Presentation of a Sedation Standard Using the Example of Transesophageal Echocardiographies (TEE) in Pediatric Outpatients.

Introduction Most pediatric patients require deep sedation for a TEE examination. We analyzed the data of our sedation protocols relating to all outpatient TEEs in patients under 18 years of age for the year 2011. On the basis of the data records of a total of 40 patients, we will describe our standard and compare it with the findings of the international literature. Material and Methods In a retrospective analysis, we inspected our sedation protocols in terms of patient-related data, vital parameters, drug applications, occurring complications and necessary interventions as well as nausea and vomiting during the post-sedative monitoring phase. Results In line with our standard, we applied atropine, midazolam, S-ketamine and propofol; complications occurred in 5 patients. They could be handled using simple measures. With regard to the vital parameters, no severe complications occurred. Dizziness was observed in 4 patients during the recovery phase; one patient complained about nausea and vomiting during the first fluid intake. All patients could be discharged 4 h after the termination of sedation. Conclusion Our standard is a practicable and safe procedure for preforming TEE examinations in pediatric outpatients.

Treatment of digital pyogenic flexor tenosynovitis: single open debridement, irrigation, and primary wound closure followed by antibiotic therapy.

INTRODUCTION: Digital pyogenic flexor tenosynovitis requires fast, aggressive treatment. Although this infection occurs frequently, treatment consensus is lacking. MATERIALS AND METHODS: Between 2011 and 2015, 22 patients with acute pyogenic flexor tenosynovitis were treated with a single open debridement followed by irrigation; the incision was closed and a 10-day antibiotic course was administered. The average incision-to-suture time was 25 min, and the average hospital stay was 4 days. Recovery was uncomplicated for 20 patients, while two were reoperated, one due to germ resistance and the other due to necrotizing fasciitis. At an average of 30 month postoperatively, 21 of the 22 patients were available for follow-up. The affected finger was inspected, and sensibility, range of motion, and grip force were compared with the opposite side, and the DASH score was determined. Each patient documented pain in the affected finger at rest and during activity, and rated overall satisfaction with the treatment on a visual analogue scale. RESULTS: Almost all patients were free of pain at follow-up and very satisfied. Compared to the contralateral side, each of the affected fingers had the same range of motion and sensibility. Grip force was similar on both sides. The average DASH score was 35 points. CONCLUSION: A single open debridement with irrigation and primary wound closure followed by 10 days of antibiotic treatment resolved uncomplicated pyogenic flexor tenosynovitis. After 2 and a half years, the treatment yielded high patient satisfaction with neither functional nor subjective impairment of the affected finger.

Gastric ghrelin, GOAT, leptin, and leptinR expression as well as peripheral serotonin are dysregulated in humans with obesity.

BACKGROUND: Gastrointestinal hormone release and the regulation of appetite and body weight are thought to be dysbalanced in obesity. However, human data investigating the expression of gastrointestinal hormones in the obese are rare. We studied the expression of ghrelin, leptin, and the serotonergic system in stomach tissue and serum of obese and non-obese individuals. METHODS: Gastric tissue and serum were collected from 29 adult obese (BMI 48.7 ± 10.6 kg/m(2) ; mean ± SD) who underwent laparoscopic sleeve gastrectomy. Gastric biopsies, surgery specimen or serum was obtained from 35 adult non-obese humans (BMI 22.7 ± 1.9 kg/m(2) ). Ghrelin, ghrelin O-acyl transferase (GOAT), leptin, leptin receptor, and tryptophan hydroxylase 1 (TPH1) mRNA expression were measured by qRT-PCR. Serotonin (5HT) and leptin protein concentration were quantified in tissue extracts and serum; GOAT and ghrelin-positive cells were immunohistologically quantified in tissue. Additionally, 21 blood immune markers were analyzed. KEY RESULTS: In gastric tissue, GOAT-positive cells were reduced (p < 0.01), but ghrelin-positive cells and mRNA were increased (both p < 0.05) in obese compared with non-obese individuals. Gastric leptin (p < 0.001) and leptin receptor (p < 0.001) mRNA expression, as well as leptin concentrations in serum (p < 0.001), were increased in obese compared with non-obese individuals. Serum 5HT was reduced (p < 0.05), while tissue 5HT and TPH1 mRNA were reduced only by trend. Interleukin 1 receptor a (IL1Ra), IL-8, IL-12, and monocyte chemoattractant protein 1 (IL1Ra) were increased and IL1Ra correlated negatively with serum leptin. CONCLUSIONS & INFERENCES: Our data indicate that obesity causes a dysregulation of gastrointestinal hormones at the tissue level and serum, including a negative correlation with an increased marker of subclinical inflammation.

