Cognitive impairment is the most consistent neurological complication of acquired and degenerative brain disorders. Historically, most focus was on dementia but now has been broadened to include the important construct of mild cognitive impairment.

Systematic search and review of articles linked quality of life (QoL) and cognitive complications of neurological disorders. We excluded QoL in dementia.

Our search identified 249 publications. Most research examined patients with brain tumours, stroke, epilepsy, head injury, Huntington's disease, motor neuron disease, multiple sclerosis and Parkinson's disease. Results suggested that the majority of patients with epilepsy, motor neuron disease, multiple sclerosis, Parkinson's disease, stroke and head injury have subtle cognitive deficits early in their disease course. These cognitive complaints are often overlooked by clinicians. In many cases, the cognitive impairment is progressive but it can also be relapsing-remitting and in some cases reversible. Despite the importance of severe cognitive impairment in the form of dementia, there is now increasing recognition of a broad spectrum of impairment, including those with subclinical or mild cognitive impairment. Even mild cognitive difficulties can have functional and psychiatric consequences–especially when they are persistent and untreated. Specific cognitive deficits such an inattention, dysexecutive function and processing speed may affect a number of quality of life (QoL) domains. For example, cognitive impairment influences return to work, interpersonal relationships and leisure activities. In addition, fear of future cognitive decline may also impact upon QoL.

We recommend further development of simple tools to screen for cognitive impairments in each neurological condition. We also recommend that a thorough cognitive assessment should be a part of routine clinical practice in those caring for individuals with neurological disorders.

To investigate for the first time in a prospective study the relationship between depressive state and the neuropathological hallmarks of Alzheimer's disease, using a scale for depressive symptoms in dementia, while controlling for clinical severity of dementia.

Within the framework of a prospective longitudinal study of depression in Alzheimer's disease, patients with dementia underwent a clinical evaluation every six months during the last years of their lives, using the Cornell scale for depression in dementia to assess depressive symptoms and using the Functional Assessment Staging scale to control for clinical severity of dementia. The brains of 43 Alzheimer patients were obtained. The last clinical evaluations prior to death together with post-mortem neuropathology measures were analysed.

We found a correlation between the Cornell scores and the sum score for the density of neuritic plaques in the entire cortex (p = 0.027), and even stronger in the temporal cortex (p = 0.012). The observed correlations were independent of sex, age of death, clinical dementia severity and duration of Alzheimer's disease.

This study shows a positive relationship between depressive state at time of death and the presence of neuritic plaques in Alzheimer's disease, which is independent of the clinical severity of dementia.

We investigated whether 24-item Hamilton Rating Scale for Depression (HamD24)-based melancholia ratings correlated with treatment outcome, with special focus on whether electroconvulsive therapy (ECT) was used in depressed patients treated on an in-patient mood disorders unit.

We analysed the data on ECT- versus non-ECT-treated patients' outcomes relative to melancholia subscale scores. Two HamD24-based melancholia rating scale scores were computed for 201 depressed in-patients at admission and discharge. Baseline melancholia ratings were analysed to see if they correlated with improvement in total HamD24 scores. We also tested to see if the melancholia subscales followed unimodal or bimodal distributions.

Melancholic symptoms as assessed by one of the HamD24-based subscales directly correlated with overall improvement. Although ECT treatment was associated with greater improvement than was noted in non-ECT-treated patients, severity of melancholia ratings did not affect this relationship. Finally, both melancholia subscale scores followed approximately unimodal distributions.

HamD24-based methods to assess severity of melancholic symptoms have limited clinical utility on an in-patient mood disorders unit in general, and for predicting ECT response in particular. Furthermore, these methods do not seem to identify bimodal populations of depressed patients (i.e. melancholic vs. non-melancholic).

Recently, a reduction in efferent vagal regulation has been found in schizophrenic patients.

Therefore, the brainstems of nine schizophrenic patients and nine normal controls were stereologically analysed. The number of neurons using the optical fractionator method and nuclear volumes applying the Cavalieri principle was estimated in Nissl stained sections of the dorsal motor nucleus of the vagus (DMNV) and the hypoglossal nucleus.

The neurons in the right DMNV were significantly increased in the schizophrenic group compared to normal controls (p = 0.047), while the volumes of the DMNV did not differ. In contrast, no such differences were found in the hypoglossal nucleus.

Although this pilot study is limited by its small sample size, the analysis of the solitarius–ambiguus–vagus system in schizophrenic patients is an interesting target in schizophrenia research. The most reasonable background for increased neuron numbers in the DMNV could be a system-specific neurodevelopmental disturbance in schizophrenia.