Update: Bilateral chronic subdural hematoma

Data on bilateral chronic subdural hematomas (CSHs) are scant 1) , including information on the frequency of symptoms, response to various treatments, and postoperative complications, compared with data on unilateral CSH. Bilateral CSHs constitute a fair portion of CSHs, especially in patients older than 75 years and in those with coagulopathy.

Clinical features

The presenting symptoms are those of raised intracranial pressure and mass effect.

The frequency of focal neurological deficits was found to be lesser in patients with bilateral CSDH, and it may confound the diagnosis and delay treatment 2).

Diagnosis

Computed tomography

Bilateral hematomas may lead to medial compression of both ventricles resulting in a narrow, slit-like elongated ventricle (the anterior horns sharply pointed and approaching one another so called ‘squeezed ventricle,’ ‘hare’s ears sign, or ‘rabbit’s ears’) 3) 4)5) 6).

see also Bilateral isodense chronic subdural hematoma

Magnetic resonance imaging

Magnetic resonance imaging is a more sensitive modality.

Differential diagnosis

If the lesion is placed more anteriorly and medially, hyperdense in intensity and enclosed in thick capsule, it may look biconvex in shape and can mimic extradural hematoma. This location of the lesion will also displace the frontal horns of the lateral ventricles laterally than medially, as in the present case. To avoid this confusion, if available, magnetic resonance imaging (MRI) would be better than CT in identifying these lesions 7) 8) 9) 10) 11).

Treatment

Occasionally patients with bilateral CSDH undergo unilateral surgery because the contralateral hematoma is deemed to be asymptomatic, and in some of these patients the contralateral hematoma may subsequently enlarge, requiring additional surgery.

Treatment of bilateral CSHs presents its own unique set of problems. New hemorrhage on the contralateral side and shift of midline structures are concerns and can be avoided by simultaneous bilateral decompression 12) 13). and significantly lowers the risk of retreatment compared with unilateral intervention and should be considered when choosing a surgical procedure 14).

To prevent neurological deterioration resulting from the thicker hematomas, early surgical decompression for bilateral CSDH should be implemented 15).

Outcome

Mixed high and low intensity in T2WI or low intensity in T1WI is the most predictable factor to show rapid aggravation 16).

Clinicians must be aware of the higher recurrent rate of bilateral CSDH after burr hole craniostomy 17).

Case series

2017

Two hundred ninety-one patients with bCSDH were identified, and 264 of them underwent unilateral (136 patients) or bilateral (128 patients) surgery. The overall retreatment rate was 21.6% (57 of 264 patients). Cases treated with unilateral surgery had twice the risk of retreatment compared with cases undergoing bilateral surgery (28.7% vs 14.1%, respectively, p = 0.002). In accordance with previous studies, the data also showed that a separated hematoma density and the absence of postoperative drainage were independent predictors of retreatment.

In bCSDHs bilateral surgical intervention significantly lowers the risk of retreatment compared with unilateral intervention and should be considered when choosing a surgical procedure 18).


Ninety-three patients with bilateral CSDH who underwent unilateral bur hole surgery at Aizu Chuo Hospital were included in a retrospective analysis. Findings on preoperative MRI, preoperative thickness of the drained hematoma, and the influence of antiplatelet or anticoagulant drugs were considered and evaluated in univariate and multivariate analyses.

The overall growth rate was 19% (18 of 93 hematomas), and a significantly greater percentage of the hematomas that were iso- or hypointense on preoperative T1-weighted imaging showed growth compared with other hematomas (35.4% vs 2.3%, p < 0.001). Multivariate logistic regression analysis showed that findings on preoperative T1-weighted MRI were the sole significant predictor of hematoma growth, and other factors such as antiplatelet or anticoagulant drug use, patient age, patient sex, thickness of the treated hematoma, and T2-weighted MRI findings were not significantly related to hematoma growth. The adjusted odds ratio for hematoma growth in the T1 isointense/hypointense group relative to the T1 hyperintense group was 25.12 (95% CI 3.89-51.58, p < 0.01).

