Springer Science and Business Media LLC

The effect of a new, powerful diuretic on biochemical parameters, urine output, central venous pressure, blood pressure, and cerebrospinal fluid pressure in patients with supratentorial intracerebral tumors who showed signs and symptoms of increased intracranial pressure was tested. When compared to an untreated control group and to the steady-state data of each patient, CSF pressure was significantly reduced using a dose of 240 mg of the diuretic. The 120 mg dosage did not produce significant results. Normalization of increased cerebrospinal fluid pressure was not completely obtained using either dose. Used alone, this substance is not suitable for treatment of increased intracranial pressure due to brain edema in patients with intracerebral tumors. It might, however, be useful in combination with other medications.

Substantial pathophysiological questions about the relationship of brain pathologies in psychosis can only be answered by multimodal neuroimaging approaches combining different imaging modalities such as structural MRI (sMRI), functional MRI (fMRI), diffusion tensor imaging (DTI), positron emission tomography (PET) and magnetic-resonance spectroscopy. In particular, the multimodal imaging approach has the potential to shed light on the neuronal mechanisms underlying the major brain structural and functional pathophysiological features of schizophrenia and high-risk states such as prefronto-temporal gray matter reduction, altered higher-order cognitive processing, or disturbed dopaminergic and glutamatergic neurotransmission. In recent years, valuable new findings have been revealed in these fields by multimodal imaging studies mostly reflecting a direct and aligned correlation of brain pathologies in psychosis. However, the amount of multimodal studies is still limited, and further efforts have to be made to consolidate previous findings and to extend the scope to other pathophysiological parameters contributing to the pathogenesis of psychosis. Here, investigating the genetic foundations of brain pathology relationships is a major challenge for future multimodal imaging applications in psychosis research.

Several linkage analyses in schizophrenia research point to a locus on chromosome 6p22, where the gene coding for tumor necrosis factor-α (TNF-α) is located. A marked influence of antipsychotic medication on TNF-α has been described. As the involvement of an immune process in the pathophysiology of schizophrenia has been discussed, a functional TNF-α polymorphism appears to be a candidate in genetic schizophrenia research. The G308A polymorphism of the TNF-α gene was described to be associated with increased TNF-α production. Boin and colleagues have already described a significant association between the polymorphic allele and schizophrenia, investigating 84 schizophrenic patients (21 % polymorphic allele) and 138 healthy volunteers (11 % polymorphic allele), recruited in Northern Italy. We carried out a replication study including 157 schizophrenic patients and 186 healthy persons, who were recruited in Southern Germany. Psychopathology was additionally monitored by PANSS. We were not able to replicate the findings of Boin et al., as we did not find any difference in allele frequency or genotype distribution between our schizophrenic patients (13.7 % polymorphic allele) and healthy controls (16.9 % polymorphic allele). Moreover, we did not find any association between genotype and psychopathology, as measured by PANSS. The different results between these two studies may be due to ethnic differences.

Opioid addiction is a global problem that has been exacerbated in the USA and Europe by the COVID-19 pandemic. The globus pallidus (GP) plays a prominent neurobiological role in the regulation of behaviour as an output station of the striato-pallidal system. GABAergic large projection neurons are the main neuronal type in the external (EGP) and internal (IGP) parts of the GP, where addiction-specific molecular and functional abnormalities occur. In these neurons, glutamate decarboxylase (GAD) with isoforms GAD 65 and 67 is a key enzyme in GABA synthesis, and experimental studies suggest GAD dysregulation in the GP of heroin addicts. Our study, which was performed on paraffin-embedded brains from the Magdeburg Brain Bank, aimed to investigate abnormalities in the GABAergic function of large GP neurons by densitometric evaluation of their GAD 65/67-immunostained thick dendrites. The study revealed a bilaterally decreased fibres density in the EGP paralleled by the increase in the IGP in 11 male heroin addicts versus 11 healthy controls (significant U-test P values). The analysis of confounding variables found no interference of age, brain volume, and duration of formalin fixation with the results. Our findings suggest a dysregulation of GABAergic activity in the GP of heroin addicts, which is consistent with experimental data from animal models and plays potentially a role in the disturbed function of basal ganglia circuit in opioid addiction.

In 1923, Friedrich H. Lewy described dementia with Lewy bodies in a large proportion of his patients with paralysis agitans which had co-incident plaques and neurofibrillary tangles. The potential contribution of Lewy bodies to a dementia syndrome with fluctuating course, visual hallucinations, Parkinsonian features and neuroleptic hypersensitivity was rediscovered many decades later. The comorbidity of Alzheimer’s and Parkinson’s disease is not uncommon as both diseases show an exponential increase with advancing age and their coincidence is of great clinical importance. The combination of a cholinergic deficit – which is particularly severe due to the double pathology targeting the basal nucleus of Meynert – and a dopaminergic deficit requires cholinergic and cautious dopaminergic treatment. Excessive dopamine (L-dopa), antidopaminergic (neuroleptic) or anticholinergic treatment (anti-Parkinson or neuroleptic medication) may further complicate the condition, worsen extrapyramidal, psychotic or cognitive disturbances and even lead to a neuroleptic malignant syndrome.