Category Archives: Vascular

Update: Optic chiasma cavernous malformation

Optic chiasma cavernous malformation

Epidemiology

Suprasellar occurrences of cavernous malformations (CM) in the optic chiasm are extremely uncommon, representing less than 1% of all CNS CMs 1) 2).

To the best of the knowledge of Abou-Al-Shaar et al. less than 80 cases have been reported in the literature 3).

Clinical features

Patients with these lesions typically present with chiasmal apoplexy, characterized by sudden visual lossacute headaches, retroorbital pain, and nausea 4).

These symptoms typically occur after a period of transient blurry vision and headaches. In addition, hypopituitarism from direct compression of the pituitary stalk has been reported in the literature 5) 6).

Diagnosis

On CT scan, optic pathway CMs appear as well-demarcated hyperdense lesions with or without calcifications 7).

MRI

MR imaging of cavernous hemangioma of the optic chiasm 8)

MRI is considered the most sensitive and specific imaging modality for the diagnosis of CM 9).

On T1-weighted images, CMs of the optic pathway demonstrate a hypointense to isointense appearance, whereas on T2-weighted images, they appear as heterogeneous “popcorn” lesions with mixed hyperintense and hypointense signals.

The hypointensity can be delineated further in the gradient-echo T2* images due to hemosiderin deposition in and around the CM. In addition, following intravenous gadolinium administration, minimal or no enhancement can be observed in the CM 10) 11).

It has been reported that CMs of the optic nerve and tract may show nerve thickening on coronal views, whereas CMs of the optic chiasm often appear as focal round masses 12).

Angiography is usually not helpful in diagnosing CMs because it does not delineate the lesion due to the low internal flow and high incidence of thrombosis 13).

Differential diagnosis

CMs of the optic pathway are commonly misdiagnosed as optic neuritisoptic gliomameningiomacraniopharyngiomavenous angiomaarteriovenous malformation, thrombosed intracranial aneurysm, and pituitary apoplexyhistiocytosishypothalamic gliomatuber cinereum hamartoma and metastasis 14) 15).

Cavernoma should be considered when a solid suprasellar mass has hemorrhage (mimicking cystic- adamantinomatous craniopharingioma).


Cavernoma and suprasellar meningioma are rarely associated. Holland and Symon report a patient, whose recovery after removal of the meningioma was complicated by haemorrhage from the cavernoma. This occurrence has not been previously reported 16).

Treatment

Surgical removal is the recommended treatment to restore or preserve vision and to eliminate the risk of future hemorrhage. However, the anatomical location and eloquence of nearby neural structures can make these lesions difficult to access and remove.

The surgical approach should allow optimal exposure of the lesion using the shortest route and with minimal brain retraction. Various surgical approaches have been reported in the literature including pterional, orbitozygomatic, supraorbital, subfrontal, and transbasal interhemispheric approaches. Almost half of the cases reported in the literature were managed through the frontotemporal approach 17).

Biopsy is contraindicated for these lesions due to the high risk of bleeding and symptomatic worsening 18) 19).

Reviews

2006

In their meticulous review of the literature, Lehner et al. found 42 previously reported patients with vascular malformations within optic nerves, chiasm, or optic tracts, 30 of them being cavernous hemangiomas. The optic chiasma was involved in 38 patients (90.5%) and a total excision of the tumor was performed in 21 cases 20).

Case reports

2016

A 33-year-old female presented 3 months postpartum with a headache of moderate severity and progressive visual loss in both eyes. On examination, the patient’s Glasgow coma scale (GCS) was 15/15. Visual field examination showed left homonymous incomplete hemianopia. Her visual acuity was 20/25 in the right eye and 20/30 in the left eye. Her discs and macula were healthy bilaterally. Extraocular movements were intact and pupils were reactive. The rest of her examination was unremarkable. Complete endocrine workup was normal.

Magnetic resonance imaging (MRI) revealed a large heterogeneous, hyperintense, hemorrhagic right suprasellar extra-axial complex cystic structure measuring 31 × 30 × 90 mm on T1-weighted images. There was mass effect on the adjacent hypothalamus and third ventricle displacing them toward the left and superiorly in addition to the optic pathway. The pituitary stalk was displaced toward the left. The lesion encased the right posterior cerebral artery and displaced the right carotid artery laterally.

