Aneurysmal subarachnoid hemorrhage outcome

Aneurysmal subarachnoid hemorrhage outcome

Latest PubMed aneurysmal subarachnoid hemorrhage outcome related Articles

Aneurysmal subarachnoid hemorrhage (aSAH) is a complex neurovascular syndrome with profound systemic effects, associated with high rates of disability and mortality.

see also Subarachnoid hemorrhage outcome.

Aneurysmal subarachnoid hemorrhage complications

Aneurysmal subarachnoid hemorrhage complications.

Quality of life

Quality of life after aneurysmal subarachnoid hemorrhage.

Aneurysmal Subarachnoid Hemorrhage Outcome in Elderly Patients

Aneurysmal Subarachnoid Hemorrhage Outcome in Elderly Patients.

Cognitive outcome

Cognitive outcome after aneurysmal subarachnoid hemorrhage.

Obesity

Obesity in aneurysmal subarachnoid hemorrhage.

Factors

CSF metabolomics

Several studies have investigated the changes in CSF metabolomics that occur after aSAH. These studies have identified alterations in various metabolites and metabolic pathways, including those involved in energy metabolism, amino acid metabolism, and lipid metabolism.

One study found that levels of lactate, a marker of anaerobic metabolism, were significantly increased in the CSF of aSAH patients compared to controls. This suggests that there is a shift towards anaerobic metabolism in the brain following aSAH, possibly due to decreased oxygen delivery and increased metabolic demand.

Other studies have reported alterations in amino acid metabolism, particularly involving glutamate and gamma-aminobutyric acid (GABA). Glutamate is an excitatory neurotransmitter that can lead to neuronal damage when present in excess, while GABA is an inhibitory neurotransmitter that can protect against excitotoxicity. Studies have shown that CSF levels of glutamate are increased and GABA levels are decreased in aSAH patients, which may contribute to the pathophysiology of the disease.

Alterations in lipid metabolism have also been reported in aSAH patients, with decreased levels of sphingomyelins and phosphatidylcholines in the CSF. These lipids play important roles in cellular membrane structure and function, and their depletion may contribute to neuronal damage and inflammation.

Overall, the findings of metabolomics studies suggest that aSAH leads to widespread metabolic alterations in the brain, involving multiple metabolic pathways. These alterations may contribute to the pathophysiology of the disease and represent potential targets for therapeutic intervention.

There is increasing evidence suggesting that biomarkers can give insight into the aneurysmal subarachnoid hemorrhage pathogenesis and can serve as an outcome predictor 1)

NFE2L2

NFE2L2 SNP, rs10183914, is significantly associated with aneurysmal subarachnoid hemorrhage outcome. This is consistent with a clinically relevant pathophysiological role for oxidative and inflammatory brain injury due to blood and its breakdown products in aSAH. Furthermore, the findings support NRF2 as a potential therapeutic target following aSAH and other forms of intracranial hemorrhage 2)

In a study by Hammer et al. from the Paracelsus Medical University, complications like pneumonia (β = 5.11; 95% CI = 1.75-8.46; p = 0.0031), sepsis (β = 9.54; 95% CI = 3.27-15.82; p = 0.0031), hydrocephalus (β = 4.63; 95% CI = 1.82-7.45; p = 0.0014), and delayed cerebral ischemia (DCI) (β = 3.38; 95% CI = 0.19-6.56; p = 0.038) were critical factors depending on the LOS in intensive care as well as decompressive craniectomy (β = 5.02; 95% CI = 1.35-8.70; p = 0.0077). All analyzed comorbidities such as hypertension, diabetes, hypothyroidism, cholesterolemia, and smoking history had no significant impact on the LOS in intensive care. LOS in intensive care (OR = 1.09; 95% CI = 1.03-1.15; p = 0.0023), as well as World Federation of Neurosurgical Societies grading for subarachnoid hemorrhage (OR = 3.72; 95% CI = 2.23-6.21; p < 0.0001) and age (OR = 1.06; 95% CI = 1.02-1.10; p = 0.0061), were significant factors that had an impact on the outcome after 1 year. Complications in intensive care but not comorbidities are associated with higher LOS in intensive care. LOS in intensive care is a modest but significant predictor of outcomes after subarachnoid hemorrhage 3).

Aneurysmal subarachnoid hemorrhage (aSAH) occurs in about 5% of all strokes and has still a mortality of 50% and a significant morbidity in survivors 4).

The second cause of disability after the initial hemorrhage is cerebral vasospasm and the delayed cerebral ischemia which occurs in 50–70% of patients 5).

These two pathological entities seem to have different pathophysiological etiologies and cannot be detected by the same techniques. Vasospasms of the vessels of the circle of Willis can be detected by transcranial Doppler ultrasonography (TCD), whereas microcirculation disturbances can be detected by perfusion imaging techniques. Digital subtraction angiography (DSA) remains until now the gold standard of imaging vasospasms, but it is invasive, and it is proven to be associated with the risk of mild neurological deficit as well as ischemic insults 6).

As angiographic vasospasm is strongly associated with delayed cerebral ischemia (DCI) and clinical outcome, clinical trials in the last few decades focused on prevention of these angiographic spasms. Despite all efforts, no new pharmacological agents have shown to improve patient outcome. As such, it has become clear that our understanding of the pathophysiology of SAH is incomplete and we need to reevaluate our concepts on the complex pathophysiological process following SAH. Angiographic vasospasm is probably important.

The case fatality in aneurysmal subarachnoid hemorrhage (aSAH) is 50% due to the initial hemorrhage or subsequent complications like aneurysm rebleeding or delayed cerebral ischemia (DCI).

One factor that might influence the initial brain damage or subsequent complications is the use of antiplatelet medication before the initial hemorrhage.

Improvements in multidisciciplinary neurocritical care and advancements in medical and surgical treatment have contributed to a decline in the case fatality rate of aneurysmal subarachnoid hemorrhage 7).

A greater proportion of patients, therefore, are surviving their initial hemorrhagic event but remain at increased risk of a number of complications.

see Aneurysmal subarachnoid hemorrhage complications.

The case fatality after aneurysmal haemorrhage is 50%; one in eight patients with subarachnoid haemorrhage dies outside hospital. Rebleeding is the most imminent danger; a first aim is therefore occlusion of the aneurysm 8).

Prothrombotic states of early brain injury (EBI) and delayed cerebral ischemia (DCI) after aSAH determine morbidity and mortality.

The outcome depends on their condition on arrival at the hospital. However, a small number of patients recover from an initially poor condition.

Associated with intracerebral hematoma (ICH) typically has a poor outcome. SAH with ICH tends to have a worse prognosis than SAH alone.

It has a high socioeconomic impact as it tends to affect younger patients. The NCEPOD study looking into management of aSAH has recommended that neurovascular units in the United Kingdom should aim to secure cerebral aneurysms within 48 h and that delays because of weekend admissions can increase the mortality and morbidity attributed to aSAH.

A study provides important data showing excess in-Hospital mortality of patients with SAH on weekend admissions served by the United Kingdom’s National Health Service.; However, there were no effects of weekend admission on long-term outcomes 9).

Prediction models

Clinical prediction models were developed with individual patient data from 10 936 patients and validated with data from 3355 patients after development of the model. In the validation cohort, a core model including patient age, premorbid hypertension, and neurological grade on admission to predict risk of functional outcome had good discrimination, with an area under the receiver operator characteristics curve (AUC) of 0.80 (95% confidence interval 0.78 to 0.82). When the core model was extended to a “neuroimaging model,” with inclusion of clot volume, aneurysm size, and location, the AUC improved to 0.81 (0.79 to 0.84). A full model that extended the neuroimaging model by including treatment modality had AUC of 0.81 (0.79 to 0.83). Discrimination was lower for a similar set of models to predict risk of mortality (AUC for full model 0.76, 0.69 to 0.82). All models showed satisfactory calibration in the validation cohort.

The prediction models reliably estimate the outcome of patients who were managed in various settings for ruptured intracranial aneurysms that caused subarachnoid haemorrhage. The predictor items are readily derived at hospital admission. The web based SAHIT prognostic calculator (http://sahitscore.com) and the related app could be adjunctive tools to support management of patients 10).

Scales

National Institute of Health Stroke Scale

Barthel Index

Extended Glasgow Outcome Scale.

Modified Rankin Scale

Systematic reviews for clinical prognostic factors and clinical prediction tools in aneurysmal subarachnoid hemorrhage (aSAH) face a number of methodological challenges. These include within and between study patient heterogeneity, regional variations in treatment protocols, patient referral biases, and differences in treatment, and prognosis viewpoints across different cultures 11).

It is critical to determine the neural basis for executive deficits in aSAH, in order to better understand and improve patient outcomes.

In a tertiary care center in India, despite recent advances in the treatment of patients with aSAH, the morbidity and mortality rates have failed to improve significantly in unselected patients and natural cohorts. This may be attributed to the natural history of aSAH, and calls for new strategies to diagnose and treat such patients before the catastrophe 12).

In the series of Nieuwkamp et al., despite an increase in the mean age of patients with SAH, case-fatality rates have decreased by 17% between 1973 and 2002 and show potentially important regional differences. This decrease coincides with the introduction of improved management strategies 13).

The case fatality after aneurysmal haemorrhage is 50%; one in eight patients with subarachnoid haemorrhage dies outside hospital.

Mortality is 10% within first few days

30-day mortality rate was 46% in one series, and in others over half the patients died within 2 weeks of their SAH.

overall mortality is 45% (range: 32—67%)

causes of mortality

neurogenic stunned myocardium

about 8% die from progressive deterioration from the initial hemorrhage

of those reaching neurosurgical care, vasospasm kills 7%, and causes severe deficit in another 7%.

about 30% of survivors have moderate to severe disability.

about 66 % of those who hove successful aneurysm clipping never return to the same quality of life as before the SAH.

With the limitation of an explorative cohort study the results indicate that routine transcranial doppler (TCD) studies do not improve the overall outcome of patients after aSAH 14).

Ventricular hemorrhage

Quantitative imaging indicators of ventricular hemorrhage (standard deviation of third ventricular hemorrhage density, minimum density of fourth ventricular hemorrhage, and left ventricular sphericity) are helpful to predict the poor prognosis of patients with aSAH with ventricular hemorrhage. The dimensional fusion model has greater value in predicting the poor prognosis of patients 15)

Amount of Bleeding

Quantitative estimation of the hemorrhage volume associated with aneurysm rupture is a tool of assessing prognosis.

A prospective cohort of 206 patients consecutively admitted with the diagnosis of aneurysmal subarachnoid hemorrhage to Hospital 12 de Octubre were included in the study. Subarachnoid, intraventricular, intracerebral, and total bleeding volumes were calculated using analytic software. For assessing factors related to prognosis, univariate and multivariate analysis (logistic regression) were performed. The relative importance of factors in determining prognosis was established by calculating their proportion of explained variation. Maximum Youden index was calculated to determine the optimal cut point for subarachnoid and total bleeding volume.

