Vascular risk factors including hypertension, diabetes and dyslipidaemia promote diverse pathological mechanisms in the brain leading to cerebral hypoperfusion and ultimately cognitive decline in people. Medial temporal, medial frontal and anterior cingulate atrophy has been closely associated with diabetes and medial temporal lobe atrophy is associated with hypertension in people with Alzheimer’s disease (AD).

To assess if hypertension, diabetes and dyslipidaemia have differential effects on different brain locations using brain imaging in people with AD.

The current study is based on [18F] fluorodeoxyglucose- positron emission tomography (FDG-PET) data of 970 participants from two large Phase III multi-centre clinical trials of a novel tau aggregation inhibitor drug Leuco-Methylthioninium (LMTX)meeting research criteria for mild to moderate AD. Vascular risk factor data including hypertension, diabetes and dyslipidaemia were collected and quantification of FDG PET hypo-metabolism was done by calculating Standardized Uptake Value Ratio(SUVR).

Hypertension, diabetes and dyslipidaemia were found to have differential effects on brain locations in people with AD. When people with hypertension, diabetes and dyslipidaemia were compared to those without, mean SUVR was increased significantly in both left and right parietal and occipital lobes and decreased in left and right anterior cingulate gyri in hypertensives. SUVR was significantly higher in both left and right temporal lobes in diabetics andlower in both left and right anterior cingulate gyri in people with dyslipidaemia.

Vascular risk factors including hypertension, diabetes and dyslipidaemia have differential effects on different brain regions, measured using SUVR analysis of FDG-PET.

The FDG-PET data was taken from participants of two large phase III clinical trials sponsored by TauRx Therapeutics (Singapore). TauRx Therapeutics has contributed towards my studentship during my PhD but the data related to drug used in the clinical tria

Obsessive-compulsive disorder (OCD) is a chronic, prevalent, and highly impairing psychiatric illness. While its aetiology remains unknown, several infectious agents have been associated to obsessive-compulsive symptoms, including herpes simplex virus 1 (HSV-1) and Toxoplasma gondii.

To evaluate the serostatus for HSV-1 and Toxoplasma gondii in sample of patients with OCD, as well as its clinical and brain imaging correlates.

Twenty-six patients with OCD and 30 healthy controls recruited in Lisbon were assessed for sociodemographic and clinical characteristics using the Yale-Brown Obsessive-Compulsive Scale-II (YBOCS-II) and the Beck Depression Inventory-II (BDI-II). Seropositivity for HSV-1 and Toxoplasma gondii was assessed in serum using ELISA, and volumes of cortical and subcortical structures were assessed using T1-weighted magnetic resonance imaging.

YBOCS-II and BDI-II scores were significantly higher in patients, while age, sex, smoking status, and seropositivity for HSV-1 and Toxoplasma gondii were similar between the two groups. Among OCD patients, those seropositive for HSV-1 had significantly lower volumes of total white-matter, total grey-matter, left and right putamen, while for HSV-1 seropositive healthy controls, only the last two were significantly smaller. In multiple regression analyses to control for age, associations between HSV-1 and brain volumes were conserved, while the effect of age was not significant. No significant differences were found in brain volumes of patients with OCD according to seropositivity for Toxoplasma gondii.

Our preliminary results suggest that in patients with OCD, seropositivity to HSV-1 is associated with smaller volumes of total white- and grey-matter in the brain.

No significant relationships.

Balance deficits are heterogeneous among children with Developmental Coordination Disorder (DCD). Balance performance depends on different balance domains, each associated with specific underlying neurological systems. In DCD, any of these domains can be affected, but the control mechanisms are poorly understood. The mirror neuron system (MNS) seems to play a key-role in DCD-related deficits. To understand the role of MNS as a control mechanism underlying the balance deficits, simultaneous registration of cortical MNS activity while performing balance tasks is imperative. Therefore, a protocol for combining real-time registration of cortical MNS activity during functional balance tasks in children with DCD, CP and TD is introduced. Methods: Children with DCD, CP and TD (n=108) aged 5-10yr perform preselected tasks of the Kids-BESTest, representing specific balance domains (mixed design): leaning with eyes closed (stability limits/verticality), single-leg-stance, alternate stair touching (anticipatory balance), in-place response, compensatory stepping backward (reactive balance) and walking over obstacles (gait stability). Simultaneously, functional Near-Infrared Spectroscopy (fNIRS) monitors cortical activity involving the MNS: premotor, inferior and superior parietal cortex and supplementary motor area. An 8-8-optode bundle, making 22 channels, targets this region of interest. Outcome measures are: (de)oxygenated hemoglobin concentration changes per task per channel. Results: In this ongoing research, the protocol was already feasible in 19 children (7.52±1.19). Conclusion: Simultaneous registration of cortical MNS activity (fNIRS) and Kids-BESTest scores will help increase the understanding of the control mechanisms underlying the heterogeneous balance problems in DCD. Consequently, first steps are made to confirm whether DCD shows deviant or delayed development.

No significant relationships.

Several neuroimaging studies on psychosis spectrum have been published in the last decades, most of them based on schizophrenia. In the context of neuroanatomical dysfunctions, clinical and prognosis implications have been reported. Nevertheless, only a few studies have been focused on delusional disorder (DD).

To present the case of a patient diagnosed with DD who suffered from two cerebrovascular events after the onset of the psychiatric disease. Our aim is to elucidate potential implications of those lesions on the course of DD. We also reviewed the literature to assess evidence for specific changes in DD on brain structures and functions.

Case report and non-systematic narrative review in PubMed (2000-2020).

