Evaluation of the anterior processes of the parotid gland: an ultrasonographic study.

OBJECTIVES: This study aimed to determine the prevalence of anterior extensions of the parotid gland (AEPG), namely the accessory parotid gland (APG) and the facial process of the parotid gland (FP), using ultrasonography. STUDY DESIGN: A total of 338 parotid glands were scanned bilaterally. APG was defined as a soft tissue mass with the same echogenic features as the main parotid gland (MPG) and not in contact with it, while FP was defined as an extension that exceeded the anterior border of the mandibular ramus and was continuous with the MPG. The anteroposterior, mediolateral, superoinferior dimensions and the mean distance from the MPG to the APG were measured. RESULTS: The prevalence of APG and FP were 19.5% and 36%, respectively, resulting in an AEPG prevalence of 55.6%. The presence of APG was statistically higher in females than in males (p = 0.039). The mean anteroposterior, mediolateral, and superoinferior dimensions of the APG were 18.1 ± 0.57 mm, 0.35 ± 0.17 mm, and 12.3 ± 0.36 mm, respectively, and the mean distance from the MPG was measured as 12.1 ± 0.87 mm. CONCLUSION: This study can raise awareness among clinicians about the presence of AEPG in the differential diagnosis of mid-cheek masses.

Changes in brain size during the menstrual cycle.

BACKGROUND: There is increasing evidence for hormone-dependent modification of function and behavior during the menstrual cycle, but little is known about associated short-term structural alterations of the brain. Preliminary studies suggest that a hormone-dependent decline in brain volume occurs in postmenopausal, or women receiving antiestrogens, long term. Advances in serial MR-volumetry have allowed for the accurate detection of small volume changes of the brain. Recently, activity-induced short-term structural plasticity of the brain was demonstrated, challenging the view that the brain is as rigid as formerly believed. METHODOLOGY/PRINCIPAL FINDINGS: We used MR-volumetry to investigate short-term brain volume changes across the menstrual cycle in women or a parallel 4 week period in men, respectively. We found a significant grey matter volume peak and CSF loss at the time of ovulation in females. This volume peak did not correlate with estradiol or progesterone hormone levels. Men did not show any significant brain volume alterations. CONCLUSIONS/SIGNIFICANCE: These data give evidence of short-term hormone-dependent structural brain changes during the menstrual cycle, which need to be correlated with functional states and have to be considered in structure-associated functional brain research.

Positional brain deformation visualized with magnetic resonance morphometry.

OBJECTIVE: To assess and visualize gravitational effects on brain morphology and the position of the brain within the skull by magnetic resonance (MR) morphometry in order to identify confounding effects and possible sources of error for accurate planning of neurosurgical interventions. METHODS: Three-dimensional MR imaging data sets of 13 healthy adults were acquired in different positions in the scanner. With a morphometric approach, data sets were evaluated by deformation field analysis and the brain boundary shift integral. Distortions of the brain were assessed comparing right versus left and prone versus supine positioning, respectively. RESULTS: Two effects could be differentiated: 1) greatest brain deformation of up to 1.7 mm predominantly located around central brain structures in the lateral direction and a less pronounced change after position changes in posterior-anterior direction, and 2) the brain boundary shift integral depicted position-dependent brain shift relative to the inner skull. CONCLUSION: Position-dependent effects on brain structure may undermine the accuracy of neuronavigational and other neurosurgical procedures. Furthermore, in longitudinal MR volumetric studies, gravitational effects should be kept in mind and the scanning position should be rigidly controlled for.

Psychosis following anti-obesity treatment with rimonabant.

BACKGROUND: In this report, we present the case of a patient with a relapse of schizophrenia following an episode of depression and increased anxiety after antiobesity treatment with rimonabant, a cannabinoid type 1 receptor antagonist. CASE REPORT: After 4 weeks of treatment the patient developed psychiatric symptoms, i.e. depressed mood and elevated anxiety. Four months after the discontinuation of rimonabant, the patient presented with psychotic symptoms fulfilling ICD-10 criteria of paranoid schizophrenia. Antipsychotic treatment with quetiapine was initialized. A stable recovery took further 4 weeks in which combined treatment with quetiapine and ziprasidone was given. CONCLUSION: The course of the illness suggests that the continuous affective symptoms, which were most likely a side effect of rimonabant, may have triggered the psychosis analogous to the stress-diathesis model of schizophrenia. As a consequence, rimonabant may not be the first choice in obese patients with a history of schizophrenia due to a potentially increased risk of a relapse via an indirect mechanism.

Olfactory impairment in monozygotic twins discordant for schizophrenia.

OBJECTIVE: Several studies demonstrated olfactory dysfunction in patients with schizophrenia, some reported deficient olfaction in unaffected relatives of schizophrenics as well. This study differentially assessed olfactory acuity as well as smell identification and smell discrimination in monozygotic twins discordant for schizophrenia and healthy, monozygotic control twins, to determine the genetic basis of different olfactory modalities and their association to schizophrenia. METHOD: The Sniffin'Sticks test,a comprehensive and standardized olfactory test, was employed to assess the olfactory function of 10 monozygotic twin pairs discordant for schizophrenia versus 10 age- and sexmatched healthy,monozygotic twin pairs. RESULTS: Olfaction of affected monozygotic twins was globally impaired. Partial olfactory impairment of their unaffected co-twins may point to a genetic cause of olfactory impairment in schizophrenia. The influence of genetic factors was most evident for olfactory acuity and least evident for smell identification. All olfactory functions declined with duration of illness. Side of stimulus presentation did not influence olfactory performance. CONCLUSIONS: Genetic factors associated with olfactory dysfunction may contribute to schizophrenia. The degree of the genetic influence on olfaction depends on the olfactory domain under examination.