Computed tomography (CT) arteriography demonstrated a completely thrombosed center. The imaging findings were compatible with suprasellar CM.

The patient underwent right frontal craniotomy and gross total resection of her suprasellar intrachiasmatic large infiltrative hemorrhagic CM. Organizing blood clots with reactive fibrohistiocytic and inflammatory reaction admixed with some ectatic vascular channels suggestive of a vascular malformation were noted. There were small foci admixed with granulation tissue, showing some dilated cavernous spaces that would be compatible with a vascular malformation such as cavernous angioma. On immunohistochemistry, the lesion was CD163+, CD20 rare, CD3+, CD34+, CD31+, CD38+, CTK−, EMA plasma cells, GFAP−, S100 dendritic cells, SMA vascular smooth muscle.

The patient had an uneventful operative course. Her visual acuity improved to 20/20 in both eyes. Extraocular muscles showed mild limitation of both eyes in an upward gaze. Otherwise, she was stable with no neurological deficits. Follow-up MRI at 12 months revealed complete removal of the suprasellar hemorrhagic CM with no evidence of a residual lesion or recurrence 21).


Cavernous malformation of the optic chiasm: Neuro-endoscopic removal 22).


Trentadue et al. report a case in which the finding was incidentally detected in a 49-year-old man. They describe the imaging characteristics of the lesion in such a rare location, highlighting the role of magnetic resonance imaging (MRI) (specifically 3 Tesla) in the management of asymptomatic patients 23).

2015

A 48-year-old female presented with an insidious history of progressive visual loss. Magnetic resonance imaging (MRI) showed a CM in the suprasellar region. The patient was operated via a right pterional approach with a complete lesion removal. The postoperative course was uneventful. Early postoperative ophthalmological examination revealed minimal improvement of the vision in the left eye 24).

2014

The case of a 60-year-old woman from our institution with acute-on-chronic visual disturbance secondary to visual pathway CM is presented. Including the current patient, 70 cases of anterior visual pathway CM have been published to our knowledge. The average patient age is 34.8 ± standard deviation of 14.2 years, with a female preponderance (n = 37, 52.9%). The majority of patients had an acute (n = 44; 62.9%; 95% confidence interval [CI] 0.51-0.73) onset of symptoms. In at least 55.6% (n = 40) of patients, the cause of visual disturbance was initially misdiagnosed. The majority (91.4%; n = 64) of patients underwent craniotomy, with complete resection and subtotal resection achieved in 53.1% (n = 34; 95%CI 0.41-0.65) and 17.2% (n = 11; 95%CI 0.10-0.28) of all surgical patients, respectively. Comparing surgically managed patients, complete resection improved visual deficits in 59.0% (n = 20; 95%CI 0.42-0.75), while subtotal resection improved visual deficits in 50.0% (n = 5; 95%CI 0.24-0.76; p = 0.62). CM is an important differential diagnosis for suprasellar lesions presenting with visual disturbance. A high index of suspicion is required in its diagnosis. Expeditious operative management is recommended to improve clinical outcomes 25).

2012

Ning et al. report a 28-year-old male presenting with left homonymous hemianopsia. Magnetic resonance imaging (MRI) revealed an occupied lesion located in the right side of the optic chiasm, and a clinical diagnosis of chiasmal CM was made. Microsurgical excision was performed via anterolateral pterional craniotomy. The patient showed good recovery with slight improvement of the visual field deficits after the operation. No CM recurrence was discovered during the follow-up MRI scans 26).

