽  
O. Henriksen

The brain of 142 healthy volunteers aged 21 to 80 years were investigated using MR imaging. The number and size of the white matter hyperintensity lesions (WMHL) in the cerebral hemispheres were determined. Furthermore, the volume of the cerebral hemispheres and of the lateral ventricles was measured. An almost linear increase in the number of volunteers with WMHL was seen with aging for males and females. With aging a significant decrease in the volume of the cerebral hemispheres was found for males, and a significant increase in the volume of the lateral ventricles was seen for both males and females. Our results suggest that with aging central atrophy increases more (relatively) than cortical atrophy. No correlation was found between the decreasing volume of the cerebral hemispheres and the increasing number and size of WMHL, nor between the increasing volume of the lateral ventricles and the increasing number and size of WMHL.


2003 ◽  
Vol 16 (3) ◽  
pp. 435-437
Author(s):  
M.G. Egitto ◽  
C. Uggetti ◽  
R. Bergamaschi ◽  
C. Livieri

We describe the results of a study on 21 patients with adrenogenital syndrome without neurological symptoms who underwent neurological examination, neurophysiological tests and MR scan. Only five patients (23.8%) had a negative neuroradiological examination, whereas 14 (66.3%) presented focal or diffuse white matter hyperintensity, ten (47.6%) had supratentorial cortical atrophy and seven (33.3%) inferior ectopia of the cerebellar tonsils. The frequency of white matter changes was not a chance finding and the lesions are speculated to be demyelinating. This hypothesis is interesting because the gene responsible for a deficit of the 21 beta-hydroxylase enzyme implicated in adrenogenital syndrome is near to the TNF gene implicated in the origin of multiple sclerosis. The possible causes of supratentorial atrophy and tonsillar ectopia are also discussed.


2004 ◽  
Vol 25 ◽  
pp. S11
Author(s):  
Antao Du ◽  
Norbert Schuff ◽  
Linda L. Chao ◽  
John Kornak ◽  
Frank Ezekiel ◽  
...  

2021 ◽  
Author(s):  
Miracle Ozzoude ◽  
Brenda Varriano ◽  
Derek Beaton ◽  
Joel Ramirez ◽  
Melissa F Holmes ◽  
...  

Introduction: Change in empathy is an increasingly recognised symptom of neurodegenerative diseases and contributes to caregiver burden and patient distress. Empathy impairment has been associated with brain atrophy but its relationship to white matter hyperintensities (WMH) is unknown. We aimed to investigate the relationships amongst WMH, brain atrophy, and empathy deficits in neurodegenerative and cerebrovascular diseases. Methods: 513 participants with Alzheimers Disease/Mild Cognitive Impairment, Amyotrophic Lateral Sclerosis, Frontotemporal Dementia (FTD), Parkinsons Disease, or Cerebrovascular Disease (CVD) were included. Empathy was assessed using the Interpersonal Reactivity Index. WMH were measured using a semi-automatic segmentation and FreeSurfer was used to measure cortical thickness. Results: A heterogeneous pattern of cortical thinning was found between groups, with FTD showing thinning in frontotemporal regions and CVD in left superior parietal, left insula, and left postcentral. Results from both univariate and multivariate analyses revealed that several variables were associated with empathy, particularly cortical thickness in the fronto-insulo-temporal and cingulate regions, sex(female), global cognition, and right parietal and occipital WMH. Conclusions: Our results suggest that cortical atrophy and WMH may be associated with empathy deficits in neurodegenerative and cerebrovascular diseases. Future work should consider investigating the longitudinal effects of WMH and atrophy on empathy deficits in neurodegenerative and cerebrovascular diseases.


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