Format

Send to

Choose Destination
Am J Nucl Med Mol Imaging. 2014 Dec 15;5(1):83-94. eCollection 2015.

Hippocampal MR spectroscopic abnormalities in a cohort of syphilitic patients with HIV and neurosyphilis infection.

Author information

1
Department of Diagnostic Radiology, The University of Hong Kong Hong Kong Special Administrative Region, China.
2
Social Hygiene Service, Centre for Health Protection, Department of Health Hong Kong Special Administrative Region, China.

Abstract

Co-infection of human immunodeficiency virus (HIV) and neurosyphilis (NS) has become a rising trend, but the extent of brain damage associated with the concomitant infections remains unknown. Proton magnetic resonance spectroscopy ((1)H-MRS) can evaluate metabolic changes underlying early brain infections. 25 syphilitic patients (7 HIV-positive with NS; 6 HIV-positive without NS; 5 HIV-negative with NS; 7 non-HIV, non-NS) and 17 healthy controls (HC) underwent single-voxel (1)H-MRS in the bilateral hippocampi. Absolute concentrations of major metabolites were measured using a 3T MRI scanner. No significant structural abnormality was detected in all patients. However, metabolic changes were found in the left hippocampus of both the HIV-positive and NS subgroups, showing significantly higher choline (Cho), creatine (Cr) and myo-inositol (mI) compared to HC. In the right hippocampus, HIV-positive subgroup showed significantly higher Cr and reduced NAA, while NS subgroup only showed significantly reduced NAA compared to HC. The non-HIV, non-NS syphilitic subgroup showed no significant difference compared to HC. Substantial metabolic changes occurred in bilateral hippocampi in HIV and NS co-infections. NAA reduction might represent early neuronal damage, while mI/Cho elevation reflects gliosis/inflammatory changes. (1)H-MRS could serve as a non-invasive tool to triage patients suspected of NS for lumbar puncture in non-HIV syphilitic patients.

KEYWORDS:

HIV; co-infection; hippocampus; magnetic resonance spectroscopy; neurosyphilis

PMID:
25625030
PMCID:
PMC4299779

Supplemental Content

Full text links

Icon for PubMed Central
Loading ...
Support Center