Childhood trauma, family history, and their association with mood disorders in early adulthood.

OBJECTIVE: To assess the prevalence of childhood trauma and types of trauma on mood disorders among young adults in a population-based sample. We further gathered data on family history of mood disorders to test the hypothesis that childhood trauma is a mediating factor for the association between family history of mood disorder and mood disorder in adulthood. METHOD: This is a cross-sectional study, including young adults with bipolar disorder, major depressive disorder, and matched controls without any mood disorder. Childhood trauma was assessed using the Childhood Trauma Questionnaire (CTQ). The Hicks and Tingley implementation was employed to assess whether trauma is a mediator of the effect of family history on diagnosis of any mood disorder. RESULTS: All types of trauma were associated with both major depression and bipolar disorder, with the exception of sexual abuse, which was only associated with bipolar disorder. Moreover, family history of psychiatric illness was also associated with mood disorder in adulthood and with childhood trauma. Using the presence of any mood disorder as the outcome, a third of the effect of having any family history of mood disorder was mediated via childhood trauma. CONCLUSION: This investigation provides further support, in a population-based sample of young adults, of the association between childhood trauma and mood disorders, with sexual abuse being specifically linked with bipolar disorder. The hypothesis that childhood trauma would function as a partial mediator of the association between family history of mood disorder and mood disorder in adulthood was also confirmed.

Brain-derived neurotrophic factor and inflammatory markers in school-aged children with early trauma.

OBJECTIVE: The impact of childhood trauma (CT) on brain-derived neurotrophic factor (BDNF) and cytokines levels remains unclear. We investigated the association between CT and changes in BDNF and cytokines plasma levels in children. METHOD: We recruited 36 children with trauma (CT+) and 26 children without trauma (CT-). The presence of CT was based on a clinical interview and by Criteria A of DSM-IV criteria for PTSD. Blood samples were drawn from all children to assess BDNF and cytokines. ancova was performed with psychiatric symptoms and BMI as covariates to evaluate group differences in plasma levels. RESULTS: CT+ showed increased levels of BDNF and TNF-α after excluding children with history of inflammatory disease (P<0.05) when compared with those CT-. IL-12p70, IL-6, IL-8, IL-10, and IL-1ß levels were not statistically different between groups. CONCLUSION: CT+ showed increased BDNF and proinflammatory cytokines levels. The increase in BDNF levels may be an attempt to neutralize the negative effects of CT, while an increase in TNF-a levels be associated with a proinflammatory state after CT. How these changes associated with trauma relate to other biological changes and illness trajectory later in life remain to be further studied.

Damage-associated molecular patterns and immune activation in bipolar disorder.

OBJECTIVE: Immune activation in bipolar disorder (BD) has been frequently reported. Damage-associated molecular patterns (DAMPs) are key players in the immune activation reaction. The aim of this study was to assess DAMP levels in drug-free patients with BD during acute episodes. METHOD: Serum levels of a predetermined set of DAMPs were assessed in drug-free patients with BD (n = 20) during an acute mood episode. We also included two control groups: healthy subjects, used as a negative control (n = 20); and patients with sepsis, used as a positive control for severe immune activation (n = 20). RESULTS: Multivariate analysis using generalized linear mixed model indicated that all DAMPs differed as a function of group membership after controlling for age and addressing multiplicity (P < 0.0006 for all comparisons). Follow-up analyses showed higher levels in BD subjects of circulating cell-free (ccf) nuclear (n)DNA (P = 0.02), HSP70 (P = 0.03) and HSP90α (P = 0.02) as compared to healthy subjects. Also, patients with BD showed lower levels of ccf nDNA (P = 0.04), HSP60 (P = 0.03), HSP70 (P = 0.01), and HSP90α (P = 0.002) as compared to patients with sepsis and higher levels of ccf mitochondrial DNA (P < 0.0001). CONCLUSION: The present findings may be linked to the inflammatory activity previously described among patients with BD and may help in the development of more targeted and personalized treatments for patients under acute episodes of BD.

Val66Met polymorphism and serum brain-derived neurotrophic factor in bipolar disorder: an open-label trial.