Variables independently related to prognosis were clinical grade at admission, age, and the different bleeding volumes. The proportion of variance explained is higher for subarachnoid bleeding. The optimal cut point related to poor prognosis is a volume of 20 mL both for subarachnoid and total bleeding.

Volumetric measurement of subarachnoid or total bleeding volume are both independent prognostic factors in patients with aneurysmal subarachnoid hemorrhage. A volume of more than 20 mL of blood in the initial noncontrast computed tomography is related to a clear increase in poor outcome risk 16).

Acute respiratory distress syndrome

Acute lung injury or acute respiratory distress syndrome (ALI/ARDS) is a common complication after aneurysmal subarachnoid hemorrhage (aSAH), and is associated with worse neurologic outcomes and longer hospitalization. However, the effect of ALI/ARDS in SAH has not been well elucidated. The purpose of this study was to determine the incidence of ALI/ARDS in a cohort of patients with SAH and to determine the risk factors for ALI/ARDS and their impact on patient prognosis. We performed a retrospective analysis of 167 consecutive patients with aSAH enrolled. ALI/ARDS patients were rigorously adjudicated using North American-European Consensus Conference definition. Regression analyses were used to test the risk factors for ALI/ARDS in patients with SAH. A total of 167 patients fulfilled the inclusion criteria, and 27% patients (45 of 167) developed ALI. Among all 45 ALI patients, 33 (20%, 33 of 167) patients met criteria for ARDS. On multivariate analysis, elderly patients, lower glasgow coma scale (GCS), higher Hunt-Hess grade, higher simplified acute physiology score (SAPS) II score, pre-existing pneumonia, gastric aspiration, hypoxemia, and tachypnea were the strongest risk factor for ALI/ARDS. Patients with ALI/ARDS showed worse clinical outcomes measured at 30 days. Development of ALI/ARDS was associated with a statistically significant increasing the odds of tracheostomy and hospital complications, and increasing duration of mechanical ventilation, intensive care unit (ICU) length and hospitalization stay. Development of ALI/ARDS is a severe complication of SAH and is associated with a poor clinical outcome, and further studies should focus on both prevention and management strategies specific to SAH-associated ALI/ARDS 17).

C-reactive protein

see C-reactive protein for aneurysmal subarachnoid hemorrhage outcome.

IL-6

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 18).

APOΕε4 polymorphism

The APOΕε4 polymorphism was analysed in 147 patients with aSAH. Allele and genotype frequencies were compared to those found in a gender- and area-matched control group of healthy individuals (n = 211). Early cerebral vasospasm (CVS) was identified and treated according to neurointensive care unit (NICU) guidelines. Neurological deficit(s) at admittance and at 1-year follow-up visit was recorded. Neurological outcome was assessed by the National Institute of Health Stroke Scale, Barthel Index and the Extended Glasgow Outcome Scale.

APOEε4 and non-APOEε4 allele frequencies were similar in aSAH patients and healthy individuals. The presence of APOEε4 was not associated with the development of early CVS. We could not find an influence of the APOE polymorphism on 1-year neurological outcome between groups. Subgroup analyses of patients treated with surgical clipping vs endovascular coiling did not reveal any associations.

For Csajbok et al. APOEε4 polymorphism has no major influence on risk of aSAH, the occurrence of CVS or long-term neurological outcome after aSAH 19).

For Cheng et al., Apolipoprotein E (APOEε4) may induce cerebral perfusion impairment in the early phase, contributing to early brain injury (EBI) following aneurysmal subarachnoid hemorrhage (aSAH), and assessment of APOE genotypes could serve as a useful tool in the prognostic evaluation and therapeutic management of aSAH 20).

Direct oral anticoagulants or vitamin K antagonists

Iatrogenic coagulopathy caused by Direct oral anticoagulants or vitamin K antagonists was not associated with more severe radiological or clinical subarachnoid hemorrhage or worse clinical outcomes in hospitalized SAH patients 21).

Brain edema in aneurysmal subarachnoid hemorrhage

Brain edema in aneurysmal subarachnoid hemorrhage

Myosteatosis was found to be associated with poor physical condition directly after the onset of aSAH. Skeletal muscle atrophy and myosteatosis were however irrelevant to outcome in the Western-European aSAH patient. Future studies are needed to validate these finding 22).

Aneurysmal subarachnoid hemorrhage length of stay

Aneurysmal subarachnoid hemorrhage length of stay.

Brain Tissue Oxygenation Monitoring

A low PbtO2 value is associated with a worse prognosis, and an increase in the PbtO2 value in response to treatment is a marker of a good outcome 23).

Blood pressure

The inverse correlation between mean arterial pressure and mean transit time (MTT) in early perfusion computed tomography, increasing with the severity of aSAH, suggests an increasing disturbance of cerebral autoregulation with the severity of early brain injury. The results emphasize the importance of maintaining physiological blood pressure values in the early phase of aSAH and preventing hypotension, especially in patients with poor-grade aSAH 24)

References

1)

Ho WM, Schmidt FA, Thomé C, Petr O. CSF metabolomics alterations after aneurysmal subarachnoid hemorrhage: what do we know? Acta Neurol Belg. 2023 Apr 30. doi: 10.1007/s13760-023-02266-2. Epub ahead of print. PMID: 37121932.
2)

Gaastra B, Duncan P, Bakker MK, Hostettler IC, Alg VS, Houlden H, Ruigrok YM, Galea I, Tapper W, Werring D, Bulters D. Genetic variation in NFE2L2 is associated with outcome following aneurysmal subarachnoid haemorrhage. Eur J Neurol. 2022 Sep 23. doi: 10.1111/ene.15571. Epub ahead of print. PMID: 36148820.
3)

Hammer A, Ranaie G, Erbguth F, Hohenhaus M, Wenzl M, Killer-Oberpfalzer M, Steiner HH, Janssen H. Impact of Complications and Comorbidities on the Intensive Care Length of Stay after Aneurysmal Subarachnoid Haemorrhage. Sci Rep. 2020 Apr 10;10(1):6228. doi: 10.1038/s41598-020-63298-9. PubMed PMID: 32277142.
4)

Malhotra K, Conners JJ, Lee VH, Prabhakaran S. Relative changes in transcranial Doppler velocities are inferior to absolute thresh- olds in prediction of symptomatic vasospasm after subarachnoid hemorrhage. J Stroke Cerebrovasc Dis. 2014;23:31–6.
5)

Jabbarli R, Gläsker S, Weber J, Taschner C, Olschewski M, Velthoven VV. Predictors of severity of cerebral vasospasm caused by aneurysmal subarachnoid hemorrhage. J Stroke Cerebrovasc Dis. 2013;22:1332–9.
6)

Zhang H, Zhang B, Li S, Liang C, Xu K, Li S. Whole brain CT perfusion combined with CT angiography in patients with sub- arachnoid haemorrhage and cerebral vasospasm. Clin Neurol Neurosurg. 2013;115:2496–501.
7)

Mackey J, Khoury JC, Alwell K, Moomaw CJ, Kissela BM, Flaherty ML, et al: Stable incidence but declining case-fatali- ty rates of subarachnoid hemorrhage in a population. Neurol- ogy 87:2192–2197, 2016
8)

van Gijn J, Kerr RS, Rinkel GJ. Subarachnoid haemorrhage. Lancet. 2007 Jan 27;369(9558):306-18. Review. PubMed PMID: 17258671.
9)

Deshmukh H, Hinkley M, Dulhanty L, Patel HC, Galea JP. Effect of weekend admission on in-Hospital mortality and functional outcomes for patients with acute subarachnoid haemorrhage (SAH). Acta Neurochir (Wien). 2016 May;158(5):829-35. doi: 10.1007/s00701-016-2746-z. Epub 2016 Mar 1. PubMed PMID: 26928730; PubMed Central PMCID: PMC4826657.
10)

Jaja BNR, Saposnik G, Lingsma HF, Macdonald E, Thorpe KE, Mamdani M, Steyerberg EW, Molyneux A, Manoel ALO, Schatlo B, Hanggi D, Hasan D, Wong GKC, Etminan N, Fukuda H, Torner J, Schaller KL, Suarez JI, Stienen MN, Vergouwen MDI, Rinkel GJE, Spears J, Cusimano MD, Todd M, Le Roux P, Kirkpatrick P, Pickard J, van den Bergh WM, Murray G, Johnston SC, Yamagata S, Mayer S, Schweizer TA, Macdonald RL; SAHIT collaboration. Development and validation of outcome prediction models for aneurysmal subarachnoid haemorrhage: the SAHIT multinational cohort study. BMJ. 2018 Jan 18;360:j5745. doi: 10.1136/bmj.j5745. PubMed PMID: 29348138.
11)

Lo BW, Fukuda H, Nishimura Y, Farrokhyar F, Thabane L, Levine MA. Systematic review of clinical prediction tools and prognostic factors in aneurysmal subarachnoid hemorrhage. Surg Neurol Int. 2015 Aug 11;6:135. doi: 10.4103/2152-7806.162676. eCollection 2015. PubMed PMID: 26322245.
12)

Sodhi HB, Savardekar AR, Mohindra S, Chhabra R, Gupta V, Gupta SK. The clinical profile, management, and overall outcome of aneurysmal subarachnoid hemorrhage at the neurosurgical unit of a tertiary care center in India. J Neurosci Rural Pract. 2014 Apr;5(2):118-26. doi: 10.4103/0976-3147.131650. PubMed PMID: 24966547.
13)

Nieuwkamp DJ, Setz LE, Algra A, Linn FH, de Rooij NK, Rinkel GJ. Changes in case fatality of aneurysmal subarachnoid haemorrhage over time, according to age, sex, and region: a meta-analysis. Lancet Neurol. 2009 Jul;8(7):635-42. doi: 10.1016/S1474-4422(09)70126-7. Epub 2009 Jun 6. PubMed PMID: 19501022.
14)

Ehrlich G, Kirschning T, Wenz H, Hegewald AA, Groden C, Schmiedek P, Scharf J, Seiz-Rosenhagen M. Is there an influence of routine daily transcranial doppler examination on clinical outcome in patients after aneurysmal subarachnoid hemorrhage? World Neurosurg. 2016 Jan 5. pii: S1878-8750(15)01714-3. doi: 10.1016/j.wneu.2015.11.091. [Epub ahead of print] PubMed PMID: 26768855.
15)

Liang JJ, Zhang ZQ, Zhang QR, Li CY, Zheng LJ, Lu GM. [Predictive performance for prognosis of aneurysmal subarachnoid hemorrhage with ventricular hemorrhage by imaging combined with clinical and laboratory quantitative index model]. Zhonghua Yi Xue Za Zhi. 2023 Mar 21;103(11):842-849. Chinese. doi: 10.3760/cma.j.cn112137-20221101-02280. PMID: 36925118.
16)