2011

Rheinboldt and Blase report the case of a 31-year-old male who presented to the ER with a 1-week history of progressively worsening, throbbing, left retro-orbital headache, ptosis, and subjective worsening of short-term memory function. Initial review of systems and laboratory data were noncontributory. Non-contrasted CT demonstrated a large hyperdense mass centered in the suprasellar cistern without evidence of dissecting extra-axial hemorrhage. Though the initial appearance mimicked a basilar tip aneurysm or another primary extra-axial suprasellar pathology such as a hemorrhagic or proteinaceous craniopharyngioma, germinoma, or optic glioma, a second smaller, clearly intra-axial, hyperdense lesion was observed in the left periventricular forceps major white matter. Consideration for multiple cavernomas versus hypervascular metastatic disease such as renal malignancy, thyroid malignancy, or melanoma was raised. CTA confirmed normal intracranial vasculature. Subsequent MRI images showed an acutely hemorrhagic mass centered at the left paramedian hypothalamus and tuber cinereum with numerous secondary foci, demonstrating mature hemorrhagic elements and confirming the diagnosis of multiple cavernomas 27).

2008

A 33-year-old female who suffered from a recurrence of an intrachiasmatic cavernous malformation is presented. She had already undergone surgery in 1991 and 2001 and was admitted to our hospital with reduced vision in the right eye. After MRI, and diagnosis of recurrence of the cavernoma, a neurosurgical operation was performed using the pterional approach. The intraoperative situation was documented with micro photographs. The postoperative course was uneventful. The female described a minimal improvement of her vision. No postoperative complications were observed. To our knowledge, microsurgically complete extirpation of a recurrence of an intrachiasmatic cavernoma has not yet been reported in the literature 28).

2007

Santos-Ditto et al. present the case of a female patient who developed chiasmatic apoplexy and menstrual alterations. CT scanning showed a suprasellar hemorrhage. She underwent surgery with the presumptive diagnosis of pituitary tumor. At surgery, we find a brown-grayish lesion involving left optic nerve and chiasm. Cavernous angioma was diagnosed by histopathology. Cavernous angiomas constitute nearly 15% of all central nervous system vascular malformations. Location at the optic pathway is very rare, but must to be ruled out in the diagnosis of a patient with chiasmatic and/or optic apoplexy. Surgery is useful in preventing worsening of the previous deficit or a new visual defect 29).


A 15-year-old boy presented with an extremely rare optochiasmatic cavernous angioma. He was admitted to a special hospital with the complaint of blurred vision persisting for 1 month. Magnetic resonance imaging and biopsy of the lesion were inconclusive. He was admitted to the neurosurgical clinic after worsening of the visual symptoms 9 months later. Repeat magnetic resonance imaging showed optochiasmatic cavernous angioma which had doubled in size. The lesion was removed completely without any problem. Postoperatively his visual complaints remained stable, but had improved after 1 year. Optochiasmatic cavernous malformation should be treated by surgical excision, whereas biopsy is useless and may result in enlargement 30).


A 38-year-old male patient who suffered from acute onset of severe headache and progressive loss of vision. The vascular malformation of the optic pathways was completely removed via a pterional approach. This is the first reported instance of complete resection of a cavernoma involving the optic nerve, the chiasm, and the optic tract 31).

2006

Muta et al. report a 14-year-old boy with cavernous malformation of the optic chiasm. He had a 2-year history of gradually worsening visual disturbance. Computed tomography (CT) and magnetic resonance imaging (MRI) revealed a suprasellar mass, findings compatible with craniopharyngioma. The mass was biopsied and histological examination confirmed cavernous malformation. On the second day after the biopsy, he suffered chiasmal apoplexy due to intratumoural haemorrhage, lost visual acuity and developed a field cut. Cavernous malformations arising from the optic nerve and chiasm are extremely rare; only 29 cases have been reported to date. Most patients manifested acute visual acuity and visual field disturbances. Although MRI findings of cavernous malformations in the brain parenchyma have been reported, MRI findings on the optic nerve and chiasm may not be completely diagnostic. Of the 29 documented patients, 16 underwent total resection of the lesion without exacerbation of their preoperative symptoms; in some cases, resection was complicated by risk of damage to the surrounding neural tissue. As patients may suffer intratumoural haemorrhage after biopsy or partial removal of the lesion, the advisability of surgical treatment of cavernous malformations of the optic nerve and chiasm must be considered carefully 32).