OBJECTIVE: Brain-derived neurotrophic factor (BDNF) is consistently associated with acute mood episodes in bipolar disorder, but there is a lack of longitudinal data to support this hypothesis. In this 16-week open-label clinical trial, we tested the predictive role of BDNF Val66Met polymorphism on serum BDNF levels and the relationship of serum BDNF and clinical response in people with bipolar disorder during an acute illness episode. METHOD: Sixty-four people with bipolar disorder who were medication-free at baseline and in an acute mood episode were recruited. They were matched with 64 healthy controls. Clinical evaluation, serum BDNF, and BDNF Val66Met polymorphism were determined at baseline, and change in serum BDNF was assessed in patients at weeks 2, 4, 8 and 16. RESULTS: There were no differences between patients and controls in serum BDNF or in frequencies of the BDNF Val66Met polymorphism genotype at baseline. The multivariable model showed that Met carriers had a significantly different change in BDNF levels compared with Val homozygotes. Not achieving a complete remission was also associated with lower prospectively assessed BDNF levels. CONCLUSION: This study provides the first longitudinal evidence that both the BDNF Val66Met polymorphism and remission status predict change in circulating BDNF levels.

DDT-induced inhibition of avian shell gland carbonic anhydrase: a mechanism for thin eggshells.

The shell-forming glands of Japanese quail fed p,p'-DDT or p,p'-DDE had carbonic anhydrase activity 16 to 19 percent lower than shell glands of quail on a diet free of pesticides.

Nonconversion of o,p'-DDT to p,p'-DDT in rats, sheep, chickens, and quail.

The finding of appreciable quantities of p,p'-DDT after feeding o,p'-DDT to rats led to the proposal of a theory, that an isomeric metabolic conversion occurs. The presence of p,p'-DDT as an impurity in supposedly pure samples of o,p'-DDT is the correct explanation for the appearance of p,p'-DDT. Purified o,p'-DDT and (14)C-labeled o,p'-DDT yielded no data to support the idea that o,p'-DDT is converted to the p,p'-DDT isomer.

Estrogenic activity of o,p'-DDT in the mammalian uterus and avian oviduct.

When rats and birds were treated with o, p-DDT, their reproductive tissues exhibited the same response as when they were treated with estrogen. Weight, water content, glycogen, and RNA increased in uteri and oviducts of rats, chickens, and quail receiving o, p-DDT; p, p-DDT produced little if any response. The o, p-DDT did not accumulate in the reproductive or adipose tissues to a greater extent than p, p-DDT.

Perturbations in the apoptotic pathway and mitochondrial network dynamics in peripheral blood mononuclear cells from bipolar disorder patients.

Bipolar disorder (BD) is a severe psychiatric disorder characterized by phasic changes of mood and can be associated with progressive structural brain change and cognitive decline. The numbers and sizes of glia and neurons are reduced in several brain areas, suggesting the involvement of apoptosis in the pathophysiology of BD. Because the changes in mitochondrial dynamics are closely related with the early process of apoptosis and the specific processes of apoptosis and mitochondrial dynamics in BD have not been fully elucidated, we measured the apoptotic pathway and the expression of mitochondrial fission/fusion proteins from BD patients and healthy controls. We recruited 16 patients with BD type I and sixteen well-matched healthy controls and investigated protein levels of several pro-apoptotic and anti-apoptotic factors, as well as the expression of mitochondrial fission/fusion proteins in peripheral blood mononuclear cells (PBMCs). Our results showed that the levels of the anti-apoptotic proteins Bcl-xL, survivin and Bcl-xL/Bak dimer were significantly decreased, while active caspase-3 protein levels were significantly increased in PBMCs from BD patients. Moreover, we observed the downregulation of the mitochondrial fusion-related proteins Mfn2 and Opa1 and the upregulation of the fission protein Fis1 in PBMCs from BD patients, both in terms of gene expression and protein levels. We also showed a significantly decrease in the citrate synthase activity. Finally, we found a positive correlation between Mfn2 and Opa1 with mitochondrial content markers, as well as a negative correlation between mitochondrial fission/fusion proteins and apoptotic markers. Overall, data reported here are consistent with the working hypothesis that apoptosis may contribute to cellular dysfunction, brain volume loss and progressive cognitive in BD. Moreover, we show an important relationship between mitochondrial dynamics and the cell death pathway activation in BD patients, supporting the link between mitochondrial dysfunction and the pathophysiology of BD.

Integrated transcriptome and methylome analysis in youth at high risk for bipolar disorder: a preliminary analysis.

