Cervical Sympathetic Nerve Block for cerebral vasospasm

Cervical Sympathetic Nerve Block for cerebral vasospasm

Sympathetic perivascular nerve fibers originate from the superior cervical ganglion (SCG) to innervate the cerebral vasculature, with activation resulting in vasoconstriction. Sympathetic pathways are thought to be a significant contributor to cerebral vasospasm 1).


A simple treatment such as a cervical sympathetic nerve block may be an effective therapy but is not routinely performed as cerebral vasospasm treatment/DCI. cervical sympathetic nerve block consists of injecting local anesthetic at the level of the cervical sympathetic trunk, which temporarily blocks the innervation of the cerebral arteries to cause arterial vasodilatation. cervical sympathetic nerve block is a local, minimally invasive, low cost and safe technique that can be performed at the bedside and may offer significant advantages as a complementary treatment in combination with more conventional neurointerventional surgery interventions. Bombardieri et al. reviewed the literature that describes cervical sympathetic nerve block for vasospasm/DCI prevention or treatment in humans after aSAH. The studies outlined in this review show promising results for a cervical sympathetic nerve block as a treatment for vasospasm/DCI. Further research is required to standardize the technique, explore how to integrate a cervical sympathetic nerve block with conventional neurointerventional surgery treatments of vasospasm and DCI, and study its long-term effect on neurological outcomes 2).


SCG was surgically identified in 15 swine and were electrically stimulated to achieve sympathetic activation. CT perfusion scans were performed to assess for changes in cerebral blood flow (CBF), cerebral blood volume (CBV), mean transit time (MTT), and time-to-maximum (TMax). Syngo. via software was used to determine regions of interest and quantify perfusion measures.

Results: SCG stimulation resulted in 20-30% reduction in mean ipsilateral CBF compared to its contralateral unaffected side (p < 0.001). Similar results of hypoperfusion were seen with CBV, MTT and TMax with SCG stimulation. Prior injection of lidocaine to SCG inhibited the effects of SCG stimulation and restored perfusion comparable to baseline (p > 0.05).

Conclusion: In swine, SCG stimulation resulted in significant cerebral perfusion deficit, and this was inhibited by prior local anesthetic injection into the SCG. Inhibiting sympathetic activation by targeting the SCG may be an effective treatment for sympathetic-mediated cerebral hypoperfusion 3).


Hu et al. investigated the therapeutic effects of SGB in a rat model of subarachnoid hemorrhage (SAH) complicated by delayed CVS and explore the underlying mechanisms. The SAH model was established by the double injection of autologous arterial blood into the cisterna magna. They simulated SGB by transection of the cervical sympathetic trunk (TCST), and measured changes in the diameter, perimeter, and cross-sectional area of the basilar artery (BA) and middle cerebral artery (MCA) to evaluate its vasodilatory effect. To investigate the underlying mechanisms, we determined the expression level of vasoactive molecules endothelin-1 (ET-1) and calcitonin gene-related peptide (CGRP) in the plasma, and apoptotic modulators Bcl-2 and Bax in the hippocampus. We found a significant increase in the diameter, perimeter, and cross-sectional area of the BA and right MCA in SAH rats subjected to TCST. Application of SGB significantly reduced the expression of ET-1 while increasing that of CGRP in SAH rats. We also found a significant increase in the expression of Bcl-2 and a decrease in the expression of Bax in the hippocampus of SAH rats subjected to TCST, when compared to untreated SAH rats. The mechanism of action of SGB is likely mediated through alterations in the ratio of ET-1 and CGRP, and Bax and Bcl-2. These results suggest that SGB can alleviate the severity of delayed CVS by inducing dilation of intracerebral blood vessels, and promoting anti-apoptotic signaling. Our findings provide evidence supporting the use of SGB as an effective and well-tolerated approach to the treatment of CVS in various clinical settings 4)


After successful modeling of cervical sympathetic block, 18 healthy male white rabbits were randomly divided into three groups (n=6), ie, sham operation group (Group A), SAH group (Group B) and SAH with cervical sympathetic block group (Group C). Models of delayed CVS were established by puncturing cisterna magna twice with an injection of autologous arterial blood in Groups B and C. A sham injection of blood through cisterna magna was made in Group A. 0.5 ml saline was injected each time through a catheter for cervical sympathetic block after the first injection of blood three times a day for 3 d in Group B (bilateral alternating). 0.5 ml of 0.25% bupivacaine was injected each time through a catheter for cervical sympathetic block after the first injection of blood three times a day for 7 d in Group B. 2 ml venous blood and cerebrospinal fluid were obtained before (T1), 30 min (T2) and 7 d (T3) after the first injection of blood, respectively, and conserved in a low temperature refrigerator. Basilar artery value at T1, T2 and T3 was measured via cerebral angiography. The degree of damage to nervous system at T1 and T3 was recorded.

Results: There was no significant difference in diameter of basilar artery at T1 among three groups. The diameters of basilar artery at T2 and T3 of Groups B and C were all smaller than that in Group A, which was smaller than Group C, with a significant difference. There was no significant difference in NO and NOS in plasma and cerebrospinal fluid among three groups. The NO and NOS contents at T2 and T3 of Groups B and C were all lower than Group A; Group C was higher than Group B, with a significant difference. The nerve function at T3 of Groups B and C were all lower than Group A and that of Group C higher than Group B, with a significant difference.

Cervical sympathetic block can relieve cerebral vasospasm after subarachnoid hemorrhage and increase NO content and NOS activity in plasma and cerebrospinal fluid to promote neural functional recovery 5)


1) , 3)

Kim WJ, Dacey M, Samarage HM, Zarrin D, Goel K, Chan C, Qi X, Wang AC, Shivkumar K, Ardell J, Colby GP. Sympathetic nervous system hyperactivity results in potent cerebral hypoperfusion in swine. Auton Neurosci. 2022 Sep;241:102987. doi: 10.1016/j.autneu.2022.102987. Epub 2022 May 6. PMID: 35567916; PMCID: PMC9659432.
2)

Bombardieri AM, Albers GW, Rodriguez S, Pileggi M, Steinberg GK, Heit JJ. Percutaneous cervical sympathetic block to treat cerebral vasospasm and delayed cerebral ischemia: a review of the evidence. J Neurointerv Surg. 2022 Dec 6:jnis-2022-019838. doi: 10.1136/jnis-2022-019838. Epub ahead of print. PMID: 36597947.
4)

Hu N, Wu Y, Chen BZ, Han JF, Zhou MT. Protective effect of stellate ganglion block on delayed cerebral vasospasm in an experimental rat model of subarachnoid hemorrhage. Brain Res. 2014 Oct 17;1585:63-71. doi: 10.1016/j.brainres.2014.08.012. Epub 2014 Aug 13. PMID: 25128600.
5)

Chun-jing H, Shan O, Guo-dong L, Hao-xiong N, Yi-ran L, Ya-ping F. Effect of cervical sympathetic block on cerebral vasospasm after subarachnoid hemorrhage in rabbits. Acta Cir Bras. 2013 Feb;28(2):89-93. doi: 10.1590/s0102-86502013000200001. PMID: 23370920.

Delirium Diagnosis

Delirium Diagnosis


Unlike dementiadelirium has an acute onset, motor signs (tremormyoclonusasterixis), slurred speech, altered consciousness (hyperalert/agitated or lethargic, or fluctuations), hallucinations may be florid.

Consultation-liaison psychiatry could improve the recognition rate of postoperative delirium in elderly patients, and shorten hospitalization time. The training of mental health knowledge for non-psychiatrists could improve the ability of early identify and treatment of delirium 1).


It is a corollary of the criteria that a diagnosis of delirium usually cannot be made without a previous assessment, or knowledge, of the affected person’s baseline level of cognitive function. In other words, a mentally disabled person who is suffering from this will be operating at their own baseline level of mental ability and would be expected to appear delirious without a baseline mental functional status against which to compare.

Early detection is crucial because the longer a patient experiences delirium the worse it becomes and the harder it is to treat. Currently, identification is through intermittent clinical assessment using standardized tools, like the Confusion Assessment Method for the Intensive Care Unit. Such tools work well in clinical research but do not translate well into clinical practice because they are subjective, intermittent, and have low sensitivity. As such, healthcare providers using these tools fail to recognize delirium symptoms as much as 80% of the time.

EEG shows pronounced diffuse slowing.

