OBJECTIVE: To measure the changes in cerebral cortical thickness in patients with herpes zoster (HZ) and postherpetic neuralgia (PHN) by surface-based morphometry (SBM) and further estimate its correlation with clinical scores.
METHODS: Twenty-nine HZ patients, 30 PHN patients and 30 well-matched healthy controls (HCs) were included. Magnetic resonance imaging (MRI) data from all subjects were collected and then analyzed by SBM. The changes in cortical thickness among the HZ, PHN and HC groups were analyzed by ANOVA and correlated with clinical scores.
RESULTS: The thickness of the bilateral primary visual cortex (V1, V2) and right primary visual cortex (V3), left somatosensory cortex (L3A), right anterior cingulate gyrus and medial prefrontal cortex (RS32) increased in PHN group, and the thickness the left insular and frontal opercular cortex (LFOP4), left motor cortex (L3B), and right superior temporal visual cortex (RSTV) were decreased in the HZ and PHN groups compared to the HC group. The thickness measurements of RS32, LFOP4, and (L3B) in HZ and PHN patients were correlated with the duration of disease. In HZ and PHN patients, the Hamilton Anxiety Scale (HAMA) and Hamilton Depression Scale (HAMD) scores were significantly positively correlated.
CONCLUSIONS: Changes in cortical thickness in the areas related to sensory, motor, and cognitive/emotional changes in patients with PHN affect the neuroplasticity process of the brain, which may be the reason for the transformation of HZ into PHN and provide a possible explanation for the neuropathological mechanism of pain persistence in PHN patients.

We aimed to delineate common principles of reorganization after infarcts of the subcortical vestibular circuitry related to the clinical symptomatology. Our hypothesis was that the recovery of specific symptoms is associated with changes in distinct regions within the core vestibular, somatosensory, and visual cortical and subcortical networks.
We used voxel- and surface-based morphometry to investigate structural reorganization of subcortical and cortical brain areas in 42 patients with a unilateral, subcortical infarct with vestibular and ocular motor deficits in the acute phase. The patients received structural neuroimaging and clinical monitoring twice (acute phase and after 6 months) to detect within-subject changes over time.
In patients with vestibular signs such as tilts of the subjective visual vertical (SVV) and ocular torsion in the acute phase, significant volumetric increases in the superficial white matter around the parieto-opercular (retro-)insular vestibular cortex (PIVC) were found at follow-up. In patients with SVV tilts, spontaneous nystagmus, and rotatory vertigo in the acute phase, gray matter volume decreases were located in the cerebellum and the visual cortex bilaterally at follow-up. Patients with saccade pathology demonstrated volumetric decreases in cerebellar, thalamic, and cortical centers for ocular motor control.
The findings support the role of the PIVC as the key hub for vestibular processing and reorganization. The volumetric decreases represent the reciprocal interaction of the vestibular, visual, and ocular motor systems during self-location and egomotion detection. A modulation in vestibular and ocular motor as well as visual networks was induced independently of the vestibular lesion site.

Moyamoya disease (MMD) is an uncommon cerebrovascular disease which leads to progressive stenosis and occlusion of the bilateral internal carotid artery and main intracerebral arteries. Concerns are always on how the hemisphere with infarction affects cognitive function, while little attention is paid to the role that the non-infarcted hemisphere plays. Therefore, we aimed to detect cortical indexes, especially cortical complexity in the left or right hemisphere separately in patients with MMD after stroke.
28 patients with MMD (14 males, 14 females) and 14 healthy controls were included in this study. All participants underwent cognitive tests and magnetic resonance imaging (MRI) scan. The preprocessing of three-dimensional T1 weighted images were performed by standard surface-based morphometry. Surface-based morphometry statistical analysis was carried out with a threshold of False Discovery Rate (FDR) P < 0.05 and fractal dimension (FD) was used to provide a quantitative description of cerebral cortical complexity.
Widespread cognitive dysfunctions were found in MMD patient with stroke. Extensive FD reduction in the left hemisphere with right-sided infarction, mainly in the superior temporal, inferior frontal, and insula, while the post central gyrus, superior parietal, and inferior parietal gyrus also showed a wide range of significant differences (FDR corrected P < 0.05). Meanwhile, FD changes in the right hemisphere with left-sided infarction are restricted to the precuneus and cingulate isthmus (FDR corrected P < 0.05).
Extensive cognitive impairment was reconfirmed in Moyamoya disease with stroke, while wild and asymmetrical decrease of cortical complexity is observed on both sides. These differences could be relative to unbalanced cognitive dysfunction, and may be the result of a long-term chronic ischemia and compensatory of the contralateral hemisphere to the infarction.

In the present pilot study, we aimed to characterize the brain surface differences between 42 sporadic healthy individuals with AVHs (Hi-AVHs) and 50 healthy individuals without AVHs. The Auditory Hallucinations Rating Scale (AHRS) was used to assess the severity of AVHs, while the gyrification index and fractal dimensions were used to evaluate cerebral cortex complexity. We observed a significant increase of the gyrification index was located in the left superior temporal gyrus, the left temporoparietal junction, the left superior frontal gyrus, and the left parietal lobe. The fractal dimensions had significantly increased in the left Wernicke\'s area, the left Broca\'s areas and the left parietal lobe. Our pilot findings indicated gyrification index and fractal dimensions differences were only located in the left hemisphere between the groups of Hi-with and without AVHs. However, these differences did not correlate with the AVHs symptoms, and the non-hallucinating healthy individuals did not demonstrate corresponding reverse changes; hence we cannot postulate that cerebral cortex complexity alterations are related to AVHs. Our pilot study provides a clue for further studies aimed at investigating the brain features of Hi-AVHs.

Amblyopia is generally considered a neurodevelopmental disorder that results from abnormal visual experiences in early childhood and may persist to adulthood. The neural basis of amblyopia has been a matter of interest for many decades, but the critical neural processing sites in amblyopia are not entirely understood. Although many functional neuroimaging studies have found abnormal neuronal responses both within and beyond V1, few studies have focused on the neurophysiologic abnormalities in the visual cortex from the viewpoint of potential structural reorganization. In this study, we used a well-validated and highly accurate surface-based method to examine cortical morphologic changes in the visual cortex using multiple parameters (including cortical thickness, surface area, volume and mean curvature).
The cortical thicknesses of the bilateral V1, left V2, left ventral V3, left V4 and left V5/MT+ in patients were significantly thinner than that in controls. The mean curvature of the bilateral V1 was significantly increased in the patients compared with the controls. For the surface area and gray matter volume, no significant differences were found between patients and controls in all region of interests. The cortical thicknesses of the bilateral V1 were both negatively correlated with the amount of anisometropia. No significant correlations were found between any other surface parameters and clinical variables.
In addition to cortical thickness, the altered mean curvature of the cortex may indicate neuroanatomic impairments of the visual cortex in patients with anisometropic amblyopia. Moreover, the structural changes were bilateral in the primary visual cortex but were unilateral in the secondary and more senior visual cortex.