Journal of Neuroinfectious Diseases
Open Access

Behcet’s disease (BD) is an inflammatory multisystem illness characterised by recurring oral-genital ulcers, skin lesions, and uveitis. Neuro-disease Behcet’s (NBD) is a central nervous system involvement in BD that has been recorded in 1.3%-59% of BD patients. It is split into two fundamental clinical categories: parenchymal Neuro-disease Behcet’s (PNBD) and non-parenchymal (vascular) Neuro-disease Behcet’s (PNBD) (VNBD) [1].

The results of magnetic resonance imaging for PNBD are not specific. In patients with PNBD, conventional MRI may reveal abnormalities and atrophy of the brainstem, cerebral hemispheres, hypothalamus area, basal ganglia, cerebellum, and spinal cord. Despite the fact that conventional MRI scans are normal, sophisticated MR imaging (MR spectroscopy [MRS], diffusion weighted imaging [DWI], and MR perfusion [MRP]) has revealed subclinical parenchymal involvement in BD patients with or without neurological impairment [2]. The pathophysiology of NBD is unknown, although the most common signs include perivascular inflammation in the absence of apparent vasculitic infiltration. Intermittent perivascular inflammation may contribute to the loss of CNS parenchyma, resulting in neuronal dysfunction.

There are few studies in the literature that evaluate quantitative morphological alterations in BD patients’ brains. These research looked at the brainstem and subcortical areas of Neuro-disease Behçet’s patients. These investigations, however, did not look at quantitative alterations in the cortex and BD individuals who did not have parenchymal damage. Cortical thickness is an important morphological metric of neuronal density, cell architecture, and cerebral cortex hierarchy. Cortical thinning has been demonstrated to develop in neurodegenerative disorders such as Alzheimer’s and Parkinson’s before symptoms appear. Cortical thinning in multiple sclerosis (MS) patients has been shown to be related with clinical impairment and is independent of white matter abnormalities [3]. The auto-inflammatory condition in BD may result in cortical thinning, neurodegeneration, and cognitive test failure. Behcet patients had worse cognitive test scores even if they do not have any neurological symptoms, according to research.

Autopsy investigations on BD patients have revealed that the condition not only causes atrophy in the brainstem but also damages the white and grey matter. Limited imaging investigations in BD have revealed reduced perfusion in cortical grey matter [4]. All of these data indicate the possibility of cortical involvement in BD. However, to the best of our knowledge, no research has been published in the literature that investigate cortical thickness alterations in BD.

Given the therapeutic relevance of early identification and therapy in BD patients, it might be anticipated that detecting cortical abnormalities before they appear in standard MRIs may enhance disease management and a patient’s prognosis [5]. The purpose of this study was to look at changes in cortical abnormalities in BD patients with and without neurological involvement, as well as the mechanism driving neurological dysfunction in BD patients.

Materials and Method

This study was planned in advance and was authorised by a local ethics commission. All participants were well informed and provided written informed consent. Before each examination, each patient provided written informed consent [6]. STROBE (Strengthening the Reporting of Observational Studies in Epidemiology) criteria were strictly followed.

Clinical-demographic information

There were no variations in age or gender between the patient and control groups. The median illness duration for patients with BD without neurological involvement was 7.5 (IQR, 3-15) years, and 11.5 (IQR, 4.75-16.75) years for patients with PNBD. For PNBD patients, the median duration of neurological symptoms was 4.5 (IQR, 2-11) years. Other clinical results are discussed [7-8].

Patients with BD without neurological involvement vs healthy controls

We found significant decreases in cortical thickness in various regions, such as the right superior frontal gyrus (p = 0.014

Discussion

In this prospective study we looked at cortical thickness alterations in the brain in BD without clinical neurological involvement and PNBD. We discovered significant cortical thinning in the brains of PNBD patients and certain regions of BD patients who did not have symptomatic neurological involvement [9]. We also discovered that PNBD patients had widespread cortical thinning as compared to BD patients without neurological involvement [10]. Disease duration was adversely associated to bilateral pericalcarine, left cuneus, and left. We created and validated a novel user-friendly nomogram to predict the likelihood of CAUTIs in Neurocritical unwell patients in this study. The nomogram primarily comprised clinical risk variables at entry and length of stay in the neuro-ICU [10]. The prediction model has a high overall predictive value. This project will help to reduce CAUTIs, which are common nosocomial infections in ICU patients, particularly in neuro-ICU patients [11].