First-degree relatives of patients with bipolar disorder (BD), particularly their offspring, have a higher risk of developing BD and other mental illnesses than the general population. However, the biological mechanisms underlying this increased risk are still unknown, particularly because most of the studies so far have been conducted in chronically ill adults and not in unaffected youth at high risk. In this preliminary study we analyzed genome-wide expression and methylation levels in peripheral blood mononuclear cells from children and adolescents from three matched groups: BD patients, unaffected offspring of bipolar parents (high risk) and controls (low risk). By integrating gene expression and DNA methylation and comparing the lists of differentially expressed genes and differentially methylated probes between groups, we were able to identify 43 risk genes that discriminate patients and high-risk youth from controls. Pathway analysis showed an enrichment of the glucocorticoid receptor (GR) pathway with the genes MED1, HSPA1L, GTF2A1 and TAF15, which might underlie the previously reported role of stress response in the risk for BD in vulnerable populations. Cell-based assays indicate a GR hyporesponsiveness in cells from adult BD patients compared to controls and suggest that these GR-related genes can be modulated by DNA methylation, which poses the theoretical possibility of manipulating their expression as a means to counteract the familial risk presented by those subjects. Although preliminary, our results suggest the utility of peripheral measures in the identification of biomarkers of risk in high-risk populations and further emphasize the potential role of stress and DNA methylation in the risk for BD in youth.

Newer insights into the role of miRNA a tiny genetic tool in psychiatric disorders: focus on post-traumatic stress disorder.

Post-traumatic stress disorder (PTSD) is a mental disorder occurring in about 2-9% of individuals after their exposure to life-threatening events, such as severe accidents, sexual abuse, combat or a natural catastrophe. Because PTSD patients are exposed to trauma, it is likely that epigenetic modifications have an important role in disease development and prognosis. For the past two decades, abnormal expression of the epigenetic regulators microRNAs (miRs) and miR-mediated gene regulation have been given importance in a variety of human diseases, such as cancer, heart disease and viral infection. Emerging evidence supports a role for miR dysregulation in psychiatric and neurological disorders, including schizophrenia, bipolar disorder, anxiety, major depressive disorder, autism spectrum disorder and Tourette's syndrome. Recently mounting of evidence supports the role of miR both in preclinical and clinical settings of psychiatric disorders. Abnormalities in miR expression can fine-tune the expression of multiple genes within a biological network, suggesting that miR dysregulation may underlie many of the molecular changes observed in PTSD pathogenesis. This provides strong evidence that miR not only has a critical role in PTSD pathogenesis, but can also open up new avenues for the development of diagnostic tools and therapeutic targets for the PTSD phenotype. In this review, we revisit some of the recent evidence associated with miR and PTSD in preclinical and clinical settings. We also discuss the possible clinical applications and future use of miRs in PTSD therapy.

The role of inflammation and microglial activation in the pathophysiology of psychiatric disorders.

Psychiatric disorders, including major depressive disorder (MDD), bipolar disorder (BD) and schizophrenia, affect a significant percentage of the world population. These disorders are associated with educational difficulties, decreased productivity and reduced quality of life, but their underlying pathophysiological mechanisms are not fully elucidated. Recently, studies have suggested that psychiatric disorders could be considered as inflammatory disorders, even though the exact mechanisms underlying this association are not known. An increase in inflammatory response and oxidative stress may lead to inflammation, which in turn can stimulate microglia in the brain. Microglial activation is roused by the M1 phenotype, which is associated with an increase in interleukin-1ß (IL-1ß) and tumor necrosis factor-α (TNF-α). On the contrary, M2 phenotype is associated with a release of anti-inflammatory cytokines. Thus, it is possible that the inflammatory response from microglial activation can contribute to brain pathology, as well as influence treatment responses. This review will highlight the role of inflammation in the pathophysiology of psychiatric disorders, such as MDD, BD, schizophrenia, and autism. More specifically, the role of microglial activation and associated molecular cascades will also be discussed as a means by which these neuroinflammatory mechanisms take place, when appropriate.

Increased serum levels of eotaxin/CCL11 in late-stage patients with bipolar disorder: An accelerated aging biomarker?