In their meticulous review of the literature, Lehner et al. found 42 previously reported patients with vascular malformations within optic nerves, chiasm, or optic tracts, 30 of them being cavernous hemangiomas. The optic chiasma was involved in 38 patients (90.5%) and a total excision of the tumor was performed in 21 cases. Lehner et al. published a patient with a cavernous haemangioma of the optic chiasma and left optic tract who presented with an acute defect of the right visual field and severe retro-orbital pain. They succeeded in total excision of the malformation via a neuronavigationally guided approach. In the postoperative course, vision of our patient improved immediately and was found to be completely normal three months after the surgical intervention. Considering this patient and the published cases in the literature, they are of the opinion that microsurgical excision is a safe and efficient treatment for these rare pathologies 33).

2005

Shkarubo et al. describe a rare case of chiasmatic apoplexy whose cause was chiasmatic cavernoma. In addition to acute visual disorders suggesting the involvement of the left optic nerve, chiasma, and left visual pathway, 23-year-old patient had endocrine disorders as polyuria, polydipsia, which first suggests craniopharyngioma and glioma of the chiasma. A capsule and hematomic clots were removed from the thickened left optic nerve and left chiasmatic half during surgery. Only did a morphological study involving immunohistochemical analysis permit identification of the process as hemorrhage from cavernous micromalformation with the formation of hematoma 34).

1989

Three patients with cavernomas of the optic nerve, chiasm, or optic tract are presented. All suffered progressive visual loss due to local hemorrhage and the space-occupying effects of the vascular malformation. Computed tomography scans revealed small lesions with mild contrast enhancement in the suprasellar and parasellar cisterns, whereas angiography was unremarkable. Magnetic resonance imaging was helpful in our cases both for diagnosis and for planning surgical approach, showing typical signs of cavernomas as confirmed by subsequent surgery and histological examination. The clinical and intraoperative findings are presented 35).

1984

Buonaguidi et al. report a very rare case of an intrasellar cavernous hemangioma mimicking, clinically and neuroradiologically, the presence of a nonfunctioning pituitary adenoma. It was possible to diagnose this benign, congenital vascular malformation only through a histological examination36).

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Venkataramana NK, Rao SA, Arun LN, Krishna C. Cavernous malformation of the optic chiasm: Neuro-endoscopic removal. Asian J Neurosurg. 2016 Jan-Mar;11(1):68-9. doi: 10.4103/1793-5482.145114. PubMed PMID: 26889286; PubMed Central PMCID: PMC4732249.
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Update: Unruptured intracranial aneurysm treatment score

Unruptured intracranial aneurysm treatment score

Etminan et al. endeavored to develop an unruptured intracranial aneurysm treatment score (UIATS) model that includes and quantifies key factors involved in clinical decision-making in the management of UIAs and to assess agreement for this model among specialists in Unruptured intracranial aneurysm (UIA) management and research.

An international multidisciplinary (neurosurgery, neuroradiology, neurology, clinical epidemiology) group of 69 specialists was convened to develop and validate the UIATS model using a Delphi consensus. For internal (39 panel members involved in identification of relevant features) and external validation (30 independent external reviewers), 30 selected UIA cases were used to analyze agreement with UIATS management recommendations based on a 5-point Likert scale (5 indicating strong agreement). Interrater agreement (IRA) was assessed with standardized coefficients of dispersion (vr*) (vr* = 0 indicating excellent agreement and vr* = 1 indicating poor agreement).

The UIATS accounts for 29 key factors in UIA management. Agreement with UIATS (mean Likert scores) was 4.2 (95% confidence interval [CI] 4.1-4.3) per reviewer for both reviewer cohorts; agreement per case was 4.3 (95% CI 4.1-4.4) for panel members and 4.5 (95% CI 4.3-4.6) for external reviewers (p = 0.017). Mean Likert scores were 4.2 (95% CI 4.1-4.3) for interventional reviewers (n = 56) and 4.1 (95% CI 3.9-4.4) for noninterventional reviewers (n = 12) (p = 0.290). Overall IRA (vr*) for both cohorts was 0.026 (95% CI 0.019-0.033).

This novel UIA decision guidance study captures an excellent consensus among highly informed individuals on UIA management, irrespective of their underlying specialty. Clinicians can use the UIATS as a comprehensive mechanism for indicating how a large group of specialists might manage an individual patient with a UIA 1) 


The purpose of the study of Ravindra et al. was to compare the unruptured intracranial aneurysm treatment score (UIATS) recommendations with the real-world experience in a quaternary academic medical center with a high volume of patients with unruptured intracranial aneurysms (UIAs).

