Hearing loss after microvascular decompression for hemifacial spasm

Hearing loss after microvascular decompression for hemifacial spasm

Risk factors

The cochlear nerve function is at risk during microvascular decompression for hemifacial spasm.

Cause and risk factors are highly variable.

A study strongly suggested a correlation between the cerebellar retraction factors, especially retraction depth and duration, and possibility of hearing loss following MVD for HFS 1).

Intradural compression due to overinfusion of saline may lead to postoperative hearing loss, although the incidence is low, and immediate decompression by drainage may be required 2).


Intraoperative monitoring of brainstem auditory evoked potentials (BAEPs) can be a useful tool to decrease the danger of hearing loss 3) 4) 5).

It is important to emphasize the need for clean exposure of the lower cranial nerves (except for cranial nerve VIII) to obtain enough working space, sharp arachnoid dissection, minimal cerebellar retraction, and proper responses to changes identified during intraoperative monitoring 6).


Prolongation of the inter-peak latency of waves I-III seems to be associated with the occurrence of delayed hearing loss. It is possible that BAEP changes may predict delayed hearing loss, but confirmatory evidence is not available as yet. Analysis of more cases is necessary to determine the utility of BAEP monitoring to predict delayed hearing loss after MVD and to identify its exact cause 7).

Case series

Lee et al., from the Samsung Medical Center in a study aimed to analyze cases of delayed hearing loss after microvascular decompression (MVD) for hemifacial spasm and identify the characteristic features of these patients.

They retrospectively reviewed the medical records of 3462 patients who underwent MVD for hemifacial spasm between January 1998 and August 2017.

Among these, there were 5 cases in which hearing was normal immediately postoperatively but delayed hearing loss occurred. None of the 5 patients reported any hearing disturbance immediately after the operation. However, they developed hearing problems suddenly after some time (median, 22 days; range 10-45 days). On examination, sensorineural hearing loss was confirmed. High-dose corticosteroid treatment was prescribed. Preoperative hearing levels were restored after several months (median duration from the time of the operation, 45 days; range 22-118 days). Interestingly, the inter-peak latency of waves I-III in the brainstem auditory evoked potentials (BAEP) was prolonged during the surgery, but recovered within a short time.

Delayed hearing loss may occur after MVD for HFS. Prolongation of the inter-peak latency of waves I-III seems to be associated with the occurrence of delayed hearing loss. It is possible that BAEP changes may predict delayed hearing loss, but confirmatory evidence is not available as yet. Analysis of more cases is necessary to determine the utility of BAEP monitoring to predict delayed hearing loss after MVD and to identify its exact cause 8).

Nine hundred and thirty-two patients with HFS who underwent MVD with intraoperative monitoring (IOM) of BAEP were analyzed. Park et al., used a 43.9 Hz/s stimulation rate and 400 averaging trials to obtain BAEP. To evaluate HL, pure-tone audiometry and speech discrimination scoring were performed before and one week after surgery. We analyzed the incidence for postoperative HL according to BAEP changes and calculated the diagnostic accuracy of significant warning criteria.

Only 11 (1.2%) patients experienced postoperative HL. The group showing permanent loss of wave V showed the largest percentage of postoperative HL (p < 0.001). No patient who experienced only latency prolongation (≥1 ms) had postoperative HL. Loss of wave V and latency prolongation (≥1 ms) with amplitude decrement (≥50%) were highly associated with postoperative HL.

Loss of wave V and latency prolongation of 1 ms with amplitude decrement ≥50% were the critical warning signs of BAEP for predicting postoperative HL 9).

Jung et al., retrospectively analyzed the medical records of patients with HFS who underwent MVD with the same surgeon from March 2003 to October 2016, and reviewed the pertinent literature. Patients who were followed up for more than 6 months were selected, resulting in the analysis of 1434 total patients. Postoperative hearing complications were evaluated audiometrically and subjectively (patient-reported symptoms). Clinical factors such as the intraoperative findings were reviewed to identify their correlation with auditory function.

