Serial cerebrospinal fluid neurofilament concentrations in bacterial meningitis

Matsushige, Takeshi; Ichiyama, Takashi; Kajimoto, Madoka; Okuda, Masayuki; Fukunaga, Shinnosuke; Furukawa, Susumu

doi:10.1016/j.jns.2009.01.021

Cited by 16 publications

(16 citation statements)

References 20 publications

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“…There were 3 cases with bacterial meningitis and 2 with sepsis. Bacterial meningitis may increase NFL concentration in CSF but CSF T-tau is unaffected which corroborates with our data [24,25] . The increase in CSF NFL in meningitis has been interpreted as a sign of neuronal injury regardless of the presence or absence of neurological sequelae.…”

Section: Discussionsupporting

confidence: 92%

Seizures, CSF neurofilament light and tau in patients with subarachnoid haemorrhage

et al. 2017

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Section: Discussionsupporting

confidence: 92%

Seizures, CSF neurofilament light and tau in patients with subarachnoid haemorrhage

et al. 2017

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“…Accordingly, CSF levels of MMP-9, an effector molecule of tissue damage that is released in the function of cytokine expression [ 35 , 36 ], were also quantitatively linked to the amount of NfL release. The correlation of CSF cytokines and CSF cell counts has been described elsewhere [ 37 , 38 ] while no correlation has been demonstrated between CSF cell counts and CSF NF in patients with BM [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

“…Only one study has evaluated NFs as a biomarker for neuronal injury in BM across an array of infectious agents. CSF concentrations of NF heavy chain were increased by 85% (22/26) children with BM; peak levels in patients with neurological sequelae were significantly higher than in those without [25].…”

Section: Introductionmentioning

confidence: 91%

Evaluation of neurofilament light chain in the cerebrospinal fluid and blood as a biomarker for neuronal damage in experimental pneumococcal meningitis

Muri

Grandgirard

et al. 2020

J Neuroinflammation

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Background Pneumococcal meningitis (PM) remains a global public health concern and affects all age groups. If acquired during infancy or childhood, permanent neurofunctional deficits including cognitive impairment, cerebral palsy, and secondary epilepsy are typical sequelae of neuronal injury. Determination of patients at risk for the development of brain injury and subsequent neurofunctional sequelae could help to identify patients for focused management. Neurofilament light chain (NfL) is an axonal cytoskeletal protein released upon neuronal injury into the cerebrospinal fluid (CSF) and blood. As little is known about the course of neurofilament release in the course of PM, we measured CSF and serum NfL levels longitudinally in experimental PM (ePM). Methods Eleven-day-old infant Wistar rats were infected intracisternally with Streptococcus pneumoniae and treated with ceftriaxone. At 18 and 42 h post-infection (hpi), the blood and CSF were sampled for NfL measurements by a single molecule array technology. Inflammatory cytokines and MMP-9 in CSF were quantified by magnetic bead multiplex assay (Luminex®) and by gel zymography, respectively. Results In ePM, CSF and serum NfL levels started to increase at 18 hpi and were 26- and 3.5-fold increased, respectively, compared to mock-infected animals at 42 hpi (p < 0.0001). CSF and serum NfL correlated at 18 hpi (p < 0.05, r = 0.4716) and 42 hpi (p < 0.0001, r = 0.8179). Both CSF and serum NfL at 42 hpi strongly correlated with CSF levels of IL-1β, TNF-α, and IL-6 and of MMP-9 depending on their individual kinetics. Conclusion Current results demonstrate that during the peak inflammatory phase of ePM, NfL levels in CSF and serum are the highest among CNS disease models studied so far. Given the strong correlation of CSF versus serum NfL, and its CNS-specific signal character, longitudinal measurements to monitor the course of PM could be performed based on blood sample tests, i.e., without the need of repetitive spinal taps. We conclude that NfL in the serum should be evaluated as a biomarker in PM.

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“…Furthermore, an increase of NfL level in the CSF, as well as the serum, has been observed after CNS infections with varicella-zoster virus [58]. It has further been seen in pneumococcal meningitis in an experimental model [59] as well as for childhood bacterial meningitis [60]. To date, CSF levels of NfL after TBE have been described in one study.…”

Section: Discussionmentioning

confidence: 94%

Tick-Borne Encephalitis Affects Sleep-Wake Behavior and Locomotion in Infant Rats

Chiffi¹,

Grandgirard²,

Stöckli³

et al. 2021

Preprint

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Background/Aims: Tick-borne encephalitis (TBE) is a disease affecting the central nervous system. Over the last decade, the incidence of TBE has steadily increased in Europe and Asia despite the availably of effective vaccines. Up to 50% of patients after TBE suffer from post-encephalitic syndrome that may develop into long-lasting morbidity. Altered sleep-wake functions have been reported by patients after TBE. The mechanisms causing these disorders in TBE are largely unknown to date. As a first step toward a better understanding of the pathology of TBEV-inducing sleep dysfunctions, we assessed parameters of sleep structure in an established infant rat model of TBE.Methods: 13-day old Wistar rats were infected with 1 x 106 FFU Langat virus (LGTV). On day 4, 9, and 21 post infection, Rotarod (balance and motor coordination) and open field tests (general locomotor activity) were performed and brains from representative animals were collected in each subgroup. On day 28 the animals were implanted with a telemetric EEG/EMG system. Sleep recording was continuously performed for 24 consecutive hours starting at day 38 post infection and visually scored for Wake, NREM, and REM in 4 seconds epochs.Results: As a novelty of this study, infected animals showed a significant larger percentage of time spend awake during the dark phase and less NREM and REM compared to the control animals (p < 0.01 for all comparisons). Furthermore, it was seen, that during the dark phase the wake bout length in infected animals was prolonged (p = 0.043) and the fragmentation index decreased (p = 0.0085) in comparison to the control animals. LGTV-infected animals additionally showed a reduced rotarod performance ability at day 4 (p = 0.0011) and day 9 (p = 0.0055) and day 21 (p = 0.0037). A lower locomotor activity was also seen at day 4 (p = 0.0196) and day 9 (p = 0.0473). Conclusion: Our data show that experimental TBE in infant rats affects sleep-wake behavior, leads to decreased spontaneous locomotor activity, and impaired moto-coordinative function.

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Serial cerebrospinal fluid neurofilament concentrations in bacterial meningitis

Cited by 16 publications

References 20 publications

Seizures, CSF neurofilament light and tau in patients with subarachnoid haemorrhage

Seizures, CSF neurofilament light and tau in patients with subarachnoid haemorrhage

Evaluation of neurofilament light chain in the cerebrospinal fluid and blood as a biomarker for neuronal damage in experimental pneumococcal meningitis

Tick-Borne Encephalitis Affects Sleep-Wake Behavior and Locomotion in Infant Rats

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