Delirium-related biochemical derangement leads to electrical changes in electroencephalographic (EEG) patterns followed by behavioral signs and symptoms. However, continuous EEG monitoring is not feasible due to the cost and the need for skilled interpretation. Studies using limited-lead EEG show large differences between patients with and without delirium while discriminating delirium from other causes. The Ceribell is a limited-lead device that analyzes EEG. If it is capable of detecting delirium, it would provide an objective physiological monitor to identify delirium before symptom onset. This pilot study was designed to explore relationships between Ceribell and delirium status. Completion of this study will provide a foundation for further research regarding delirium status using the Ceribell data 2).


Hut SC, Dijkstra-Kersten SM, Numan T, Henriquez NR, Teunissen NW, van den Boogaard M, Leijten FS, Slooter AJ. EEG and clinical assessment in delirium and acute encephalopathy. Psychiatry Clin Neurosci. 2021 May 16. doi: 10.1111/pcn.13225. Epub ahead of print. PMID: 33993579.


Early neutrophil-to-lymphocyte ratio (NLR) elevation may also predict delayed-onset delirium, potentially implicating systemic inflammation as a contributory delirium mechanism 3).

Older age, headache, coagulopathy, decreased level of consciousness, seizures, and history of falls. Conversely, infection was associated with a reduced yield.

In higher-risk patients and settings, there should be a push toward earlier neuroimaging as indicated by clinical examinations and individual risk factors. In the meta-analysis, the yield of head CT was higher in ICU patients and those who had focal neurological deficits in addition to altered mental status and was especially high in neuro ICU settings 4)

Neuroimaging should not replace a clinical exam, even in ICU settings; ICU patients should have their sedation reduced to properly test for delirium 5).

Delirium has a complex and fluctuating course with underlying causes that are often multifactorial; identifying a CNS lesion does not necessarily exclude other causes, and vice-versa 6).

The risks of neuroimaging need to be considered in the decision-making process 7).

The use of CT head to diagnose the etiology of delirium and AMS varied widely and yield has declined. Guidelines and clinical decision support tools could increase the appropriate use of CT head in the diagnostic etiology of delirium/AMS 8).


1)

Xie Q, Liu XB, Jing GW, Jiang X, Liu H, Zhong BL, Li Y. The Effect of Consultation-Liaison Psychiatry on Postoperative Delirium in Elderly Hip Fracture Patients in the General Hospital. Orthop Surg. 2023 Jan 3. doi: 10.1111/os.13501. Epub ahead of print. PMID: 36597675.
2)

Mulkey MA, Hardin SR, Munro CL, Everhart DE, Kim S, Schoemann AM, Olson DM. Methods of identifying delirium: A research protocol. Res Nurs Health. 2019 May 30. doi: 10.1002/nur.21953. [Epub ahead of print] PubMed PMID: 31148216.
3)

Reznik ME, Kalagara R, Moody S, Drake J, Margolis SA, Cizginer S, Mahta A, Rao SS, Stretz C, Wendell LC, Thompson BB, Asaad WF, Furie KL, Jones RN, Daiello LA. Common biomarkers of physiologic stress and associations with delirium in patients with intracerebral hemorrhage. J Crit Care. 2021 Mar 23;64:62-67. doi: 10.1016/j.jcrc.2021.03.009. Epub ahead of print. PMID: 33794468.
4)

MadsenTE, KhouryJ, Cadena R, et al. Potentially missed diagnosis of ischemic stroke in the Emergency Department in the Greater Cincinnati/Northern Kentucky stroke study.Acad Emerg Med. 2016;23(10):1128-1135. doi:10.1111/acem.13029
5)

Venkat A, Cappelen-Smith C, Askar S, et al. Factors associated with stroke misdiagnosis in the emergency department: a retrospective case-control study. Neuroepidemiology. 2018;51(3–4):123-127. doi:10.1159/000491635
6)

The 2019 American Geriatrics Society Beers Criteria®UpdateExpert Panel. American Geriatrics Society 2019 updated AGSbeers criteria for potentially inappropriate medication use in older adults. J Am Geriatr Soc. 2019;67(4):674-694. doi:10.1111/jgs.15767
7)

Reznik ME, Rudolph JL. “Yield” to the time-brain dilemma: The case for neuroimaging in delirium. J Am Geriatr Soc. 2023 Jan 6. doi: 10.1111/jgs.18206. Epub ahead of print. PMID: 36606371.
8)

Akhtar H, Chaudhry SH, Bortolussi-Courval É, Hanula R, Akhtar A, Nauche B, McDonald EG. Diagnostic yield of CT head in delirium and altered mental status-A systematic review and meta-analysis. J Am Geriatr Soc. 2022 Nov 26. doi: 10.1111/jgs.18134. Epub ahead of print. PMID: 36434820.

Spinal cord injury epidemiology

Spinal cord injury epidemiology


see also Cervical spine fracture epidemiology.


Thoracolumbar spine fracture epidemiology


Pediatric cervical spine injury epidemiology.


Spinal cord injury epidemiology is changing as preventative interventions reduce injuries in younger individuals, and there is an increased incidence of incomplete injuries in aging populations. With decompressive surgery and proactive interventions to improve spinal cord perfusion, early treatment has become more intensive. Accurate data, including specialized outcome measures, are crucial to understanding the impact of epidemiological and treatment trends. Dedicated SCI clinical research and data networks and registries have been established in the United States, Canada, Europe, and several other countries.


Traumatic spinal cord injuries (TSCIs) affect up to 500,000 people worldwide each year, and their high morbidity is associated with substantial individual and societal burden and socioeconomic impact 1) 2).

TSCIs most commonly affect young males and result from road traffic accidents, but recent reports also highlight their increasing incidence in older adults as a result of low-energy falls 3) 4) 5).


Kelly-Hedrick et al. reviewed four registry networks, The NACTN Spinal Cord Injury RegistryThe Spinal Cord Injury Model Systems (SCIMS) Database, The Rick Hansen Spinal Cord Injury Registry (RHSCIR), and the European Multi-Center Study about Spinal Cord Injury Study (EMSCI). They compared the registries’ focuses, data platforms, advanced analytics use, and impacts. They also describe how registries’ data can be combined with EHR or shared using federated analysis to protect registrants’ identities. These registries have identified changes in epidemiology, recovery patterns, complication incidence, and the impact of practice changes like early decompression. They’ve also revealed latent disease-modifying factors, helped develop clinical trial stratification models and served as matched control groups in clinical trials. Advancing SCI clinical science for personalized medicine requires advanced analytical techniques, including machine learning, counterfactual analysis, and the creation of digital twins. Registries and other data sources help drive innovation in SCI clinical science 6).


1)

WHO. Spinal Cord Injury, Fact Sheet. Available at 2013 http://www.who.int/mediacentre/factsheets/fs384/en/
2)

Singh A., Tetreault L., Kalsi-Ryan S., Nouri A., Fehlings M.G. (2014). Global prevalence and incidence of traumatic spinal cord injury. Clin. Epidemiol. 6, 309–331
3)

Noonan V.K., Fingas M., Farry A., Baxter D., Singh A., Fehlings M.G., Dvorak M.F. (2012). Incidence and prevalence of spinal cord injury in Canada: a national perspective. Neuroepidemiology 38, 219–226
4)

Selvarajah S., Hammond E.R., Haider A.H., Abularrage C.J., Becker D., Dhiman N., Hyder O., Gupta D., Black J.H., 3rd, Schneider E.B. (2014). The burden of acute traumatic spinal cord injury among adults in the United States: an update. J. Neurotrauma 31, 228–238
5)

Wyndaele M., Wyndaele J.J. (2006). Incidence, prevalence and epidemiology of spinal cord injury: what learns a worldwide literature survey? Spinal Cord 44, 523–529
6)

Kelly-Hedrick M, Abd-El-Barr M, Aarabi B, Curt A, Howley SP, Harrop JS, Kirshblum S, Neal CJ, Noonan VK, Park C, Ugiliweneza B, Tator C, Toups EG, Fehlings MG, Williamson T, Guest J. The Importance of Prospective Registries and Clinical Research Networks in the Evolution of Spinal Cord Injury Care. J Neurotrauma. 2022 Dec 28. doi: 10.1089/neu.2022.0450. Epub ahead of print. PMID: 36576020.

Brain abscess

Brain abscess

J.Sales-Llopis

Neurosurgery Service, Alicante University General Hospital, Alicante Institute for Health and Biomedical Research (ISABIAL – FISABIO Foundation), Alicante, Spain.


A brain abscess is a focal area of necrosis starting in an area of cerebritis surrounded by a membrane.

Brain abscesses are suppurative infections of the brain parenchyma surrounded by a vascularized capsule.

see also Intracranial abscess.