Symptoms in 1333/1434 patients (93.0%) resolved more than 90% from their preoperative state. Among them, 16 patients (1.1%) complained of hearing impairment after surgery. Most impairment was transient, although 6/1333 patients (0.4%) required additional interventions for persistent hearing deficits (one surgical intervention and five hearing aids). A >50% decrease in the amplitude of brainstem auditory evoked potentials during the operation was significantly associated with postoperative hearing deficits.

Few auditory complications, mostly transient, result from MVD. Although MVD is a commonplace surgical technique, to reduce complications it is important to emphasize the need for clean exposure of the lower cranial nerves (except for cranial nerve VIII) to obtain enough working space, sharp arachnoid dissection, minimal cerebellar retraction, and proper responses to changes identified during intraoperative monitoring 10)

Three hundred thirty-one patients with HFS underwent MVD from March 2009 to October 2010.

Brain stem auditory evoked potential (BAEP) was monitored during the surgery. Before completion of the dural closure, the surgical field was routinely filled with warm saline to avoid postoperative pneumocephalus and epidural hematoma.

Seven patients experienced a change in wave V amplitude and latency after the dural closure. In 2 patients, the amplitudes decreased by less than 50%, and latencies were delayed by less than 1.0 ms, ipsilaterally in 1 patient and contralaterally in the other. In 1 patient, decreased amplitude and delayed latency appeared bilaterally with more severity on the operated side, accompanied by delayed ipsilateral permanent hearing loss. In 4 of the 7 patients, an ipsilateral response of BAEP was completely absent. Of these 4 patients, 2 experienced permanent hearing loss, and another 2 patients who underwent dural reopening and saline drainage had restoration of their normal hearing.

Intradural compression due to overinfusion of saline may lead to postoperative hearing loss, although the incidence is low, and immediate decompression by drainage may be required 11).

668 patients (95.7%) had no hearing loss immediately after surgery (group 1). 17 patients (2.4%) had a postoperative decrease in PTA exceeding 15 dB and a decrease in SDS which was proportional to the postoperative PTA thresholds (group 2). Eight patients (1.2%) had poor SDS that appeared to be out of proportion to the degree of hearing loss depicted by the postoperative PTA thresholds, suggesting retrocochlear or cochlear nerve pathology (group 3). Five patients (0.7%) had total deafness after surgery (group 4). In group 2, 12 patients (70.6%) returned to their preoperative hearing capacity. However, among the eight patients in group 3 and five in group 4, only two (25%) and none (0%) have returned to their preoperative hearing status, respectively.

In this large study, permanent hearing loss occurred in 16 patients (2.2%). Patients with a mild hearing loss with a good SDS (cochlear type) demonstrated much better prognosis than those with poor SDS (retrocochlear type) or total deafness. In addition, total deafness after surgery had no chance of recovery to preoperative hearing capacity 12).

Auditory function was studied before and after surgery in 143 consecutive patients who were operated on for hemifacial spasm by microvascular decompression of the intracranial portion of the facial nerve. The acoustic reflex was abnormal preoperatively in 41% of the patients, indicating that the vascular abnormalities that caused the hemifacial spasm also affected the auditory nerve. Three patients suffered a profound hearing loss in the ear on the operated side, and one lost hearing function totally. In addition, 24 patients had a moderate elevation in the pure-tone threshold at one or more octave frequencies. Of these, 16 patients experienced a hearing loss at only one frequency (8000 Hz), while eight had a threshold evaluation of no more than 20 dB in the speech frequency range (500, 1000, and 2000 Hz). Two patients were deaf on the side of the spasm before the operation. Three patients were not tested postoperatively, and one patient was tested only after surgery. Thus, in this series of 143 patients, only 2.8% suffered a significant hearing loss as a complication of facial nerve decompression to relieve hemifacial spasm 13).

Case reports

Onoda et al., reported two unusual cases of delayed hearing loss after microvascular decompression (MVD) for hemifacial spasm. In the first case, A 59-year-old female noted left hearing loss one week after receiving MVD for left hemifacial spasm. In the second case, A 39-year-old male also noticed ipsilateral hearing loss on the 7th day after MVD for right hemifacial spasm. Both cases were treated by steroid. Two months after the onset, their hearing function improved dramatically. These cases indicated that the delayed hearing loss after MVD for hemifacial spasm can occur, even when gentle microsurgical technique is used, but the prognosis for this condition is fairly good 14).



