Lewy body dementia, consisting of both dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD), is considerably under-recognised clinically compared with its frequency in autopsy series.

This study investigated the clinical diagnostic pathways of patients with Lewy body dementia to assess if difficulties in diagnosis may be contributing to these differences.

We reviewed the medical notes of 74 people with DLB and 72 with non-DLB dementia matched for age, gender and cognitive performance, together with 38 people with PDD and 35 with Parkinson's disease, matched for age and gender, from two geographically distinct UK regions.

The cases of individuals with DLB took longer to reach a final diagnosis (1.2 v. 0.6 years, P = 0.017), underwent more scans (1.7 v. 1.2, P = 0.002) and had more alternative prior diagnoses (0.8 v. 0.4, P = 0.002), than the cases of those with non-DLB dementia. Individuals diagnosed in one region of the UK had significantly more core features (2.1 v. 1.5, P = 0.007) than those in the other region, and were less likely to have dopamine transporter imaging (P < 0.001). For patients with PDD, more than 1.4 years prior to receiving a dementia diagnosis: 46% (12 of 26) had documented impaired activities of daily living because of cognitive impairment, 57% (16 of 28) had cognitive impairment in multiple domains, with 38% (6 of 16) having both, and 39% (9 of 23) already receiving anti-dementia drugs.

Our results show the pathway to diagnosis of DLB is longer and more complex than for non-DLB dementia. There were also marked differences between regions in the thresholds clinicians adopt for diagnosing DLB and also in the use of dopamine transporter imaging. For PDD, a diagnosis of dementia was delayed well beyond symptom onset and even treatment.

Temporal lobe epilepsy is associated with a significant risk of psychosis but there are only limited studies investigating the underlying neurobiology.

To characterise neuroanatomical changes in temporal lobe epilepsy and comorbid psychosis.

The study population comprised all individuals with temporal lobe epilepsy on the epilepsy database at the National Centre for Epilepsy and Epilepsy Neurosurgery in Ireland (Beaumont Hospital) between 2002 and 2006. Ten people with temporal lobe epilepsy with psychosis were matched for age, gender, handedness, epilepsy duration, seizure laterality, severity of epilepsy and anti-epileptic medication with ten comparison participants with temporal lobe epilepsy only. Participants received a magnetic resonance imaging scan and voxel-based morphometry analyses were applied to grey and white matter anatomy.

Significant grey matter reduction was found bilaterally in those with temporal lobe epilepsy with psychosis in the temporal lobes in the inferior, middle and superior temporal gyri and fusiform gyri, and unilaterally in the left parahippocampal gyrus and hippocampus. Significant extra-temporal grey matter reduction was found bilaterally in the insula, cerebellum, caudate nuclei and in the right cingulum and left inferior parietal lobule. Significant white matter reduction in those with temporal lobe epilepsy with psychosis was found bilaterally in the hippocampus, parahippocampal/fusiform gyri, middle/inferior temporal gyri, cingulum, corpus callosum, posterior thalamic radiation, anterior limb of internal capsule and white matter fibres from the caudate nuclei, and unilaterally in the left lingual gyrus and right midbrain and superior temporal gyrus.

Significant grey and white matter deficits occur in temporal lobe epilepsy with psychosis. These encompass the medial temporal lobe structures but also extend to lateral temporal and extra-temporal regions. Some of these deficits overlap with those found in schizophrenia.

A non-optimal foetal environment, reflected in smaller birth size and shorter duration of gestation, is a risk factor for compromised health later in life.

To examine whether smaller birth size and shorter gestation predict depressive symptoms.

A total of 1371 members of a cohort born between 1934 and 1944 at term (259–294 days' gestation) in Helsinki, Finland, completed the Beck Depression Inventory (BDI) and the Center for Epidemiological Studies Depression scale (CES–D) at an average age of 61.5 years (BDI) and 63.4 years (BDI and CES–D).

Gestational length predicted depressive symptoms linearly and independently of gender and birth weight: per day decrease in gestational length, depressive symptoms scores increased by 0.8-0.9% (95% CI 0.2-1.4, P<0.009). Weight, length and head circumference at birth showed no linear association with depression, adjusted for gender and gestational length. The results did not change when further controlled for socioeconomic characteristics at birth and in adulthood, age and body mass index in adulthood.

Susceptibility to depressive symptoms may relate to shorter length of gestation.

Low birth weight is a risk factor for coronary heart disease, diabetes, stroke and hypertension. Depression is highly associated with these conditions.

To examine the association between birth weight and depression in late life.

A total of 882 singleton term births in the 1920s had contemporary records of birth weight and weight at 1 year. At 68 years all completed the Geriatric Depression Scale and 867 completed the Geriatric Mental State Examination. A logistic regression was used to analyse the associations between depression, birth weight and weight at 1 year while adjusting for known risk factors.

Current social class, social class at birth, recent bereavement, social isolation and physical illness increased the risk of depression. After adjusting for these and weight at 1 year, the odds ratios for depression among men, but not women, rose incrementally with decreasing birth weight (1.0, 12.8; for continuous variable, P < 0.007).

Foetal undernutrition predisposes men to depression in late adult life. If replicated, these results would suggest a neurodevelopmental aetiology of depression, possibly mediated by programming of the hypothalamic–pituitary–adrenal axis.