The findings of preoperative MRI, namely T1-weighted sequences, may be useful in predicting the growth of hematomas that did not undergo bur hole surgery in patients with bilateral CSDH 19).

2013

Huang et al., identified 25 of 98 CSDH (25.51%). The patients with bilateral lesions had a lower incidence of hemiparesis than those having unilateral lesions (p = 0.004). Analysis of the neuro-images revealed significant differences in the presence of a midline shift (p = 0.001) and thickness of the hematoma (p < 0.001).

The mean Markwalder grading score at admission was 1.89 ± 0.66 and 1.64 ± 0.49 in the unilateral and bilateral hematoma groups, respectively (p = 0.010). After a minimum follow-up period of 6 months, the mean Glasgow Outcome Scale was not significantly different (p = 0.060). The recurrence rate of up to 28.00% observed for the bilateral disease was found to be higher than 9.59% observed for the unilateral disease (p = 0.042) 20).

Case reports

2017

A 72-year-old man with bilateral chronic subdural hematomas was admitted and treated using a YL-1 type hematoma aspiration needle. The treatment was complicated by hemorrhage of the basal ganglia and brainstem. This patient had no history of hypertension. Chen et al evaluated the relevant literature to analyze the causes of cerebral hemorrhage in similar patients.

This case report illustrates that the stability of the intracranial pressure should be closely monitored during the surgical treatment of chronic subdural hematomas, and large fluctuations in the cerebral perfusion pressure should be avoided during the operation. They also propose improvements in the technical details of the operative treatment of chronic subdural hematomas 21).


Calcified chronic subdural hematomas are an occurrence rarely seen in neurosurgical clinical practice. And when they occur bilaterally, the radiologic image they present is fascinating, as is the clinical presentation, but their management may be challenging. They have been reported to present with a multitude of neurologic deficits but never with diabetes insipidus, which is described by Siddiqui et al.

Due to the rarity of this pathology, the management protocol is not well defined, though there have been quite a few papers on this condition. This review article gathers information published over the years on this rare entity to suggest a treatment protocol 22).

2006

An 81-year-old man suffered blunt trauma to his chest resulting from a road traffic accident. On admission a chest X-ray showed multiple rib fractures but a computerized tomography scan of the head ruled out any post-traumatic lesion. He had a background diagnosis of mild Alzheimer’s dementia for which he was being treated with galantamine. He lived a reasonably independent life with his wife and was driving the car himself when the accident occurred. After a fortnight he was discharged from hospital.

Two months later he developed progressive deterioration in mobility. His wife noted an increasing level of forgetfulness and intermittent episodes of confusion. His general practitioner noted a shuffling gait and rigidity affecting lower limbs and made a working diagnosis of parkinsonism. A trial of Madopar (Levodopa and benserazide: 62.5 mg three times a day for 2 weeks) was given by the GP but this failed to improve the situation and he became virtually bed-bound. He was referred back to the hospital for further investigation.

On admission he was confused and marked rigidity affecting upper and lower limbs was detected. No resting tremor was noted but gait could not be tested, as he was unable to get out of bed. In view of the clinical presentation a computerized tomography scan of the head was repeated which showed bilateral fronto-parietal chronic subdural haematoma (Figure 1a,b). He was referred to the regional neurosurgical centre where he underwent bilateral burrhole drainage. Postoperative recovery was unremarkable and on examination there was complete resolution of previous rigidity affecting upper and lower limbs. He was able to converse normally with his wife and began walking with the aid of a stick by third postoperative day. A week later he was discharged from the hospital having regained his previous level of mobility and independence with activities of daily living 23).