Li N, Zhao WG, Pu CH, Yang WL. Quantitative study of the correlation between cerebellar retraction factors and hearing loss following microvascular decompression for hemifacial spasm. Acta Neurochir (Wien). 2018 Jan;160(1):145-150. doi: 10.1007/s00701-017-3368-9. Epub 2017 Oct 26. PubMed PMID: 29075904.
2) , 11)

Jo KW, Lee JA, Park K, Cho YS. A new possible mechanism of hearing loss after microvascular decompression for hemifacial spasm. Otol Neurotol. 2013 Sep;34(7):1247-52. doi: 10.1097/MAO.0b013e31829b5786. PubMed PMID: 23942352.
3) , 7) , 8)

Lee MH, Lee S, Park SK, Lee JA, Park K. Delayed hearing loss after microvascular decompression for hemifacial spasm. Acta Neurochir (Wien). 2019 Mar;161(3):503-508. doi: 10.1007/s00701-018-3774-7. Epub 2018 Dec 19. PubMed PMID: 30569226.
4) , 9)

Park SK, Joo BE, Lee S, Lee JA, Hwang JH, Kong DS, Seo DW, Park K, Lee HT. The critical warning sign of real-time brainstem auditory evoked potentials during microvascular decompression for hemifacial spasm. Clin Neurophysiol. 2018 May;129(5):1097-1102. doi: 10.1016/j.clinph.2017.12.032. Epub 2018 Jan 4. PubMed PMID: 29342440.

El Damaty A, Rosenstengel C, Matthes M, Baldauf J, Dziemba O, Hosemann W, Schroeder HWS. A New Score to Predict the Risk of Hearing Impairment After Microvascular Decompression for Hemifacial Spasm. Neurosurgery. 2017 Nov 1;81(5):834-843. doi: 10.1093/neuros/nyx111. PubMed PMID: 28973677.
6) , 10)

Jung NY, Lee SW, Park CK, Chang WS, Jung HH, Chang JW. Hearing Outcome Following Microvascular Decompression for Hemifacial Spasm: Series of 1434 Cases. World Neurosurg. 2017 Dec;108:566-571. doi: 10.1016/j.wneu.2017.09.053. Epub 2017 Sep 18. PubMed PMID: 28927910.

Park K, Hong SH, Hong SD, Cho YS, Chung WH, Ryu NG. Patterns of hearing loss after microvascular decompression for hemifacial spasm. J Neurol Neurosurg Psychiatry. 2009 Oct;80(10):1165-7. doi: 10.1136/jnnp.2007.136713. PubMed PMID: 19762909.

Møller MB, Møller AR. Loss of auditory function in microvascular decompression for hemifacial spasm. Results in 143 consecutive cases. J Neurosurg. 1985 Jul;63(1):17-20. PubMed PMID: 4009269.

Onoda K, Ono S, Miyoshi Y, Tokunaga K, Date I. [Delayed hearing loss after microvascular decompression for hemifacial spasm: report of two cases]. No Shinkei Geka. 2006 Oct;34(10):1045-9. Review. Japanese. PubMed PMID: 17052017.