[Supplementary arthrolysis of the proximal interphalangeal joint of fingers in surgical treatment of Dupuytren's contracture]. / Die ergänzende Mittelgelenkarthrolyse bei der operativen Behandlung einer Dupuytren'schen Beugekontraktur am Finger.

OBJECTIVE: Correction of residual flexion deformity of the proximal interphalangeal (PIP) joint after excision of diseased connective tissue in Dupuytren's contracture by stepwise arthrolysis. INDICATIONS: Flexion deformity of the PIP joint of 20° or more after excision of the diseased connective tissue in Dupuytren's contracture. CONTRAINDICATIONS: Joint deformities, osteoarthrosis, intrinsic muscle contracture, instability of the PIP joint. SURGICAL TECHNIQUE: Arthrolysis of the PIP joint is performed by six consecutive steps: dissection of the remaining skin ligaments, opening the flexor tendon sheath by transverse incision at the distal end of the A2 pulley, dissection of the checkrein ligaments, dissection of the accessory collateral ligaments, releasing the palmar plate proximally, releasing the palmar plate up to its insertion at the middle phalanx base. POSTOPERATIVE MANAGEMENT: Dorsal plaster of Paris with extended fingers and compressive dressing in the palm for 2 days, occupational/physical therapy, static and possible dynamic extension splint several weeks/months. RESULTS: A total of 31 fingers in 28 patients with Dupuytren's contracture were evaluated an average of 22 months after arthrolysis of the PIP joint. In all, 26 joints with an average recurrent flexion contracture of 29° were improved compared to the preoperative flexion contracture of 81°; 4 PIP joints with a recurrent flexion contracture averaging 60° were worse. In one patient, PIP flexion contracture of 90° was unchanged at follow-up although the joint could be extended intraoperatively to 10° of flexion.

[Acute Carpal Tunnel Syndrome due to Spontaneous Bleeding after Taking Rivaroxaban (Xarelto®)]. / Akutes Karpaltunnelsyndrom durch spontane Blutung nach Einnahme von Rivaroxaban (Xarelto®).

A 64-year-old man suffered from acute carpal tunnel syndrome of his right hand without explainable reason. An emergency operation drained a pronounced haematoma. There is a strong suspicion this was a bleeding complication related to taking rivaroxaban (Xarelto(®)).

[Experiences of stigma and discrimination in patients with first-episode schizophrenia]. / Erleben von Stigma und Diskriminierung bei ersterkrankten Schizophreniepatienten.

BACKGROUND: Patients with mental illnesses, especially with schizophrenia, suffer from stigma and discrimination. In addition, the stigma is a barrier to recognising and treating patients with first-episode psychosis; however, a self-rating instrument that assesses the general burden due to stigma experiences is still lacking. MATERIAL AND METHODS: A total of N = 48 patients with first-episode schizophrenia who were participants in the multicenter first-episode (long-term) study within the German Research Network on Schizophrenia, completed a newly developed self-rating questionnaire to assess the burden due to stigma experiences (B-STE). The following variables were analyzed as possible correlates: psychopathology (CGI, PANSS, CDSS and HAM-D), global functioning (GAF), social adjustment (SAS), self-esteem (FSKN), as well as quality of life (LQLP), subjective well-being under neuroleptic treatment (SWN) and anticipated stigma (PDDQ). RESULTS: Of the participants 25 % showed an increased burden due to stigma experiences, which correlated with a lower quality of life, lower subjective well-being under neuroleptic treatment, lower self-esteem and higher anticipated stigma. The results indicate that patients rated higher on the CGI scale who are at the same time better socially adjusted (SAS), are more intensely affected by the burden due to stigma experiences. CONCLUSION: The short self-rating instrument burden due to stigma experiences (B-STE) can help to identify patients who might benefit from therapeutic or educational interventions to support coping with stigma experiences.

ZNF804A genetic variation (rs1344706) affects brain grey but not white matter in schizophrenia and healthy subjects.