All patients with UIAs evaluated during a 3-year period were included. All factors included in the UIATS were abstracted, and patients were scored using the UIATS. Patients were categorized in a contingency table assessing UIATS recommendation versus real-world treatment decision. The authors calculated the percentage of misclassification, sensitivity, specificity, and area under the receiver operating characteristic (ROC) curve. RESULTS A total of 221 consecutive patients with UIAs met the inclusion criteria: 69 (31%) patients underwent treatment and 152 (69%) did not. Fifty-nine (27%) patients had a UIATS between -2 and 2, which does not offer a treatment recommendation, leaving 162 (73%) patients with a UIATS treatment recommendation. The UIATS was significantly associated with treatment (p < 0.001); however, the sensitivity, specificity, and percentage of misclassification were 49%, 80%, and 28%, respectively. Notably, 51% of patients for whom treatment would be recommended by the UIATS did not undergo treatment in the real-world cohort and 20% of patients for whom conservative management would be recommended by UIATS had intervention. The area under the ROC curve was 0.646.

Compared with the authors’ experience, the UIATS recommended overtreatment of UIAs. Although the UIATS could be used as a screening tool, individualized treatment recommendations based on consultation with a cerebrovascular specialist are necessary. Further validation with longitudinal data on rupture rates of UIAs is needed before widespread use 2).

1)

Etminan N, Brown RD Jr, Beseoglu K, Juvela S, Raymond J, Morita A, Torner JC, Derdeyn CP, Raabe A, Mocco J, Korja M, Abdulazim A, Amin-Hanjani S, Al-Shahi Salman R, Barrow DL, Bederson J, Bonafe A, Dumont AS, Fiorella DJ, Gruber A, Hankey GJ, Hasan DM, Hoh BL, Jabbour P, Kasuya H, Kelly ME, Kirkpatrick PJ, Knuckey N, Koivisto T, Krings T, Lawton MT, Marotta TR, Mayer SA, Mee E, Pereira VM, Molyneux A, Morgan MK, Mori K, Murayama Y, Nagahiro S, Nakayama N, Niemelä M, Ogilvy CS, Pierot L, Rabinstein AA, Roos YB, Rinne J, Rosenwasser RH, Ronkainen A, Schaller K, Seifert V, Solomon RA, Spears J, Steiger HJ, Vergouwen MD, Wanke I, Wermer MJ, Wong GK, Wong JH, Zipfel GJ, Connolly ES Jr, Steinmetz H, Lanzino G, Pasqualin A, Rüfenacht D, Vajkoczy P, McDougall C, Hänggi D, LeRoux P, Rinkel GJ, Macdonald RL. The unruptured intracranial aneurysm treatment score: a multidisciplinary consensus. Neurology. 2015 Sep 8;85(10):881-9. doi: 10.1212/WNL.0000000000001891. Epub 2015 Aug 14. PubMed PMID: 26276380; PubMed Central PMCID: PMC4560059.
2)

Ravindra VM, de Havenon A, Gooldy TC, Scoville J, Guan J, Couldwell WT, Taussky P, MacDonald JD, Schmidt RH, Park MS. Validation of the unruptured intracranial aneurysm treatment score: comparison with real-world cerebrovascular practice. J Neurosurg. 2017 Oct 6:1-7. doi: 10.3171/2017.4.JNS17548. [Epub ahead of print] PubMed PMID: 28984518.

Update: Spontaneous intracerebral hemorrhage expansion

Spontaneous intracerebral hemorrhage expansion

Spontaneous intracerebral hemorrhage expansion occurs in about 30% of patients and is related to poor outcome 1).

Patient with prior Warfarin use and intraventricular hemorrhage (IVH) are at risk of hematoma expansion. Aggressive measures to prevent hematoma growth are important in these patients 2).

Hematoma volume HV>16, hematoma heterogeneity HH, 1.5 h-systolic BP SBP>160) can be a practical tool for prediction of ICH growth in the acute stage. Further prospective studies are warranted to validate the ability of this model to predict clinical outcome 3).

