Cerebrospinal Fluid Abnormalities in Viral Encephalitis

Ekmekçi, Hakan; Ege, Fahrettin; Öztürk, Şerefnur

doi:10.5772/54590

Cited by 5 publications

(6 citation statements)

References 19 publications

(19 reference statements)

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“…Lower glucose (< 50 mg/dl) and relatively higher protein (> 50 mg/dl) levels noted in anti-HAV IgM-positive CSF samples were in agreement with those reported earlier in acute infections with herpes, varicella zoster and mumps viruses (Hammond et al, 1982;Ekmekci et al, 2013). Further, CSF pleocytosis associated with anti-HAV IgM/IgG positivity in the CSF of AES patients was in concurrence with that of the previously reported HAV-associated encephalitis cases (Davis et al, 1993;Lee et al, 2011) and suggested active inflammatory response in this group of patients.…”

Section: Discussionsupporting

confidence: 91%

Evidence of hepatitis A virus infection in the patients with acute encephalitis syndrome in Gorakhpur region, North India

Joshi¹,

Tandale²,

Gore³

et al. 2018

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The etiological agent remained unidentified in a large number of patients hospitalized for acute encephalitis syndrome (AES) in 2008-2009 in Uttar Pradesh and Bihar, north India. All patients were found to present with fever and altered sensorium, while 28%, 19% and 13% showed hepatomegaly, splenomegaly and meningeal signs, respectively. Involvement mostly of children with abnormal hepatic features prompted us to undertake an exploratory study on viral hepatitis A to determine its association, if any, with hepatic derangements. AES patients (n = 2515) and healthy children (n = 167) were investigated for the presence of serum anti-hepatitis A virus (anti-HAV) IgM and anti-Japanese encephalitis (anti-JE) virus IgM by ELISA. Cerebrospinal fluids (CSFs, n = 595) and rectal swabs (n = 182) were examined for anti-HAV IgM and/or HAV RNA. Anti-HAV IgM was detected in the sera of 14.6% patients as against 6.6% of healthy children (p = 0.0042). Anti-JE virus IgM positivity was Keywords: acute encephalitis syndrome; cerebrospinal fluid; hepatitis A virus; anti-HAV IgM; non-Japanese encephalitis.

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Section: Discussionsupporting

confidence: 91%

Evidence of hepatitis A virus infection in the patients with acute encephalitis syndrome in Gorakhpur region, North India

Joshi¹,

Tandale²,

Gore³

et al. 2018

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“…[1][2][3]6,7 A significant amount of evidence exists showing that other viruses and coronaviruses specifically can invade the CNS and induce neurological symptoms. [52][53][54][55][56][57][58][59][60][61] In addition, one study of 18 autopsies positive for SARS-COV-1 found that viral "genome sequences were detected in the brains of all SARS autopsies with real-time reverse transcriptase-polymerase chain reaction (RT-PCR) assays." 62 The route of initial SARS-CoV-1 infection to the brain remains unclear, but the viral presence was definitively established in the CNS.…”

Section: F I G U R Ementioning

confidence: 99%

Potential neuroinvasive pathways of SARS‐CoV‐2: Deciphering the spectrum of neurological deficit seen in coronavirus disease‐2019 (COVID‐19)

Baig

Sanders

2020

Journal of Medical Virology

129

131

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Coronavirus disease‐2019 (COVID‐19) was declared a global pandemic on 11 March 2020. Scientists and clinicians must acknowledge that severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) has the potential to attack the human body in multiple ways simultaneously and exploit any weaknesses of its host. A multipronged attack could potentially explain the severity and extensive variety of signs and symptoms observed in patients with COVID‐19. Understanding the diverse tactics of this virus to infect the human body is both critical and incredibly complex. Although patients diagnosed with COVID‐19 have primarily presented with pulmonary involvement, viral invasion, and injury to diverse end organs is also prevalent and well documented in these patients, but has been largely unheeded. Human organs known for angiotensin‐converting enzyme 2 (ACE2) expression including the gastrointestinal tract, kidneys, heart, adrenals, brain, and testicles are examples of extra pulmonary tissues with confirmed invasion by SARS‐CoV‐2. Initial multiple organ involvement may present with vague signs and symptoms to alert health care professionals early in the course of COVID‐19. Another example of an ongoing, yet neglected element of the syndromic features of COVID‐19, are the reported findings of loss of smell, altered taste, ataxia, headache, dizziness, and loss of consciousness, which suggest a potential for neural involvement. In this review, we further deliberate on the neuroinvasive potential of SARS‐CoV‐2, the neurologic symptomology observed in COVID‐19, the host‐virus interaction, possible routes of SARS‐CoV‐2 to invade the central nervous system, other neurologic considerations for patients with COVID‐19, and a collective call to action.

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“…Depending on the patient's history, physical examination, signs and symptoms and laboratory findings, if a CNS infection is suspected then immediate action to confirm diagnosis should be done by performing supplementary tests such as imaging and lumbar puncture if necessary. CSF cell count as well as CSF biomarkers (such as IFN-γ, TNF-α, IL-2, IL-6, CD8, MIF, NfH-SM135, GFAP-SM126, S100B) analysis are necessary to confirm the presence of inflammatory process in CNS [2], but since these CSF findings in most of the inflammatory states are similar, a differential diagnosis becomes challenging based on the CSF cell analysis therefore further steps such as image acquisition is needed to be able to proceed further. The physical findings such as meningeal irritation signs (Brudzinski's and Kernig's sign) and photosensitivity are not enough for the establishment of any type of CNS infection; even in cases where beside the above mentioned signs and symptoms, pyrexia and increased inflammatory markers are present, a definite diagnosis of CNS infection cannot be made, because conditions like subarachnoid hemorrhage (SAH) can have the very same clinical findings, and the origin of pyrexia or elevated inflammatory factors can be something rather than the CNS.…”

Section: Diagnosismentioning

confidence: 99%

Infections in Neurosurgery and Their Management

Tahaei¹,

Tahaei²,

Mencser³

et al. 2021

Infections and Sepsis Development

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Surgical site and postoperative infections are common problems in surgical wards and treating them can be challenging and very complicated. It is important to understand different types of postoperative infections and their best management. In this chapter we try to emphasis on infections which are occurring in neurosurgical units and how to approach them. Foreign body infection is another challenge that happens in neurosurgical units, and it is vital to recognize these infections in time and start the treatment as soon as possible. Atypical infections occurrence is low therefore this problem is not addressed often in textbooks or in the literature, therefore atypical infections will be discussed in this chapter too. By discussing the most common postoperative complications and their best management profile, the authors here will try to widen the perspective of readers on infections in neurosurgical units in order to understand this problem better. Untreated infections or poorly treated infections can lead to sepsis and catastrophic results.

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Cerebrospinal Fluid Abnormalities in Viral Encephalitis

Cited by 5 publications

References 19 publications

Evidence of hepatitis A virus infection in the patients with acute encephalitis syndrome in Gorakhpur region, North India

Evidence of hepatitis A virus infection in the patients with acute encephalitis syndrome in Gorakhpur region, North India

Potential neuroinvasive pathways of SARS‐CoV‐2: Deciphering the spectrum of neurological deficit seen in coronavirus disease‐2019 (COVID‐19)

Infections in Neurosurgery and Their Management

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