1)

Schaller B, Radziwill AJ, Wasner M, Gratzl O, Steck AJ. [Intermittent paraparesis as manifestation of a bilateral chronic subdural hematoma]. Schweiz Med Wochenschr. 1999 Jul 27;129(29-30):1067-72. German. PubMed PMID: 10464909.
2) , 15) , 17) , 20)

Huang YH, Yang KY, Lee TC, Liao CC. Bilateral chronic subdural hematoma: what is the clinical significance? Int J Surg. 2013;11(7):544-8. doi: 10.1016/j.ijsu.2013.05.007. Epub 2013 May 24. PubMed PMID: 23707986.
3)

Marcu H, Becker H. Computed-tomography of bilateral isodense chronic subdural hematomas. Neuroradiology. 1977;14:81–3.
4)

Ellis GL. Subdural haematoma in the elderly. Emerg Med Clin North Am. 1990;8:281–94.
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Karasawa H, Tomita S, Suzuki S. Chronic subdural haematomas: Time density curve and iodine concentrations in enhanced CT. Neuroradiology. 1987;29:36–9.
6)

Kim KS, Hemmati M, Weinberg P. Computed tomography in isodense subdural haematoma. Radiology. 1978;128:71–4.
7)

Fujisawa H, Nomura S, Kajiwara K, Kato S, Fujii M, Suzuki M. Various magnetic resonance imaging patterns of chronic subdural hematomas: indicators of the pathogenesis? Neurol Med Chir (Tokyo) 2006;46:333–9.
8)

Kelly AB, Zimmerman RD, Snow RB, Gandy SE, Heier LA, Deck MD. Head trauma: Comparison of MR and CT experience in 100 patients. AJNR Am J Neuroradiol. 1988;9:699–708.
9)

Guenot M. Chronic subdural haematoma: diagnostic imaging studies. Neurochirurgie. 2001;47:473–8.
10)

Hosoda K, Tamaki N, Masumura M, Matsumoto S, Maeda F. Magnetic resonance images of chronic subdural hematomas. J Neurosurg. 1987;67:677–83.
11)

Agrawal A. Bilateral biconvex frontal chronic subdural hematoma mimicking extradural hematoma. J Surg Tech Case Rep. 2010 Jul;2(2):90-1. doi: 10.4103/2006-8808.73625. PubMed PMID: 22091345; PubMed Central PMCID: PMC3214288.
12)

Sadrolhefazi A, Bloomfield SM. Interhemispheric and bilateral chronic subdural hematoma. Neurosurg Clin N Am. 2000 Jul;11(3):455-63. Review. PubMed PMID: 10918015.
13) , 16)

Kurokawa Y, Ishizaki E, Inaba K. Bilateral chronic subdural hematoma cases showing rapid and progressive aggravation. Surg Neurol. 2005 Nov;64(5):444-9; discussion 449. PubMed PMID: 16253697.
14) , 18)

Andersen-Ranberg NC, Poulsen FR, Bergholt B, Hundsholt T, Fugleholm K. Bilateral chronic subdural hematoma: unilateral or bilateral drainage? J Neurosurg. 2017 Jun;126(6):1905-1911. doi: 10.3171/2016.4.JNS152642. Epub 2016 Jul 8. PubMed PMID: 27392267.
19)

Fujitani S, Ishikawa O, Miura K, Takeda Y, Goto H, Maeda K. Factors predicting contralateral hematoma growth after unilateral drainage of bilateral chronic subdural hematoma. J Neurosurg. 2017 Mar;126(3):755-759. doi: 10.3171/2016.1.JNS152655. PubMed PMID: 27081904.
21)

Chen L, Dong L, Wang XD, Zhang HZ, Wei M, She L. Bilateral Chronic Subdural Hematoma Treated by YL-1 Type Hematoma Aspiration Needle Complicated by Hemorrhage of the Basal Ganglia and Brainstem. World Neurosurg. 2017 Jan;97:761.e11-761.e13. doi: 10.1016/j.wneu.2016.09.074. PubMed PMID: 27702707.
22)

Siddiqui SA, Singh PK, Sawarkar D, Singh M, Sharma BS. Bilateral Ossified Chronic Subdural Hematoma Presenting as Diabetes Insipidus-Case Report and Literature Review. World Neurosurg. 2017 Feb;98:520-524. doi: 10.1016/j.wneu.2016.11.031. Review. PubMed PMID: 27867130.
23)

Suman S, Meenakshisundaram S, Woodhouse P. Bilateral chronic subdural haematoma: a reversible cause of parkinsonism. J R Soc Med. 2006 Feb;99(2):91-2. PubMed PMID: 16449784; PubMed Central PMCID: PMC1360497.