Lagares A, Jiménez-Roldán L, Gomez PA, Munarriz PM, Castaño-León AM, Cepeda S, Alén JF. Prognostic Value of the Amount of Bleeding After Aneurysmal Subarachnoid Hemorrhage: A Quantitative Volumetric Study. Neurosurgery. 2015 Dec;77(6):898-907. doi: 10.1227/NEU.0000000000000927. PubMed PMID: 26308629.
17)

Wu J, Gao W, Zhang H. Development of acute lung injury or acute respiratory distress syndrome after subarachnoid hemorrhage, predictive factors, and impact on prognosis. Acta Neurol Belg. 2023 Mar 15. doi: 10.1007/s13760-023-02207-z. Epub ahead of print. PMID: 36922484.
18)

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.
19)

Csajbok LZ, Nylén K, Öst M, Blennow K, Zetterberg H, Nellgård P, Nellgård B. Apolipoprotein E polymorphism in aneurysmal subarachnoid haemorrhage in West Sweden. Acta Neurol Scand. 2015 Sep 16. doi: 10.1111/ane.12487. [Epub ahead of print] PubMed PMID: 26374096.
20)

Cheng C, Jiang L, Yang Y, Wu H, Huang Z, Sun X. Effect of APOE Gene Polymorphism on Early Cerebral Perfusion After Aneurysmal Subarachnoid Hemorrhage. Transl Stroke Res. 2015 Sep 14. [Epub ahead of print] PubMed PMID: 26370543.
21)

Veldeman M, Rossmann T, Weiss M, Conzen-Dilger C, Korja M, Hoellig A, Virta JJ, Satopää J, Luostarinen T, Clusmann H, Niemelä M, Raj R. Aneurysmal Subarachnoid Hemorrhage in Hospitalized Patients on Anticoagulants-A Two Center Matched Case-Control Study. J Clin Med. 2023 Feb 13;12(4):1476. doi: 10.3390/jcm12041476. PMID: 36836011; PMCID: PMC9958876.
22)

Shen Y, Levolger S, Zaid Al-Kaylani AHA, Uyttenboogaart M, van Donkelaar CE, Van Dijk JMC, Viddeleer AR, Bokkers RPH. Skeletal muscle atrophy and myosteatosis are not related to long-term aneurysmal subarachnoid hemorrhage outcome. PLoS One. 2022 Mar 4;17(3):e0264616. doi: 10.1371/journal.pone.0264616. PMID: 35245308.
23)

Gouvea Bogossian E, Battaglini D, Fratino S, Minini A, Gianni G, Fiore M, Robba C, Taccone FS. The Role of Brain Tissue Oxygenation Monitoring in the Management of Subarachnoid Hemorrhage: A Scoping Review. Neurocrit Care. 2023 Feb 17. doi: 10.1007/s12028-023-01680-x. Epub ahead of print. PMID: 36802011.
24)

Hofmann BB, Donaldson DM, Fischer I, Karadag C, Neyazi M, Piedade GS, Abusabha Y, Muhammad S, Rubbert C, Hänggi D, Beseoglu K. Blood Pressure Affects the Early CT Perfusion Imaging in Patients with aSAH Reflecting Early Disturbed Autoregulation. Neurocrit Care. 2023 Feb 17. doi: 10.1007/s12028-023-01683-8. Epub ahead of print. PMID: 36802010.

Basal ganglia hemorrhage surgery

Basal ganglia hemorrhage surgery

Latest Pubmed Related Articles

Techniques

The main surgical techniques for spontaneous basal ganglia hemorrhage include stereotactic aspiration, endoscopic aspiration, and craniotomy. However, credible evidence is still needed to validate the effect of these techniques.

Craniotomy

Craniotomy for basal ganglia hemorrhage evacuation.

Decompressive craniectomy

Outcome analysis was stratified using hematoma volume, ICH score, preoperative GCS score, and decompressive craniectomy (DC).

Results: The mean hematoma volume was 70.8 mL, and 68 patients (26.9%) underwent DC. The mean postoperative ICP was 28.8 ± 6.7 mmHg for patients without DC, and only 17.5 ± 8.6 mmHg for patients with DC. Twenty-five patients (9.9%) died within 30 days of the operation, and 88 patients (34.8%, GOS ≥ 4) had good outcome 3 months after surgery. ICH volume > 50 mL, preoperative GCS score ≤ 8, and ICH score ≥ 3 are risk factors for unfavorable outcomes.

Conclusions: DC can be used for patients with low preoperative GCS score, and it effectively reduces ICP and 30-day mortality. Hematoma volume, preoperative GCS score, and ICH score are of predictive value for surgical outcome of large basal ganglia hemorrhage 1).

Stereotactic aspiration

Stereotactic aspiration for basal ganglia hemorrhage evacuation.

Endoscopic aspiration

Endoscopic aspiration for basal ganglia hemorrhage evacuation.

Laser navigation combined with XperCT technology-assisted puncture

A total of 61 patients with hypertensive basal ganglia hemorrhage were recruited at the Binzhou Medical University Hospital, between October 2019 and January 2021, and their clinical information was retrospectively analyzed. Based on the surgical approach used, patients were assigned into either laser navigation or small bone window groups depending on the surgical approach. Then, they compared the operation times, intraoperative blood loss, clinic stay, Glasgow Outcome Scale (GOS) rating at 30 days, Barthel index (BI) rating at 6 months, postoperative pneumonia incidences, and intracranial contamination complications between groups. Intraoperative blood loss, operation time, and sanatorium were significantly low in the laser navigation group, relative to the small bone window group. At the same time, there were no significant differences between the groups with regard to postoperative hematoma volume, lung contamination, cerebrospinal fluid (CSF) leak, and intracranial contamination, as well as the 6-month BI and 30-day GOS rating. There were no deaths in either group. Compared with traditional small bone window surgery, laser-guided puncture, and drainage is a low-cost, accurate, and safe method for the treatment of basal ganglia hemorrhage, which is suitable for promotion in developing countries and economically underdeveloped areas 2)

Complications

Postoperative hemorrhage is a severe complication, and it’s relative to neurosurgical techniques.

The favorable outcome group was slightly younger (p-value 0.050*). Also, the volume and extension of hematoma into the ventricular system, hydrocephalic dilatation, and midline shift greater than 5 mm had a significantly worse outcome with a statistically significant difference.

The early surgical management with the removal of the hematoma led to a dramatic reduction of ICP and improved the prognosis. Patients with signs of brain herniation, a midline shift > 5 mm, hydrocephalic dilatation, ventricular hemorrhage, and a depressed level of consciousness have a poor prognosis 3)

References

1)

Li Q, Yang CH, Xu JG, Li H, You C. Surgical treatment for large spontaneous basal ganglia hemorrhage: retrospective analysis of 253 cases. Br J Neurosurg. 2013 Oct;27(5):617-21. doi: 10.3109/02688697.2013.765938. Epub 2013 Feb 14. PMID: 23406426.
2)

Yuan Z, Wei Q, Chen Z, Xing H, Zhang T, Li Z. Laser navigation combined with XperCT technology-assisted puncture of basal ganglia intracerebral hemorrhage. Neurosurg Rev. 2023 May 5;46(1):104. doi: 10.1007/s10143-023-02015-2. PMID: 37145343.
3)

khallaf, M., Abdelrahman, M. Surgical management for large hypertensive basal ganglionic hemorrhage: single center experience. Egypt J Neurosurg 34, 19 (2019). https://doi.org/10.1186/s41984-019-0044-9

Superior sagittal sinus dural arteriovenous fistula

Superior sagittal sinus dural arteriovenous fistula

Latest Pubmed Related Articles

A intracranial dural arteriovenous fistula (dAVF) involving the superior sagittal sinus (SSS) is relatively rare, and its clinical course is usually aggressive. Its concomitance with a tumor has rarely been reported.

Supratentorial dural arteriovenous fistula DVAs mostly drained in the superior sagittal sinus (80%), while all of infratentorial/combined DVAs drained in deep ependymal veins of the 4th ventricle. All the supratentorial dAVFs drained into the superior sagittal sinus, while the infratentorial/combined dAVFs mostly drained in the jugular bulb, Vein of Rosenthal, or transverse-sigmoid sinuses (75%) 1).

Gigliotti et al. reported the first case of a superior sagittal sinus DAVF occurring after surgical resection of a parasagittal meningioma 2).

Literature Review

https://www.thieme-connect.de/products/ejournals/pdf/10.1055/s-0041-1731594.pdf

Case reports

A case of SSS dAVF due to meningioma invasion, which was treated with sinus reconstruction and endovascular embolization. A 75-year-old man who had undergone tumor resection for parasagittal meningioma 4 years prior presented with intra-ventricular hemorrhage. Computed tomography angiography and magnetic resonance imaging revealed recurrent tumor invasion into the SSS causing occlusion. Cerebral angiography revealed multiple shunts along the occluded segment of the SSS, diffuse deep venous congestion, and cortical reflux. Borden type 3 SSS dAVF was diagnosed. We first performed direct tumor resection, followed by stenting for the occluded SSS and partial embolization of the shunts. After a 6-month interval, transvenous occlusion of the SSS was performed along the stent, resulting in complete obliteration of the dAVF. Sinus reconstruction therapy was effective in the immediate improvement of venous hypertension, obtaining the access route to the fistulas, and eradicating the shunts 3)

A 78-year-old man presented after trauma with basal and cortical subarachnoid hemorrhage (SAH). Computed tomography revealed a parietal bone fracture overlying the superior sagittal sinus (SSS). Catheter angiography performed within 24 hours of the injury demonstrated an SSS dAVF supplied by the middle meningeal artery, adjacent to the fracture.

Lessons: The authors present the case of an acute traumatic dAVF adjacent to a calvarial fracture. In this case, the authors proprose that the underlying pathogenesis is suggestive of direct vessel injury rather than the pathway commonly associated with this pathology 4)

Spontaneous closure of a superior sagittal sinus dural arteriovenous fistula after treatment of subarachnoid hemorrhage and secondary hydrocephalus 5).

A 61-year-old male with a history of meningioma previously managed with subtotal resection and stereotactic radiosurgery presented with progressive right-sided vision loss and bilateral papilledema. Initial imaging suggested possible sinus occlusion. Catheter angiogram revealed a Borden-Shucart grade III DAVF of the superior sagittal sinus and elevated venous pressures and the patient subsequently underwent endovascular transarterial intervention twice. We report on the first case of a superior sagittal sinus DAVF occurring after surgical resection of a parasagittal meningioma 6).

A sagittal sinus dural arteriovenous fistula manifesting as dysphonia secondary to vocal cord paresis. The patient presented with a 6-week history of hoarseness. Imaging studies demonstrated findings suggestive of a dural arteriovenous fistula affecting the superior sagittal sinus. Direct laryngoscopy demonstrated paresis of the right vocal fold. We hypothesized that pressure on the vagus nerve from a dilated and arterialized internal jugular vein within the jugular foramen was responsible for the cranial neuropathy. The patient’s dysphonia resolved with embolization of the fistula, and repeat laryngoscopy showed resolution of the vocal fold paresis 7).