Hydrocephalus after posterior fossa decompression for Chiari type 1 deformity

Hydrocephalus after posterior fossa decompression for Chiari type 1 deformity

Hydrocephalus may be seen in association with Chiari type 1 deformity, likely because of disruptions in normal CSF flow. Although patients sometimes demonstrate evidence of hydrocephalus during their initial presentation for CM-I, a subset of patients appear to develop hydrocephalus only after posterior fossa decompression. These patients may present with evidence of raised intracranial pressure, ventricular dilation on imaging, or persistent cerebrospinal fluid leakage postoperatively. To date, there are no reports in the literature investigating what factors are associated with the need for CSF diversion after PFD is performed to treat CM-I.
Guan et al. performed a retrospective clinical chart review of all patients who underwent PFD surgery and duraplasty for CM-I at the Primary Children’s Hospital in Utah from June 1, 2005, through May 31, 2015. Patients were dichotomized based on the need for long-term CSF diversion after PFD. Analysis included both univariate and multivariable logistic regression analyses.
The authors identified 297 decompressive surgeries over the period of the study, 22 of which required long-term postoperative CSF diversion. On multivariable analysis, age < 6 years old (OR 3.342, 95% CI 1.282-8.713), higher intraoperative blood loss (OR 1.003, 95% CI 1.001-1.006), and the presence of a fourth ventricular web (OR 3.752, 95% CI 1.306-10.783) were significantly associated with the need for long-term CSF diversion after decompressive surgery.
Younger patients, those with extensive intraoperative blood loss, and those found during surgery to have a fourth ventricular web were at higher risk for the development of CRH. Clinicians should be alert to evidence of CRH in this patient population after PFD surgery. 1) 2).
Elton et al. present three patients who developed infratentorial supracerebellar hygromas causing acute hydrocephalus after posterior cranial fossa decompression 3).
A 34-year-old woman presented with strain-related suboccipital headache and myelopathy for 6 months. Imaging revealed tonsillar herniation up to C2 level and cervical syringomyelia. A standard FMD, C1 posterior arch removal, and tonsillar reduction was performed. After an initial uneventful postoperative course, she had 2 readmissions with headache, vomiting, and ataxia. Imaging showed a tense pseudomeningocele and concomitant supratentorial and infratentorial (initially right-sided, followed by left-sided) SDHs with ventriculomegaly. She was conservatively managed with antiedema measures and had excellent relief of symptoms. For the literature review, only cases with concomitant supratentorial and infratentorial SDHs with hydrocephalus were searched online and analyzed.
Including this, 10 cases have been reported. Mean age was 25.3 years. The male-to-female ratio was 1:2.3. Symptoms appeared an average of 12.6 days postoperatively. Treatment was with conservative management in 3 cases, and 3 cases required permanent cerebrospinal fluid diversions. Mean follow-up duration was 9.4 months (range, 1-27 months).
Coexistent supratentorial and infratentorial SDHs with hydrocephalus after Chiari decompression is a very rare occurrence. Treatment needs to be individualized based on the predominant symptomatic lesion, and surgical options need to be judiciously considered. Good prognosis is the rule in most cases 4).

A 2-year-old girl with the Chiari 1 malformation underwent FMD, including suboccipital craniotomy, C1 laminectomy and durotomy without opening the arachnoid.
After initial postoperative improvement, the patient deteriorated, developing subdural hygromas and hydrocephalus. These were treated successfully with observation and acetazolamide.
Subdural hygromas may complicate FMD. A slit valve opening in the arachnoid might be part of the pathophysiology. While surgical intervention may be necessary in some circumstances, non-operative measures may be effective as well 5).

Guan J, Riva-Cambrin J, Brockmeyer DL. Chiari-related hydrocephalus: assessment of clinical risk factors in a cohort of 297 consecutive patients. Neurosurg Focus. 2016 Nov;41(5):E2. PubMed PMID: 27798986.

Pereira EA, Magdum SA. Foramen magnum decompression – from hygromas to hydrocephalus. Br J Neurosurg. 2016 Jun;30(3):355. doi: 10.3109/02688697.2016.1173198. Epub 2016 Apr 21. PubMed PMID: 27100816.

Elton S, Tubbs RS, Wellons JC 3rd, Blount JP, Grabb PA, Oakes WJ. Acute hydrocephalus following a Chiari I decompression. Pediatr Neurosurg. 2002 Feb;36(2):101-4. PubMed PMID: 11893893.

Prasad GL, Menon GR. Coexistent Supratentorial and Infratentorial Subdural Hygromas with Hydrocephalus After Chiari Decompression Surgery: Review of Literature. World Neurosurg. 2016 Sep;93:208-14. doi: 10.1016/j.wneu.2016.06.025. Epub 2016 Jun 16. Review. PubMed PMID: 27319314.

Filis AK, Moon K, Cohen AR. Symptomatic Subdural Hygroma and Hydrocephalus following Chiari I Decompression. Pediatr Neurosurg. 2009;45(6):425-8. doi: 10.1159/000270159. Epub 2009 Dec 24. PubMed PMID: 20051703.