Conclusion

In this work, we created a simple nomogram to predict the likelihood of CAUTIs in neuro-ICU patients in everyday clinical practise, using only a few easily accessible characteristics. The nomogram primarily included clinical risk variables at admission (age, admission diagnosis, and albumin levels) as well as the length of stay in the neuro-ICU [12]. The nomogram is a useful tool for promoting more individualised nursing for neuro-ICU patients as well as the avoidance of nosocomial infections.

Acknowledgment

The authors appreciate and thank all laboratory personnel as well as all physicians and staff at the neurosurgical critical care unit.

1. Glaser CAC, Glaser A, Honarmand S, Anderson L J, Schnurr D P, et al. (2006) Beyond viruses: clinical profiles and etiologies associated with encephalitis. Clin Infect Dis 43: 1565 -1577.

                Indexed at, Google Scholar, Crossref

2. Granerod J, Ambrose Helen E, Davies Nicholas WS, Clewley Jonathan P ,Walsh Amanda L , et al. (2010) Causes of encephalitis and differences in their clinical presentations in England: a multicentre, population-based prospective study. Lancet Infect Dis 10: 835-844.

               Indexed at, Google Scholar, Crossref

3.  Granerod J, Simon  Cousen , Nicholas WS , Davies, Natasha S, et al. (2013) New estimates of incidence of encephalitis in England. Emerg Infect Dis19: 9.

Indexed at, Google Scholar, Crossref

4. Jmor F, Hedley CA Emsley, Marc Fischer, Tom Solomon, Penny Lewthwaite (2008) The incidence of acute encephalitis syndrome in Western industrialised and tropical countries. Virol J 5: 134.

        Indexed at, Google Scholar, Crossref

5. Ho Dang Trung N, Nghia Ho Dang Trung, Tu Le Thi Phuong, Marcel Wolbers, Hoang Nguyen Van Minh, et al. (2012) Aetiologies of central nervous system infection in Viet Nam: a prospective provincial hospital-based descriptive surveillance study. PLoS One 7: e37825.

Indexed at, Google Scholar, Crossref

6. Giri A, Amit Arjyal, Samir Koirala, Abhilasha Karkey, Sabina Dongol, et al. (2013) Aetiologies of central nervous system infections in adults in Kathmandu, Nepal: a prospective hospital-based study. Sci Rep 3: 2382.

Indexed at, Google Scholar, Crossref

7. Bastos MS, Natália Lessa, Felipe G Naveca, Rossicléia L Monte, Wornei S Brag, et al. (2014) Detection of Herpesvirus, Enterovirus, and Arbovirus infection in patients with suspected central nervous system viral infection in the Western Brazilian Amazon. J Med Virol 86: 1522-1527.

Indexed at, Google Scholar, Crossref

8. Srey VH, Helene Sadones, Sivuth Ong, Mony Mam, Chantham Yim, et al. (2002) Etiology of encephalitis syndrome among hospitalized children and adults in Takeo, Cambodia, 1999-2000. Am J Trop Med Hyg 66: 200-207.

Indexed at, Google Scholar, Crossref

9. Weber T, Frye S , Bodemer M , Otto M , Lüke W, et al. (1996) Clinical implications of nucleic acid amplification methods for the diagnosis of viral infections of the nervous system.J Neurovirol 2: 175-190

Indexed at, Google Scholar, Crossref

10. Selim HS, El-Barrawy AM, Rakha EM, Yingst LS, Baskharoun FM (2007) Microbial study of meningitis and encephalitis cases. J Egypt Public Health Assoc 82: 1-19.

        Google Scholar

11. Rathore SK, Dwibedi B , Kar Sk, Dixit S, Sabat J, et al. (2014) Viral aetiology and clinico-epidemiological features of acute encephalitis syndrome in eastern India. Epidemiol Infect 142: 2512-2514.

Indexed at, Google Scholar, Crossref

12. Ghannad MS, Solgi G, Hashemi SH , Zebarjady-Bagherpour J , Hemmatzadeh A, et al. (2013) Herpes simplex virus encephalitis in Hamadan, Iran. Iran J Microbiol 5: 272–277.

Indexed at, Google Scholar