BACKGROUND: Genetic variation in the gene encoding ZNF804A, a risk gene for schizophrenia, has been shown to affect brain functional endophenotypes of the disorder, while studies of white matter structure have been inconclusive. METHOD: We analysed effects of ZNF804A single nucleotide polymorphism rs1344706 on grey and white matter using voxel-based morphometry (VBM) in high-resolution T1-weighted magnetic resonance imaging scans of 62 schizophrenia patients and 54 matched healthy controls. RESULTS: We found a significant (p < 0.05, family-wise error corrected for multiple comparisons) interaction effect of diagnostic group x genotype for local grey matter in the left orbitofrontal and right and left lateral temporal cortices, where patients and controls showed diverging effects of genotype. Analysing the groups separately (at p < 0.001, uncorrected), variation in rs1344706 showed effects on brain structure within the schizophrenia patients in several areas including the left and right inferior temporal, right supramarginal/superior temporal, right and left inferior frontal, left frontopolar, right and left dorsolateral/ventrolateral prefrontal cortices, and the right thalamus, as well as effects within the healthy controls in left lateral temporal, right anterior insula and left orbitofrontal cortical areas. We did not find effects of genotype of regional white matter in either of the two cohorts. CONCLUSIONS: Our findings demonstrate effects of ZNF804A genetic variation on brain structure, with diverging regional effects in schizophrenia patients and healthy controls in frontal and temporal brain areas. These effects, however, might be dependent on the impact of other (genetic or non-genetic) disease factors.

Reciprocal causation models of cognitive vs volumetric cerebral intermediate phenotypes for schizophrenia in a pan-European twin cohort.

In aetiologically complex illnesses such as schizophrenia, there is no direct link between genotype and phenotype. Intermediate phenotypes could help clarify the underlying biology and assist in the hunt for genetic vulnerability variants. We have previously shown that cognition shares substantial genetic variance with schizophrenia; however, it is unknown if this reflects pleiotropic effects, direct causality or some shared third factor that links both, for example, brain volume (BV) changes. We quantified the degree of net genetic overlap and tested the direction of causation between schizophrenia liability, brain structure and cognition in a pan-European schizophrenia twin cohort consisting of 1243 members from 626 pairs. Cognitive deficits lie upstream of the liability for schizophrenia with about a quarter of the variance in liability to schizophrenia explained by variation in cognitive function. BV changes lay downstream of schizophrenia liability, with 4% of BV variation explained directly by variation in liability. However, our power to determine the nature of the relationship between BV deviation and schizophrenia liability was more limited. Thus, while there was strong evidence that cognitive impairment is causal to schizophrenia liability, we are not in a position to make a similar statement about the relationship between liability and BV. This is the first study to demonstrate that schizophrenia liability is expressed partially through cognitive deficits. One prediction of the finding that BV changes lie downstream of the disease liability is that the risk loci that influence schizophrenia liability will thereafter influence BV and to a lesser extent. By way of contrast, cognitive function lies upstream of schizophrenia, thus the relevant loci will actually have a larger effect size on cognitive function than on schizophrenia. These are testable predictions.

Non-neurological, steroid-related adverse events in very low birth weight infants: a prospective audit.

BACKGROUND AND STUDY PURPOSE: To assess the incidence of cardiac and metabolic adverse events in very low birth weight (VLBW) infants receiving systematic steroids. PATIENTS AND METHODS: Prospective single centre audit in VLBW infants (<1,500 g) at the neonatal intensive care unit at the University Children's Hospital of Saarland, Germany. RESULTS: A total of 72 VLBW infants (38 female) were included in this report (mean birth weight: 967 ± 338 g; range: 320-1490 g). Birth weight, gestational age and Apgar scores were significantly lower in the steroid group (p <0.01). Mortality rate was 8/72 (7/34 in the steroid treated vs nontreated 1/38; odds ratio [OR]: 9.6; 95% confidence interval [CI]: 1.1-82.6 p = 0.02). In 34/72 infants, steroids were given (22 hydrocortisone alone; 12 combination of hydrocortisone and dexamethasone). The most common indication for use of steroids was respiratory distress syndrome (RDS) and respiratory insufficiency (30/34). Adverse events that occurred more often in the steroid group included hypertrophic cardiomyopathy (14/34 vs 0/38; p <0.001); thrombus formation (8/34 vs 1/38; OR: 11.4; 95% CI: 1.3-96.6; p <0.05), hyperglycaemia (27/34 vs 3/38; OR: 45.0; 95% CI: 10.6-190.4; p <0.01), hypernatraemia (15/34 vs 7/38; OR: 3.5; 95% CI: 1.2-10.1; p <0.05), and sepsis/infections (8/34 vs 1/38; OR: 11.4; 95% CI: 1.3-96.6; p <0.05). No significant differences were seen between hydrocortisone alone and the combination of hydrocortisone with dexamethasone. Birth weight and severity of RDS were predictors of steroid use (p <0.01). CONCLUSIONS: The use of steroids was significantly associated with severe short-term adverse events - most importantly hypertrophic cardiomyopathy and thrombus formation. These complications must be taken into consideration when administering steroids to VLBW infants.

