Individuals with a family history of bipolar disorder are at increased risk of developing affective psychopathology. Longitudinal imaging studies in young people with familial risk have been limited, and cortical developmental trajectories in the progression towards illness remain obscure.

To establish high-resolution longitudinal differences in cortical structure that are associated with risk of bipolar disorder.

Using structural magnetic resonance imaging data from 217 unrelated ‘Bipolar Kids and Sibs study’ participants (baseline n = 217, follow-up n = 152), we examined changes over a 2-year period in cortical area, thickness and volume, measured at each vertex across the cortical surface. Groups comprised 105 ‘high-risk’ participants with a first-degree relative with bipolar disorder (female n = 64; age in years: M (mean) = 20.9, s.d. = 5.5) and 112 controls with no familial psychiatric history (females n = 60; age in years: M = 22.4, s.d. = 3.7).

Accelerated thickness and volume reductions over time were observed in ‘high-risk’ individuals across multiple cortical regions, relative to controls, including right lateral orbitofrontal thickness (β = 0.033, P < 0.001) and inferior frontal volume (β = 0.021, P < 0.001). These differences were observed after controlling for age, sex, ancestry, current medication status, lifetime psychiatric diagnoses and measures of gross brain morphology.

Longitudinal group differences suggest the presence of thicker cortex in familial ‘high-risk’ individuals at earlier developmental stages, followed by accelerated thinning towards the typical age of bipolar disorder onset. Future examination of genetic and environmental components of familial risk and the mechanistic nature (pathological or protective) of cortical-trajectory differences over time may facilitate the identification of prodromal biomarkers and opportunities for early clinical intervention.

This study examined children at the onset of tic disorder (tics for less than 9 months: NT group), a population on which little research exists. Here, we investigate relationships between the baseline shape and volume of subcortical nuclei, diagnosis, and tic symptom outcomes.

187 children were assessed at baseline and a 12-month follow-up: 88 with NT, 60 tic-free healthy controls (HC), and 39 with chronic tic disorder/Tourette syndrome (TS), using T1-weighted MRI and total tic scores (TTS) from the Yale Global Tic Severity Scale to evaluate symptom change. Subcortical surface maps were generated using FreeSurfer-initialized large deformation diffeomorphic metric mapping. Linear regression models correlated baseline structural shapes with follow-up TTS while accounting for covariates, with relationships mapped onto structure surfaces.

We found that the NT group had a larger right hippocampus compared to HC. Surface maps illustrate distinct patterns of inward deformation in the putamen and outward deformation in the thalamus for NT compared to controls. We also found patterns of outward deformation in almost all studied structures when comparing the TS group to controls. The NT group also showed consistent outward deformation compared to TS in the caudate, accumbens, putamen, and thalamus. Subsequent analyses including clinical symptoms revealed that a larger pallidum and thalamus at baseline correlated with less improvement of tic symptoms at follow-up.

These observations constitute some of the first prognostic biomarkers for tic disorders and suggest that these subregional shape and volume differences may be associated with the outcome of tic disorders.

Late-life depression has been associated with volume changes of the hippocampus. However, little is known about its association with specific hippocampal subfields over time.

We investigated whether hippocampal subfield volumes were associated with prevalence, course and incidence of depressive symptoms.

We extracted 12 hippocampal subfield volumes per hemisphere with FreeSurfer v6.0 using T1-weighted and fluid-attenuated inversion recovery 3T magnetic resonance images. Depressive symptoms were assessed at baseline and annually over 7 years of follow-up (9-item Patient Health Questionnaire). We used negative binominal, logistic, and Cox regression analyses, corrected for multiple comparisons, and adjusted for demographic, cardiovascular and lifestyle factors.