It is a potentially life-threatening condition requiring prompt radiological identification and rapid treatment.

The most frequent intracranial locations (in descending order of frequency) are: frontal-temporal, frontal-parietal, parietal, cerebellar, and occipital lobes.

In a article, Chen review the literature to find out how the epidemiology of this disease has changed through the years and re-visit the basic pathological process of abscess evolution and highlight the new research in the biochemical pathways that initiate and regulate this process 1).

The epidemiology of brain abscess has changed with the increasing incidence of this infection in immunocompromised patients, particularly solid organ and bone marrow transplant recipients, and the decreasing incidence of brain abscess related to sinusitis and otitis 2).

There have been several trends in the epidemiology of brain abscess over recent decades. One trend is that there appears to be a trend toward a decreasing incidence of brain abscess. In a population-based study of residents of Olmstead County, Minnesota, the incidence rate was 1.3 per 100,000 patient-years from 1935 to 1944 compared with 0.9 per 100,000 patient-years from 1965 to 1981 3).

Clinical presentation is non-specific, with many cases having no convincing inflammatory or septic symptoms.

Abscess formation should be considered in case of clinical deteriorationheadache, and any neurological deficit after febrile episodes.

Similar to any other mass lesion but tend to progress rapidly.

Symptoms of raised intracranial pressure, seizures and focal neurological deficits are the most common forms of presentation

Eventually, many abscesses rupture into the ventricular system, which results in a sudden and dramatic worsening of the clinical presentation and often heralds a poor outcome.

Cerebral abscesses result from pathogens growing within the brain parenchyma. Initial parenchymal infection is known as cerebritis, which may progress into a cerebral abscess.

Cerebral infection is commonly divided into four stages with distinct imaging and histopathologic features:

early cerebritis (a focal infection without a capsule or pus formation,can resolve or develop into frank abscess) late cerebritis

early abscess/encapsulation – may occur 10 days after infection

late abscess/encapsulation – may occur >14 days after infection

Significant advances in the diagnosis and management of bacterial brain abscess over the past several decades have improved the expected outcome of a disease once regarded as invariably fatal. Despite this, intraparenchymal abscess continues to present a serious and potentially life-threatening condition 4).

There has been a gradual improvement in the outcome of patients with brain abscess over the past 50 years, which might be driven by improved brain imaging techniques, minimally invasive neurosurgical procedures, and protocoled antibiotic treatment. Multicenter prospective studies and randomized clinical trials are needed to further advance treatment and prognosis in brain abscess patients.

Our understanding of brain abscesses has increased by meta-analysis on clinical characteristics, ancillary investigations, and treatment modalities. Prognosis has improved over time, likely due to improved brain imaging techniques, minimally invasive neurosurgical procedures, and protocoled antibiotic treatment 5).


Current evidences suggest that for encapsulated brain abscess in superficial non-eloquent area, abscess resection compared to abscess aspiration had lower post-operative residual abscess rate; lower re-operation rate; higher rate of improvement in neurological status within 1 month after surgery, shorter duration of post-operative antibiotics and average length of hospital stay. There was no statistically significant difference in the rate of improvement in neurological status at 3 months post-operative and the mortality 6).

Intraventricular rupture of brain abscess (IVROBA)

Strongly influences poor outcome in patients with cyanotic heart disease. The key to decreasing poor outcomes may be the prevention and management of IVROBA. To reduce operative and anesthetic risk in these patients, abscesses should be managed by less invasive aspiration methods guided by computed tomography. Abscesses larger than 2 cm in diameter, in deep-located or parieto-occipital regions, should be aspirated immediately and repeatedly, mainly using computed tomography-guided methods to decrease intracranial pressure and avoid IVROBA. IVROBA should be aggressively treated by aspiration methods for the abscess coupled with the appropriate intravenous and intrathecal administration of antibiotics while evaluating intracranial pressure pathophysiology 7).

Known space-occupying lesion, centered in the right frontal anterior white matter, with estimated diameters of 3.5 x 3 x 3.5 cm. It shows well-defined contours and a practically spherical shape. A predominantly hypointense signal on T1 and homogeneously hyperintense on T2, with a wall with hypointense behavior on T2-weighted sequences. After contrast administration, only enhancement of its wall was observed, in a fine and linear way, without identifying solid poles. The lesion shows diffusion sequence restriction and low values ​​of rVSC in perfusion. Marked surrounding vasogenic edema, which causes a mass effect on the neighboring sulci, as well as mild subfalcian herniation, with a deviation from the midline of approximately 6 mm (significant improvement compared to previous CT control). The discrete mass effect is also on the knee of the corpus callosum and the frontal horn of the right ventricle. The findings are compatible with a brain abscess. A small solution of continuity is observed in its anterior wall, in contact with the meninge, which is thickened in a laminar manner in relation to inflammatory involvement, without clearly identifying empyema. Extensive occupation of the frontal sinus bilaterally, with an enhancement of its wall. Retrospectively, the CT study showed slight permeation on the posterior wall of one of the loculations of the frontal sinus close to the abscess. Small hyperintense foci in subcortical and periventricular white matter with a chronic ischemic profile of a small vessel, to a mild degree. Diagnostic impression: Findings compatible with a right frontal parenchymal abscess, 3.5 cm in diameter, with inflammatory changes and thickening of the adjacent pachymeninge, although without clear associated empyema.


1)

Chen M, Low DCY, Low SYY, Muzumdar D, Seow WT. Management of brain abscesses: where are we now? Childs Nerv Syst. 2018 Oct;34(10):1871-1880. doi: 10.1007/s00381-018-3886-7. Epub 2018 Jul 3. PubMed PMID: 29968000.
2)

Calfee DP, Wispelwey B. Brain abscess. Semin Neurol. 2000;20(3):353-60. Review. PubMed PMID: 11051299.
3)

Nicolosi A, Hauser WA, Musicco M, Kurland LT: Incidence and prognosis of brain abscess in a defined population: Olmsted County, Minnesota, 1935-1981. Neuroepidemiology 1991;10:122-131.
4)

atel K, Clifford DB. Bacterial brain abscess. Neurohospitalist. 2014 Oct;4(4):196-204. doi: 10.1177/1941874414540684. PubMed PMID: 25360205; PubMed Central PMCID: PMC4212419.
5)

Brouwer MC, van de Beek D. Epidemiology, diagnosis, and treatment of brain abscesses. Curr Opin Infect Dis. 2016 Nov 8. [Epub ahead of print] PubMed PMID: 27828809.
6)

Zhai Y, Wei X, Chen R, Guo Z, Raj Singh R, Zhang Y. Surgical outcome of encapsulated brain abscess in superficial non-eloquent area: A systematic review. Br J Neurosurg. 2015 Nov 16:1-6. [Epub ahead of print] PubMed PMID: 26569628.
7)

Takeshita M, Kagawa M, Yato S, Izawa M, Onda H, Takakura K, Momma K. Current treatment of brain abscess in patients with congenital cyanotic heart disease. Neurosurgery. 1997 Dec;41(6):1270-8; discussion 1278-9. PubMed PMID: 9402578.

Trigone ventricular meningioma

Trigone ventricular meningioma

Thirty patients with trigone meningiomas were enrolled in this retrospective study. Conventional MRI was performed in all patients; SWI (17 cases), dynamic contrast-enhanced PWI (10 cases), and dynamic susceptibility contrast PWI (6 cases) were performed. Demographics, conventional MRI features, SWI- and PWI-derived parameters were compared between different grades of trigone meningiomas.

On conventional MRI, the irregularity of tumor shape (ρ = 0.497, P = 0.005) and the extent of peritumoral edema (ρ = 0.187, P = 0.022) might help distinguish low-grade and high-grade trigone meningiomas. On multiparametric functional MRI, rTTPmax (1.17 ± 0.06 vs 1.30 ± 0.05, P = 0.048), Kep, Ve, and iAUC demonstrated their potentiality to predict World Health Organization grades I, II, and III trigone meningiomas.

Conventional MRI combined with dynamic susceptibility contrast and dynamic contrast-enhanced can help predict the World Health Organization grade of trigone meningiomas 1).

A 65-year-old female refers to a speech disorder (slowed speech and stuttering) for months of evolution, the reason for which an MRI study was performed. Refers to impaired reading (blurred vision of some letters) associated.