Case report: A 66-year-old female with DD presenting, during the course of the disease, general atrophy and consecutive ischemic lesions on parietal, occipital and cerebellar areas. Clinical stabilization was achieved 12-16 months after risperidone 1.5mg/day treatment. Review: 19 studies were included: Structural brain data (n=15), Functional data (n=13). Most of the structural neuroimaging studies reported white and gray matter abnormalities, particularly in temporal, parietal and frontal lobes, and in limbic structures. Functional neuroimaging studies pointed to temporal and parietal lobes, as well as basal ganglia and limbic related structures.

Temporal, parietal, frontal, basal ganglia and limbic-related structures, as well as dysfunctions in other specific brain regions, may be implicated in the core symptoms of DD. These findings might be further investigated as potential neuroimaging markers of prognosis, such as partial or delayed response to antipsychotic treatment, as presented in our case.

Spontaneous cerebrospinal fluid leak of the temporal bone is an emerging clinical entity for which prompt and accurate diagnosis is difficult given the subtle signs and symptoms that patients present with. This study sought to describe the key temporal bone abnormalities in patients with spontaneous cerebrospinal fluid leak.

A retrospective cohort study was conducted of adult patients with biochemically confirmed spontaneous cerebrospinal fluid leak. Demographics and radiological features identified on computed tomography imaging of the temporal bones and/or magnetic resonance imaging were analysed.

Sixty-one patients with spontaneous cerebrospinal fluid leak were identified. Fifty-four patients (88.5 per cent) underwent both temporal bone computed tomography and magnetic resonance imaging. Despite imaging revealing bilateral defects in over 75 per cent of the cohort, only two patients presented with bilateral spontaneous cerebrospinal fluid leaks. Anterior tegmen mastoideum defects were most common, with an average size of 2.5 mm (range, 1–10 mm).

Temporal bone computed tomography is sensitive for the identification of defects when suspicion exists. In the setting of an opacified middle ear and/or mastoid, close examination of the skull base is crucial given that this fluid is potentially cerebrospinal fluid.

Catatonia is a frequent, complex and severe identifiable syndrome of motor dysregulation. However, its pathophysiology is poorly understood.

We aimed to provide a systematic review of all brain imaging studies (both structural and functional) in catatonia.

We identified 137 case reports and 18 group studies representing 186 individual patients with catatonia. Catatonia is often associated with brain imaging abnormalities (in more than 75% of cases). The majority of the case reports show diffuse lesions of white matter, in a wide range of brain regions. Most of the case reports of functional imaging usually show frontal, temporal, or basal ganglia hypoperfusion. These abnormalities appear to be alleviated after successful treatment of clinical symptoms. Structural brain magnetic resonance imaging studies are very scarce in the catatonia literature, mostly showing diffuse cerebral atrophy. Group studies assessing functional brain imaging after catatonic episodes show that emotional dysregulation is related to the GABAergic system, with hypoactivation of orbitofrontal cortex, hyperactivation of median prefrontal cortex, and dysconnectivity between frontal and motor areas.

In catatonia, brain imaging is abnormal in the majority of cases, and abnormalities more frequently diffuse than localised. Brain imaging studies published so far suffer from serious limitations and for now the different models presented in the literature do not explain most of the cases. There is an important need for further studies including a better clinical characterisation of patients with catatonia, functional imaging with concurrent catatonic symptoms and the use of novel brain imaging techniques.

To provide a review of the available literature about the functional neuroimaging of anorexia nervosa, and to summarize the possible role of neurobiological factors in its pathogenesis.

A systematic review of the literature was performed using PubMed and Medline electronic database (1950–September 2009). Eligible studies were restricted to those involving the main parameters of cerebral activity and functional neuroimaging techniques. Findings of the reviewed studies have been grouped on a diagnostic subtype basis, and their comparison has been interpreted in terms of concordance.

We found a high level of concordance among available studies with regard to the presence of frontal, parietal and cingulate functional disturbances in both anorexia nervosa restricting and binge/purging subtypes. Concordance among studies conducted regardless of the anorexia nervosa subtypes suggests an alteration in temporal and parietal functions and striatal metabolism.

The most consistent alterations in anorexia nervosa cerebral activity seem to involve the dorsolateral prefrontal cortex, the inferior parietal lobule, the anterior cingulate cortex and the caudate nucleus. They may affect different neural systems such as the frontal visual system, the attention network, the arousal and emotional processing systems, the reward processing network, and the network for the body schema.

Structural neuroimaging studies have revealed a consistent pattern of volumetric reductions in both the hippocampus and the anterior cingulate cortex (ACC) of individuals with a major depressive episode (MDE). This study investigated hippocampal and ACC volume differences in the elderly comparing currently depressed individuals and individuals with a past lifetime history of MDE versus healthy controls.

We studied non-demented individuals from a cohort of community-dwelling people aged 65 and over (ESPRIT study). T1-weighted magnetic resonance images were used to acquire anatomical scans from 150 currently depressed individuals, 79 individuals with at least one past MDE, and 310 healthy controls. We derived quantitative regional estimates of subcortical volume of hippocampus and ACC using FreeSurfer Software (automated method). Concerning hippocampus, we also used a manual method of measurement. General Linear Model was used to study brain volumes in current and past depression adjusting for gender, age, education level, total brain volume, and anxiety disorder comorbidity.

After adjustment, current depression was associated with a lower left posterior hippocampal volume (F = 10.38, P = 0.001) using manual estimation of volume. No other significant differences were observed. A positive correlation was found between time since the last MDE and left posterior hippocampal volume.

The finding of left posterior hippocampal volume reduction in currently depressed individuals but not in those with a past MDE compared to healthy controls could be related to brain neuroplasticity. Additionally, our results suggest manual measures to be more sensitive than automated methods.

The authors have not supplied their declaration of competing interest.