Beer-Furlan A, Joshi KC, Dasenbrock HH, Chen M. Endovascular management of complex superior sagittal sinus dural arteriovenous fistula. Neurosurg Focus. 2019 Apr 1;46(Suppl_2):V11. doi: 10.3171/2019.2.FocusVid.18687. PMID: 30939439.

Song W, Sun H, Liu J, Liu L, Liu J. Spontaneous Resolution of Venous Aneurysms After Transarterial Embolization of a Variant Superior Sagittal Sinus Dural Arteriovenous Fistula: Case Report and Literature Review. Neurologist. 2017 Sep;22(5):186-195. doi: 10.1097/NRL.0000000000000137. Review. PubMed PMID: 28859024.

A DAVF of the SSS in a patient who presented uniquely with increasing dizziness and disequilibrium who was treated with a single modality, endovascular embolization with ethyl vinyl alcohol co-polymer (Onyx, EV3, Irvine, CA). The patient underwent staged embolization in 2 sessions with no complications. An angiographic cure was achieved and the patient’s symptoms were ameliorated. Single modality therapy with endovascular embolization of a SSS DAVF can be achieved. Careful attention to technique during embolization with Onyx is required, but complete obliteration is possible without the need for adjunctive surgical resection 8)

A 61-year-old man who had been treated with anticoagulation for a known SSS thrombosis presented with a sudden onset of headache. CT scan revealed an intraventricular hemorrhage and cerebral angiography revealed DAVFs involving the SSS which had severe venous congestion and sinus occlusion. We treated this case with a staged endovascular approach which consisted of stent placement for the occluded sinus and transarterial intravenous embolization resulting in complete eradication of DAVFs. Recanalization of an occluded sinus by stent placement can reduce venous congestion and transarterial intravenous embolization can obliterate dural arteriovenous shunts. This staged strategy is feasible and should be considered a first option of treatment, especially for DAVFs which presented with intracranial hemorrhage and aggressive venous hypertension 9)

A case report and review of the literature of 16 dural arteriovenous fistulas (DAVFs) involving the superior sagittal sinus region are presented. In the case, magnetic resonance angiography detected the DAVF with multiple arterial feeding vessels from both external carotid arteries. The patient was successfully treated endovascularly, with complete occlusion of arterial feeders and a total resolution of symptoms 10).

References

1)

Agosti E, De Maria L, Panciani PP, Serioli S, Mardighian D, Fontanella MM, Lanzino G. Developmental venous anomaly associated with dural arteriovenous fistula: Etiopathogenesis and hemorrhagic risk. Front Surg. 2023 Mar 21;10:1141857. doi: 10.3389/fsurg.2023.1141857. PMID: 37025268; PMCID: PMC10071040.
2) , 6)

Gigliotti MJ, Patel N, Simon S. Superior sagittal sinus dural arteriovenous fistula caused by treatment of meningioma masquerades as sinus thrombosis. J Cerebrovasc Endovasc Neurosurg. 2021 Sep;23(3):260-265. doi: 10.7461/jcen.2021.E2021.01.002. Epub 2021 Aug 25. PMID: 34428863; PMCID: PMC8497717.
3)

Shima S, Sato S, Kushi K, Okada Y, Niimi Y. Sinus reconstruction therapy for superior sagittal sinus dural arteriovenous fistula caused by parasagittal meningioma invasion: a case report. Neuroradiol J. 2023 May 4:19714009231173103. doi: 10.1177/19714009231173103. Epub ahead of print. PMID: 37142419.
4)

Pryce ML, Chung KHC, Zeineddine HA, Dawes BH. Acute traumatic dural arteriovenous fistula of the superior sagittal sinus: illustrative case. J Neurosurg Case Lessons. 2023 Apr 10;5(15):CASE2392. doi: 10.3171/CASE2392. PMID: 37039291.
5)

Endo H, Ishizuka T, Murahashi T, Oka K, Nakamura H. Spontaneous closure of a superior sagittal sinus dural arteriovenous fistula after treatment of subarachnoid hemorrhage and secondary hydrocephalus. Neurol Sci. 2023 Mar 30. doi: 10.1007/s10072-023-06786-w. Epub ahead of print. PMID: 36995470.
7)

Rinaldo L, Ekbom DC, Lanzino G. Sagittal sinus dural arteriovenous fistula manifesting as unilateral vocal fold paresis. Clin Neurol Neurosurg. 2021 Aug 2;208:106856. doi: 10.1016/j.clineuro.2021.106856. Epub ahead of print. PMID: 34365240.
8)

Chong BW, Demaerschalk BM. Unusual Presentation of a Dural Arteriovenous Fistula of the Superior Sagittal Sinus and Single Modality Therapy with Onyx. Radiol Case Rep. 2015 Nov 6;3(1):158. doi: 10.2484/rcr.v3i1.158. PMID: 27303511; PMCID: PMC4896129.
9)

Ohara N, Toyota S, Kobayashi M, Wakayama A. Superior sagittal sinus dural arteriovenous fistulas treated by stent placement for an occluded sinus and transarterial embolization. A case report. Interv Neuroradiol. 2012 Sep;18(3):333-40. doi: 10.1177/159101991201800314. Epub 2012 Sep 10. PMID: 22958774; PMCID: PMC3442309.
10)

Kurl S, Saari T, Vanninen R, Hernesniemi J. Dural arteriovenous fistulas of superior sagittal sinus: case report and review of literature. Surg Neurol. 1996 Mar;45(3):250-5. doi: 10.1016/0090-3019(95)00361-4. PMID: 8638222.

Glioblastoma

Glioblastoma

J.Sales-Llopis

Neurosurgery Service, Alicante University General Hospital, Spain.

Definition

While glioblastoma was historically classified as isocitrate dehydrogenase (IDH)-wildtype and IDH-mutant groups, the Consortium to Inform Molecular and Practical Approaches to CNS Tumor Taxonomy (cIMPACT-NOW) and the World Health Organization Classification of Tumors of the Central Nervous System 2021 clearly updated the nomenclature to reflect glioblastoma to be compatible with wildtype IDH status only. Therefore, glioblastoma is now defined as “a diffuse, astrocytic glioma that is IDH-wildtype and H3-wildtype and has one or more of the following histological or genetic features: microvascular proliferation, necrosis, TERT promoter mutation, Epidermal growth factor receptor gene amplification, +7/-10 chromosome copy-number changes (CNS WHO grade 4) 1).

History

see Glioblastoma History.

Epidemiology

see Glioblastoma epidemiology.

Prior malignancies in patients harboring glioblastoma

Patients who develop Glioblastoma following a prior malignancy constitute ~8% of patients with Glioblastoma. Despite significant molecular differences these two cohorts appear to have a similar overall prognosis and clinical course. Thus, whether or not a patient harbors a malignancy prior to diagnosis of Glioblastoma should not exclude him or her from aggressive treatment or for consideration of novel investigational therapies 2).

Classification

see Glioblastoma classification.

Glioblastoma cell lines

Glioblastoma cell lines.

Glioblastoma stem-like cells

Glioblastoma stem-like cells

Glioblastoma biology

Glioblastoma biology

Pathogenesis

see Glioblastoma pathogenesis.

Pathophysiology

Glioblastoma Pathophysiology.

Molecular pathways in the development of glioblastoma

Genome-wide profiling studies have shown remarkable genomic diversity among glioblastomas.

Molecular studies have helped identify at least 3 different pathways in the development of glioblastomas.

● 1st pathway: dysregulation of growth factor signaling through amplification and mutational activation of receptor tyrosine kinase (RTK) genes. RTKs are transmembrane proteins that act as receptors for an epidermal growth factor (EGF), vascular endothelial growth factor (VEGF) & platelet-derived growth factor (PDGF). They can also act as receptors for cytokines, hormones, and other signaling pathways

● 2nd pathway: activation of the Phosphoinositide 3 kinase (PI3K)/AKT/mTOR, which is an intracellular signaling pathway that is essential in regulating cell survival

● 3rd pathway: inactivation of the p53 and retinoblastoma (Rb) tumor suppressor pathways

Risk factors

Glioblastomas are intrinsic brain tumors thought to originate from a neuroglial stem or progenitor cells. More than 90% of glioblastomas are isocitrate dehydrogenase (IDH)-wildtype tumors. Incidence increases with age, males are more often affected. Beyond rare instances of genetic predisposition and irradiation exposure, there are no known glioblastoma risk factors.

Biomarkers

Glioblastoma biomarker.

Microcirculation patterns

Vessels with different microcirculation patterns are required for glioblastoma (Glioblastoma) growth. However, details of the microcirculation patterns in Glioblastoma remain unclear.

Mei et al. examined the microcirculation patterns of Glioblastoma and analyzed their roles in patient prognosis together with two well-known GMB prognosis factors (O6 -methylguanine DNA methyltransferase [MGMT] promoter methylation status and isocitrate dehydrogenase [IDH] mutations).

Eighty Glioblastoma clinical specimens were collected from patients diagnosed between January 2000 and December 2012. The microcirculation patterns, including endothelium-dependent vessels (EDVs), extracellular matrix-dependent vessels (ECMDVs), Glioblastoma cell-derived vessels (GDVs), and mosaic vessels (MVs), were evaluated by immunohistochemistry (IHC) and immunofluorescence (IF) staining in both Glioblastoma clinical specimens and xenograft tissues. Vascular density assessments and three-dimensional reconstruction were performed. MGMT promoter methylation status was determined by methylation-specific PCR, and IDH1/2 mutations were detected by Sanger sequencing. The relationship between the microcirculation patterns and the patient prognosis was analyzed by the Kaplan-Meier method.

All 4 microcirculation patterns were observed in both Glioblastoma clinical specimens and xenograft tissues. EDVs was detected in all tissue samples, while the other three patterns were observed in a small number of tissue samples (ECMDVs in 27.5%, GDVs in 43.8%, and MVs in 52.5% tissue samples). GDV-positive patients had a median survival of 9.56 months versus 13.60 months for GDV-negative patients (P = 0.015). In MGMT promoter-methylated cohort, GDV-positive patients had a median survival of 6.76 months versus 14.23 months for GDV-negative patients (P = 0.022).

GDVs might be a negative predictor for the survival of Glioblastoma patients, even in those with MGMT promoter methylation 3).

Pathology

Glioblastoma Pathology.

Genetics

see Glioblastoma Genetics.

Growth

see Glioblastoma growth.

Radioresistance

Glioblastoma Radioresistance

Clinical Features

It generally presents with epilepsy, cognitive decline, headache, dysphasia, or progressive hemiparesis. 4).

Seizures as the presenting symptom of glioblastoma predicted longer survival in adults younger than 60 years. The IDH1 R132H mutation and p53 overexpression (>40%) were associated with seizures at presentation. Seizures showed no relationship with the tumor size or proliferation parameters 5).