Brain MRI:

In the left hemisphere, a rounded tumor of 28 mm in greater diameter is located inside the lateral ventricle. It is a tumor slightly hypointense on T1, slightly hyperintense on Flair, and practically isointense on T2. The lesion uptakes contrast intense and relatively uniform way. The posterior horn of the ventricle appears dilated and there is a modification of the signal intensity of the adjacent tissue. However, the midline does not appear displaced. the ventricle right lateral and third ventricles are dilated

General anesthesia. Right lateral decubitus position with Mayfield skull clampIncision and craniotomy location with craniometric points (intraparietal point). Left parietal craniotomy with the high-speed motor. U-shaped dural opening with a sagittal sinus base. The postcentral sulcus and intraparietal sulcus are visualized in the cortex. Location of the atrium and tumor with intraoperative ultrasound. Approach through the intraparietal sulcus in its lower portion until the ventricle was opened and a pinkish-colored tumor with a rubbery consistency visible, macroscopically compatible with meningioma. Dissection of the edges at the intraventricular level, separating the choroid plexus and coagulating and sectioning several nutrient arteries. Tumor dissection with CUSA until leaving a small fragment that is dissected from the medial wall of the ventricle and excised. Macroscopically complete resection. Careful hemostasis and abundant washing. Dural closure is almost hermetic and sealed with TachosilBone replacement with titanium trephine plates and plugs. Cutaneous closure by planes. Stapled skin. The sample is sent to pathology.


1)

Yang X, Xiao Z, Xing Z, Lin X, Wang F, Cao D. Grading Trigone Meningiomas Using Conventional Magnetic Resonance Imaging With Susceptibility-Weighted Imaging and Perfusion-Weighted Imaging. J Comput Assist Tomogr. 2022 Jan-Feb 01;46(1):103-109. doi: 10.1097/RCT.0000000000001256. PMID: 35027521.

Linezolid in Neurosurgery

Linezolid in Neurosurgery

Relevant studies were identified through searches of the PubMed, Current Contents, and Cochrane databases (publications archived until October 2006).

Case reports, case series, prospective and retrospective studies, and randomized controlled trials were eligible for inclusion in our review if they evaluated the effectiveness and safety of linezolid for the treatment of patients with CNS infections.

In 18 (42.9%) of the 42 relevant cases identified, patients had undergone neurosurgical operations and/or had prosthetic devices. Meningitis was the most common CNS infection, accounting for 20 (47.6%) cases. Other CNS infections included brain abscesses (14; 33.3%), ventriculitis (5; 11.9%), and ventriculo-peritoneal shunt infection (3; 7.1%). In the 39 patients in whom the responsible pathogen was isolated, those predominantly responsible for the CNS infections were: penicillin-nonsusceptible Streptococcus pneumoniae (7; 17.9%), vancomycin-resistant enterococci (6; 15.4%), Nocardia spp. (5; 12.8%), methicillin-resistant Staphylococcus epidermidis (4; 10.3%), and methicillin-resistant Staphylococcus aureus (3; 7.7%). Of the 42 patients who received linezolid for the treatment of CNS infections, 38 (90.5%) were either cured or showed clinical improvement of the infection. The mean duration of follow-up was 7.2 months; no recurrent CNS infection was reported.

The limited published data suggest that linezolid may be considered for the treatment of patients with CNS infections in cases of failure of previously administered treatment or limited available options 2).

To evaluate the efficacy and safety of SAT with oral linezolid in patients with NSI and to analyse the cost implications, an observational, non-comparative, prospective cohort study was conducted on clinically stable consecutive adult patients at the Neurosurgical Service. Following intravenous treatment, patients were discharged with SAT with oral linezolid.

A total of 77 patients were included. The most common NSIs were: 41 surgical wound infections, 20 subdural empyemas, 18 epidural abscesses, and 16 brain abscesses. Forty-four percent of patients presented two or more concomitant NSIs. Aetiological agents commonly isolated were: Propionibacterium acnes (36 %), Staphylococcus aureus (23 %), Staphylococcus epidermidis (21 %) and Streptococcus spp. (13 %). The median duration of the SAT was 15 days (range, 3-42). The SAT was interrupted in five cases due to adverse events. The remainder of the patients were cured at the end of the SAT. A total of 1,163 days of hospitalisation were saved. An overall cost reduction of €516,188 was attributed to the SAT. Eight patients with device infections did not require removal of the device, with an additional cost reduction of €190,595. The mean cost saving per patient was €9,179.

SAT with linezolid was safe and effective for the treatment of NSI. SAT reduces hospitalisation times, which means significant savings of health and economic resources 3).


Seventeen patients were included in the study. The main comorbidities among these patients included one or more of the following: subarachnoidal or intraventricular hemorrhage (n=8), solid neurological cancer (n=7), corticosteroids(n=9), and hydrocephalus (n=6). Eight patients underwent a craniotomy and fourteen patients had external ventricular drainage (EVD) as a predisposing factor for infection. Meningitis was the most common infection (11; 64.7%), followed by ventriculitis (4; 23.5%) and brain abscesses (2;11.8%). The main causative organisms were coagulase-negative Staphylococcus spp. (13; 76.5%). Linezolid was used as the initial therapy in 8 episodes, after therapy failure in 6, and for other reasons in 3. The oral route was used in 9 (52.9%) episodes; linezolid was initiated orally in 2 cases. The mean duration of treatment was 26.5 days (range 15-58). No adverse events were reported. Sixteen (94.1%) patients were considered cured. There was one recurrence. The mean length of hospital stay was 45.6 (range 15-112) days and the mean duration of follow-up was 7.2 (range 0.4-32) months. No related deaths occurred during active episodes.

Linezolid was mainly indicated in post-neurosurgical EVD-associated infections due to coagulase-negative Staphylococcus spp. It was used as initial therapy in most cases. A high rate of clinical cure was observed and no related adverse events were reported. More than half of the patients benefited from the advantages of the oral route of administration 4).


In order to study the penetration of this antimicrobial into the cerebrospinal fluid (CSF) of such patients, the disposition of linezolid in serum and CSF was studied in 14 neurosurgical patients given linezolid at 600 mg twice daily (1-h intravenous infusion) for the treatment of CNS infections caused by gram-positive pathogens or for prophylactic chemotherapy. Serum and CSF linezolid steady-state concentrations were analyzed by high-pressure liquid chromatography, and the concentration-time profiles obtained were analyzed to estimate pharmacokinetic parameters. The mean +/- standard deviation (SD) linezolid maximum and minimum measured concentrations were 18.6 +/- 9.6 microg/ml and 5.6 +/- 5.0 microg/ml, respectively, in serum and 10.8 +/- 5.7 microg/ml and 6.1 +/- 4.2 microg/ml, respectively, in CSF. The mean +/- SD areas under the concentration-time curves (AUCs) were 128.7 +/- 83.9 microg x h/ml for serum and 101.6 +/- 59.6 microg x h/ml for CSF, with a mean penetration ratio for the AUC for CSF to the AUC for serum of 0.66. The mean elimination half-life of linezolid in CSF was longer than that in serum (19.1 +/- 19.0 h and 6.5 +/- 3.6 h, respectively). The serum and CSF linezolid concentrations exceeded the pharmacodynamic breakpoint of 4 microg/ml for susceptible target pathogens for the entire dosing interval in the majority of patients. These findings suggest that linezolid may achieve adequate concentrations in the CSF of patients requiring antibiotics for the management or prophylaxis of CNS infections caused by gram-positive pathogens 5).


1)

Jahoda D, Nyc O, Pokorný D, Landor I, Sosna A. [Linezolid in the treatment of antibiotic-resistant gram-positive infections of the musculoskeletal system]. Acta Chir Orthop Traumatol Cech. 2006 Oct;73(5):329-33. Czech. PubMed PMID: 17140514.
2)

Ntziora F, Falagas ME. Linezolid for the treatment of patients with central nervous system infection. Ann Pharmacother. 2007 Feb;41(2):296-308. Epub 2007 Feb 6. Review. PubMed PMID: 17284501.
3)

Martín-Gandul C, Mayorga-Buiza MJ, Castillo-Ojeda E, Gómez-Gómez MJ, Rivero-Garvía M, Gil-Navarro MV, Márquez-Rivas FJ, Jiménez-Mejías ME. Sequential antimicrobial treatment with linezolid for neurosurgical infections: efficacy, safety and cost study. Acta Neurochir (Wien). 2016 Oct;158(10):1837-43. doi: 10.1007/s00701-016-2915-0. Epub 2016 Aug 13. PubMed PMID: 27520361.
4)

Sousa D, Llinares P, Meijide H, Gutiérrez JM, Miguez E, Sánchez E, Castelo L, Mena A. Clinical experience with linezolid for the treatment of neurosurgical infections. Rev Esp Quimioter. 2011 Mar;24(1):42-7. PMID: 21412669.
5)

Myrianthefs P, Markantonis SL, Vlachos K, Anagnostaki M, Boutzouka E, Panidis D, Baltopoulos G. Serum and cerebrospinal fluid concentrations of linezolid in neurosurgical patients. Antimicrob Agents Chemother. 2006 Dec;50(12):3971-6. doi: 10.1128/AAC.00051-06. Epub 2006 Sep 18. PMID: 16982782; PMCID: PMC1694012.

