Cerebrospinal fluid tau proteins in status epilepticus

Monti, Giulia; Tondelli, Manuela; Giovannini, Giada; Bedin, Roberta; Nichelli, Paolo Frigio; Trenti, Tommaso; Meletti, Stefano; Chiari, Annalisa

doi:10.1016/j.yebeh.2015.04.030

Cited by 35 publications

(28 citation statements)

References 39 publications

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“…Only few studies evaluated the potential of tau protein as a prognosis biomarker of seizure‐related neuronal damage . CSF levels of tau protein were evaluated in patients with SE and correlated with prognosis . Of 28 patients with SE without acute brain injury, CNS infection, or neurodegenerative disorders, CSF tau levels were increased in 14 patients.…”

Section: Acute Axonal Injurymentioning

confidence: 99%

Cerebrospinal fluid and blood biomarkers of status epilepticus

et al. 2019

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Status epilepticus is a condition resulting either from the failure of the mechanisms responsible for seizure termination or from the initiation of mechanisms that lead to abnormally prolonged seizures and require urgent administration of antiepileptic drugs. Refractory status epilepticus requires anesthetics drugs and may lead to brain injury with molecular and cellular alterations (eg, inflammation, and neuronal and astroglial injury) that could induce neurologic sequels and further development of epilepsy. Outcome scores based on demographic, clinical, and electroencephalography (EEG) condition are available, allowing prediction of the risk of mortality, but the severity of brain injury in survivors is poorly evaluated. New biomarkers are needed to predict with higher accuracy the outcome of patients admitted with status in an intensive care unit. Here, we summarize the findings of studies from patients and animal models of status epilepticus. Specific protein markers can be detected in the cerebrospinal fluid and the blood. One of the first described markers of neuronal death is the neuron‐specific enolase. Gliosis resulting from inflammatory responses after status can be detected through the increase of S100‐beta, or some cytokines, like the High Mobility Group Box 1. Other proteins, like progranulin may reflect the neuroprotective mechanisms resulting from the brain adaptation to excitotoxicity. These new biomarkers aim to prospectively identify the severity and development of disability, and subsequent epilepsy of patients with status. We discuss the advantages and disadvantages of each biomarker, by evaluating their brain specificity, stability in the fluids, and sensitivity to external interferences, such as hemolysis. Finally, we emphasize the need for further development and validation of such biomarkers in order to better assess patients with severe status epilepticus.

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Section: Acute Axonal Injurymentioning

confidence: 99%

Cerebrospinal fluid and blood biomarkers of status epilepticus

et al. 2019

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“…Accumulation of pTau was reported in brain specimens obtained from patients with focal cortical dysplasia or acquired epilepsy (eg, post-traumatic), 47,[54][55][56] as well as in temporal lobe epilepsy patients with no history of TBI. 57,58 Results were corroborated by using experimental models of epilepsy 59 or of TBI associated with the development of seizures. 60,61 pTau has been implicated in the regulation of neuronal network synchronization 62,63 and in neuroplasticity changes 64,65 resulting in hyperexcitability.…”

Section: Box 2: Ptau Accumulation and Neuronal Hyperexcitabilitymentioning

confidence: 81%

Central nervous system lymphatic unit, immunity, and epilepsy: Is there a link?

Noè

Marchi

2019

Epilepsia Open

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Summary The recent definition of a network of lymphatic vessels in the meninges surrounding the brain and the spinal cord has advanced our knowledge on the functional anatomy of fluid movement within the central nervous system (CNS). Meningeal lymphatic vessels along dural sinuses and main nerves contribute to cerebrospinal fluid (CSF) drainage, integrating the cerebrovascular and periventricular routes, and forming a circuit that we here define as the CNS‐lymphatic unit. The latter unit is important for parenchymal waste clearance, brain homeostasis, and the regulation of immune or inflammatory processes within the brain. Disruption of fluid drain mechanisms may promote or sustain CNS disease, conceivably applicable to epilepsy where extracellular accumulation of macromolecules and metabolic by‐products occur in the interstitial and perivascular spaces. Herein we address an emerging concept and propose a theoretical framework on: (a) how a defect of brain clearance of macromolecules could favor neuronal hyperexcitability and seizures, and (b) whether meningeal lymphatic vessel dysfunction contributes to the neuroimmune cross‐talk in epileptic pathophysiology. We propose possible molecular interventions targeting meningeal lymphatic dysfunctions, a potential target for immune‐mediated epilepsy.

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“…However, CSF levels of 14-3-3 protein and/ or tau protein are reportedly elevated in both sCJD and status epilepticus with non-prion disease. 1,2 In addition, cortical hyper-intensity in diffusion-weighted MR images (DW-MRI) is observed during the acute phases of status eplepticus 3 and CJD. Furthermore, V180I genetic CJD (gCJD) exhibits cortical-edematous hyper-intensities on DW-MRI, 4,5 which is similar to the acute phase of status epilepticus.…”

Section: Introductionmentioning

confidence: 99%

An autopsy-verified case of steroid-responsive encephalopathy with convulsion and a false-positive result from the real-time quaking-induced conversion assay

Hayashi

Iwasaki

Yagi

et al. 2017

Prion

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We report an autopsy-verified case of steroid-responsive encephalopathy with convulsion and a false-positive result from the real-time quaking-induced conversion (RT-QUIC) assay. A 61-year-old Japanese man presented with acute onset of consciousness disturbance, and convulsions, but without a past medical or family history of progressive dementia, epilepsy, or prion disease. Brain diffusion and fluid-attenuated inverted recovery MR images revealed edematous cortical hyper-intensity, which diminished after the acute phase. Steroid pulse therapy was partially effective, although he continued to have dementia with myoclonus and psychiatric symptoms, despite resolution of the consciousness disturbance. Cerebrospinal fluid (CSF) analysis revealed a normal cell count, with significantly elevated levels of 14-3-3 protein and total tau protein. In addition, prion protein in the CSF was slowly amplified by the RT-QUIC assay. PRNP gene analysis revealed methionine homozygosity at codon 129 without mutation. The patient died of sudden cardiac arrest at 3 months after the onset of symptoms. The positive result from the RT-QUIC assay led us to suspect involvement of prion disease, although a postmortem assessment revealed that he had pathological changes after convulsion, and no prion disease. This case indicates that convulsion may cause false-positive RT-QUIC results, and that a postmortem evaluation remains the gold standard for diagnosing similar cases.

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Cerebrospinal fluid tau proteins in status epilepticus

Cited by 35 publications

References 39 publications

Cerebrospinal fluid and blood biomarkers of status epilepticus

Cerebrospinal fluid and blood biomarkers of status epilepticus

Central nervous system lymphatic unit, immunity, and epilepsy: Is there a link?

An autopsy-verified case of steroid-responsive encephalopathy with convulsion and a false-positive result from the real-time quaking-induced conversion assay

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