Omega-3 fatty acid supplementation changes intracellular phospholipase A2 activity and membrane fatty acid profiles in individuals at ultra-high risk for psychosis.

The identification of an ultra-high risk (UHR) profile for psychosis and a greater understanding of its prodrome have led to increasing interest in early intervention to delay or prevent the onset of psychotic illness. In a randomized placebo-controlled trial, we have identified long-chain ω-3 (ω-3) polyunsaturated fatty acid (PUFA) supplementation as potentially useful, as it reduced the rate of transition to psychosis by 22.6% 1 year after baseline in a cohort of 81 young people at UHR of transition to psychosis. However, the mechanisms whereby the ω-3 PUFAs might be neuroprotective are incompletely understood. Here, we report on the effects of ω-3 PUFA supplementation on intracellular phospholipase A2 (inPLA(2)) activity, the main enzymes regulating phospholipid metabolism, as well as on peripheral membrane lipid profiles in the individuals who participated in this randomized placebo-controlled trial. Patients were studied cross-sectionally (n=80) and longitudinally (n=65) before and after a 12-week intervention with 1.2 g per day ω-3 PUFAs or placebo, followed by a 40-week observation period to establish the rates of transition to psychosis. We investigated inPLA(2) and erythrocyte membrane FAs in the treatment groups (ω-3 PUFAs vs placebo) and the outcome groups (psychotic vs non-psychotic). The levels of membrane ω-3 and ω-6 PUFAs and inPLA(2) were significantly related. Some of the significant associations (that is, long-chain ω-6 PUFAs, arachidonic acid) with inPLA(2) activity were in opposite directions in individuals who did (a positive correlation) and who did not (a negative correlation) transition to psychosis. Supplementation with ω-3 PUFA resulted in a significant decrease in inPLA(2) activity. We conclude that ω-3 PUFA supplementation may act by normalizing inPLA(2) activity and δ-6-desaturase-mediated metabolism of ω-3 and ω-6 PUFAs, suggesting their role in neuroprogression of psychosis.

Common variation in NCAN, a risk factor for bipolar disorder and schizophrenia, influences local cortical folding in schizophrenia.

BACKGROUND: Recent studies have provided strong evidence that variation in the gene neurocan (NCAN, rs1064395) is a common risk factor for bipolar disorder (BD) and schizophrenia. However, the possible relevance of NCAN variation to disease mechanisms in the human brain has not yet been explored. Thus, to identify a putative pathomechanism, we tested whether the risk allele has an influence on cortical thickness and folding in a well-characterized sample of patients with schizophrenia and healthy controls. METHOD: Sixty-three patients and 65 controls underwent T1-weighted magnetic resonance imaging (MRI) and were genotyped for the single nucleotide polymorphism (SNP) rs1064395. Folding and thickness were analysed on a node-by-node basis using a surface-based approach (FreeSurfer). RESULTS: In patients, NCAN risk status (defined by AA and AG carriers) was found to be associated with higher folding in the right lateral occipital region and at a trend level for the left dorsolateral prefrontal cortex. Controls did not show any association (p > 0.05). For cortical thickness, there was no significant effect in either patients or controls. CONCLUSIONS: This study is the first to describe an effect of the NCAN risk variant on brain structure. Our data show that the NCAN risk allele influences cortical folding in the occipital and prefrontal cortex, which may establish disease susceptibility during neurodevelopment. The findings suggest that NCAN is involved in visual processing and top-down cognitive functioning. Both major cognitive processes are known to be disturbed in schizophrenia. Moreover, our study reveals new evidence for a specific genetic influence on local cortical folding in schizophrenia.

[Psychiatric psychotherapeutic research in Germany: taking stock and international comparison]. / Psychiatrisch-psychotherapeutische Forschung in Deutschland : Bestandsaufnahme und internationaler Vergleich.