Frontal sinus cranialization

Frontal sinus cranialization


Cranialization refers to the removal of the posterior table of the frontal sinus with occlusion of the inlet into the frontonasal ducts and allowing the neural structures, mainly frontal lobes of the brain and the intact dura, to move directly posterior to the anterior table of the frontal bone 1).

Frontal sinus cranialization with closure via bifrontal pericranial flaps is the gold standard for separating the nasofrontal recess from the intracranial cavity for posterior table defects. Despite the high success rate, cerebrospinal fluid (CSF) leak may persist and is particularly challenging when vascularized reconstructive options from the bicoronal incision are exhausted.

For appropriately selected patients with extensive frontal injuries, cranialization is a procedure that provides an excellent margin of long-term safety and a satisfactory esthetic outcome. Individual surgeons will continue to differ at times as to the appropriate management of a particular frontal injury. Nevertheless, for the most severe of these, cranialization continues to be the definitive treatment 2).


In the case series of Donath and Sindwani indications included extensive frontal sinus fractures involving the posterior table (78.9%), mucocele (10.5%), arteriovenous malformation (5.3%), and frontal bone osteomyelitis (5.3%). 3).


For Calis et al. it seems that isolated anterior table fractures with a maximum amount of displacement of less than 4.5 mm can be treated conservatively without leading to contour deformities. CSF leakage in the acute setting might not always require cranialization and this may spontaneously resolve within 10 days. Cranialization should be considered whenever CSF leakage lasts longer than 10 days 4).


For Echo et al. the first step in assessing frontal sinus fractures involves the assessment of the posterior table of the frontal sinus and determining the need for cranialization. Criteria for cranialization include severe posterior table fracture, CSF leak greater than 1 to 2 weeks, or in any situation where a craniotomy is otherwise indicated. Any patient who meets these criteria would undergo a cranialization of the frontal sinus, obliteration of the nasofrontal outflow tracts, and reconstruction of the anterior table 5).


Using a pedicle vascularized pericranial flap as an extra layer and an autologous fence above the dura adds more protection to the brain. This flap may reduce the risk of CSF leak and perioperative infections and improve the overall results. Yet, more prospective and randomized trials are recommended 6).


Cranialization of the frontal sinus appears to be a good option for the prevention of secondary mucocele development after open excision of benign frontal sinus lesions 7).

A retrospective review of 3 patients (all male; ages 42, 43, and 69 yr) with persistent CSF leak despite frontal sinus cranialization and repair with bifrontal pericranium was performed. Etiology of injury was traumatic in 2 patients and iatrogenic in 1 patient after anaplastic meningioma treatment. To create space for the flap and repair the nasofrontal ducts, endoscopic Draf III (Case 1, 3) or Draf IIb left frontal sinusotomy (Case 2) was performed. The forearm flap was harvested, passed through a Caldwell-Luc exposure, and placed within the Draf frontal sinustomy. The flap vessels were tunneled to the left neck and anastomosed to the facial vessels by the mandibular notch.

Intraoperatively, the flaps were well-seated and provided a watertight seal. Postoperative hospital courses were uncomplicated. There were no new CSF leaks or flap necrosis at 12, 14, and 16 mo.

Endoscopic endonasal free flap reconstruction through a Draf procedure is a novel viable option for persistent CSF leak after failed frontal sinus cranialization 8).


Soto et al. presented the outcome data from 28 cases of frontal sinus trauma due to gunshot wounds. There was a statistically significant difference (P = 0.049) in the type reconstructive strategy employed with each type of flap, with pericranial flaps primarily used in cranialization, temporal grafts were more likely to be used in obliteration, and free flaps were more likely to be used in cranialization. The overall major complication rate was 52% (P = 0.248), with the most common acute major complication being cerebrospinal fluid leak (39%) and the major chronic was an abscess (23.5%).

This report explores the management of frontal sinus trauma and presents short-term outcomes of treatment for penetrating gunshot wounds at a tertiary referral center 9).


Shin et al. suggested a combination flap of galea and reverse temporalis muscle as a method for reconstruction of huge skull base defect.

From 2016 to 2019, a retrospective review was conducted, assessing 7 patients with bone defect which is not just opening of frontal sinus but extends to frontal sinus and cribriform plate. Reconstructions were done by combination of galeal flap and reverse temporalis muscle flap transposition.

Defects were caused by nasal cavity tumor with intracranial extension or brain tumor with nasal cavity extension. There was no major complication in every case. During the follow up period, no patient had signs of complication such as ascending infection, herniation and CSF rhinorrhea. Postoperative radiologic images of all patients that were taken at least 6 months after the surgery showed that flaps maintained the lining and the volume well.

Conventional reconstruction of skull base defect with galeal flap is not effective enough to cover the large sized defect. In conclusion, galeal flap in combination with reverse temporalis muscle flap can effectively block the communication of nasal cavity and intracranium 10).


19 patients underwent (bilateral) frontal sinus cranialization with the pericranial flap between 2000 and 2005. Indications included extensive frontal sinus fractures involving the posterior table (78.9%), mucocele (10.5%), arteriovenous malformation (5.3%), and frontal bone osteomyelitis (5.3%). There were no intraoperative complications. A postoperative cerebrospinal fluid leak occurred in one patient with extensive skull base injuries. This was repaired endoscopically. Follow-up ranged from 9 to 55 months.

The pericranial flap is easily harvested and versatile. Using this vascularized tissue during cranialization affords added protection by providing an extra barrier between the intracranial cavity and the frontal bone and sinonasal tract. This technique is inexpensive, safe, and effective and should be considered when cranialization of the frontal sinus is performed 11).

A 47-year-old man with adenoid cystic carcinoma who underwent secondary reconstruction of the frontal bone with a split-iliac crest bone flap based on the deep circumflex iliac artery. The patient’s course following an initial ablative procedure was complicated by recurrent periorbital cellulitis, radiation, and eventual recurrence of the malignancy. Reconstructive requirements included restoration of the superior orbital rim, cranialization of the frontal sinus, and reconstruction of a sizeable frontal bone defect. In this setting, the iliac crest served as an excellent reconstructive option owing to its natural curvature and large surface area. The split-iliac crest deep circumflex iliac artery bone flap offers a robust and valuable reconstructive option for calvarial defects in hostile surgical fields 12).


2)

Ruggiero, F. P., & Zender, C. A. (2010). Frontal sinus cranialization. Operative Techniques in Otolaryngology-Head and Neck Surgery, 21(2), 143-146. https://doi.org/10.1016/j.otot.2010.03.001
3) , 11)

Donath A, Sindwani R. Frontal sinus cranialization using the pericranial flap: an added layer of protection. Laryngoscope. 2006 Sep;116(9):1585-8. doi: 10.1097/01.mlg.0000232514.31101.39. PMID: 16954984.
4)

Calis M, Kaplan GO, Küçük KY, Altunbulak AY, Akgöz Karaosmanoğlu A, Işıkay Aİ, Mavili ME, Tunçbilek G. Algorithms for the management of frontal sinus fractures: A retrospective study. J Craniomaxillofac Surg. 2022 Oct 4:S1010-5182(22)00144-5. doi: 10.1016/j.jcms.2022.09.007. Epub ahead of print. PMID: 36220677.
5)

Echo A, Troy JS, Hollier LH Jr. Frontal sinus fractures. Semin Plast Surg. 2010 Nov;24(4):375-82. doi: 10.1055/s-0030-1269766. PubMed PMID: 22550461; PubMed Central PMCID: PMC3324222.
6)

Hammad W, Mahmoud B, Alsharif S. Frontal sinus cranialization using pericranial flap: Experience in thirty cases. Saudi J Otorhinolaryngol Head Neck Surg 2021;23:55-9
7)

Horowitz G, Amit M, Ben-Ari O, Gil Z, Abergel A, Margalit N, et al. (2013) Cranialization of the Frontal Sinus for Secondary Mucocele Prevention following Open Surgery for Benign Frontal Lesions. PLoS ONE 8(12): e83820. https://doi.org/10.1371/journal.pone.0083820
8)