Diagnosis

see Glioblastoma diagnosis.

Differential diagnosis

Glioblastoma Differential Diagnosis

Scores

SHORT score.

Treatment

see Glioblastoma treatment.

Outcome

see Glioblastoma outcome

Diet

see Ketogenic Diet in glioblastoma.

Complications

see Glioblastoma complications.

Case series

see Glioblastoma case series.

Case reports

Glioblastoma case reports.

1)

Chen J, Han P, Dahiya S. Glioblastoma: Changing concepts in the WHO CNS5 classification. Indian J Pathol Microbiol. 2022 May;65(Supplement):S24-S32. doi: 10.4103/ijpm.ijpm_1109_21. PMID: 35562131.
2)

Zacharia BE, DiStefano N, Mader MM, Chohan MO, Ogilvie S, Brennan C, Gutin P, Tabar V. Prior malignancies in patients harboring glioblastoma: an institutional case-study of 2164 patients. J Neurooncol. 2017 May 27. doi: 10.1007/s11060-017-2512-y. [Epub ahead of print] Review. PubMed PMID: 28551847.
3)

Mei X, Chen YS, Zhang QP, Chen FR, Xi SY, Long YK, Zhang J, Cai HP, Ke C, Wang J, Chen ZP. Association between glioblastoma cell-derived vessels and poor prognosis of the patients. Cancer Commun (Lond). 2020 May 2. doi: 10.1002/cac2.12026. [Epub ahead of print] PubMed PMID: 32359215.
4)

Thomas DGT,Graham DI, McKeran RO,Thomas DGT. The clinical study of gliomas. In: Brain tumours: scientific basis, clinical investigation and current therapy. In: Thomas DGT, Graham DI eds. London: Butterworths, 1980:194–230.
5)

Toledo M, Sarria-Estrada S, Quintana M, Maldonado X, Martinez-Ricarte F, Rodon J, Auger C, Aizpurua M, Salas-Puig J, Santamarina E, Martinez-Saez E. Epileptic features and survival in glioblastomas presenting with seizures. Epilepsy Res. 2016 Dec 26;130:1-6. doi: 10.1016/j.eplepsyres.2016.12.013. [Epub ahead of print] PubMed PMID: 28073027.

Pituitary neuroendocrine tumor

Pituitary neuroendocrine tumor

Latest Pubmed Related Articles

History

Pituitary neuroendocrine tumor history

Risk factors

Pituitary tumors have very few known risk factors, and these are related to genetics. There are no known environmental or lifestyle-related risk factors for pituitary tumors. Though science has suggested that people who are overweight or obese might be at increased risk.

Youn et al. discovered that a 3’untranslated region (3’UTR) variant, rs181031884 of CDKN2B (Asian-specific variant), had significant association with the risk of pituitary neuroendocrine tumor (PA) (Odds ratio = 0.58, P = 0.00003). Also, rs181031884 appeared as an independent causal variant among the significant variants in CDKN2A and CDKN2B, and showed dose-dependent effects on PA.

Although further studies are needed to verify the impact of this variant on pituitary neuroendocrine tumor susceptibility, the results may help to understand CDKN2B polymorphism and the risk of pituitary neuroendocrine tumor 1).

Epidemiology

Pituitary neuroendocrine tumor epidemiology.

Classification

Pituitary neuroendocrine tumor classification.

Natural History

Pituitary Neuroendocrine Tumor Natural History.

Genetic syndromes

Multiple endocrine neoplasia type 1

Multiple endocrine neoplasia type 4

McCune-Albright syndrome

Carney complex

Pathogenesis

Pituitary neuroendocrine tumor pathogenesis.

Clinical features

Pituitary neuroendocrine tumor clinical features.

Diagnosis

pituitary neuroendocrine tumor Diagnosis.

Treatment

Pituitary neuroendocrine tumor treatment

Outcome

Pituitary Neuroendocrine Tumor Outcome.

Case series

Pituitary neuroendocrine tumor case series

Case reports

A 45-year-old woman who suffered from limb edema for 2 months. Dong et al. focused on tumor recurrence and other common potential diseases based on the pituitary neuroendocrine tumor history. However, none of the examinations showed any abnormality. Later, her continuous complaints about the family relationship and depressed mood came into sight, and a psychiatry consultation was arranged. Following that, she was diagnosed with major depressive disorder. After several days of Melitracen and tandospirone treatment, the patient’s limb edema dramatically subsided. This is the first case of limb edema associated with depression. This highlights the importance of awareness of mental illness for non-psychiatrists, especially in patients with severe somatic symptoms, but with negative results 2).

Recurrence

Pituitary neuroendocrine tumor recurrence

Pituitary neuroendocrine tumor General University Hospital of Alicante Cases

A 39-year-old woman reports visual loss (blurred vision) in both eyes for 2 months, the left worse than the right. Refers to headache (twice a week) that subsides with paracetamol In the last 15 days, he has woken up at night several days due to headaches.

Migraines under control by Neurology

Antiphospholipid syndrome antibody/hypercoagulability in follow-up by Hematology

APA is positive at low titer.

Bilateral superior external quadrantanopia

Treatment with Zolmitriptan

Computed tomography

Suprasellar mass is observed that occupies and expands the sella turcica, difficult to define, which produces a break in the continuity of the floor of the sella turcica and a complete occupation of the sphenoid sinus, which also presents an expansion of the same and thinning of its bony walls. It has maximum measurements of 3.5 x 2.8 x 1.2 cm (craniocaudal by transverse by anteroposterior). These findings seem compatible with an aggressive pituitary neuroendocrine tumor

The mass ascends through the sellar diaphragm and compresses the optic chiasm, and in the lateral areas, it completely encompasses both intracavernous carotid arteries and both cavernous sinuses bilaterally.

Brain MRI

A large sellar lesion with a marked isointense suprasellar extension on T1 and heterogeneous on T2 with multiple hyperintense foci on T2, especially the cystic-necrotic suprasellar portion in relation to macroadenoma. The lesion measures approximately 4 cm in diameter craniocaudal, 3.9 anteroposterior, and 4.2 cm transverse. It extends to both cavernous sinuses and surrounds the right internal carotid artery for more than 180° and the left for approximately 180°. It causes a mass effect on the optic chiasm, displacing it superiorly. The pituitary stalk seems to be located anterior to the lesion with a slight right lateralization, although it is difficult to locate it due to the large size of the lesion.

HORMONES

FREE T4 1.7 ng/dL

FSH 5.3 U/L

LH 3.4 U/L

PROLACTIN 8.3ng/mL

ESTRADIOL 32.0 pg/mL

CORTISOL MORNING 10.9 µg/dL

IGF-1 231 ng/mL

Under general anesthesia, orotracheal intubation, and antibiotic prophylaxis with cefazolin 2 gr IV. Supine position with neutral head resting on a donut-type pillow. Preoperative topical intranasal oxymetazoline was applied with lectins.

nasal phase: Right middle turbinate resection. Preparation of a nasoseptal flap with mucosa from the right septum. It is left lodged in the right choana. Posterior septostomy and communication of both nostrils. In the ostium, a tumor is visualized that completely occupies the sphenoid sinus. Wide anterior sphenoidotomy with the help of a laminotome and cutting burr. Profuse bleeding throughout the nasal phase comes from the tumor. Part of the left paramedian septum that was encompassed by the tumor was removed.

Excision phase: Excision of the tumor part contained in the sphenoid sinus until the bony limits of the sella turcica were visualized. With the help of neuronavigation and Doppler, both ICAs were located. Clivus partly eroded. In the most inferior and posterior part, a bone area corresponding to the posterior clinoid is observed, which is moth-eaten and loose, encompassed by a tumor. Intracapsular excision of the tumor is started by way of debulking, and sending tumor samples for AP analysis. The tumor shows a friable consistency and a purplish color compatible with a pituitary neuroendocrine tumor. Central excision until visualizing gradual descent of sellar and arachnoid diagrams in the sellar cavity with contained low-flow fistula. Exeresis in the posterior region until observing the dura mater of the posterior fossa. Excision of the lateral walls and part of the cavernous sinus. Hemostasis with Floseal.

Reconstruction phase: Tachosil is placed covering the arachnoid in the area of ​​the contained fistula. A nasoseptal flap is placed in contact with the bone defect around the sellar opening. The flap is fixed with surgicel and tissucol. Rapid -Rhino binasal tires are left. The free mucosa of the middle turbinate is left covering the part of the septum from which the flap has been removed.

1)

Youn BJ, Cheong HS, Namgoong S, Kim LH, Baek IK, Kim JH, Yoon SJ, Kim EH, Kim SH, Chang JH, Kim SH, Shin HD. Asian-specific 3’UTR variant in CDKN2B associated with risk of pituitary neuroendocrine tumor. Mol Biol Rep. 2022 Sep 12. doi: 10.1007/s11033-022-07796-1. Epub ahead of print. PMID: 36097105.
2)

Dong X, Fang S, Li W, Li X, Zhang S. Deanxit and tandospirone relieved unexplained limb edema in a depressed pituitary neuroendocrine tumor survivor: A case report. Front Psychiatry. 2022 Nov 10;13:965495. doi: 10.3389/fpsyt.2022.965495. PMID: 36440410; PMCID: PMC9685525.

Aneurysmal subarachnoid hemorrhage (aSAH)

Aneurysmal subarachnoid hemorrhage (aSAH)

Type of spontaneous subarachnoid hemorrhage.

Aneurysmal subarachnoid hemorrhage algorithm

see Aneurysmal subarachnoid hemorrhage algorithm.

Classification

Aneurysmal subarachnoid hemorrhage classification.

Miscellaneous facts about SAH

Subarachnoid hemorrhage (SAH) following aneurysm bleeding accounts for 6% to 8% of all cerebrovascular accidents.

The anterior communicating artery aneurysm cause aneurysmal subarachnoid hemorrhage, about 21.0%~25.5% of percent of spontaneous subarachnoid hemorrhage 1) 2) 3).

The peak age for aneurysmal subarachnoid hemorrhage aSAH is 55-60 years, about 20% of cases occur between ages 15-45 yrs.

30% of aSAHs occurs during sleep

50% of patients with aneurysms have warning symptoms, usually 6-20 days before SAH

headache ls lateralized in 30%, most to the side of the aneurysm.

soft evidence suggests that rupture incidence is higher in spring and autumn

patients > 70 yrs age have a higher proportion with a severe neurologic grade.

Epidemiology

see Aneurysmal subarachnoid hemorrhage epidemiology.

Risk factors

see Aneurysmal subarachnoid hemorrhage risk factors.

Meteorological influence

The inherent variability in the incidence and presentation of ruptured cerebral aneurysms has been investigated in association with seasonality, circadian rhythm, lunar cycle, and climate factors.