Update: Interleukin 6 after aneurysmal subarachnoid hemorrhage

Interleukin 6 after aneurysmal subarachnoid hemorrhage

After rupture of a intracranial aneurysm, high CSF Interleukin 6 levels were found to associate with vasospasm 1) 2) 3).
This aneurysmal subarachnoid hemorrhage (SAH) has been reported to induce an intrathecal inflammatory reaction reflected by cytokine release, particularly interleukin 6 (IL-6), which correlates with early brain damage and poor outcome.
Results provide strong evidence that IL-6 and TNF-α CSF levels are elevated in SAH patients and may participate in SAH development. Thus, these two cytokines could be important biomarkers for early diagnosis and disease monitoring in SAH patients 4).
Higher early IL6 serum levels after aSAH are associated with poor outcome at discharge. In addition, involvement of leukemia inhibitory factor (LIF) in the early inflammatory reaction after aSAH has been demonstrated 5).
CSF IL-6 values of ≥10,000 pg/ml in the early post-SAH period may be a useful diagnostic tool for predicting shunt dependency in patients with acute posthemorrhagic hydrocephalus. The development of shunt-dependent posthemorrhagic hydrocephalus remains a multifactorial process 6).

Case series


The concentrations of serum biomarkers and markers in the CSF were collected in 63 consecutive patients with aSAH and external ventricular drainage. Arithmetical means and standard deviations, area under the curve (AUC), cutoff values (C-OFF), sensitivity (SE), and specificity (SP) were calculated for markers and their correlation with SAHw/o/c, cVSSAH, and VCSAH. RESULTS: Clinical courses included 27 patients with cVSSAH, 17 with VCSAH, and 19 with SAHw/o/c. Mean ± standard deviationCSFIL-6 values were 7588 ± 4580 pg/mL at onset of VCSAH and 4102 ± 4970 pg/mL for cVSSAH and higher than 234 ± 239 pg/mL in SAHw/o/c (P < 0.001). CSFIL-6 showed excellent diagnostic potential for differing between VCSAH and SAHw/o/c (AUC, 1.00; C-OFF, 707; SE, 100%; SP, 100%), and a moderate diagnostic potential for differing VCSAH from cVSSAH (AUC, 0.757; C-OFF, 3100 pg/Ml; SE, 86.7%; SP, 70.6%). The concentration of CSFIL-6 within the cVSSAH group was significantly increased compared with SAHw/o/c (AUC, 0.937; C-OFF, 530 pg/mL; SE, 87.5%; SP, 91.7%).
CSFIL-6 is increased after aSAH in patients with cVSSAH or VCSAH. Patients with a CSFIL-6 level higher than a C-OFF of 3100 pg/mL have an increased likelihood for VCSAH; patients with CSFIL-6 levels between 530 and 3100 pg/mL have an increased posttest probability for cVSSAH 7).


Kao et al. prospectively included 53 consecutive patients treated with platinum coil embolization of the ruptured intracranial aneurysm. Plasma IL-6 levels were measured in the blood samples at the orifices of the aneurysms and from peripheral veins. The outcome measure was the modified Rankin Scale one month after SAH. Multiple logistic regression analyses were used to evaluate the associations between the plasma IL-6 levels and the neurological outcome.
Significant risk factors for the poor outcome were old age, low Glasgow Coma Scale (GCS) on day 0, high Fisher grades, and high aneurysmal and venous IL-6 levels in univariate analyses. Aneurysmal IL-6 levels showed modest to moderate correlations with GCS on day 0, vasospasm grade and Fisher grade. A strong correlation was found between the aneurysmal and the corresponding venous IL-6 levels (ρ = 0.721; P<0.001). In the multiple logistic regression models, the poor 30-day mRS was significantly associated with high aneurysmal IL-6 level (OR, 17.97; 95% CI, 1.51-214.33; P = 0.022) and marginally associated with high venous IL-6 level (OR, 12.71; 95% CI, 0.90-180.35; P = 0.022) after adjusting for dichotomized age, GCS on day 0, and vasospasm and Fisher grades.
The plasma level of IL-6 is an independent prognostic biomarker that could be used to aid in the identification of patients at high-risk of poor neurological outcome after rupture of the intracranial aneurysm 8).