Mannitol for intraoperative brain relaxation

The risk of brain edema after dural opening is high in patients with midline shift undergoing supratentorial tumor surgery. Brain swelling may result in intracranial hypertension, impeded tumor exposure, and adverse outcomes. Mannitol is recommended as a first-line dehydration treatment to reduce brain edema and enable brain relaxation during neurosurgery. Research has indicated that mannitol enhanced brain relaxation in patients undergoing supratentorial tumor surgery; however, these results need further confirmation, and the optimal mannitol dose has not yet been established 1).

Some clinicians 2) 3) advocate high doses (>1.0 g/kg) of mannitol to effectively reduce intracranial pressure, while others recommend lower doses (<1.0 g/kg) 4) 5).

Treatment guidelines for using mannitol in patients with traumatic brain injury and stroke have been published and provide recommendations regarding the dose and timing of mannitol. However, there is still controversy concerning dehydration treatment with mannitol in patients with preoperatively increased intracranial pressure during brain tumor surgery.


Seo et al. sought to determine the dose of mannitol that provides adequate brain relaxation with the fewest adverse effects.

A total of 124 patients were randomized to receive mannitol at 0.25 g/kg (Group A), 0.5 g/kg (Group B), 1.0 g/kg (Group C), and 1.5 g/kg (Group D). The degree of brain relaxation was classified according to a 4-point scale (1, bulging; 2, firm; 3, adequate; and 4, perfectly relaxed) by neurosurgeons; Classes 3 and 4 were considered to indicate satisfactory brain relaxation. The osmolality gap (OG) and serum electrolytes were measured before and after mannitol administration.

The brain relaxation score showed an increasing trend in patients receiving higher doses of mannitol (p = 0.005). The incidence of satisfactory brain relaxation was higher in Groups C and D than in Group A (67.7% and 64.5% vs 32.2%, p = 0.011 and 0.022, respectively). The incidence of OG greater than 10 mOsm/kg was also higher in Groups C and D than in Group A (100.0% in both groups vs 77.4%, p = 0.011 for both). The incidence of moderate hyponatremia (125 mmol/L ≤ Na+ < 130 mmol/L) was significantly higher in Group D than in other groups (38.7% vs 0.0%, 9.7%, and 12.9% in Groups A, B, and C; p < 0.001, p = 0.008, and p = 0.020, respectively). Hyperkalemia (K+ > 5.0 mmol/L) was observed in 12.9% of patients in Group D only.

The higher doses of mannitol provided better brain relaxation but were associated with more adverse effects. Considering the balance between the benefits and risks of mannitol, the authors suggest the use of 1.0 g/kg of intraoperative mannitol for satisfactory brain relaxation with the fewest adverse effects. Clinical trial registration no.: NCT02168075 ( clinicaltrials.gov ) 6).

1)

Peng Y, Liu X, Wang A, Han R. The effect of mannitol on intraoperative brain relaxation in patients undergoing supratentorial tumor surgery: study protocol for a randomized controlled trial. Trials. 2014 May 10;15:165. doi: 10.1186/1745-6215-15-165. PubMed PMID: 24884731; PubMed Central PMCID: PMC4018619.
2)

Wise BL. High-dose mannitol. J Neurosurg. 2004;101:566–567.
3)

Cruz J, Minoja G, Okuchi K, Facco E. Successful use of the new high-dose mannitol treatment in patients with Glasgow Coma Scale scores of 3 and bilateral abnormal pupillary widening: a randomized trial. J Neurosurg. 2004 Mar;100(3):376-83. PubMed PMID: 15035271.
4)

Myburgh JA, Lewis SB. Mannitol for resuscitation in acute head injury: effects on cerebral perfusion and osmolality. Crit Care Resusc. 2000;2:14–18
5)