Fluid levels, density heterogeneity, and margin irregularity on noncontrast CT are associated with hematoma expansion at 24 hours. These markers may assist in prediction of outcomes in scenarios where CT angiography is not readily available and may be of future help in refining the predictive value of the CT angiography spot sign 4).

Large ICHs were significantly more irregular in shape, heterogeneous in density, and had greater growth. Density heterogeneity independently predicted ICH growth using some definitions 5).

The inconsistency in findings may be caused by ambiguous definition of irregular shape.


Very small hematomas are unlikely to expand and have a low spot sign prevalence. Hemostatic therapy trials may be best targeted at hemorrhages >3 mL in volume 6).

Compared with previously reported predictors for hematoma expansion on non-enhanced CT, such as blend signblack hole sign and heterogeneous density, CTA spot sign has better predictive accuracy for hematoma expansion 7) 8) 9).

However, CTA is not available to all medical centers, especially in some remote areas and non-enhanced CT is sometimes the only emergency neuroimaging examination for spontaneous ICH patients. Thus, it is still important to investigate predictors for hematoma expansion on non-enhanced CT.


A non-enhanced computed tomography (CT) based finding, termed the ‘satellite sign‘, was reported to be a novel predictor for poor outcome in spontaneous ICH. However, it is still unclear whether the presence of the satellite sign is related to hematoma expansion.

Initial computed tomography angiography (CTA) was conducted within 6h after ictus. Satellite sign on non-enhanced CT and spot sign on CTA were detected by two independent reviewers. The sensitivity and specificity of both satellite sign and spot sign were calculated. Receiver-operator analysis was conducted to evaluate their predictive accuracy for hematoma expansion.

This study included 153 patients. Satellite sign was detected in 58 (37.91%) patients and spot sign was detected in 38 (24.84%) patients. Among 37 patients with hematoma expansion, 22 (59.46%) had satellite sign and 23 (62.16%) had spot sign. The sensitivity and specificity of satellite sign for prediction of hematoma expansion were 59.46% and 68.97%, respectively. The sensitivity and specificity of spot sign were 62.16% and 87.07%, respectively. The area under the curve (AUC) of satellite sign was 0.642 and the AUC of spot sign was 0.746. (P=0.157)

The results suggest that the satellite sign is an independent predictor for hematoma expansion in spontaneous ICH. Although spot sign has the higher predictive accuracy, satellite sign is still an acceptable predictor for hematoma expansion when CTA is unavailable

Yu et al. compared the predictive values of spot sign and satellite sign for hematoma expansion. Compared with satellite sign, spot sign had higher sensitivity and specificity. In addition, spot sign had a larger AUC than satellite sign, but no significant difference existed. Thus, CTA spot sign seems to be a better predictor for hematoma expansion in spontaneous ICH patients, but satellite sign is still an acceptable predictor for hematoma expansion when CTA is unavailable.

The study has several limitations. First, this was a retrospective study with limited sample size in a single medical center. Second, the association between satellite sign and prognosis was not investigated because of insufficient follow-up data. Furthermore, the onset-to-CTA time was relatively long, which could influence the predictive accuracy of both spot sign and satellite sign.

In conclusion, the study demonstrated that the satellite sign was an independent predictor for hematoma expansion in spontaneous ICH patients. Spot sign has higher accuracy for predicting hematoma expansion, but the satellite sign is still an acceptable predictor when CTA is unavailable. Further multi-center, prospective studies with larger sample sizes are still needed to confirm the utility and validity of the satellite sign in predicting hematoma expansion in spontaneous ICH patients 10).