Lee JJ, Wick EH, Chicoine MR, Dowling JL, Leuthardt EC, Santiago P, Pipkorn P. Endonasal Free Flap Reconstruction Combined With Draf Frontal Sinusotomy for Complex Cerebrospinal Fluid Leak: A Technical Report & Case Series. Oper Neurosurg (Hagerstown). 2021 Nov 15;21(6):478-484. doi: 10.1093/ons/opab309. PMID: 34423844; PMCID: PMC8599085.
9)

Soto E, Ovaitt AK, Clark AR, Tindal RR, Chiasson KF, Aryanpour Z, Ananthasekar S, Grant JH, Myers RP. Reconstructive Management of Gunshot Wounds to the Frontal Sinus: An Urban Trauma Center’s Perspective. Ann Plast Surg. 2021 Jun 1;86(6S Suppl 5):S550-S554. doi: 10.1097/SAP.0000000000002857. PMID: 33883442; PMCID: PMC8187270.
10)

Shin D, Yang CE, Kim YO, Hong JW, Lee WJ, Lew DH, Chang JH, Kim CH. Huge Anterior Skull Base Defect Reconstruction on Communicating Between Cranium and Nasal Cavity: Combination Flap of Galeal Flap and Reverse Temporalis Flap. J Craniofac Surg. 2020 Feb 7. doi: 10.1097/SCS.0000000000006221. [Epub ahead of print] PubMed PMID: 32049922.
12)

Baudoin ME, Palines PA, Stalder MW. Frontal Cranioplasty with Vascularized Split-iliac Crest Bone Flap. Plast Reconstr Surg Glob Open. 2021 Nov 16;9(11):e3934. doi: 10.1097/GOX.0000000000003934. PMID: 34796087; PMCID: PMC8594656.

Cerebellar pilocytic astrocytoma

Cerebellar pilocytic astrocytoma

Latest news


Key concepts

● Often cystic, half of these have a mural nodule.

● Usually presents during the second decade of life (ages 10–20 yrs).

● A subtype of pilocytic astrocytoma. Formerly referred to by the nonspecific and confusing term cystic cerebellar astrocytoma.

Epidemiology

Cerebellar pilocytic astrocytoma epidemiology.

Classification

Children

see Cerebellar pilocytic astrocytoma in children.

Adult

Cerebellar pilocytic astrocytomas in adults should be treated with macroscopic complete surgical resection whenever possible. If this is achieved, long-term survival rates are excellent, whereas subtotal resection carries a high risk of tumor recurrence. Ki67 is less important prognostically than the extent of initial resection 1).

Clinical features

In the posterior fossa tumors, there is predominantly a mass effect with signs of raised intracranial pressure, especially when hydrocephalus is present. Bulbar palsy or cerebellar syndrome may also be present.

Diagnosis

Cerebellar pilocytic astrocytoma diagnosis.

Differential diagnosis

Cerebellar pilocytic astrocytoma differential diagnosis.

Treatment

see Cerebellar pilocytic astrocytoma treatment.

Outcome

Nine percent of the children in a study underwent repeated surgery due to progressive tumor recurrence, and 15% were treated for persistent hydrocephalus 2).

The long-term functional outcome of low-grade cerebellar astrocytoma is generally favourable, in the absence of post-operative complications and brainstem involvement. No major impact of neurological deficits, cognitive functions and emotional disorders on academic achievement and independent functioning was observed 3).

The good long-term outcomes suggest that it may be appropriate to do incomplete resection rather than risk additional neurological deficit 4).

There is controversy about whether patients with tumor remaining after surgery should receive radiation therapy. It is also unclear whether only patients with incomplete resection require follow-up and for how long 5).

Complications

Acute hemorrhagic presentation in pilocytic astrocytomas (PAs) has become increasingly recognized. This type of presentation poses a clinically emergent situation in those hemorrhages arising in PAs of the cerebellum, the most frequent site, because of the limited capacity of the posterior fossa to compensate for mass effect, predisposing to rapid neurological deterioration.

Complete resection

Complete resection of cerebellar astrocytoma is an important prognostic factor, indicating a more favorable prognosis than subtotal resection. This was also the conclusion of a much larger study by Villarejo et al. who reviewed 203 cases of low-grade cerebellar astrocytoma 6).

Loh et al., documented that patients with subtotal removal of cerebellar astrocytoma can have arrested tumor growth or spontaneous tumor regression during long-term follow-up. Following partial resection of pediatric cerebellar astrocytoma, they recommend that the patients be followed up a “wait and see” approach with surveillance using MRI. They found that several tumors treated with radiotherapy after surgery had malignant transformation and do not recommend adjuvant radiation treatment for children with cerebellar astrocytoma who have subtotal resection. More research is needed on the prognosis of patients with subtotal resection of cerebellar astrocytoma 7).

Pilomyxoid features and anaplasia

A subset may behave in a more aggressive fashion and clinically progress despite the use of conventional treatments. Histologic features associated with a more aggressive course include the presence of monomorphous pilomyxoid features (ie, pilomyxoid variant) and anaplasia in the form of brisk mitotic activity with or without necrosis 8).

Case series

Cerebellar pilocytic astrocytoma case series.

Case reports

Cerebellar pilocytic astrocytoma case reports.

References


1) 

Wade A, Hayhurst C, Amato-Watkins A, Lammie A, Leach P. Cerebellar pilocytic astrocytoma in adults: a management paradigm for a rare tumour. Acta Neurochir (Wien). 2013 Aug;155(8):1431-5. doi: 10.1007/s00701-013-1790-1. Epub 2013 Jun 22. PubMed PMID: 23793962.

2) 

Due-Tønnessen BJ, Lundar T, Egge A, Scheie D. Neurosurgical treatment of low-grade cerebellar astrocytoma in children and adolescents: a single consecutive institutional series of 100 patients. J Neurosurg Pediatr. 2013 Mar;11(3):245-9. doi: 10.3171/2012.11.PEDS12265. Epub 2012 Dec 14. PubMed PMID: 23240848.

3) 

Ait Khelifa-Gallois N, Laroussinie F, Puget S, Sainte-Rose C, Dellatolas G. Long-term functional outcome of patients with cerebellar pilocytic astrocytoma surgically treated in childhood. Brain Inj. 2014 Nov 10:1-8. [Epub ahead of print] PubMed PMID: 25383654.

4) 

Steinbok P, Mangat JS, Kerr JM, Sargent M, Suryaningtyas W, Singhal A, Cochrane D. Neurological morbidity of surgical resection of pediatric cerebellar astrocytomas. Childs Nerv Syst. 2013 Aug;29(8):1269-75. doi: 10.1007/s00381-013-2171-z. Epub 2013 May 29. PubMed PMID: 23715810.

5) 

Dirven CM, Mooij JJ, Molenaar WM. Cerebellar pilocytic astrocytoma: a treatment protocol based upon analysis of 73 cases and a review of the literature. Childs Nerv Syst. 1997;13:17–23. doi: 10.1007/s003810050033.

6) 

Villarejo F, Diego JMB, Riva AG. Prognosis of cerebellar astrocytoma in children. Childs Nerv Syst. 2008;24:203–210. doi: 10.1007/s00381-007-0449-8.

7) 

Loh JK, Lieu AS, Chai CY, Hwang SL, Kwan AL, Wang CJ, Howng SL. Arrested growth and spontaneous tumor regression of partially resected low-grade cerebellar astrocytomas in children. Childs Nerv Syst. 2013 Nov;29(11):2051-5. doi: 10.1007/s00381-013-2113-9. Epub 2013 May 1. PubMed PMID: 23632690; PubMed Central PMCID: PMC3825417.

8) 

Rodriguez FJ, Scheithauer BW, Burger PC, Jenkins S, Giannini C. Anaplasia in pilocytic astrocytoma predicts aggressive behavior. Am J Surg Pathol. 2010;34(2):147–160.

Microvascular decompression for hemifacial spasm

Microvascular decompression for hemifacial spasm

see also Hemifacial spasm treatment.


Many ablative procedures are effective for hemifacial spasm (HFS) (including sectioning of divisions of the facial nerve), however, this leaves the patient with some degree of facial paresis. The current procedure of choice for HFS is microvascular decompression (MVD) wherein the offending vessel is physically moved off of the nerve, and a sponge (e.g. Ivalon®, polyvinyl formyl alcohol foam) is interposed as a cushion. Other cushions may not prove to be as satisfactory (muscle may disappear, and Teflon felt may thin 1)).

