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Updated: Mar 21, 2026

Investigations on Alterations of Hippocampal Circuit Function Following Mild Traumatic Brain Injury
Published on: November 19, 2012
Cognitive dysfunction and hippocampal metabolic alterations in patients with postherpetic neuralgia
Xiaokang Ni1, Yanrong Yuan2, Jun Wang2
1Department of Psychiatry, Hangzhou Third People's Hospital, Zhejiang, China.
Objectives:
Chronic pain is closely related to cognitive function, and pain caused by different etiologies may impair diverse domains of cognition. However, the change of cognitive function and cellular metabolism in hippocampus in postherpetic neuralgia (PHN) patients have received little attention. This study aimed to investigate the cognitive function and cellular metabolism changes in bilateral hippocampus in patients with PHN.
Methods:
From July 2021 to December 2024, 41 PHN patients, 48 acute herpes zoster (HZ) patients and 43 controls were enrolled. 1H-magnetic resonance spectroscopy (1H-MRS) detected bilateral hippocampal metabolism. Cognitive function, pain intensity, depression and anxiety were assessed via Montreal Cognitive Assessment (MoCA), Numeric Rating Scale (NRS), Hamilton Depression Rating Scale (HAMD) and Hamilton Anxiety Rating Scale (HAMA), the correlation between clinical features and the cellular metabolism of bilateral hippocampal was analyzed.
Results:
Cognitive impairment occurred in 31.7% (13/41) of PHN patients, whose MoCA scores were significantly lower than HZ and control groups (p < 0.05, p < 0.01), mainly involving visualspatial executive function, attention and abstraction (all p < 0.05). Binary logistic regression analysis found that duration of disease and NRS scores were independent risk factors for cognitive impairment in PHN patients (p < 0.05). The Choline/Creatine (Cho/Cr) levels in the bilateral hippocampus of patients in the PHN group were significantly lower than those in the HZ and the control group (p < 0.05, p < 0.01), and the N-acetylaspartate/Creatine (NAA/Cr) levels in the bilateral hippocampus of patients in the PHN group were significantly lower than those in the control group (p < 0.05). The duration of disease and NRS scores of PHN patients were negatively correlated with bilateral hippocampal Cho/Cr levels and MoCA scores (p < 0.05, p < 0.01), a positive correlation between HAMD/HAMA scores (p < 0.01).
Conclusion:
PHN patients have a high incidence of cognitive impairment, mainly characterized by reduced visualspatial execution, attention and abstraction abilities, they also exhibit metabolic changes in bilateral hippocampus. Among them, PHN patients with long duration of disease and severe pain have more significant changes. For the management of PHN patients, clinicians should not only pay attention to the patient's pain symptoms, but also to their cognitive and emotional disorders.
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