1)

H.B. Brouwers, Y. Chang, G.J. Falcone, X. Cai, A.M. Ayres, T.W. Battey, A. Vashkevich, K.A. McNamara, V. Valant, K. Schwab, S.C. Orzell, L.M. Bresette, S.K. Feske, N.S. Rost, J.M. Romero, A. Viswanathan, S.H. Chou, S.M. Greenberg, J. Rosand, J.N. Goldstein, Predicting hematoma expansion after primary intracerebral hemorrhage, JAMA Neurol. 1 (2) (2014) 158–164.
2)

Yaghi S, Dibu J, Achi E, Patel A, Samant R, Hinduja A. Hematoma expansion in spontaneous intracerebral hemorrhage: predictors and outcome. Int J Neurosci. 2014 Dec;124(12):890-3. doi: 10.3109/00207454.2014.887716. Epub 2014 Feb 28. PubMed PMID: 24472073.
3)

Takeda R, Ogura T, Ooigawa H, Fushihara G, Yoshikawa S, Okada D, Araki R, Kurita H. A practical prediction model for early hematoma expansion in spontaneous deep ganglionic intracerebral hemorrhage. Clin Neurol Neurosurg. 2013 Jul;115(7):1028-31. doi: 10.1016/j.clineuro.2012.10.016. Epub 2012 Dec 14. PubMed PMID: 23245855.
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Blacquiere D, Demchuk AM, Al-Hazzaa M, Deshpande A, Petrcich W, Aviv RI, Rodriguez-Luna D, Molina CA, Silva Blas Y, Dzialowski I, Czlonkowska A, Boulanger JM, Lum C, Gubitz G, Padma V, Roy J, Kase CS, Bhatia R, Hill MD, Dowlatshahi D; PREDICT/Sunnybrook ICH CTA Study Group. Intracerebral Hematoma Morphologic Appearance on Noncontrast Computed Tomography Predicts Significant Hematoma Expansion. Stroke. 2015 Nov;46(11):3111-6. doi: 10.1161/STROKEAHA.115.010566. Epub 2015 Oct 8. PubMed PMID: 26451019.
5)

Barras CD, Tress BM, Christensen S, MacGregor L, Collins M, Desmond PM, Skolnick BE, Mayer SA, Broderick JP, Diringer MN, Steiner T, Davis SM; Recombinant Activated Factor VII Intracerebral Hemorrhage Trial Investigators. Density and shape as CT predictors of intracerebral hemorrhage growth. Stroke. 2009 Apr;40(4):1325-31. doi: 10.1161/STROKEAHA.108.536888. Epub 2009 Mar 12. PubMed PMID: 19286590.
6)

Dowlatshahi D, Yogendrakumar V, Aviv RI, Rodriguez-Luna D, Molina CA, Silva Y, Dzialowski I, Czlonkowska A, Boulanger JM, Lum C, Gubitz G, Padma V, Roy J, Kase CS, Bhatia R, Hill MD, Demchuk AM; PREDICT/Sunnybrook ICH CTA study group. Small intracerebral hemorrhages have a low spot sign prevalence and are less likely to expand. Int J Stroke. 2016 Feb;11(2):191-7. doi: 10.1177/1747493015616635. PubMed PMID: 26783310.
8)

Zheng J, Yu Z, Xu Z, Li M, Wang X, Lin S, Li H, You C. The Accuracy of the Spot Sign and the Blend Sign for Predicting Hematoma Expansion in Patients with Spontaneous Intracerebral Hemorrhage. Med Sci Monit. 2017 May 12;23:2250-2257. PubMed PMID: 28498827; PubMed Central PMCID: PMC5437917.
9)

Yu Z, Zheng J, Ma L, Guo R, Li M, Wang X, Lin S, Li H, You C. The predictive accuracy of the black hole sign and the spot sign for hematoma expansion in patients with spontaneous intracerebral hemorrhage. Neurol Sci. 2017 Jun 2. doi: 10.1007/s10072-017-3006-6. [Epub ahead of print] PubMed PMID: 28577268.
10)

Yu Z, Zheng J, Ali H, Guo R, Li M, Wang X, Ma L, Li H, You C. Significance of satellite sign and spot sign in predicting hematoma expansion in spontaneous intracerebral hemorrhage. Clin Neurol Neurosurg. 2017 Sep 20;162:67-71. doi: 10.1016/j.clineuro.2017.09.008. [Epub ahead of print] PubMed PMID: 28946021.

Update: Anticonvulsant in aneurysmal subarachnoid hemorrhage

Anticonvulsant in aneurysmal subarachnoid hemorrhage

Concerns over the possible consequences of a seizure in the setting of an unsecured intracranial aneurysm, has led to routine prophylactic administration of antiepileptic drugs (AEDs) following SAH in many centers 1) 2).