Most often, the offending vessel approaches the nerve at a right angle, and causes grooving in the nerve. Compression must occur at the root exit zone; decompression of vessels impinging distal to this area is usually ineffective.

Intra-operative brainstem auditory evoked potentials (BAER), 2) or more applicable, direct VIII nerve monitoring 3) may help prevent hearing loss during MVD for 7th or 8th nerve dysfunction. Furthermore, monitoring for the disappearance of the (delayed) synkinetic response may aid in determining when adequate decompression has been achieved (generally reserved for teaching institutions) 4).

The facial nerve should not be manipulated, and one should avoid dissection around the VII and VIII nerves near the IAC 5). Vessels must be preserved, especially the cochlear artery and small perforators. Place gentle medial traction on the cerebellum (<1 cm is recommended 6) ), and incise the arachnoid membrane between the flocculus and the eighth nerve (to avoid tension on nerves that could cause post-op deficit). The IX nerve may be followed medially from the jugular foramen to locate the origin of the VII nerve (the origin of VII is 4 mm cephalad and 2 mm anterior to that of the IX nerve 7)).


Redo MVD remains a feasible treatment option for HFS patients who have failed to benefit from prior MVD, but is associated with higher risks of cranial nerve and vascular injuries 8).

Three-dimensional reconstructions were found to provide much clearer characterization of this area than traditional preoperative imaging. Therefore, Teton et al., suggest that use of these reconstructions in the preoperative setting has the potential to help identify appropriate surgical candidates, guide preoperative planning, and thus improve outcome in patients with HFS 9).

The classic surgical position for microvascular decompression (MVD) is lateral decubitus position with the head rotated 10 degrees away from the affected side.

Ko et al. measured the angles of the posterior fossa, specifically focusing on the surgical corridors used in MVD surgery for hemifacial spasm (HFS), to identify the proper surgical position.

The following parameters were assessed on preoperative magnetic resonance images (MRI): petrous angle (PA), sigmoid angle (SA), sigmoid diameter (SD), and root exit zone-sigmoid sinus edge angle (REZ-SEA).

The mean PA was 59.7 ± 5.6 degrees, SA was 16.8 ± 8.6 degrees, SD was 13.4 ± 3.5 mm, and the mean REZ-SEA was 59.6 ± 5.8 degrees. The difference between the maximum SA to avoid cerebellar hemisphere injury and the minimum REZ-SEA required to verify the facial nerve REZ is assumed to be the usable range of angles for the operative microscope; the average midpoint of this range was 38.2 ± 6.4 degrees.

Turning the patient’s head 10 degrees away from the affected side was generally appropriate for performing MVD surgery because it provided a mean microscope angle of 48 degrees. However, some patients had corner values for the sigmoid angle, REZ-SEA, and sigmoid sinus diameter. Rotating a patient’s head based on precise calculations from preoperative MRI helps to achieve successful surgery 10).

“5–5-5” incision (5mm medial, extending 5cm up to 5cm down), used for approach to seventh/ eighth nerve complex:

A video demonstrates the surgical steps of a MVD at left facial REZ in a 41-year-old man who presented with typical hemifacial spasm on the left side due to VIIth nerve REZ compression by PICA. A classical retromastoid and infrafloccular approach was performed to avoid stretching of the VIIIth nerve and access the VIIth nerve ventro-caudally. The next step is insertion-along the brainstem, VII-VIIIth nerves REZ, and flocculus-of a plaque made of Teflon felt (Edward-type) which is semi-rigid, and by principle does not exert direct compression on the facial REZ, thus avoiding compression and/or transmission of pulsations on the VIIth nerve. The patient’s postoperative period was uneventful and clinical outcome good 11)

Postoperative neurocritical intensive care unit (NICU) admission of patients who underwent craniotomy for close observation is common practice. Hatipoglu Majernik et al. performed a comparative analysis to determine if there is a real need for NICU admission after microvascular decompression (MVD) for cranial nerve disorders or whether it may be abandoned. The study evaluates a consecutive series of 236 MVD surgeries performed for treatment of trigeminal neuralgia (213), hemifacial spasm (17), vagoglossopharyngeal neuralgia (2), paroxysmal vertigo (2), and pulsatile tinnitus (2). All patients were operated by the senior surgeon according to a standard protocol over a period of 12 years. Patients were admitted routinely to NICU during the first phase of the study (phase I), while in the second phase (phase II), only patients with specific indications would go to NICU. While 105 patients (44%) were admitted to NICU postoperatively (phase I), 131 patients (56%) returned to the ward after a short stay in a postanaesthesia care unit (PACU) (phase II). Specific indications for NICU admission in phase I were pneumothorax secondary to central venous catheter insertion (4 patients), AV block during surgery, low blood oxygen levels after extubation, and postoperative dysphagia and dysphonia (1 patient, respectively). There were no significant differences in the distribution of ASA scores or the presence of cardiac and pulmonary comorbidities like congestive heart failure, arterial hypertension, or chronic obstructive pulmonary disease between groups. There were no secondary referrals from PACU to NICU. Our study shows that routine admission of patients after eventless MVD to NICU does not provide additional value. NICU admission can be restricted to patients with specific indications. When MVD surgery is performed in experienced hands according to a standard anaesthesia protocol, clinical observation on a neurosurgical ward is sufficient to monitor the postoperative course. Such a policy results in substantial savings of costs and human resources 12).

Al Menabbawy et al. extracted retrospective data of patients who received Indocyanine green videoangiography from a prospectively maintained database for microvascular decompression. They noted relevant data including demographics, offending vessels, operative technique, outcome, and complications.

Out of the 438 patients, 15 patients with a mean age (SD) of 53 ± 10.5 years underwent intraoperative ICG angiography. Male: female was 1:1.14. The mean disease duration prior to surgery was 7.7 ± 5.3 years. The mean follow-up (SD) was 50.7 ± 42.0 months. In 14 patients, the offending vessel was an artery, and in one patient, a vein. Intraoperative readjustment of the Teflon pledget or sling was required in 20% (3/15) of the cases. No patient had any sort of brainstem ischemia. Eighty percent of the patients (12/15) experienced complete resolution of the spasms. 86.7% (13/15) of the patients reported a satisfactory outcome with marked improvement of the spasms. Three patients experienced slight hearing affection after surgery, which improved in two patients later. There was no facial or lower cranial nerve affection.

Intraoperative ICG is a safe tool for evaluating the flow within the brain stem perforators and avoiding brainstem stroke in MVD for hemifacial spasm 13).


1)

Rhoton AL. Comment on Payner T D and Tew J M: Recurrence of Hemifacial Spasm After Microvascular Decompression. Neurosurgery. 1996; 38
2)

Friedman WA, Kaplan BJ, Gravenstein D, et al. Int raoperative Brain-Stem Auditory Evoked Potentials During Posterior Fossa Microvascular Decompression. J Neurosurg. 1985; 62:552–557
3)

Moller AR, Jannetta PJ. Monitoring Auditory Functions During Cranial Nerve Microvascular Decompression Operations by Direct Recording from the Eighth Nerve. J Neurosurg. 1983; 59:493–499
4)

Moller AR, Jannetta PJ. Microvascular Decompression in Hemifacial Spasm: Intraoperative Electrophysiological Observations. Neurosurgery. 1985; 16:612–618
5) , 6)

Fukushima T, Carter LP, Spetzler RF, Hamilton MG. In: Microvascular Decompression for Hemifacial Spasm: Results in 2890 Cases. Neurovascular Surgery. New York: McGraw-Hill; 1995:1133–1145
7)

Rhoton AL. Microsurgical Anatomy of the Brainstem Surface Facing an Acoustic Neuroma. Surg Neurol. 1986; 25:326–339
8)

Lee S, Park SK, Lee JA, Joo BE, Park K. Missed Culprits in Failed Microvascular Decompression Surgery for Hemifacial Spasm and Expenses for Redo Surgery. World Neurosurg. 2019 May 31. pii: S1878-8750(19)31508-6. doi: 10.1016/j.wneu.2019.05.231. [Epub ahead of print] PubMed PMID: 31158550.
9)

Teton ZE, Blatt D, Holste K, Raslan AM, Burchiel KJ. Utilization of 3D imaging reconstructions and assessment of symptom-free survival after microvascular decompression of the facial nerve in hemifacial spasm. J Neurosurg. 2019 Jul 12:1-8. doi: 10.3171/2019.4.JNS183207. [Epub ahead of print] PubMed PMID: 31299649.
10)