BACKGROUND: Bipolar disorder (BD) is commonly comorbid with many medical disorders including atopy, and appears characterized by progressive social, neurobiological, and functional impairment associated with increasing number of episodes and illness duration. Early and late stages of BD may present different biological features and may therefore require different treatment strategies. Consequently, the aim of this study was to evaluate serum levels of eotaxin/CCL11, eotaxin-2/CCL24, IL-2, IL-4, IL-6, IL-10, IL-17, TNF-α, IFNγ, BDNF, TBARS, carbonyl, and GPx in a sample of euthymic patients with BD at early and late stages compared to controls. METHODS: Early-stage BD patients, 12 late-stage patients, and 25 controls matched for sex and age were selected. 10mL of peripheral blood was drawn from all subjects by venipuncture. Serum levels of BDNF, TBARS, carbonyl content, glutathione-peroxidase activity (GPx), cytokines (IL-2, IL-4, IL-6, IL-10, IL-17, TNF-α and IFNγ), and chemokines (eotaxin/CCL11 and eotaxin-2/CCL24) were measured. RESULTS: There were no demographic differences between patients and controls. No significant differences were found for any of the biomarkers, except chemokine eotaxin/CCL11, whose serum levels were higher in late-stage patients with BD when compared to controls (p=0.022; Mann-Whitney U test). LIMITATIONS: Small number of subjects and use of medication may have influenced in our results. CONCLUSION: The present study suggests a link between biomarkers of atopy and eosinophil function and bipolar disorder. These findings are also in line with progressive biological changes partially mediated by inflammatory imbalance, a process referred to as neuroprogression.

Distribution and kinetics of PBB residues in cattle.

Cows fed a constant amount of polybrominated biphenyl (PBB) reached a steady-state concentration in milk fat within 30 days. This concentration was approximately four times the concentration in the total diet. When feeding of PBB was stopped, the concentration in milk was adequately described as a sum of two first-order elimination rates. Biological half-life in environmentally contaminated cows, studied for 6 months about a year after contamination, was 60 days. The stage of lactation affected the rate of elimination, and in some concentrations increased shortly after calving. Residues were distributed in body tissues proportionally to concentration of fat in the tissues. Liver and brain were exceptions. Concentration in liver fat was generally higher than other tissues and possibly related to the treatment of some cows with phenobarbital. Residues in brain fat were significantly lower than all other tissues. The ratio of the concentrations in milk fat to concentration of residues in the blood of calves and fat of fetal tissues to the concentration in the corresponding tissue in the dams was 0.36:1. It was estimated that people consuming milk from the highly contaminated Michigan cows could have received PBB doses as great as 10 g from this source alone.

Endoscope-assisted brain surgery: part 1--evolution, basic concept, and current technique.

RATIONALE: The evolution of neurosurgical techniques indicates the effort to reduce surgery-related traumatization of patients. The reduction of traumatization contributes to better postoperative outcomes. The improvement of diagnostic imaging techniques facilitates not only the precise localization of lesions but also the accurate determination of topographical relations of specific lesions to individual anatomic variations of intracranial structures. This precision of diagnostic imaging should be used to perform individual surgical procedures through so-called keyhole approaches. Keyhole craniotomies are afflicted with a reduction of light intensity in the depth of the operating field, and they provide rather narrow viewing angles. Thus, objects located directly opposite the approach entrance are more visible than those in the shadow of the microscope beam. These two deficiencies of keyhole craniotomies can be compensated for by the intraoperative use of rigid rod lens endoscopes, the shaft of which remains easily controllable through the surgical microscope. CONCEPT: Endoscope-assisted microsurgery, like all routine microsurgical procedures, is performed with both hands; the endoscope is fixed in its desired position via a mechanical arm to the headholder. Because of their superior optical quality and maneuverability, only rigid lens scopes are used for endoscope-assisted brain microsurgery. There are five ways of observing the endoscopic and microscopic images at the same time: 1) observation of the microscopic image through the oculars of the microscope and observation of the endoscopic image on a video screen placed in front of the surgeon, 2) observation of the microscopic image through the oculars of the microscope and display of the endoscopic image on a head-mounted LCD screen, 3) projection of both microscopic and endoscopic images on one screen in a picture-in-picture mode, 4) projection of both microscopic and endoscopic images into specially designed microscope oculars, and 5) transmission of both microscopic and endoscopic images into a head-mounted LCD screen. DISCUSSION: With the knowledge of almost all individual anatomic and pathoanatomic details of a specific patient, it is possible to target the individual lesion through a keyhole approach using the particular anatomic windows. As the light intensity and the depiction of important anatomic details are improved by the intraoperative use of lens scopes, endoscope-assisted microsurgery during keyhole approaches may provide maximum efficiency to remove the lesion, maximum safety for the patient, and minimum invasiveness.