This article is based on an evaluation carried out by the DGPPN in 2011 surveying 50 German university and non-university institutions about the scientific research output focussing on psychiatric and psychotherapeutic research. The results of the survey show that on average there are 1 to 2 professors with 12 assistants scientifically active per institution. According to self-disclosure an estimated 1.8 million Euros of external funds are raised each year.Compared to international standards regarding the illnesses major depression, schizophrenia and alcohol abuse, Germany ranks second and third place behind the USA and the UK or Canada in terms of publication output. In terms of authors and institutions, German scientists and universities rank in the upper third to upper tenth for these illnesses. These data show that psychiatric research in Germany is not only internationally competitive but outstanding in its excellent achievements in these fields. Unfortunately, many funding programmes are limited to a 3-6 year period. In view of this fact and in order to achieve a long-term improvement in the translation of funding structures, as in the US (NIMH) or the UK (MRC) to benefit the mentally ill the implementation of a German centre for mental disorders is inevitable.

Exendin-4 protects hypoxic islets from oxidative stress and improves islet transplantation outcome.

Oxidative stress produced during pancreatic islet isolation leads to significant ß-cell damage. Homeostatic cytokines secreted subsequently to islet transplantation damage ß-cells by generating oxygen free radicals. In this study, exendin-4, a glucagon-like peptide-1 analog improved islet transplantation outcome by increasing the survival of diabetic recipient mice from 58% to 100%. We hypothesized that this beneficial effect was due to the ability of exendin-4 to reduce oxidative stress. Further experiments showed that it significantly reduced the apoptotic rate of cultured ß-cells subjected to hypoxia or to IL-1ß. Reduction of apoptotic events was confirmed in pancreatic islet grafts of exendin-4-treated mice. Exendin-4 enhanced Akt phosphorylation of ß-cells and insulin released from them. It even augmented insulin secretion from islets cultivated at hypoxic conditions. Exposure to hypoxia led to a decrease in the activation of Akt, which was reversed when ß-cells were pretreated with exendin-4. Moreover, exendin-4 increased the activity of redox enzymes in a hypoxia-treated ß-cell line and reduced reactive oxygen species production in isolated pancreatic islets. Recovery from diabetes in mice transplanted with hypoxic islets was more efficient when they received exendin-4. In conclusion, exendin-4 rescued islets from oxidative stress caused by hypoxia or due to cytokine exposure. It improved the outcome of syngenic and xenogenic islet transplantation.

Should early improvement be re-defined to better predict the maintenance of response in first-episode schizophrenia patients?

OBJECTIVE: To evaluate the predictive validity of early response in first-episode schizophrenia within a 1-year follow-up trial and to compare the resulting cutoff to the currently proposed early response definition (20% improvement by week 2). METHOD: Receiver operator characteristic (ROC) analyses were used to identify the predictive validity of the psychopathological improvement of treatment from week 1 to week 8, regarding the maintenance of response until week 52 as well as to define the most reasonable cutoff in 132 first-episode patients. The Youden Index (maximum of sensitivity and specificity) was used to compare the newly developed and the commonly used early response definition. RESULTS: Starting with week 6, a reasonable validity to predict the maintenance of response was found (area under the curve = 0.721) with the best fitting cutoff being a 51.6% PANSS total score improvement. Using this cutoff 74 patients (56%) were correctly identified to become responder and maintain response during follow-up (sensitivity: 0.747). The Youden Index was higher applying the newly developed early response cutoff featuring higher specificity compared to the commonly used early response definition. CONCLUSION: Regarding long-term treatment, it seems more appropriate to base predictions of the patient's maintenance of response not before 6 weeks of treatment.

Duplications in RB1CC1 are associated with schizophrenia; identification in large European sample sets.

Schizophrenia (SCZ) is a severe and debilitating neuropsychiatric disorder with an estimated heritability of ~80%. Recently, de novo mutations, identified by next-generation sequencing (NGS) technology, have been suggested to contribute to the risk of developing SCZ. Although these studies show an overall excess of de novo mutations among patients compared with controls, it is not easy to pinpoint specific genes hit by de novo mutations as actually involved in the disease process. Importantly, support for a specific gene can be provided by the identification of additional alterations in several independent patients. We took advantage of existing genome-wide single-nucleotide polymorphism data sets to screen for deletions or duplications (copy number variations, CNVs) in genes previously implicated by NGS studies. Our approach was based on the observation that CNVs constitute part of the mutational spectrum in many human disease-associated genes. In a discovery step, we investigated whether CNVs in 55 candidate genes, suggested from NGS studies, were more frequent among 1637 patients compared with 1627 controls. Duplications in RB1CC1 were overrepresented among patients. This finding was followed-up in large, independent European sample sets. In the combined analysis, totaling 8461 patients and 112 871 controls, duplications in RB1CC1 were found to be associated with SCZ (P=1.29 × 10(-5); odds ratio=8.58). Our study provides evidence for rare duplications in RB1CC1 as a risk factor for SCZ.