Sorani MD, Morabito D, Rosenthal G, Giacomini KM, Manley GT. Characterizing the dose–response relationship between mannitol and intracranial pressure in traumatic brain injury patients using a high-frequency physiological data collection system. J Neurotrauma. 2008;25:291–298. doi: 10.1089/neu.2007.0411.
6)

Seo H, Kim E, Jung H, Lim YJ, Kim JW, Park CK, Se YB, Jeon YT, Hwang JW, Park HP. A prospective randomized trial of the optimal dose of mannitol for intraoperative brain relaxation in patients undergoing craniotomy for supratentorial brain tumor resection. J Neurosurg. 2017 Jun;126(6):1839-1846. doi: 10.3171/2016.6.JNS16537. Epub 2016 Aug 19. PubMed PMID: 27540904.

Cystic glioblastoma

Cystic glioblastoma is a descriptive term to one form of glioblastoma that contains large cystic component, rather than being a pathological subtype.

Epidemiology

It is a rare disease whose exact prevalence is unknown. Glioblastoma is usually seen as a unilateral solid tumor more commonly in the supratentorial compartment. The presence of cyst in the GBM is rare. Bilateral large cystic GBM is still rarer 1).

Tumor cysts may be a nutrient reservoir for brain tumors, securing tumor energy metabolism and synthesis of cell constituents. Serum is one likely source of cyst fluid nutrients. Nutrient levels in tumor cyst fluid are highly variable, which could differentially stimulate tumor growth. Cyst fluid glutamate, lactate, and phosphate may act as tumor growth factors; these compounds have previously been shown to stimulate tumor growth at concentrations found in tumor cyst fluid.


GBM cysts contained glucose at 2.2 mmol/L (median value; range <0.8-3.5) and glutamine at 1.04 mmol/L (0.17-4.2). Lactate was 7.1 mmol/L (2.4-12.5) and correlated inversely with glucose level (r = -0.77; P < .001). Amino acids, including glutamate, varied greatly, but median values were similar to previously published serum values. Ammonia was 75 μmol/L (11-241). B vitamins were present at previously published serum values, and riboflavin, nicotinamide, pyridoxal 5΄-phosphate, and cobalamin were higher in cyst fluid than in cerebrospinal fluid. Inorganic phosphate was 1.25 mmol/L (0.34-3.44), which was >3 times higher than in ventricular cerebrospinal fluid: 0.35 mmol/L (0.22-0.66; P < .001). Tricarboxylic acid cycle intermediates were in the low micromolar range, except for citrate, which was 240 μmol/L (140-590). In cystic metastatic malignant melanomas and lung tumors values were similar to those in GBMs. 2).


Cystic GBM may be confused rarely on radiology with tuberculoma as both may show a mass lesion with hypodense centre surrounded by a ring of enhancement. Peroperative cytological examination of smears prepared from fluid aspirated from cysts by rapid Diff-Quik method may prove beneficial for immediate diagnosis in suspicious cases and appropriate patient management may be carried out 3).

Outcome

The presence of cystic features in glioblastoma (GBM) has been described as a favorable prognostic factor, possibly because cystic GBMs showed comparatively little infiltration of the peritumoral brain parenchyma 4).

Case series

 2011

A retrospective review of 354 consecutive patients treated with resection of primary GBM was performed using medical records and imaging information obtained at the University of California, San Francisco from 2005 to 2009. Within this cohort, 37 patients with large cysts (≥ 50% of tumor) were identified. Clinical presentations and surgical outcomes were statistically compared between the cystic and noncystic patients.

There were no statistically significant differences in clinical presentation between groups, including differences in age, sex, presenting symptoms, tumor location, or preoperative functional status, with the exception of tumor size, which was marginally larger in the cystic group. Surgical outcomes, including extent of resection and postoperative functional status, were equivalent. The median actuarial survival for the patients with cystic GBM was 17.0 months (95% CI 12.6-21.3 months), and the median survival for patients with noncystic GBM was 15.9 months (95% CI 14.6-17.2 months). There was no significant between-groups difference in survival (p = 0.99, log-rank test). A Cox multivariate regression model was constructed, which identified only age and extent of resection as independent predictors of survival. The presence of a cyst was not a statistically significant prognostic factor.