A complete data set (DHEAS and IL-6 serum levels for days 0, 1, 4, 7, 10 and 14 after aSAH) and outcome assessment at discharge according to modified Rankin Scale score (mRS) was available for 53 patients of the initially screened cohort (n = 109). Outcome assessment six months after aSAH was obtained from 41 patients. Logarithmized levels of DHEAS and IL-6 were related to dichotomized functional outcome either assessed at discharge or at six months. A mixed between-within subjects ANOVA was applied for statistical analysis (SPSS 21.0).
DHEAS and IL-6 levels across time were related to functional outcome. Regarding outcome assessment at discharge and at six months after aSAH, DHEAS levels (transformed to square root for statistical purposes) were considerably higher in patients with favorable outcome (mRS 0-2) (p = .001; p = .020). Inversely, in patients with favorable outcome either at discharge or six months after aSAH, lower IL-6 levels (logarithmized for statistical purposes) were observed across time (both p < .001).
Höllig et al. provide new evidence that DHEAS is associated with protective properties resulting in improvement of functional outcome after aSAH, possibly by influencing the inflammatory response after aSAH shown in the decreasing IL-6 serum levels. But the results for outcome six months after SAH are limited due to a high drop-out rate 9).


Daily systemic IL-6 levels were measured in the acute phase in 11 patients with non-aneurysmal perimesencephalic SAH (pmSAH), with bleeding strictly located around the midbrain, and in nine patients with non-aneurysmal non-perimesencephalic (non-pmSAH), with hemorrhage extending into adjacent cisterns (group 1). IL-6 levels were compared with those from patients suffering from aSAH with cerebral vasospasm (CVS) (group 2) and without CVS (group 3). The mean IL-6 level (±standard error of the mean) was significantly lower in group 1 compared to group 2 (9.9±1.9 vs. 29.1±6.7 pg/mL, p=0.018). The difference in mean IL-6 level between group 1 and 3 fell short of significance (9.9±1.9 vs. 14.9±1.1 pg/mL, p=0.073). Patients in group 1 had a significantly better outcome (Glasgow Outcome Scale score 4-5) compared to group 2 (p<0.001) and a trend towards better outcome compared to group 3 (p=0.102). A subgroup analysis revealed a higher mean IL-6 concentration in patients with non-pmSAH compared to patients with pm-SAH (p=0.001). We concluded that systemic IL-6 concentration reflects the severity of the inflammatory stress response and course of the illness. The more benign illness and good prognosis of patients with pmSAH or non-pmSAH in contrast to patients with aSAH is reflected by the lower concentrations of IL-6 10).


A total of 38 consecutive aSAH patients were studied prospectively within 14 days after admission and classified as asymptomatic (n = 9; WFNS grade 1 (1-2), median and quartiles) and symptomatic (n = 29; WFNS grade 4 (2-5)); the latter presenting with acute focal neurological deficits (AFND) (n = 13), delayed cerebral ischemia(DCI). (n = 10) or both (n = 6). Levels of pro-inflammatory cytokine IL-6 were determined in cerebral extracellular fluid (ECF, using cerebral microdialysis), cerebrospinal fluid (CSF) and plasma for 10 days after aSAH. Additionally, C-reactive protein (CRP) levels were measured in plasma.
High IL-6 levels in CSF, ECF and plasma were found in all patients, reflecting a pronounced local inflammatory response after aSAH, followed only in symptomatic patients by a delayed systemic inflammation (CRP P < 0.025, days 7-9 after aSAH). In all compartments, IL-6 levels appeared to be higher in symptomatic patients, accompanied also by a higher ECF lactate-pyruvate ratio (P = 0.04). Cerebral, but not plasma IL-6, levels were indicative of the development of DCI in symptomatic patients (ECF P = 0.003; CSF P = 0.001).
A pronounced initial cerebral inflammatory state was observed in patients of all WFNS grades, suggesting that IL-6 elevations are not necessarily detrimental. Cerebral, but not plasma IL-6, levels were predictive of the development of delayed ischemic deficits in symptomatic patients, suggesting that CSF or ECF are the best sampling media for future studies 11).
Ďuriš K, Neuman E, Vybíhal V, Juráň V, Gottwaldová J, Kýr M, Vašků A, Smrčka M. Early Dynamics of Interleukin-6 in Cerebrospinal Fluid after Aneurysmal Subarachnoid Hemorrhage. J Neurol Surg A Cent Eur Neurosurg. 2017 Sep 4. doi: 10.1055/s-0037-1604084. [Epub ahead of print] PubMed PMID: 28869993.

