The role of the antihypertensive therapy in preventing vascular cognitive disorders in elderly persons without a history of stroke is a matter of debate. This review focuses on cognitive disorders in elderly hypertensive patients.

Relevant papers were identified by searches in PubMed from 1946 until February 2007 using the keywords ‘cerebral blood flow autoregulation’, ‘vascular cognitive disorders’, ‘neuroimaging in hypertension’, ‘antihypertensive treatment’ and ‘neuroprotection in cerebral ischemia’.

Excessive blood pressure lowering in patients with long-standing hypertension may increase the risk of cerebral hypoperfusion, white matter lesions and consequent cognitive decline. White matter lesions have been found in the majority of patients with long-standing hypertension. They correlate with vascular cognitive disorders, particularly impairments of attention and executive function, while memory is relatively preserved. Cerebral small vessel disease in elderly patients should be taken into account when antihypertensive treatment is considered. Renin–angiotensin blockade, some calcium channel blockers and statins are thought to possess neuroprotective action.

For prevention of cerebral hypoperfusion in elderly hypertensives blood pressure lowering should be cautiously controlled. The increased risk of white matter lesions is an indication for early neuroprotection. The combination of renin–angiotensin blockade or calcium channel blockers with statins may become a promising preventive strategy against cognitive decline in elderly hypertensives. Cerebral white matter protection is a future challenge.

In consultation-liaison settings, neuropsychiatrists are commonly asked to assess patients with hallucinatory syndromes and to differentiate ‘functional’ from ‘organic’ psychotic presentations.

The occurrence and management of visual hallucinations (VH) in healthy individuals, lesion states, neurodegenerative disorders, intoxication/withdrawal states and delirium are reviewed.

The presence of VH has been shown to predict a secondary rather than primary psychotic illness and an understanding of the neurobiology of the visual system – including how and where underlying neurotransmitter systems interact in visual processing and how perturbations can result in VH – allows for appropriate clinical assessment and management.

Early environmental events may be relevant to the etiology of schizophrenia. Among such events, interest has focused especially on obstetric complications (OCs).

Aims of the study were to compare the incidence of OCs in patients, siblings and normal controls and to examine the relationship between OCs and later schizophrenia.

One hundred and thirteen patients with schizophrenia were recruited, as were 140 patients’ siblings and 113 controls without schizophrenia. The OCs history of patients, their sibs and controls was obtained through interviews with patients’ and controls’ mothers.

The results highlighted that more patients than sibs had at least one definite OC and a higher mean number of OCs; more patients had premature rupture of membranes, threatened abortion and a labor of more than 36 h.

Our data provide some evidence for a link between OCs and later schizophrenia. Furthermore, this study highlights how OCs, which may cause fetal distress through a hypoxic-ischemic mechanism, could increase the risk of schizophrenia interacting with genetic susceptibility.

Emotion perception may be impaired after stroke. No study on emotion perception after stroke has taken the influence of post-stroke depressive symptoms into account, although depressive symptoms themselves may hamper emotion perception.

To compare the perception of emotional facial expressions in stroke patients with and without depressive symptoms.

Twenty-two stroke patients participated whose depressive symptoms were classified using the Montgomery-Åsberg Depression Rating Scale (cutoff = 10) and who were compared with healthy controls. Emotion recognition was measured using morphed images of facial expressions.

Patients with depressive symptoms performed worse than controls on all emotions; patients without depressive symptoms performed at control level. Patients with depressive symptoms were less sensitive to the emotions anger, happiness and sadness compared with patients without depressive symptoms.

Post-stroke depressive symptoms impair emotion perception. This extends findings in bipolar disorder indicating that emotion perception deficits are strongly related to the level of depression.

To provide a comprehensive review and evaluation of the psychological and neurophysiological literature pertaining to mindfulness meditation.

A search for papers in English was undertaken using PsycINFO (from 1804 onward), MedLine (from 1966 onward) and the Cochrane Library with the following search terms: Vipassana, Mindfulness, Meditation, Zen, Insight, EEG, ERP, fMRI, neuroimaging and intervention. In addition, retrieved papers and reports known to the authors were also reviewed for additional relevant literature.

Mindfulness-based therapeutic interventions appear to be effective in the treatment of depression, anxiety, psychosis, borderline personality disorder and suicidal/self-harm behaviour. Mindfulness meditation per se is effective in reducing substance use and recidivism rates in incarcerated populations but has not been specifically investigated in populations with psychiatric disorders. Electroencephalography research suggests increased alpha, theta and beta activity in frontal and posterior regions, some gamma band effects, with theta activity strongly related to level of experience of meditation; however, these findings have not been consistent. The few neuroimaging studies that have been conducted suggest volumetric and functional change in key brain regions.

Preliminary findings from treatment outcome studies provide support for the application of mindfulness-based interventions in the treatment of affective, anxiety and personality disorders. However, direct evidence for the effectiveness of mindfulness meditation per se in the treatment of psychiatric disorders is needed. Current neurophysiological and imaging research findings have identified neural changes in association with meditation and provide a potentially promising avenue for future research.