This study, comprising the largest series of cases of primary cystic GBM reported in the literature to date, demonstrates that the presence of a large cyst in patients with GBM does not significantly affect overall survival as compared with survival in patients without a cyst. Preoperative discussions with patients with GBM should focus on validated prognostic factors. The presence of cystic features does not confer a survival advantage 5).

2004

A retrospective analysis was conducted in 22 patients by using imaging information and chart reviews of operative reports of GBMs with large cysts (> or = 50% of tumor volume) at The University of Texas M. D. Anderson Cancer Center between 1993 and 2002. Clinical and neurosurgical outcomes and recurrence rates were studied. A statistical comparison was made with a matching cohort of 22 patients with noncystic GBMs. No significant differences in clinical variables were found between the cohort with cystic GBMs and the matched cohort with noncystic GBMs. To avoid bias in preoperative assessment of tumor volume, the tumor burden was compared in patients whose tumors had cysts (excluding the cystic mass) and in patients whose tumors did not contain cysts. There was no statistically significant difference between the two groups (p = 0.8). In patients with cystic GBMs the median survival time after surgery was 18.2 months (95% confidence interval [CI] 11.9-24.5 months) and at 2 years 43% of the patients were still alive. In comparison, in patients with noncystic GBMs, the median survival time was 14.3 months (95% CI 12.1-16.4 months) and only 16% of patients were alive at 2 years. The median time to tumor recurrence was 7.6 months (95% CI 0.01-18 months) in patients harboring cystic GBMs and 4.2 months (95% CI 1.8-6.6 months) in the matched cohort (log-rank test, p = 0.04). In the cystic GBM group, no recurrence was observed in 53% of patients at 6 months, 45% at 1 year, and 38% at 2 years after surgery, whereas the corresponding numbers for the noncystic group were 36, 14, and 9%, respectively.

The results indicate that patients harboring a GBM that contains a large cyst survive longer and have a longer time to recurrence than those who lack such a cyst. This is the first such observation in the literature 6).

1)

Kumar S, Handa A, Sinha R, Tiwari R. Bilateral cystic glioblastoma multiforme. J Neurosci Rural Pract. 2013 Oct;4(4):476-7. doi: 10.4103/0976-3147.120196. PubMed PMID: 24347967; PubMed Central PMCID: PMC3858779.
2)

Dahlberg D, Struys EA, Jansen EE, Mørkrid L, Midttun Ø, Hassel B. Cyst Fluid From Cystic, Malignant Brain Tumors: A Reservoir of Nutrients, Including Growth Factor-Like Nutrients, for Tumor Cells. Neurosurgery. 2017 Jun 1;80(6):917-924. doi: 10.1093/neuros/nyw101. PubMed PMID: 28327992.
3)

Hasan M, Siddiqui B, Qadri S, Faridi S. Cystic glioblastoma multiforme masquerading as a cerebral tuberculoma. BMJ Case Rep. 2014 Oct 17;2014. pii: bcr2014206832. doi: 10.1136/bcr-2014-206832. PubMed PMID: 25326570; PubMed Central PMCID: PMC4202055.
4)

Utsuki S, Oka H, Suzuki S, Shimizu S, Tanizaki Y, Kondo K, Tanaka S, Kawano N, Fujii K. Pathological and clinical features of cystic and noncystic glioblastomas. Brain Tumor Pathol. 2006 Apr;23(1):29-34. PubMed PMID: 18095116.
5)

Kaur G, Bloch O, Jian BJ, Kaur R, Sughrue ME, Aghi MK, McDermott MW, Berger MS, Chang SM, Parsa AT. A critical evaluation of cystic features in primary glioblastoma as a prognostic factor for survival. J Neurosurg. 2011 Oct;115(4):754-9. doi: 10.3171/2011.5.JNS11128. Epub 2011 Jul 15. PubMed PMID: 21761969.
6)

Maldaun MV, Suki D, Lang FF, Prabhu S, Shi W, Fuller GN, Wildrick DM, Sawaya R. Cystic glioblastoma multiforme: survival outcomes in 22 cases. J Neurosurg. 2004 Jan;100(1):61-7. PubMed PMID: 14743913.