Fassbender K, Hodapp B, Rossol S, Bertsch T, Schmeck J, Schutt S, et al. Inflammatory cytokines in subarachnoid haemorrhage: association with abnormal blood flow velocities in basal cerebral arteries. J Neurol Neurosurg Psychiatry. 2001;70: 534–537.

Hendryk S, Jarzab B, Josko J. Increase of the IL-1 beta and IL-6 levels in CSF in patients with vasospasm following aneurysmal SAH. Neuro Endocrinol Lett. 2004;25: 141–147.

Schoch B, Regel JP, Wichert M, Gasser T, Volbracht L, Stolke D. Analysis of intrathecal interleukin-6 as a potential predictive factor for vasospasm in subarachnoid hemorrhage. Neurosurgery. 2007;60: 828–836; discussion 828–836.

Wu W, Guan Y, Zhao G, Fu XJ, Guo TZ, Liu YT, Ren XL, Wang W, Liu HR, Li YQ. Elevated IL-6 and TNF-α Levels in Cerebrospinal Fluid of Subarachnoid Hemorrhage Patients. Mol Neurobiol. 2015 Jun 11. [Epub ahead of print] PubMed PMID: 26063595.

Höllig A, Remmel D, Stoffel-Wagner B, Schubert GA, Coburn M, Clusmann H. Association of early inflammatory parameters after subarachnoid hemorrhage with functional outcome: A prospective cohort study. Clin Neurol Neurosurg. 2015 Aug 28;138:177-183. doi: 10.1016/j.clineuro.2015.08.030. [Epub ahead of print] PubMed PMID: 26355810.

Wostrack M, Reeb T, Martin J, Kehl V, Shiban E, Preuss A, Ringel F, Meyer B, Ryang YM. Shunt-Dependent Hydrocephalus After Aneurysmal Subarachnoid Hemorrhage: The Role of Intrathecal Interleukin-6. Neurocrit Care. 2014 May 20. [Epub ahead of print] PubMed PMID: 24840896.

Lenski M, Huge V, Briegel J, Tonn JC, Schichor C, Thon N. Interleukin 6 in the Cerebrospinal Fluid as a Biomarker for Onset of Vasospasm and Ventriculitis After Severe Subarachnoid Hemorrhage. World Neurosurg. 2017 Mar;99:132-139. doi: 10.1016/j.wneu.2016.11.131. Epub 2016 Dec 5. PubMed PMID: 27931942.

Kao HW, Lee KW, Kuo CL, Huang CS, Tseng WM, Liu CS, Lin CP. Interleukin-6 as a Prognostic Biomarker in Ruptured Intracranial Aneurysms. PLoS One. 2015 Jul 15;10(7):e0132115. doi: 10.1371/journal.pone.0132115. eCollection 2015. PubMed PMID: 26176774; PubMed Central PMCID: PMC4503596.

Höllig A, Thiel M, Stoffel-Wagner B, Coburn M, Clusmann H. Neuroprotective properties of dehydroepiandrosterone-sulfate and its relationship to interleukin 6 after aneurysmal subarachnoid hemorrhage: a prospective cohort study. Crit Care. 2015 May 21;19:231. doi: 10.1186/s13054-015-0954-1. PubMed PMID: 25993987; PubMed Central PMCID: PMC4462180.

Muroi C, Bellut D, Coluccia D, Mink S, Fujioka M, Keller E. Systemic interleukin-6 concentrations in patients with perimesencephalic non-aneurysmal subarachnoid hemorrhage. J Clin Neurosci. 2011 Dec;18(12):1626-9. doi: 10.1016/j.jocn.2011.03.022. Epub 2011 Oct 22. PubMed PMID: 22019436.

Sarrafzadeh A, Schlenk F, Gericke C, Vajkoczy P. Relevance of cerebral interleukin-6 after aneurysmal subarachnoid hemorrhage. Neurocrit Care. 2010 Dec;13(3):339-46. doi: 10.1007/s12028-010-9432-4. PubMed PMID: 20725805.
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