A total of n = 4174 participants were included (mean age 60.0 years, s.d. = 8.6, 51.8% female). Larger right hippocampal fissure volume was associated with prevalent depressive symptoms (odds ratio (OR) = 1.26, 95% CI 1.08–1.48). Larger bilateral hippocampal fissure (OR = 1.37–1.40, 95% CI 1.14–1.71), larger right molecular layer (OR = 1.51, 95% CI 1.14–2.00) and smaller right cornu ammonis (CA)3 volumes (OR = 0.61, 95% CI 0.48–0.79) were associated with prevalent depressive symptoms with a chronic course. No associations of hippocampal subfield volumes with incident depressive symptoms were found. Yet, lower left hippocampal amygdala transition area (HATA) volume was associated with incident depressive symptoms with chronic course (hazard ratio = 0.70, 95% CI 0.55–0.89).

Differences in hippocampal fissure, molecular layer and CA volumes might co-occur or follow the onset of depressive symptoms, in particular with a chronic course. Smaller HATA was associated with an increased risk of incident (chronic) depression. Our results could capture a biological foundation for the development of chronic depressive symptoms, and stresses the need to discriminate subtypes of depression to unravel its biological underpinnings.

Gerstmann syndrome is a rare neurological disorder that consist primarily of 4 neuropsychological signs that include acalculia (impairment in performing calcultaions), digital agnosia (dificulty discriminating their own fingers), agraphia (impairment or dificulty to write by hand); and left-right disorientation (impairment of distinguishing left from right.

Presentation of a case report of a patient with Gertsmann syndrome secondary to breast cancer metastasis.

We analyze the case of a 79 years-old female with a history of breast cancer in remission, with a severe depressive episode of 8 months of evolution, dysphoria, apathy, decrease in the ability to carry out basic activities of daily life, acute personality changes and sleep disruption. 15 days previous to the first examination the patient suffers gait disturbances, falling from her own height, memory impairment, suicide ideation and nomination aphasia.

At the examination we encounter digital agnosia, acalculia, agraphia, right-left disorientation, right hemiparesis. MRI are taken founding 3 tumor lesions in the left and right frontal lobe, 2 solid lesions with a necrotic appearance in the right parietal lobe, one of them in the angular gyrus of the parietal cortex. CT scan found a solid tumor-like lesion in the left pulmonary apex. CA-125 antigen 429.5 U/mL. She was sent to continue her treatment with oncology, receiving radiotherapy.

The psychiatric abnormalities secondary to Gerstmann syndrome make the relatives of this patient seek psychiatric care, requiring multidisciplinary work to reach an accurate diagnosis. Gerstmann syndrome is a rare neurological condition that can mimic lots of other clinical pictures.

No significant relationships.

Early-life interpersonal stress, particularly childhood maltreatment, is associated with neurobiological abnormalities. However, few studies have investigated the neural effects of peer victimisation.

This study examines common and specific associations between childhood maltreatment, peer victimisation and brain structural alterations in youths.

Grey matter volume (GMV) and cortical thickness data were collected from 105 age- and gender-matched youths (age range: 17–21 years). Region-of-interest and whole-brain analyses were conducted.

For the region-of-interest analyses, the childhood maltreatment group had smaller GMV than controls in left inferior frontal gyrus, bilateral anterior insula, postcentral and lingual regions, which were associated with greater emotional abuse, along with smaller insular GMV than the peer victimisation group, who had smaller left lingual and postcentral GMV than controls. At the whole-brain level, both childhood maltreatment and peer victimisation groups had smaller GMV than controls in a cluster comprising left post/precentral, inferior frontal gyrus, insula, superior parietal and supramarginal gyri. The peer victimisation group alone had increased cortical thickness in a cluster comprising left superior frontal, anterior cingulate and medial orbitofrontal gyri, which was related to greater cyberbullying.

Early-life interpersonal stress is associated with common structural alterations of the inferior frontal-limbic, sensory and lingual regions involved in cognitive control, emotion and sensory processing. The findings of childhood-maltreatment-related reduced anterior insular GMV and peer-victimisation-related increased cortical thickness in the left medial prefrontal-anterior cingulate cluster underscore the distinctive negative effects of childhood maltreatment and peer victimisation, and suggest that peer victimisation, particularly cyberbullying, could be as detrimental as childhood maltreatment.