Butterfly glioma

 

Butterfly glioma is a high grade astrocytoma, usually a glioblastoma (WHO grade IV), which crosses the midline via the corpus callosum. Other white matter commissures are also occasionally involved. The term butterfly refers to the symmetric wing like extensions across the midline.

Epidemiology

Most frequently butterfly gliomas occur in the frontal lobes, crossing via the genu of the corpus callosum, however posterior butterflies are also encountered.

Differential diagnosis

Primary central nervous system lymphoma: especially in AIDS patients

cerebral toxoplasmosis: especially in AIDS patients

tumefactive demyelination

cerebral metastases (rare)

occasionally a leptomeningeal process which fills the quadrigeminal and ambient cisterns can cause confusion.

A meningioma can mimic butterfly glioma when it arises from the falx cerebri and crosses the midline. Presence of a cerebrospinal fluid intensity cleft between the tumour and adjacent brain cortex is a useful sign to identify the extra-axial location of these lesions and differentiate them from butterfly gliomas 1).

Treatment

Gliomas invading the anterior corpus callosum are commonly deemed unresectable due to an unacceptable risk/benefit ratio, including the risk of abulia.

Burks et al. in a study presents evidence that anterior butterfly gliomas can be safely removed using a novel, attention-task based, awake brain surgery technique that focuses on preserving the anatomical connectivity of the cingulum and relevant aspects of the cingulate gyrus 2).

Current management options include biopsy only, followed by radiation and chemotherapy; surgical decompression followed by radiation and chemotherapy; or biopsy followed by palliative measures (comfort care). Management decisions are subjective, based upon physician experience and/or patient/family preferences in light of the prognosis of this disease.

Outcome

The prognosis of glioblastoma multiforme (GBM) is poor even with aggressive first-line therapy, which includes surgery, radiation therapy, and adjuvant chemotherapy. Although the ideal course of treatment for elderly patients with newly diagnosed GBM is still undecided and requires further studies, the new chemotherapeutic agents administered with or without concomitant radiation therapy have shown promising results. However, in our setting, where resources are limited and newer treatment options are expensive, it is often difficult to deliver the best care to the patient 3).

Case series

2017

Burks et al. reviewed clinical data on all patients undergoing glioma surgery performed by the senior author during a 4-year period at the University of Oklahoma Health Sciences Center. Forty patients were identified who underwent surgery for butterfly gliomas. Each patient was designated as having undergone surgery either with or without the use of awake subcortical mapping and preservation of the cingulum. Data recorded on these patients included the incidence of abulia/akinetic mutism. In the context of the study findings, the authors conducted a detailed anatomical study of the cingulum and its role within the DMN using postmortem fiber tract dissections of 10 cerebral hemispheres and in vivo diffusion tractography of 10 healthy subjects.

Forty patients with butterfly gliomas were treated, 25 (62%) with standard surgical methods and 15 (38%) with awake subcortical mapping and preservation of the cingulum. One patient (1/15, 7%) experienced postoperative abulia following surgery with the cingulum-sparing technique. Greater than 90% resection was achieved in 13/15 (87%) of these patients.

This study presents evidence that anterior butterfly gliomas can be safely removed using a novel, attention-task based, awake brain surgery technique that focuses on preserving the anatomical connectivity of the cingulum and relevant aspects of the cingulate gyrus 4).

2014

Of 336 patients with newly diagnosed GBM who were operated on, 48 (14 %) presented with bGBM, where 29 (60 %) and 19 (40 %) underwent surgical resection and biopsy, respectively. In multivariate analysis, a bGBM was independently associated with poorer survival [HR (95 % CI) 1.848 (1.250-2.685), p < 0.003]. In matched-pair analysis, patients who underwent surgical resection had improved median survival than biopsy patients (7.0 vs. 3.5 months, p = 0.03). In multivariate analysis, increasing percent resection [HR (95 % CI) 0.987 (0.977-0.997), p = 0.01], radiation [HR (95 % CI) 0.431 (0.225-0.812), p = 0.009], and temozolomide [HR (95 % CI) 0.413 (0.212-0. 784), p = 0.007] were each independently associated with prolonged survival among patients with bGBM. This present study shows that while patients with bGBM have poorer prognoses compared to non-bGBM, these patients can also benefit from aggressive treatments including debulking surgery, maximal safe surgical resection, temozolomide chemotherapy, and radiation therapy 5).