Endoscope-assisted brain surgery: part 2--analysis of 380 procedures.

OBJECTIVES: Microsurgical techniques and instruments that help to reduce intraoperative retraction of normal intracranial neuronal and vascular structures contribute to improved postoperative results. To achieve sufficient control of the operating field without retraction of neurovascular components, the resection of dura and bone edges is frequently required, which, on the other hand, increases operating time and operation-related trauma. The use of endoscopes may help to reduce retraction and, at the same time, may help to avoid additional dura and bone resection. The aim of this study is to describe the principles on which the technique of endoscope-assisted brain surgery is based, to give an impression of possible indications for endoscope-assisted microsurgical procedures, and, with illustrative cases, to delineate the advantages of endoscopes used as surgical instruments during microsurgical approaches to intracranial lesions. METHODS: During a period of 4.5 years, 380 microsurgical procedures were performed as endoscope-assisted microneurosurgical operations. This surgical series was analyzed for time of surgery, usefulness of intraoperative endoscopy, and complication rates. Lens scopes with viewing angles of 0 to 110 degrees and with diameters of 2.0 to 5.0 mm as well as newly designed "viewing dissectors" (curved, rigid fiberscopes) with diameters of 1.0 to 1.5 mm connected to a video unit were used as microsurgical instruments. The positioning of the endoscopes was achieved by retractor arms fixed to the Mayfield headholder. Thus, the surgeon was able to perform customary microsurgical manipulations with both hands under simultaneous endoscopic and microscopic control. RESULTS: The lesions treated with endoscope-assisted microsurgery comprised 205 tumors, 53 aneurysms, 86 cysts, and 36 neurovascular compression syndromes. Eighty-nine of these lesions were localized in the ventricular system, 242 in the subarachnoid space or intracerebral, and 49 in the sella. Endoscope-assisted microsurgery was advantageous to reduce the size and the operation-related tissue trauma of approaches to lesions within the ventricular system, in the brain tissue as well as in the subarachnoid space at the base of the brain. Using less retraction during tumor removal, the visual control of retrosellar, endosellar, retroclival, and infratentorial structures was improved. Video-endoscope instrumentation was especially helpful during procedures in the posterior cranial fossa and at the craniocervical junction. It allowed for inspection of channels and hidden structures (e.g., the internal auditory meatus, the ventral surface of the brain stem, the ventral aspect of root entry zones of cranial nerves, the content of the foramen magnum, and the upper cervical canal), both without retraction and without resection of dura and bone edges. Endoscope instrumentation during surgery for large or giant aneurysms was useful to dissect perforators on the back side of the aneurysms and to control the completeness of clipping. CONCLUSION: Although the results reported herein cannot be compared directly with those of exclusive microsurgical procedures performed during the same period of time, videoendoscope-assisted microsurgery can be recommended as a time-saving, trauma-reducing procedure apt to improve postoperative outcomes.

Enhanced interleukin-1 beta release and longevity of glioma-associated peripheral blood monocytes in vitro.

Interleukin-1 (IL-1) plays a controversial role in the immune response. Besides its activation of immune cells and juvenile central nervous system cells, monocyte-derived IL-1 may be able to stimulate the malignant transformation and proliferation of glial brain tumor cells expressing IL-1 receptors. The aim of this study was to determine the growth pattern and the IL-1 beta release of long-term cultured peripheral blood monocytes of glioma patients. At 6- to 7-day intervals, the vital monocytes, characterized by CD14 immunophenotyping, were counted. By the use of a specific IL-1 beta enzyme-linked immunosorbent assay, the IL-1 beta content of monocyte culture supernatants derived from 13 subjects with glioma and from 12 controls were compared at Days 7, 21, and 100 of culture. Cell clusters of monocytes derived from glioblastoma patients survived more than 250 days in culture, whereas control monocytes survived only up to 114 days. The IL-1 beta release of glioma-associated peripheral blood monocyte cultures was about 50 times higher as compared with control monocyte cultures. Dexamethasone treatment at the time of blood sampling and recurrences of the gliomas did not influence the increase in the IL-1 beta expression of glioma monocytes. It seemed that at least subsets of glioma-associated blood monocytes, although they had been removed from the circulation, remained activated for a long period of time. We conclude that increased IL-1 beta production of glioma-associated peripheral blood monocytes and their longevity in vitro may be features of aberrant immune cell subsets. In future studies, the exact phenotyping of monocyte subsets will be mandatory.

