Cyberchondria in First Year Medical Students of Yogyakarta

Abstract

Cyberchondria is a relatively new term addressing health anxiety associated with online information. Research data is scarce, as most instruments measuring anxiety do not consider online behavior an important factor. Medical students are arguably assumed to have frequent health anxieties, i.e. “medical student syndrome.” Moreover, they are exposed to large amounts of information. We aimed to measure the level of cyberchondria severity of first-year medical students. First-year medical students of the regular program at Universitas Gadjah Mada completed self-reported instruments (the Cyberchondria Severity Scale (CSS) and the Beck Anxiety Inventory (BAI)). Cut off was determined using ROC analysis to find the best score that corresponded to BAI cut off of 16. Data were analyzed using chi square and t-tests to analyze any differences between gender. Respondents were 162 students, 54 males and 108 females, with mean age 18.18-year-old ± 0.696. Based on ROC analysis, cut off of 75.5 corresponded with BAI score of 16. Mean CSS score was 70.73 ± 16.292. There was no significant difference of CSS scores between genders. Based on the analysis of individual items, compared to male students, female students more frequently searched for physical symptoms on the Internet, and afterwards, consulted the results with a General Practitioner (GP), discussed with a GP, or went to other specialists; and thus, more frequently required reassurance after online search. In contrast, male students more frequently had difficulty relaxing after searching online for physical symptoms. We concluded that there was no difference of overall cyberchondria severity score, but there were slight but significant differences of online behavior between genders.     

Association analysis of the DISC1 gene with schizophrenia in the Japanese population and DISC1 immunoreactivity in the postmortem brain

The Disrupted-in-Schizophrenia 1 (DISC1) gene plays a role in the regulation of neural development. Previous evidence from genetic association and biological studies implicates the DISC1 gene as having a role in the pathophysiology of schizophrenia. In the present study, we explored the association between DISC1 missense mutation rs821616 (Ser704Cys) single nucleotide polymorphism (SNP) and four other SNPs (rs1772702, rs1754603, rs821621, rs821624) in the related haplotype block and schizophrenia in the Japanese population. We could not find a significant association of selected SNPs with schizophrenia after correction for multiple testing. We performed a meta-analysis of the Ser704Cys variant in schizophrenia using data from the present study and five previous Japanese population studies, and found no association with schizophrenia. We also examined DISC1 immunoreactivity in postmortem prefrontal cortex specimens of schizophrenia patients compared to control samples. The immunoreactivity revealed a significant decrease of DISC1 protein expression in the schizophrenia samples after ruling out potential confounding factors. However, the Ser704Cys variant did not show effects on DISC1 immunoreactivity. These results provide evidence that this functional genetic variation of DISC1 do not underlie the pathophysiology of schizophrenia in the Japanese population.     

Association study of EP1 gene polymorphisms with suicide completers in the Japanese population

Background

Both environmental and genetic factors have been reported to be involved in suicidal behaviors. Considerable evidence indicates that impulsive aggression is one of the important risk factors that contribute to suicide. A recent study has shown that prostaglandin E2 type 1 receptor (EP1) signaling regulates impulsive-aggressive behaviors in mice under both social and environmental stresses. To test the possible involvement of the EP1 gene in suicide, we carried out an association study of EP1 gene polymorphisms with suicide completers in the Japanese population.

Methods

We studied 5 SNPs including one SNP in exon 2 (rs3745459) and four SNPs in the potential promoter region of the EP1 gene (rs3810255, rs3810254, rs3810253 and rs10416814) in 374 healthy control and 287 completed suicide victims using standard Taqman probe genotyping assays.

Results

No significant differences of the genotypic distribution, allelic frequency or haplotype distribution between controls and suicide completers were found. Gender based analysis revealed that genotypic, allelic and haplotypic distributions of rs3810255, rs3810254, rs3810253 and rs10416814 SNPs were significantly different between the female control and female suicide groups, although the differences did not withstand correction for multiple comparisons.

Conclusion

We could not find an association of EP1 gene with suicide in the Japanese population. Because several SNPs in the promoter region of the EP1 gene were nominally significantly associated with suicide in the female, further studies with a larger sample size and different population are needed to confirm this result.     

A common polymorphism in the 3′-UTR of the NOS1 gene was associated with completed suicides in Japanese male population

Background

Suicidal behavior has been widely accepted as familial. Its transmission cannot be explained by the transmission of psychiatric disorder alone and seems to be partly explained by the transmission of impulsive–aggressive behavior. Studies in laboratory animal have shown that mice lacking NOS1 manifest significant aggressive behavior. Further, several polymorphisms of neuronal nitric oxide synthase (NOS1) gene have been reported to be associated with impulsivity, aggression and suicide attempts. To further clarify the possible involvement of NOS1 with suicide, we carried out an association study of NOS1 gene polymorphisms with completed suicide.