2011

Median age was 59 years; 52 % were female; median preoperative Karnofsky performance score (KPS) was 80. Twelve patients underwent biopsy and eleven underwent surgical decompression. The median tumor volume for the biopsy group was 60.6 cm(3) and for the surgically decompressed group 40.5 cm(3). In the biopsy group, five patients received adjuvant therapy but one died prior to its completion; two died prior to the initiation of adjuvant therapy and five were lost to follow up. In the surgical decompression group, seven patients received adjuvant therapy, one died prior to the initiation of adjuvant therapy, two were treated with palliative measures only, and one was lost to follow up. Kaplan-Meier estimates of overall median post surgical-survival of the whole group was 180 days, the biopsy group 48 days, and the surgically decompressed group 265 days (p = 0.14). Our results show that there was a higher median survival in the surgically decompressed group; but a direct correlation could not be established, and that the median KPS did not improve in either group after treatment. A larger multicenter review is required to quantitatively assess the factors, including tumor biomarkers that are associated with patient outcome 6).

Case reports

A 54-year-old man presented with change in behaviour, nocturnal enuresis, abnormal limb movement and headache of one week’s duration. The diagnosis of butterfly glioma (glioblastoma multiforme) was made based on imaging characteristics and was further confirmed by biopsy findings. As the corpus callosum is usually resistant to infiltration by tumours, a mass that involves and crosses the corpus callosum is suggestive of an aggressive neoplasm 7).

1)

Watts J, Box G, Galvin A, et al. Magnetic resonance imaging of meningiomas: a pictorial review. Insights Imaging. 2014;5:113–22.
2) , 4)

Burks JD, Bonney PA, Conner AK, Glenn CA, Briggs RG, Battiste JD, McCoy T, O’Donoghue DL, Wu DH, Sughrue ME. A method for safelyresecting anterior butterfly gliomas: the surgical anatomy of the default mode network and the relevance of its preservation. J Neurosurg. 2017 Jun;126(6):1795-1811. doi: 10.3171/2016.5.JNS153006. Epub 2016 Sep 16. PubMed PMID: 27636183.
3)

Agrawal A. Butterfly glioma of the corpus callosum. J Cancer Res Ther. 2009 Jan-Mar;5(1):43-5. PubMed PMID: 19293489.
5)

Chaichana KL, Jusue-Torres I, Lemos AM, Gokaslan A, Cabrera-Aldana EE, Ashary A, Olivi A, Quinones-Hinojosa A. The butterfly effect on glioblastoma: is volumetric extent of resection more effective than biopsy for these tumors? J Neurooncol. 2014 Dec;120(3):625-34. doi: 10.1007/s11060-014-1597-9. Epub 2014 Sep 6. PubMed PMID: 25193022; PubMed Central PMCID: PMC4313925.
6)

Dziurzynski K, Blas-Boria D, Suki D, Cahill DP, Prabhu SS, Puduvalli V, Levine N. Butterfly glioblastomas: a retrospective review and qualitative assessment of outcomes. J Neurooncol. 2012 Sep;109(3):555-63. doi: 10.1007/s11060-012-0926-0. Epub 2012 Jul 18. PubMed PMID: 22806339; PubMed Central PMCID: PMC3992290.
7)

Krishnan V, Lim TC, Ho FC, Peh WC. Clinics in diagnostic imaging (175). Corpus callosum glioblastoma multiforme (GBM): butterfly glioma. Singapore Med J. 2017 Mar;58(3):121-125. doi: 10.11622/smedj.2017017. PubMed PMID: 28361164; PubMed Central PMCID: PMC5360865.