Meningiomas of the space of the cavernous sinus.

During the years 1985 to 1992, we encountered 59 patients with meningiomas involving the space of the cavernous sinus. In 29 of these patients, meningiomas were primarily located within the space of the cavernous sinus and were operated on without mortality and with low morbidity. A small subtemporal surgical approach was favored, which allowed initial tumor resection from the posterior aspect, where the Parkinson's triangle is wide, thus avoiding the additional morbidity of large-scale approaches. According to the relationships of the all-important cranial nerves passing within the lateral wall of the cavernous sinus, we divided the primary intracavernous meningiomas into four types, which reflected not only the preoperative cranial nerve deficit but also the feasibility of surgical resection. Cranial nerve function deteriorated after operations in 14% of oculomotor nerves, in one abducent nerve, in 58% of trochlear nerves, and in 21% of trigeminal nerves. We encountered improvement of function in 43% of oculomotor nerves, in 50% of abducent nerves, and in approximately 30% of the second and third but in only 7% of the first branches of trigeminal nerves. There was no improvement in trochlear nerve function. Improvement of oculomotor nerve function was observed only in moderately impaired nerves, which indicates that surgery should be undertaken early to preserve or improve oculomotor nerve function.

Contralateral and ipsilateral microsurgical approaches to carotid-ophthalmic aneurysms.

OBJECTIVE: The vicinity of carotid-ophthalmic aneurysms to the roof of the cavernous sinus, to the anterior clinoid process, and to the optic nerve or the optic chiasm requires well-defined surgical techniques. Although microsurgical techniques with ipsilateral direct approaches to these aneurysms have been described in detail, studies about contralateral strategies for the microsurgical treatment of carotid-ophthalmic aneurysms are rare and are mainly confined to case reports. The aim of this study is to describe how to decide on the ipsilateral and contralateral microsurgical approaches to such aneurysms and to demonstrate the surgical techniques for the ipsilateral and contralateral exposure of carotid-ophthalmic aneurysms. METHODS: In a series of 51 patients with 58 aneurysms of the ophthalmic segment of the internal carotid artery, nine patients with 10 aneurysms (4 large aneurysms, 6 small aneurysms) were treated via a contralateral microsurgical approach after careful preoperative planning. Preoperative planning was based on the analysis of clinical and radiographic data, including cranial computed tomography, magnetic resonance imaging, magnetic resonance angiography, and conventional cerebral angiography. RESULTS: The postoperative results were good in 38 (75%) of the patients, fair in 2 (4%), and poor in 3 (6%); 8 (15%) of the patients died after surgery. The postoperative follow-up was 4 months to 10 years. Postoperatively, 15 of 19 patients with uni- or bilateral visual deficits or visual field defects improved, 3 of the 19 patients experienced postoperative impairment of visual function, and 1 of the 19 patients had an unchanged visual field deficit. Visual impairment or unchanged visual function was observed in patients who underwent ipsilateral approaches, which was possibly caused by inappropriate intraoperative retraction of the optic nerve or chiasm. In all patients presenting with preoperative visual deficits who were treated via contralateral approaches, visual function improved in the postoperative course. CONCLUSION: Giant carotid-ophthalmic aneurysms that are eligible for surgical treatment as well as small and large aneurysms dislocating the optic nerve or the chiasm superomedially or medially should be approached via ipsilateral craniotomies. It is recommended that small and large aneurysms of the carotid-ophthalmic segment originating medially, superomedially, or superiorly, displacing the optic nerve or the chiasm superiorly, superolaterally, or laterally, be approached via contralateral craniotomies.

Suprasellar granular cell tumor.

A case of a suprasellar granular cell tumor, approximately 1.5 cm in diameter, in a 68-year-old woman is described. Diagnosis was established postoperatively by histopathological examination of the tumor tissue. The preoperative computed tomographic scan revealed a slightly hyperdense suprasellar mass with strong contrast enhancement. There was no evidence of calcification. The T1-weighted image on magnetic resonance imaging scan showed an isointense tumor with non-homogeneous enhancement after intravenous gadolinium diethylene-triamine-pentaacetic acid. In the proton-weighted image, the suprasellar mass presented a non-homogeneously enhanced signal. A non-homogeneous signal reduction was seen in the T2-weighted image.