Ko HC, Lee SH, Shin HS. Proper Head Rotation when Performing Microvascular Decompression for Hemifacial Spasm: An Orthometric Consideration Based on Preoperative MRI. J Neurol Surg A Cent Eur Neurosurg. 2022 Feb 15. doi: 10.1055/s-0041-1725950. Epub ahead of print. PMID: 35170003.
11)

Sindou M, Esqueda-Liquidano M, Brinzeu A. Microvascular Decompression for Hemifacial Spasm. Neurosurgery. 2014 Sep 24. [Epub ahead of print] PubMed PMID: 25255262.
12)

Hatipoglu Majernik G, Wolff Fernandes F, Al-Afif S, Heissler HE, Palmaers T, Atallah O, Scheinichen D, Krauss JK. Routine postoperative admission to the neurocritical intensive care unit after microvascular decompression: necessary or can it be abandoned? Neurosurg Rev. 2022 Dec 9;46(1):12. doi: 10.1007/s10143-022-01910-4. PMID: 36482263.
13)

Al Menabbawy A, Refaee EE, Shoubash L, Matthes M, Schroeder HWS. The value of intraoperative indocyanine green angiography in microvascular decompression for hemifacial spasm to avoid brainstem ischemia. Acta Neurochir (Wien). 2022 Oct 27. doi: 10.1007/s00701-022-05389-2. Epub ahead of print. Erratum in: Acta Neurochir (Wien). 2022 Nov 28;: PMID: 36289111.

Pediatric traumatic brain injury outcome

Pediatric traumatic brain injury outcome


Neuropsychological and behavioral outcomes for injured children vary with the severity of the injury, child age at injury, premorbid child characteristics, family factors, and the family’s socioeconomic status. Each of these factors needs to be taken into account when designing rehabilitation strategies and assessing factors related to outcomes 1)


The Functional Status Score (FSS) can be implemented as part of routine practice in two different healthcare systems and the relationships observed between the FSS and patient characteristics can serve as a baseline for work going forward in the coming years. As a field, establishing which outcomes tests can be readily administered while also measuring relevant outcomes for various populations of children with TBI is an essential next step in developing therapies for this disorder that is highly prevalent and morbid 2).


The multi-center, prospectively collected CENTER-TBI core and registry databases were screened and patients were included when younger than 18 years at enrollment and admitted to the regular ward (admission stratum) or intensive care unit (ICU stratum) following TBI. Patient demographics, injury causes, clinical findings, brain CT imaging details, and outcome (GOSE at 6 months follow-up) were retrieved and analyzed. Injury characteristics were compared between patients admitted to the regular ward and ICU and a multivariate analysis of factors predicting an unfavorable outcome (GOSE 1-4) was performed. Results from the core study were compared to the registry dataset which includes larger patient numbers but no follow-up data. Results: Two hundred and twenty-seven patients in the core dataset and 687 patients in the registry dataset were included in this study. In the core dataset, road-traffic incidents were the most common cause of injury overall and in the ICU stratum, while incidental falls were most common in the admission stratum. Brain injury was considered serious to severe in the majority of patients and concurrent injuries in other body parts were very common. Intracranial abnormalities were detected in 60% of initial brain CTs. Intra- and extracranial surgical interventions were performed in one-fifth of patients. The overall mortality rate was 3% and the rate of unfavorable outcomes was 10%, with those numbers being considerably higher among ICU patients. GCS and the occurrence of secondary insults could be identified as independent predictors of an unfavorable outcome 3).


There are few specific prognostic models specifically developed for the pediatric traumatic brain injury (TBI) population.


Fang et al. aimed to combine multiple machine learning approaches to building hybrid models for predicting the prognosis and length of hospital stay for adults and children with TBI.

They collected relevant clinical information from patients treated at the Neurosurgery Center of the Second Affiliated Hospital of Anhui Medical University between May 2017 and May 2022, of which 80% was used for training the model and 20% for testing via screening and data splitting. They trained and tested the machine learning models using 5 cross-validations to avoid overfitting. In the machine learning models, 11 types of independent variables were used as input variables and the Glasgow Outcome Scale score, was used to evaluate patients’ prognosis, and patient length of stay was used as the output variable. Once the models were trained, we obtained and compared the errors of each machine-learning model from 5 rounds of cross-validation to select the best predictive model. The model was then externally tested using clinical data of patients treated at the First Affiliated Hospital of Anhui Medical University from June 2021 to February 2022.

Results: The final convolutional neural network-support vector machine (CNN-SVM) model predicted the Glasgow Outcome Scale score with an accuracy of 93% and 93.69% in the test and external validation sets, respectively, and an area under the curve of 94.68% and 94.32% in the test and external validation sets, respectively. The mean absolute percentage error of the final built convolutional neural network-support vector regression (CNN-SVR) model predicting inpatient time in the test set and external validation set was 10.72% and 10.44%, respectively. The coefficient of determination (R2) was 0.93 and 0.92 in the test set and external validation set, respectively. Compared with a back-propagation neural network, CNN, and SVM models built separately, our hybrid model was identified to be optimal and had high confidence.

This study demonstrates the clinical utility of 2 hybrid models built by combining multiple machine learning approaches to accurately predict the prognosis and length of stay in hospital for adults and children with TBI. Application of these models may reduce the burden on physicians when assessing TBI and assist clinicians in the medical decision-making process 4).


Mikkonen et al., tested the predictive performance of existing prognostic tools, originally developed for the adult TBI population, in pediatric TBI patients requiring stays in the ICU.

They used the Finnish Intensive Care Consortium database to identify pediatric patients (< 18 years of age) treated in 4 academic ICUs in Finland between 2003 and 2013. They tested the predictive performance of 4 classification systems-the International Mission for Prognosis and Analysis of Clinical Trials (IMPACT) TBI model, the Helsinki CT score, the Rotterdam CT score, and the Marshall CT classification-by assessing the area under the receiver operating characteristic curve (AUC) and the explanatory variation (pseudo-R2 statistic). The primary outcome was 6-month functional outcome (favorable outcome defined as a Glasgow Outcome Scale score of 3-5).

Overall, 341 patients (median age 14 years) were included; of these, 291 patients had primary head CT scans available. The IMPACT core-based model showed an AUC of 0.85 (95% CI 0.78-0.91) and a pseudo-R2 value of 0.40. Of the CT scoring systems, the Helsinki CT score displayed the highest performance (AUC 0.84, 95% CI 0.78-0.90; pseudo-R2 0.39) followed by the Rotterdam CT score (AUC 0.80, 95% CI 0.73-0.86; pseudo-R2 0.34).

Prognostic tools originally developed for the adult TBI population seemed to perform well in pediatric TBI. Of the tested CT scoring systems, the Helsinki CT score yielded the highest predictive value 5).


1)

Keenan HT, Bratton SL. Epidemiology and outcomes of pediatric traumatic brain injury. Dev Neurosci. 2006;28(4-5):256-63. doi: 10.1159/000094152. PMID: 16943649.
2)

Bell MJ. Outcomes for Children With Traumatic Brain Injury-How Can the Functional Status Scale Contribute? Pediatr Crit Care Med. 2016 Dec;17(12):1185-1186. doi: 10.1097/PCC.0000000000000950. PMID: 27918390; PMCID: PMC5142208.
3)

Riemann L, Zweckberger K, Unterberg A, El Damaty A, Younsi A; Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) Investigators and Participants. Injury Causes and Severity in Pediatric Traumatic Brain Injury Patients Admitted to the Ward or Intensive Care Unit: A Collaborative European Neurotrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) Study. Front Neurol. 2020 Apr 30;11:345. doi: 10.3389/fneur.2020.00345. PMID: 32425879; PMCID: PMC7205018.
4)

Fang C, Pan Y, Zhao L, Niu Z, Guo Q, Zhao B. A Machine Learning-Based Approach to Predict Prognosis and Length of Hospital Stay in Adults and Children With Traumatic Brain Injury: Retrospective Cohort Study. J Med Internet Res. 2022 Dec 9;24(12):e41819. doi: 10.2196/41819. PMID: 36485032.
5)

Mikkonen ED, Skrifvars MB, Reinikainen M, Bendel S, Laitio R, Hoppu S, Ala-Kokko T, Karppinen A, Raj R. Validation of prognostic models in intensive care unit-treated pediatric traumatic brain injury patients. J Neurosurg Pediatr. 2019 Jun 7:1-8. doi: 10.3171/2019.4.PEDS1983. [Epub ahead of print] PubMed PMID: 31174193.