Rosenbaum et al., aimed to identify an association between solar activity (solar flux and sunspots) and the incidence of aneurysmal SAH, all of which appear to behave in periodic fashions over long time periods. The Nationwide Inpatient Sample (NIS) provided longitudinal, retrospective data on patients hospitalized with SAH in the United States, from 1988 to 2010, who underwent aneurysmal clipping or coiling. Solar activity and SAH incidence data were modeled with the cosinor methodology and a 10-year periodic cycle length. The NIS database contained 32,281 matching hospitalizations from 1988 to 2010. The acrophase (time point in the cycle of highest amplitude) for solar flux and for sunspots were coincident. The acrophase for aneurysmal SAH incidence was out of phase with solar activity determined by non-overlapping 95% confidence intervals (CIs). Aneurysmal SAH incidence peaks appear to be delayed behind solar activity peaks by 64 months (95% CI; 56-73 months) when using a modeled 10-year periodic cycle. Solar activity (solar flux and sunspots) appears to be associated with the incidence of aneurysmal SAH. As solar activity reaches a relative maximum, the incidence of aneurysmal SAH reaches a relative minimum. These observations may help identify future trends in aneurysmal SAH on a population basis. 4).

By using high-quality meteorological data analyzed with a sophisticated and robust statistical method no clearly identifiable meteorological influence for the SAH events considered can be found. Further studies on the influence of the investigated parameters on SAH incidence seem redundant 5).

Pathogenesis

Aneurysmal subarachnoid hemorrhage pathogenesis.

Pathophysiology

Aneurysmal subarachnoid hemorrhage pathophysiology

Clinical features

see Subarachnoid hemorrhage clinical features

Diagnosis

see Subarachnoid hemorrhage diagnosis.

Scales

Subarachnoid hemorrhage scales.

Outcome

see Aneurysmal subarachnoid hemorrhage outcome

Intracerebral hematoma and aneurysmal subarachnoid hemorrhage

see Intracerebral hematoma and aneurysmal subarachnoid hemorrhage

Complications

see Aneurysmal subarachnoid hemorrhage complications.

Treatment

see Aneurysmal subarachnoid hemorrhage treatment.

Anticonvulsant in aneurysmal subarachnoid hemorrhage

Anticonvulsant in aneurysmal subarachnoid hemorrhage

Croatia

Evidence based information on the epidemiology, risk factors and prognosis, as well as recommendations on diagnostic work up, monitoring and management are provided, with regard to treatment possibilities in Croatia in the article of Solter et al. 6) 7).

Spain

There is high variability in the election of treatment modality among centres in Spain. Endovascular treatment allows more patients to have their aneurysm treated. Guideline adherence is moderate 8).

Guidelines

see Aneurysmal Subarachnoid Hemorrhage Guidelines.

Case series

Aneurysmal subarachnoid hemorrhage case series.

1)

Suzuki M, Fujisawa H, Ishihara H, Yoneda H, Kato S, Ogawa A. Side selection of pterional approach for anterior communicating artery aneurysms–surgical anatomy and strategy. Acta Neurochir (Wien) 2008;150:31–39. 39.
2)

Kimura T, Morita A, Shirouzu I, Sora S. Preoperative evaluation of unruptured cerebral aneurysms by fast imaging employing steady-state acquisition image. Neurosurgery. 2011;69:412–419. discussion 419-420.
3)

Kwon SC, Park JB, Shin SH, Sim HB, Lyo IU, Kim Y. The Efficacy of Simultaneous Bilateral Internal Carotid Angiography during Coil Embolization for Anterior Communicating Artery Aneurysms. J Korean Neurosurg Soc. 2011;49:257–261
4)

Rosenbaum BP, Weil RJ. Aneurysmal Subarachnoid Hemorrhage: Relationship to Solar Activity in the United States, 1988-2010. Astrobiology. 2014 Jun 30. [Epub ahead of print] PubMed PMID: 24979701.
5)

Neidert MC, Sprenger M, Wernli H, Burkhardt JK, Krayenbühl N, Bozinov O, Regli L, Woernle CM. Meteorological influences on the incidence of aneurysmal subarachnoid hemorrhage – a single center study of 511 patients. PLoS One. 2013 Dec 2;8(12):e81621. doi: 10.1371/journal.pone.0081621. eCollection 2013. PubMed PMID: 24312565; PubMed Central PMCID: PMC3847045.
6)

Solter VV, Breitenfeld T, Roje-Bedeković M, Supanc V, Lovrencić-Huzjan A, Serić V, Antoncić I, Basić S, Beros V, Bielen I, Soldo SB, Kadojić D, Lusić I, Maldini B, Marović A, Paladino J, Poljaković Z, Radanović B, Rados M, Rotim K, Vukić M, Zadravec D, Kes VB. General recommendations for the management of aneurysmal subarachnoid hemorrhage. Acta Clin Croat. 2014 Mar;53(1):139-52. PubMed PMID: 24974676.
7)

Solter VV, Roje-Bedeković M, Breitenfeld T, Supanc V, Lovrencić-Huzjan A, Serić V, Antoncić I, Basić S, Beros V, Bielen I, Soldo SB, Kadojić D, Lusić I, Maldini B, Marović A, Paladino J, Poljaković Z, Radanović B, Rados M, Rotim K, Vukić M, Zadravec D, Kes VB. Recommendations for the management of medical complications in patients following aneurysmal subarachnoid hemorrhage. Acta Clin Croat. 2014 Mar;53(1):113-38. PubMed PMID: 24974675.
8)

Lagares A, Munarriz PM, Ibáñez J, Arikán F, Sarabia R, Morera J, Gabarrós A, Horcajadas Á; el Grupo de Patología Vascular de la SENEC. [Variability in the management of aneurysmal subarachnoid haemorrhage in Spain: Analysis of the prospective multicenter database from the Working Group on Neurovascular Diseases of the Spanish Society of Neurosurgery.]. Neurocirugia (Astur). 2015 Jan 15. pii: S1130-1473(14)00153-5. doi: 10.1016/j.neucir.2014.11.005. [Epub ahead of print] Spanish. PubMed PMID: 25599868.

Subarachnoid hemorrhage (SAH)

Subarachnoid hemorrhage (SAH)

A subarachnoid hemorrhage is a hemorrhage in the subarachnoid space. Subarachnoid hemorrhage (SAH) is a medical emergency that requires immediate intervention. The etiology varies between cases; however, rupture of an intracranial aneurysm accounts for 80% of medical emergencies. Early intervention and treatment are essential to prevent long-term complications. Over the years, treatment of SAH has drastically improved, which is responsible for the rapid rise in SAH survivors. Post-SAH, a significant number of patients exhibit impairments in memory and executive function and report high rates of depression and anxiety that ultimately affect daily living, return to work, and quality of life. Given the rise in SAH survivors, rehabilitation post-SAH to optimize patient outcomes becomes crucial 1)

Epidemiology

Spontaneous subarachnoid hemorrhage epidemiology.

Etiology

Subarachnoid Hemorrhage Etiology.

Classification

see Subarachnoid hemorrhage classification.

Scales

Subarachnoid hemorrhage scales

Clinical features

see Subarachnoid hemorrhage clinical features.

Diagnosis

see Subarachnoid hemorrhage diagnosis.

Outcome

see Subarachnoid hemorrhage outcome.

Complications

see Aneurysmal subarachnoid hemorrhage complications.

Treatment

see Subarachnoid hemorrhage treatment.

Models

The Rabbit Blood-shunt Model for the Study of Acute and Late Sequelae of Subarachnoid Hemorrhage 2).

3) 4) 5) 6) 7) 8) 9) 10)

Outcome

Subarachnoid hemorrhage (SAH) has a substantial impact on quality of life and future risk for mortality in patients who survive the initial injury and hospitalization. Poor neurological status and advanced age on admission have been recognized as poor clinical prognostic factors and is one of the life-threatening diseases with high morbidity and mortality rate 11).

A neurological disease that was disgraceful fifty years ago has lost any disquieting and embarrassing significance in the present time to the light of evolution of vascular neurosurgery 12)

Hospital case volume may be associated with improved outcomes after subarachnoid hemorrhage (SAH)

High SAH patient volume is robustly and strongly associated with lower inpatient mortality, fewer poor outcomes, and more discharges to home. The observed SAH patient volume association does not plateau until facilities are treating more than 100 SAH patients per year. This is a considerably higher patient volume threshold than the 20 SAH/year/facility set forth by the Joint Commission for CSC Certification.

Short-term SAH outcomes have improved. High-volume hospitals have more favorable outcomes than low-volume hospitals. This effect is substantial, even for hospitals conventionally classified as high volume. 13).

Using the Get With The Guidelines Stroke registry, Prabhakaran et al., analyzed patients with a discharge diagnosis of SAH between April 2003 and March 2012 and assessed the association of annual SAH case volume with in-hospital mortality by using multivariate logistic regression adjusting for relevant patient, hospital, and geographic characteristics.

Among 31,973 patients with SAH from 685 hospitals, the median annual case volume per hospital was 8.5 (25th-75th percentile, 6.7-12.9) patients. Mean in-hospital mortality was 25.7%, but was lower with increasing annual SAH volume: 29.5% in quartile 1 (range, 4-6.6), 27.0% in quartile 2 (range, 6.7-8.5), 24.1% in quartile 3 (range, 8.5-12.7), and 22.1% in quartile 4 (range, 12.9-94.5). Adjusting for the patient and hospital characteristics, hospital SAH volume was independently associated with in-hospital mortality (adjusted odds ratio 0.79 for quartile 4 vs 1, 95% confidence interval, 0.67-0.92). The quartile of SAH volume also was associated with length of stay but not with discharge home or independent ambulatory status.

