Brain metastases from cervical carcinoma are rare. Accompanying symptoms depend on the location of the metastatic lesions. Penduncular hallucinosis is a vivid form of hallucination with clinical findings indicating a lesion of the upper midbrain. We hereby report a probable first case of peduncular hallucinosis associated with brain metastases from cervical cancer.

A 42-year-old woman had been diagnosed with adenocarcinoma of cervix. On admission for her increasing pelvic pain, she had complex visual hallucinations comprising cartoon children, figurative people and a foggy room. Magnetic resonance imaging of the head revealed a lesion in the left mesencephalothalamic area.

Peduncular hallucinosis is well known for its vivid and life-like characteristics associated with a mesencephalic area lesion, and recognition of this may be useful of its diagnosis and differential diagnosis from confusion and other hallucinations.

Identification of candidate genes for schizophrenia may be more successful than genome screens as the latter have not found consistent linkages.

To assist in the gene search, a model of schizophrenia based on resistance to infectious diseases, rather than susceptibility, is proposed. The theory blends the geography of schizophrenia with the assumption that genes that cause schizophrenia likely evolved and persist from selection pressure. The theory includes the notion that schizophrenia enhances biological survival at the cost of psychological and social functioning.

To demonstrate the utility of using this model, the Medline literature was searched for resistance genes, mostly identified in mice.

Based on homologous locations in the human genome, these resistance genes are shown to be located in human chromosome regions linked significantly, in at least one genome screen, with schizophrenia or some physiologically related function or condition associated with schizophrenia.

The infectious disease resistance theory of schizophrenia is offered as a viable model for understanding the origins of schizophrenia. The theory also allows for the inclusion of persistent infections, seasonal variability and translational pathophysiology to contribute to the etiology of schizophrenia.

This study assessed the changes in the isoprenoid pathway and its metabolites in seizure disorder (ILAE classification – I generalized – idiopathic generalized epilepsy with age-related onset – epilepsy with generalized tonic clonic seizures on awakening) and the metabolic cascade produced by isoprenoid pathway dysregulation.

The following parameters were assessed in seizure disorder: isoprenoid pathway metabolites, tyrosine and tryptophan catabolites, glycoconjugates metabolism and red blood cell (RBC) membrane composition.

There was elevation in plasma HMG-CoA reductase activity, serum digoxin and dolichol and a reduction in RBC membrane Na-K+ ATPase activity, serum magnesium and ubiquinone levels. Serum tryptophan, serotonin, strychnine, nicotine and quinolinic acid were elevated while tyrosine, dopamine, morphine and norepinephrine were decreased. The total serum glycosaminoglycans and glycosaminoglycan fractions (except dermatan sulfate), the activity of glycosaminoglycans (GAG) degrading enzymes and glycohydrolases, carbohydrate residues of glycoproteins and serum glycolipids were elevated. Total serum cholesterol, LDL cholesterol and free fatty acids were increased while HDL cholesterol and triglycerides were unaltered. The concentration of membrane hexose, fucose, cholesterol and phospholipids in the RBC membrane decreased significantly but the total RBC membrane GAG was unaltered.

Epileptogenesis could be due to a dysfunctional isoprenoidal pathway and paroxysmal hypothalamic digoxin hypersecretion.

Cryotherapy has a long tradition in somatic medicine. Yet we know very little about its impact on psyche and mood disturbances in particular. Therefore there is a real need for scientific investigations into this problem.

The study reported here was an initial approach to whole-body cryotherapy (WBCT) as a potential treatment modality for depression and was expected to provide rough data helping to design a future project with extended methodology, larger sample groups and longer follow-up.

Twenty-three patients aged 37–70 years gave informed consent to participate in the study. Ten WBCT procedures (160 s, −150°C) were applied within 2 weeks. Participants were recruited from depressed day hospital patients. Antidepressive medication was not ceased. Symptoms were rated at the beginning and end of this intervention using the 21-item Hamilton Depression Rating Scale (HDRS). Changes in scores were analyzed in the group of patients for every item separately as well as for the sum of all items for each patient.

Almost for each individual HDRS item, the overall score for all patients together was significantly lower after WBCT. This means that all symptoms, except for day–night mood fluctuations, were presumably positively influenced by cryotherapy. The HDRS sum-score for each patient after WBCT was lower than that of the baseline and reached statistical significance in a paired samples t-test. Every patient was therefore considerably relieved after WBCT.

It appears that WBCT helps in alleviating depression symptoms. Should this be confirmed in the extended study we are currently implementing, WBCT may become an auxiliary treatment in depression.

Tolerability, safety and effectiveness of quetiapine in an in-patient group with a relapse of schizophrenia and the possible role of plasma amino acid concentrations, 5-HT parameters and HVA in the prediction of response to treatment were investigated in an open-label baseline-controlled trial of 14 weeks in 21 hospitalized schizophrenic patients. Responders were defined as those patients who exhibit at least a 40% reduction of BPRS total scores. Secondary efficacy measures were the PANSS, the Clinical Global Impression (CGI)-severity scale and the MADRS. Extrapyramidal side-effects were evaluated with the AIMS. Other side-effects were monitored at regular intervals. Amino acids and the derived tryptophan and tyrosine ratios, as well as monoaminergic parameters, were assessed in plasma at baseline and at weeks 3, 6 and 14.

Treatment with quetiapine resulted in the predefined treatment effect in 10 out of the 17 patients who completed at least 4 weeks of treatment. Effect in responders was observed on all efficacy parameters, including lower MADRS scores. No extrapyramidal side-effects emerged. Clinical and biochemical parameters did not predict response to treatment.

This study demonstrates the moderate antipsychotic efficacy of quetiapine on preferentially positive symptoms in a group of relatively young schizophrenics. Some observed changes in biochemical parameters are discussed.

To find out whether the neurodevelopmental disorders autism and childhood-onset schizophrenia have a common developmental pathway and whether the abnormalities detected are ‘disorder-specific’, by reviewing magnetic resonance imaging (MRI) studies.

As a result of a Medline search, we were able to access 28 studies on autism and 12 studies on childhood-onset schizophrenia, which focused on children and adolescents.

Larger lateral ventricles were found to be a common abnormality in both disorders. ‘Disorder-specific’ abnormalities in patients with autism were larger brains, a larger thalamic area, and a smaller right cingulate gyrus. Subjects with childhood-onset schizophrenia were found to have smaller brains, a smaller amygdalum and thalamus, and a larger nucleus caudatus. In subjects with childhood-onset schizophrenia, abnormalities appeared to progress over a limited period of time.

Because the study designs varied so much, the results should be interpreted cautiously. Before abnormalities found in the disorders can be designated as equal or ‘disorder-specific’, it will be essential to perform large longitudinal and cross-sectional follow-up studies.