To critically examine the relationship between evolutionary and developmental influences on human neocortex and the properties of the conscious mind it creates.

Using PubMed searches and the bibliographies of several monographs, we selected 50 key works, which offer empirical support for a novel understanding of the organization of the neocortex.

The cognitive gulf between humans and our closest primate relatives has usually been taken as evidence that our brains evolved crucial new mechanisms somehow conferring advanced capacities, particularly in association areas of the neocortex. In this overview of neocortical development and comparative brain morphometry, we propose an alternative view: that an increase in neocortical size, alone, could account for novel and powerful cognitive capabilities. Other than humans’ very large brain in relation to the body weight, the morphometric relations between neocortex and all other brain regions show remarkably consistent exponential ratios across the range of primate species, including humans. For an increase in neocortical size to produce new abilities, the developmental mechanisms of neocortex would need to be able to generate an interarchy of functionally diverse cortical domains in the absence of explicit specification, and in this respect, the mammalian neocortex is unique: its relationship to the rest of the nervous system is unusually plastic, allowing great changes in cortical organization to occur in relatively short periods of evolution. The fact that even advanced abilities like self-recognition have arisen in species from different mammalian orders suggests that expansion of the neocortex quite naturally generates new levels of cognitive sophistication. Our cognitive and behavioural sophistication may, therefore, be attributable to these intrinsic mechanisms’ ability to generate complex interarchies when the neocortex reaches a sufficient size.

Our analysis offers a parsimonious explanation for key properties of the human mind based on evolutionary influences and developmental processes. This view is perhaps surprising in its simplicity, but offers a fresh perspective on the evolutionary basis of mental complexity.

To conduct a comprehensive literature review of the area of neural stem cells and neuropsychiatry.

‘Neural stem cells’ (NSCs) and ‘neurogenesis’ were used as keywords in Medline (1966 – November 2006) to identify relevant papers in the areas of Alzheimer’s disease (AD), depression, schizophrenia and Parkinson’s disease (PD). This list was supplemented with papers from reference lists of seminal reviews.

The concept of a ‘stem cell’ continues to evolve and is currently defined by operational criteria related to symmetrical renewal, multipotency and functional viability. In vivo adult mammalian neurogenesis occurs in discrete niches in the subventricular and subgranular zones – however, functional precursor cells can be generated in vitro from a wide variety of biological sources. Both artificial and physiological microenvironment is therefore critical to the characteristics and behaviour of neural precursors, and it is not straightforward how results from the laboratory can be extrapolated to the living organism. Transplant strategies in PD have shown that it is possible for primitive neural tissue to engraft into neuropathic brain areas, become biologically functional and lead to amelioration of clinical signs and symptoms. However, with long-term follow-up, significant problems related to intractable side-effects and potential neoplastic growth have been reported. These are therefore the potentials and pitfalls for NSC technology in neuropsychiatry. In AD, the physiology of amyloid precursor protein may directly interact with NSCs, and a role in memory function has been speculated. The role of endogenous neurogenesis has also been implicated in the etiology of depression. The significance of NSCs and neurogenesis for schizophrenia is still emerging.

There are a number of technical and conceptual challenges ahead before the promise of NSCs can be harnessed for the understanding and treatment of neuropsychiatric disorders. Further research into fundamental NSC biology and how this interacts with the neuropsychiatric disease processes is required.

One of the most popular approaches in cognitive neuroscience has been to study the normal adult human brain. However, there are likely to be limits to the knowledge that can be obtained from such studies. If we assume that no single approach can ever provide us with knowledge of causative processes whereby the mind emerges from the brain, then we need to consider how to combine more disparate approaches. I aim to illustrate here how the parallel study of brain phylogeny, ontogeny and dysfunction may bring us towards an integrative understanding of fundamental aspects of cognitive neuroscience.

A review of published literature in these research areas was carried out and representative articles selected.

Comparative approaches, utilizing the extraordinary behavioural abilities as well as the structural and functional variants that evolution has thrown up across diverse groups of species, can inform the core neural systems that may be necessary and sufficient to support specific cognitive processes. Similarly, detailed studies of human brain development, focusing on structural and functional maturation correlated with temporal mapping of cognitive processes as they come ‘on-line’, may provide unique mechanistic insights. Finally, the study of brain dysfunction in neurological and psychiatric disorders such as Huntington’s disease, Alzheimer’s disease, schizophrenia and depression, may have the beneficial side-effect of greatly enhancing our understanding of healthy brain function.

Each approach has its own epistemological advantages and disadvantages, but combined they may lead to more sophisticated, and empirically testable, models. In this review, I outline evidence for their utility, illustrate the approaches using specific examples and suggest how new advances in fields such as genomics, neurophysiology and neuroimaging may provide unprecedented opportunities in cognitive neuroscience.