Methods

We examined 7 single nucleotide polymorphisms (SNPs) of the NOS1 gene which were previously studied in several neuropsychiatric disorders (rs2682826, rs6490121, rs3782206, rs561712, rs3782219, rs3782221, and rs41279104), in age and gender matched 287 healthy control subjects and 284 completed suicides using the TaqMan probe assays.

Results

We found that both the genotypic distribution and the allelic frequencies of rs2682826 SNP were significantly different between the completed suicide and control groups (P = 0.0007 and 0.0005, respectively). The odd ratio for the minor allele of the SNP was 0.653 (95% CI 0.513–0.832). The significance was remained even after correction for multiple testing. Gender-based analysis showed that the significances were appeared in males only.

Conclusion

Our study raises a possibility that a genetic variation of NOS1 may be implicated in the pathophysiology of suicide in Japanese population, especially in males. Further studies on more NOS1 genetic variants are needed to confirm our observations.     

Relationships between brain water content and diffusion tensor imaging parameters (apparent diffusion coefficient and fractional anisotropy) in multiple sclerosis

Fifteen multiple sclerosis patients were examined by diffusion tensor imaging (DTI) to determine fractional anisotropy (FA) and apparent diffusion coefficient (ADC) in a superventricular volume of interest of 8×8×2 cm³ containing gray matter (GM) and white matter (WM) tissue. Point resolved spectroscopy 2D-chemical shift imaging of the same volume was performed without water suppression. The water contents and DTI parameters in 64 voxels of 2 cm³ were compared. The water content was increased in patients compared with controls (GM: 244±21 vs. 194±10 a.u.; WM: 245±32 vs. 190±11 a.u.), FA decreased (GM: 0.226±0.038 vs. 0.270±0.020; WM: 0.337±0.044 vs. 0.402±0.011) and ADC increased [GM: 1134±203 vs. 899±28 (×10⁻⁶ mm²/s); WM: 901±138 vs. 751±17 (×10⁻⁶ mm²/s)]. Correlations of water content with FA and ADC in WM were strong (r=−0.68, P<0.02; r=0.75; P<0.01, respectively); those in GM were weaker (r=−0.50, P<0.05; r=0.45, P<0.1, respectively). Likewise, FA and ADC were more strongly correlated in WM (r=−0.88; P<0.00001) than in GM (r=−0.69, P<0.01). The demonstrated relationship between DTI parameters and water content in multiple sclerosis patients suggests a potential for therapy monitoring in normal-appearing brain tissue.     

MR spectroscopy and diffusion tensor imaging of the brain in congenital muscular dystrophy with merosin deficiency: metabolite level decreases, fractional anisotropy decreases, and apparent diffusion coefficient increases in the white matter

Brain magnetic resonance spectroscopy (MRS) and diffusion tensor imaging (DTI) in one patient with merosin-deficient congenital muscular dystrophy (MDCMD) revealed significant metabolite (choline, creatine, N-acetyl aspartate) level reductions, fractional anisotropy (FA) reduction and increased apparent diffusion coefficient (ADC) in the white matter (p<0.01, all). In the gray matter, the MRS properties did not differ significantly from those in controls. The ADC and FA, however, differed significantly as in the white matter, although the differences were less pronounced. This is the first quantitative MR study of the brain in a patient with MDCMD, which revealed that the concentrations of all MRS measured metabolites were decreased only in the white matter. This observation, combined with the DTI observed ADC increases and FA decrease, indicated a presence of vasogenic edema in the white matter.     

Analysis of the human brain in primary progressive multiple sclerosis with mapping of the spatial distributions using 1H MR spectroscopy and diffusion tensor imaging

Primary progressive multiple sclerosis (ppMS; n=4) patients and controls (n=4) were examined by 1H magnetic resonance spectroscopy (MRS) and diffusion tensor imaging (DTI) in order to map choline (Cho), creatine and N-acetylaspartate (NAA), the fractional anisotropy (FA) and the apparent diffusion constant (ADC). After chemical shift imaging (point-resolved spectroscopy, repetition time/echo time 1,500 ms/135 ms) of a supraventricular volume of interest of 8×8×2 cm³ (64 voxels) MRS peak areas were matched to the results of DTI for the corresponding volume elements. Mean FA and NAA values were reduced in the ppMS patients (P<0.01, both) and the ADC increased (P<0.02). The spatial distribution of NAA showed strong correlation to ADC in both ppMS patients and controls (r =–0.74 and r= –0.70; P<0.00001, both), and weaker correlations to FA (r=0.49 and r=0.41; P<0.00001, all). FA and ADC also correlated significantly with Cho in patients and controls (P<0.00001, all). The relationship of Cho and NAA to the ADC and the FA and thus to the content of neuronal structures suggests that these metabolite signals essentially originate from axons (NAA) and the myelin sheath (Cho). This is of interest in view of previous reports in which Cho increases were associated with demyelination and the subsequent breakdown of neurons.