In a large nationwide registry, they observed that patients treated at hospitals with higher volumes of SAH patients have lower in-hospital mortality, independent of patient and hospital characteristics suggesting that experienced centers may provide more optimized care for SAH patients. 14)

Studies

ICONS study

1)

Nwafor DC, Kirby BD, Ralston JD, Colantonio MA, Ibekwe E, Lucke-Wold B. Neurocognitive Sequelae and Rehabilitation after Subarachnoid Hemorrhage: Optimizing Outcomes. J Vasc Dis. 2023 Jun;2(2):197-211. doi: 10.3390/jvd2020014. Epub 2023 Apr 1. PMID: 37082756; PMCID: PMC10111247.
2)

Andereggen L, Neuschmelting V, von Gunten M, Widmer HR, Takala J, Jakob SM, Fandino J, Marbacher S. The Rabbit Blood-shunt Model for the Study of Acute and Late Sequelae of Subarachnoid Hemorrhage: Technical Aspects. J Vis Exp. 2014 Oct 2;(92). doi: 10.3791/52132. PubMed PMID: 25350004.
3)

Mori K, Fujii K, Tomura S, Ueno H, Wada K, Otani N, Osada H, Tomiyama A. Canine double hemorrhage model of experimental subarachnoid hemorrhage. Acta Neurochir Suppl. 2015;120:347-51. doi: 10.1007/978-3-319-04981-6_60. PubMed PMID: 25366650.
4)

Fathi AR, Bakhtian KD, Marbacher S, Fandino J, Pluta RM. Blood Clot Placement Model of Subarachnoid Hemorrhage in Non-human Primates. Acta Neurochir Suppl. 2015;120:343-6. doi: 10.1007/978-3-319-04981-6_59. PubMed PMID: 25366649.
5)

Marbacher S, Fathi AR, Muroi C, Coluccia D, Andereggen L, Neuschmelting V, Widmer HR, Jakob SM, Fandino J. The rabbit blood shunt subarachnoid haemorrhage model. Acta Neurochir Suppl. 2015;120:337-42. doi: 10.1007/978-3-319-04981-6_58. PubMed PMID: 25366648.
6)

Kikkawa Y. A rabbit cisterna magna double-injection subarachnoid hemorrhage model. Acta Neurochir Suppl. 2015;120:331-5. doi: 10.1007/978-3-319-04981-6_57. PubMed PMID: 25366647.
7)

Güresir E, Schuss P, Borger V, Vatter H. Rat cisterna magna double-injection model of subarachnoid hemorrhage – background, advantages/limitations, technical considerations, modifications, and outcome measures. Acta Neurochir Suppl. 2015;120:325-9. doi: 10.1007/978-3-319-04981-6_56. PubMed PMID: 25366646.
8)

Sehba FA. The rat endovascular perforation model of subarachnoid hemorrhage. Acta Neurochir Suppl. 2015;120:321-4. doi: 10.1007/978-3-319-04981-6_55. PubMed PMID: 25366645.
9)

Attia MS, Macdonald RL. Anterior circulation model of subarachnoid hemorrhage in mice. Acta Neurochir Suppl. 2015;120:311-4. doi: 10.1007/978-3-319-04981-6_53. PubMed PMID: 25366643.
10)

Marbacher S. Foreword Chapter Animal Models of SAH. Acta Neurochir Suppl. 2015;120:309. doi: 10.1007/978-3-319-04981-6_52. PubMed PMID: 25366642.
11)

Kooijman E, Nijboer CH, van Velthoven CT, Kavelaars A, Kesecioglu J, Heijnen CJ. The rodent endovascular puncture model of subarachnoid hemorrhage: mechanisms of brain damage and therapeutic strategies. J Neuroinflammation. 2014;11:2.
12)

Longatti P, Giombelli E, Pavesi G, Carteri A, Feletti A. Management of subarachnoid hemorrhage in two important Italian political leaders: a paradigm of ethical and technological evolution of neurosurgery during the past half-century. World Neurosurg. 2016 Jan 13. pii: S1878-8750(16)00007-3. doi: 10.1016/j.wneu.2015.12.089. [Epub ahead of print] Review. PubMed PMID: 26775232.
13)

Pandey AS, Gemmete JJ, Wilson TJ, Chaudhary N, Thompson BG, Morgenstern LB, Burke JF. High Subarachnoid Hemorrhage Patient Volume Associated With Lower Mortality and Better Outcomes. Neurosurgery. 2015 Sep;77(3):462-70. doi: 10.1227/NEU.0000000000000850. PubMed PMID: 26110818.
14)

Prabhakaran S, Fonarow GC, Smith EE, Liang L, Xian Y, Neely M, Peterson ED, Schwamm LH. Hospital case volume is associated with mortality in patients hospitalized with subarachnoid hemorrhage. Neurosurgery. 2014 Nov;75(5):500-8. doi: 10.1227/NEU.0000000000000475. PubMed PMID: 24979097.

Adamantinomatous craniopharyngioma diagnosis

Adamantinomatous craniopharyngioma diagnosis

Latest Pubmed Related Articles

Diagnosis of adamantinomatous craniopharyngioma (ACP) is predominantly determined through invasive pathological examination of a neurosurgical biopsy specimen.

▷ ESSENTIAL ◁

Tumor in the sellar region

Squamous non-keratinizing epithelium, benign

AND

stellate reticulum and/or wet keratin

▷ DESIRABLE ◁

▶ Nuclear immunoreactivity for β-catenin

▶ Mutation in CTNNB1

▶ Absence of BRAF p.V600E mutation

Adamantinomatous craniopharyngiomas typically have a lobulated contour as a result of usually being multiple cystic lesions. Solid components are present, but often form a relatively minor part of the mass and enhance vividly on both CT and MRI. Overall, calcification is very common, but this is only true of the adamantinomatous subtype (~90% are calcified).

These tumors have a predilection to being large, extending superiorly into the third ventricle, encasing vessels, and even adhering to adjacent structures.

CT

Contrast enhancement, cyst formation, and calcification are the three characteristic features of craniopharyngiomas on computed tomographic scans. More than 90% of suprasellar craniopharyngiomas exhibit at least two of these three features, thus providing easy radiologic detection. Imaging mnemonic: “90% rule” 90% of adamantinomatous craniopharyngiomas exhibit at least 2 of the following “C” features: cyst formation, prominent calcifications. 1)

Magnetic resonance imaging

Cysts

T1: iso- to hyperintense to the brain (due to high protein content “motor oil cysts”)

T2: variable but ~80% are mostly or partly T2 hyperintense

Solid component

T1 C+ (Gd): vivid enhancement

T2: variable or mixed

Calcification

Difficult to appreciate on conventional imaging

Susceptible sequences may better demonstrate calcification

MR angiography

May show displacement of the A1 segment of the anterior cerebral artery (ACA)

MR spectroscopy

Cyst contents may show a broad lipid spectrum, with an otherwise flat baseline.

Clinical experts can distinguish ACP from Magnetic Resonance Imaging (MRI) with an accuracy of 86%, and 9% of ACP cases are diagnosed this way. Classification using deep learning (DL) provides a solution to support a non-invasive diagnosis of ACP through neuroimaging, but it is still limited in implementation, a major reason being the lack of predictive uncertainty representation. We trained and tested a DL classifier on preoperative MRI from 86 suprasellar tumor patients across multiple institutions. We then applied a Bayesian DL approach to calibrate our previously published ACP classifier, extending beyond point-estimate predictions to predictive distributions. Our original classifier outperforms random forest and XGBoost models in classifying ACP. The calibrated classifier underperformed our previously published results, indicating that the original model was overfitting. The mean values of the predictive distributions were not informative regarding model uncertainty. However, the variance of predictive distributions was indicative of predictive uncertainty. We developed an algorithm to incorporate predicted values and the associated uncertainty to create a classification abstention mechanism. Our model accuracy improved from 80.8% to 95.5%, with a 34.2% abstention rate. We demonstrated that calibration of DL models can be used to estimate predictive uncertainty, which may enable the clinical translation of artificial intelligence to support the non-invasive diagnosis of brain tumors in the future 2).

1)

Johnson LN, Hepler RS, Yee RD, Frazee JG, Simons KB. Magnetic resonance imaging of craniopharyngioma. Am J Ophthalmol. 1986 Aug 15;102(2):242-4. doi: 10.1016/0002-9394(86)90152-2. PMID: 3740186.
2)

Prince EW, Ghosh D, Görg C, Hankinson TC. Uncertainty-Aware Deep Learning Classification of Adamantinomatous Craniopharyngioma from Preoperative MRI. Diagnostics (Basel). 2023 Mar 16;13(6):1132. doi: 10.3390/diagnostics13061132. PMID: 36980440; PMCID: PMC10047069.

Anterior communicating artery

Anterior communicating artery

see anterior communicating artery aneurysm.

Connect one anterior cerebral artery with the other, within and along the floor of the cerebral vault.

The local anatomy of the anterior communicating artery aneurysms is very complex and there are 13 arteries in them.

ACCEPTED ANATOMIC STUDIES have indicated that the anterior communicating artery has no branches or a single variable branch 1) 2) 3) During microsurgery in this region, Yasargil noted and spared several branches of the anterior communicating artery 4).

The anatomy of the anterior communicating artery complex plays a critical role in surgical treatment of anterior circulation aneurysms. Female subjects have a higher incidence of variations in the anterior communicating artery complex. There is a higher incidence of anterior communicating artery aplasia among women 5).

Perforators of the anterior communicating artery

see Perforators of the anterior communicating artery.

The anterior communicating artery was studied with the operating microscope in 10 autopsy cases. This vessel was present in all cases with reduplication in three. Arterial diameter ranged from 0.8 to 2.3 mm, with lengths of 5 to 10 mm. Branches of the anterior communicating artery were found in every case (range 3-13, average 5.4). Most branches were small (50-250 mu), but at least one large branch (250-1000 mu) was invariably present. Small ventral branches ramified on the optic chiasm. Small and large dorsal branches distributed themselves to lamina terminalis, hypothalamus, parolfactory areas, columns of fornix, and corpus callosum.

The regularity and destinations of these branches suggest an important physiologic function. Subarachnoid bleeding from an aneurysm in this location could produce mechanical disruption or vasospasm of these branches, and thus could account for serious disturbances of function in the territory of supply. Obliteration of the anterior communicating artery, once advocated in the therapy of anterior communicating artery aneurysms, probably leads to adverse psycho-organic syndromes by interruption of these important perforant branches. Careful sparing of these branches is recommended during aneurysm surgery 6).

The anterior communicating artery (ACoA) and its branches were examined in 22 human brains after injecting Indian ink or methylmethacrylate. The ACoA branches were divided into the small and the large. Small branches were from 1 to 5 in number (mean 2), and from 70 to 270 microns in diameter (mean 151 microns). Seventy-six percent of the branches originated directly from the ACoA. They tended to arise closer to the left than to the right anterior cerebral artery. Fourteen percent of them arose from the junctional site of the ACoA with the anterior cerebral arteries, and 10% from the site of origin of the subcallosal artery. Large branches were identified as the median artery of the corpus callosum, and the subcallosal artery, respectively. The former vessel was present in 9% of the patients, and the latter in 91%. The subcallosal artery was from 320 to 640 microns in size (mean 486 microns). It tended to arise from the middle of the ACoA. In spite of the very frequent anastomoses involving the ACoA branches, care must be taken to avoid injury to these important vessels during operations of the ACoA aneurysms 7).

The microsurgical anatomy of these branches was studied on 60 fixed human brains, with special attention to their number, caliber, and vascular territory. The direction of the branches was evaluated, measuring the angle formed by them with the postcommunicating segment of the anterior cerebral artery 8).

Variations

In 30 cadaver brains, the anterior communicating artery aneurysm and its branches were examined under magnification using a surgical microscope.

The ACoA was evident in all specimens and had variations consisting of plexiform (33%), dimple (33%), fenestration (21%), duplication (18%), string (18%), fusion (12%), median artery of the corpus callosum (6%), and azygous anterior cerebral artery (3%). The perforating branches were also observed in all cadaver brains. They were classified into subcallosal, hypothalamic, and chiasmatic branches according to their vascular territories. The subcallosal branch, usually single and the largest, supplied the bilateral subcallosal areas, branching off to the hypothalamic area. The hypothalamic branches, multiple and of small caliber, terminated in the hypothalamic area.