Heart rate variability in the irritable bowel syndrome: a review of the literature.

BACKGROUND: Patients with irritable bowel syndrome (IBS) often present with disturbances of bowel habits (diarrhea, constipation) and abdominal pain/discomfort that are modulated by the autonomic nerve system (ANS). In this narrative review, we analyzed studies that measured ANS functioning in IBS by means of heart rate variability (HRV). METHODS: The PUBMED was searched with the keywords 'irritable bowel syndrome' AND ('heart rate variability' OR 'autonomic function'). We included only papers that used 'traditional' HRV indices and diagnosed IBS based on Manning or Rome criteria. Studies were sub-grouped according to methodological features of HRV analysis (24-h monitoring, short-term laboratory records, records during sleep). KEY RESULTS: Most studies reported no difference in HRV when the IBS population was compared to healthy controls. Dividing the IBS sample into subgroups--according to their predominant bowel symptoms, the severity of clinical course, the presence of depressive symptoms, or a history of abuse in the past--revealed changes in autonomic functioning. CONCLUSIONS & INFERENCES: Patients with IBS appear to experience symptoms that may be the result of changes in ANS functioning. HRV measures in clinical routine may allow assessing these changes, but further studies performed in a standardized fashion should improve the validity of HRV measures for clinical research first.

A vegan or vegetarian diet substantially alters the human colonic faecal microbiota.

BACKGROUND/OBJECTIVES: Consisting of ≈10(14) microbial cells, the intestinal microbiota represents the largest and the most complex microbial community inhabiting the human body. However, the influence of regular diets on the microbiota is widely unknown. SUBJECTS/METHODS: We examined faecal samples of vegetarians (n=144), vegans (n=105) and an equal number of control subjects consuming ordinary omnivorous diet who were matched for age and gender. We used classical bacteriological isolation, identification and enumeration of the main anaerobic and aerobic bacterial genera and computed absolute and relative numbers that were compared between groups. RESULTS: Total counts of Bacteroides spp., Bifidobacterium spp., Escherichia coli and Enterobacteriaceae spp. were significantly lower (P=0.001, P=0.002, P=0.006 and P=0.008, respectively) in vegan samples than in controls, whereas others (E. coli biovars, Klebsiella spp., Enterobacter spp., other Enterobacteriaceae, Enterococcus spp., Lactobacillus spp., Citrobacter spp. and Clostridium spp.) were not. Subjects on a vegetarian diet ranked between vegans and controls. The total microbial count did not differ between the groups. In addition, subjects on a vegan or vegetarian diet showed significantly (P=0.0001) lower stool pH than did controls, and stool pH and counts of E. coli and Enterobacteriaceae were significantly correlated across all subgroups. CONCLUSIONS: Maintaining a strict vegan or vegetarian diet results in a significant shift in the microbiota while total cell numbers remain unaltered.

Temporal and right frontal lobe alterations in panic disorder: a quantitative volumetric and voxel-based morphometric MRI study.

BACKGROUND: With regard to current neurobiological theories, the aim of our study was to examine possible alterations of temporal and frontal lobe volume in panic disorder (PD). METHOD: Seventeen in-patients with PD and a group of healthy control subjects (HC) matched for age and gender were investigated by quantitative volumetric magnetic resonance imaging (MRI). Structures of interest were: the temporal lobe, the amygdala-hippocampus complex (AHC) and the frontal lobe. In addition, a voxel-based morphometry (VBM) analysis implemented in Statistical Parametric Mapping 5 (SPM5) was used for a more detailed assessment of possible volume alterations. Modulated grey matter (GM) images were used to test our a priori hypotheses and to present the volumetric results. RESULTS: Quantitative volumetric MRI revealed a bilateral reduction in temporal lobe volume in patients with PD compared to HC subjects. The AHC was normal. The right frontal lobe volume was also decreased. Using VBM we detected a significant GM volume reduction in the right middle temporal gyrus [Brodmann area (BA) 21] in patients with PD. In addition, there was a reduction in GM volume in the medial part of the orbitofrontal cortex (BA 11). CONCLUSIONS: Our results of reduced temporal and frontal lobe volume in PD are in agreement with prior studies. By using a recent VBM approach we were able to assess the abnormalities more precisely. The location of GM volume reduction in the right middle temporal gyrus and medial orbitofrontal cortex lends further support to recent aetiological models of PD.