The incidence of anomalous ACoA was higher than has been previously reported, and any segment of the anomalous ACoA may have perforating branches regardless of diameter.

Despite the variable anatomy of the anterior communicating artery (AcoA) complex, three main perforating branches can be typically identified the largest of which being the subcallosal artery (ScA).

This artery is very important because it feeds bilateral subcallosal areas branching to the hypothalamic area 9).

Absence

Latest Pubmed Related Articles

The absence of the ACoA is a rare congenital anomaly that occurs when this artery fails to form or is underdeveloped.

When the ACoA is absent, blood flow between the two hemispheres of the brain is disrupted, which can lead to various neurological symptoms. Some people with ACoA absence may not experience any symptoms, while others may develop conditions such as aneurysms, cognitive impairment, or neurological deficits.

A 61-year-old male patient, a rare anatomic variant was found to be associated with a previously unreported one. Both ACAs had symmetrical horizontal and vertical segments, but the AComA was absent from the usual location. The right ACA continued as callosomarginal artery (CMA) without sending off a pericallosal artery. A median artery of corpus callosum (MACC) left from the horizontal segment of the left ACA. Then the left ACA continued as CMA. At 1.9 cm from its origin, the MACC was united to the right CMA by a high, interhemispheric AComA. Therefore, an AComA should be regarded as absent only after documenting the bilateral anastomoses within the interhemispheric fissure. A third interhemispheric main artery, such as a rarely occurring MACC, could be accurately documented by computed tomography angiogram to avoid unpleasant intraoperative hemorrhage or to establish a personalized endovascular route to the anterior cerebral system 10).

Pathology

see Anterior communicating artery aneurysm

1)

Critchley M: The anterior cerebral artery, and its syndromes. Brain 53: 120-165. 1930
2)

Gillilan LA: The arterial and venous blood supplies to the forebrain (including the internal capsule) of primates. Neurology 18: 653-670, 1968
3)

Stephens RB. Stillwell DL: In: Arteries and Veins of the Human Brain. C C Thomas, Springfield, II.1
4)

Yasargil MG, Fox JL, Ray MW: The operative approach to aneurysms of the anterior communicating artery. In Krayenbiihl H. (ed.). Advances and Technical Standards in Neurosurgery, vol. 2. Vienna, Springer Verlag, pp. 115-128, 1975
5)

Krzyżewski RM, Tomaszewski KA, Kochana M, Kopeć M, Klimek-Piotrowska W, Walocha JA. Anatomical variations of the anterior communicating artery complex: gender relationship. Surg Radiol Anat. 2014 May 22. [Epub ahead of print] PubMed PMID: 24849465.
6)

Crowell RM, Morawetz RB. The anterior communicating artery has significant branches. Stroke. 1977 Mar-Apr;8(2):272-3. PubMed PMID: 847795.
7)

Marinković S, Milisavljević M, Marinković Z. Branches of the anterior communicating artery. Microsurgical anatomy. Acta Neurochir (Wien). 1990;106(1-2):78-85. PubMed PMID: 2270791.
8)

Vincentelli F, Lehman G, Caruso G, Grisoli F, Rabehanta P, Gouaze A. Extracerebral course of the perforating branches of the anterior communicating artery: microsurgical anatomical study. Surg Neurol. 1991 Feb;35(2):98-104. PubMed PMID: 1990488.
9)

Serizawa T, Saeki N, Yamaura A. Microsurgical anatomy and clinical significance of the anterior communicating artery and its perforating branches. Neurosurgery. 1997 Jun;40(6):1211-6; discussion 1216-8. PubMed PMID: 9179894.
10)

Rusu MC, Lazăr M, Toader C. False Absence of the Anterior Communicating Artery and a Median Artery of Corpus Callosum. J Craniofac Surg. 2023 Apr 24. doi: 10.1097/SCS.0000000000009316. Epub ahead of print. PMID: 37088893.

Burr hole trephination for chronic subdural hematoma

Burr hole trephination for chronic subdural hematoma

Burr hole trephination for drainage of chronic subdural hematomas are routine operative procedures done by neurosurgery residents.

Burr hole trephination for chronic subdural hematoma with a closed drainage system

Double burr hole trepanation combined with a subperiostal passive closed-drainage system is a technically easy, highly effective, safe, and cost-efficient treatment strategy for symptomatic chronic subdural hematomas. The absence of a drain in direct contact with the hematoma capsule may moderate the risk of postoperative seizure and limit the secondary spread of infection to intracranial compartments 1).

The main aim of surgery should be a complete removal of the aggressive liquid. In case of many membranes that separate the hematoma into chambers like honeycomb an open procedure cannot be avoided. Nevertheless, the preferred operative therapy for most of CSDH is a burr hole craniostomy with a closed drainage system 2) 3).

Surgical Technique

Surgical safety checklist

see Surgical safety checklist.

Preoperative antibiotic prophylaxis

see Preoperative antibiotic prophylaxis.

Skin Preparation

see Skin Preparation.

Positioning

Preferably under general anesthesia the surgical approach should be over the thickest part of the hematoma and the patients positioned in a way that the burr hole comes to the highest point to avoid pneumocephalus.

Therefore, the head is rotated and the ipsilateral shoulder is usually padded.

The supine position is used with the patient‘s head rotated for temporal access. Extremes of head rotation can obstruct the jugular venous drainage, and a shoulder roll can combat this problem or lateral positioning (park bench position).

Skin incision

Sites of predilection are frontal about 1 cm anterior to the coronal suture or parietal posterior to the parietal eminence. The area around Kocher’s point offers a safe entry without injury of branches of the middle meningeal artery or the motor strip. Additionally, the skin incision should be brought, if possible, into alignment with an eventual future skin flap for craniotomy. A curved flap avoids a burr hole position directly under the skin cut and a possible impaired wound-healing as a consequence. Further, the base of the C-shaped incision should be opposite of the planned direction of the drain tip. Obviously, a kinking of the drain is obviated 4).

Burr Holes

A performed burr hole with a diameter of 14 mm enables a sufficient angulation of the drain tip and allows an insertion of the drainage close to the calvaria.

Diren and Ozdemir found that an increase in the width of burr hole craniotomy (BHC), especially the posterior BHC, contributed to the improvement in midline shift 5).

Dura mater opening

The dura mater is coagulated and cut in a stellate fashion.

Technical issues

Under direct vision, the external membrane is perforated by the tips of the bipolar forceps. In general, there are the open or the closed ways of evacuation of the hematoma after the drain is inserted 6)

The open variant should be chosen only if irrigation is desired: the dura and external membrane are opened widely so that the fluid of the hematoma and irrigation can drip out beside the drain during rinsing. Removal of the fluid enriched with inflammatory mediators is considered obviously as an advantage, although a remaining pneumocephalus is seen as an approved factor of recurrence 7) 8).

In the closed way the aim is that no air enters the subdural space. Before the dural opening the drain is tunneled beneath the galea in the direction towards the middle of the base of the skin flap. A distance from the burr hole to the drain’s exit point of at least 5 cm prevents infection 9).

Then the dura and external membrane are incised. This opening should have the same diameter as the drain to allow for a watertight and airtight drain introduction. The hematoma can therefore be evacuated only through the drain: the more fluid that is going to be collected, the more negative pressure that will be built up, which helps the brain to unfold again.

The dura is covered with a small piece of a gelatin sponge and the burr hole is filled and with bone chips collected at the beginning.

The last steps are to connect the drain to a closed collecting system and secure the connection and the exit point from the skin with sutures.

Drain insertion after CSDH drainage is important, but position (subgaleal or subdural) and duration did not appear to influence recurrence rate or clinical outcomes. Similarly, drain location did not influence recurrence rate nor outcomes where both parietal and frontal burr holes were made. Further prospective cohort studies or randomized controlled trials could provide further clarification 10).

Videos

References

1)

Zumofen D, Regli L, Levivier M, Krayenbühl N. Chronic subdural hematomas treated by burr hole trepanation and a subperiostal drainage system. Neurosurgery. 2009 Jun;64(6):1116-21; discussion 1121-2. doi: 10.1227/01.NEU.0000345633.45961.BB. PubMed PMID: 19487891.
2)

Santarius T, Kirkpatrick PJ, Ganesan D, Chia HL, Jalloh I, Smielewski P, Richards HK, Marcus H, Parker RA, Price SJ, Kirollos RW, Pickard JD, Hutchinson PJ (2009) Use of drains versus no drains after burr-hole evacuation of chronic subdural haematoma: a randomised controlled trial. Lancet 374:1067–1073
3)

Weigel R, Schmiedek P, Krauss JK (2003) Outcome of contemporary surgery for chronic subdural haematoma: evidence based review. J Neurol Neurosurg Psychiatry 74:937–943
4)

Emich S, Dollenz M, Winkler PA. Burr hole is not burr hole: technical considerations to the evacuation of chronic subdural hematomas. Acta Neurochir (Wien). 2015 Jan 13. [Epub ahead of print] PubMed PMID: 25578345.
5)

Diren F, Ozdemir O. The effectiveness of Burr-hole sizes on midline shift and hematoma thickness in the treatment of chronic subdural hematoma. World Neurosurg. 2023 Apr 20:S1878-8750(23)00546-6. doi: 10.1016/j.wneu.2023.04.062. Epub ahead of print. PMID: 37087033.
6)

Tosaka M, Sakamoto K, Watanabe S, Yodonawa M, Kunimine H, Aishima K, Fujii T, Yoshimoto Y (2013) Critical classification of craniostomy for chronic subdural hematoma; safer technique for hematoma aspiration. Neurol Med Chir (Tokyo) 53:273–278
7)

Mori K, Maeda M (2001) Surgical treatment of chronic subdural hematoma in 500 consecutive cases: clinical characteristics, surgical outcome, complications, and recurrence rate. Neurol Med Chir (Tokyo) 41:371–381
8)

Stanišić M, Hald J, Rasmussen IA, Pripp AH, Ivanović J, Kolstad F, Sundseth J, Züchner M, Lindegaard KF (2013) Volume and densities of chronic subdural haematoma obtained from CT imaging as predictors of postoperative recurrence: a prospective study of 107 operated patients. Acta Neurochir 155:323–333
9)

Berghauser Pont LM, Dammers R, Schouten JW, Lingsma HF, Dirven CM (2012) Clinical factors associated with outcome in chronic subdural haematoma: a retrospective cohort study of patients on preoperative corticosteroid therapy. Neurosurgery 70:873–880
10)

Glancz LJ, Poon MTC, Coulter IC, Hutchinson PJ, Kolias AG, Brennan PM. Does Drain Position and Duration Influence Outcomes in Patients Undergoing Burr-Hole Evacuation of Chronic Subdural Hematoma? Lessons from a UK Multicenter Prospective Cohort Study. Neurosurgery. 2019 Oct 1;85(4):486-493. doi: 10.1093/neuros/nyy366. PubMed PMID: 30169738.