In a review, the Department of Clinical Pharmacy, University of Tennessee Health Science Center, College of Pharmacy, Knoxville, describes the evidence associated with the use of AEDs for seizure prophylaxis in patients with intracerebral tumors, traumatic brain injury, aneurysmal subarachnoid hemorrhage, craniotomy, ischemic stroke, and intracerebral hemorrhage. Clear evidence indicates that the short-term use of AEDs for seizure prophylaxis in patients with traumatic brain injury and aneurysmal subarachnoid hemorrhage may be beneficial; however, evidence to support the use of AEDs in other disease states is less clear 3).

Anticonvulsant prophylaxis remains controversial, with studies suggesting a brief course may be adequate and longer exposure may be associated with worse outcomes. Nonetheless, in the absence of controlled trials to inform practice, patients continue to receive variable chemoprophylaxis 4).

Current practice regarding seizure prophylaxis in aneurysmal subarachnoid hemorrhage across academic centers

An eight question survey was sent to 25 US centers with high volume aSAH cases (>100 annually). Respondents were asked about institutional practices regarding use, duration, and type of seizure prophylaxis.

13 (52%) respondents endorsed the utility of seizure prophylaxis while 10 (40%) did not, and two (8%) were unsure. Among respondents using prophylaxis, levetiracetam was the firstline medication for the majority (94%) while phenytoin was used as a primary agent at one (4%) center and as a secondary agent at four (16%) centers. Duration of levetiracetam prophylaxis ranged from 1 day to 6 weeks following SAH (mean 13.2; median 11). Only a single center employed EEG routinely in all aSAH patients but most supported EEG use when the neurologic examination was unreliable or inexplicably declining. 24 (96%) respondents agreed that a trial randomizing patients to levetiracetam or no antiseizure medication is warranted at this time, and all 25 (100%) believed that such a trial would be appropriate or ethically sound.

The routine use of seizure prophylaxis following aSAH is controversial. Among a sampling of 25 major academic centers, most administer prophylaxis, while a significant proportion does not. The majority believes a trial randomizing patients to receive seizure prophylaxis is both timely and ethical 5)

Complications

Literature has suggested increased adverse effects associated with post-hemorrhagic AED exposure; including serious drug related complications as well as worse cognitive and functional outcomes 6).

Up to 21% of those receiving AED prophylaxis suffered adverse medication side effects, including impaired liver function, thrombocytopenia, rash, and Stevens-Johnson syndrome. Few studies to date have specifically evaluated prophylactic AED treatment protocols, and only one has detailed the incidence and risk factors of clinical seizures in patients not receiving prophylactic AED medications 7).

Reviews

2013

Raper et al. performed a MEDLINE (1985-2011) search to identify randomized controlled trials and retrospective series of aSAH. Statistical analyses of categorical variables such as presentation and early and late seizures were carried out using χ(2) and Fisher exact tests.

They included 25 studies involving 7002 patients. The rate of early postoperative seizure was 2.3%. The rate of late postoperative seizure was 5.5%. The average time to late seizure was 7.45 months. Patients who experienced a late seizure were more likely to have MCA aneurysms, be Hunt/Hess grade III, and be repaired with microsurgical clipping than endovascular coiling.

Despite improved microsurgical techniques and antiepileptic drug prophylaxis, a significant proportion of patients undergoing aneurysm clipping still experience seizures. Seizures may occur years after aneurysm repair, and careful monitoring for late complications remains important. Furthermore, routine perioperative AED use does not seem to prevent seizures after SAH 8).


Marigold et al. searched the Cochrane Epilepsy Group Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL) (2013, Issue 1) in The Cochrane Library, and MEDLINE (1946 to 12th March 2013). We checked the reference lists of articles retrieved from these searches.

They considered all randomised and quasi-randomised controlled trials in which patients were assigned to a treatment (one or more AEDs) or placebo.

Two review authors (RM and JK) independently screened and assessed the methodological quality of the studies. If studies were included, one author extracted the data and the other checked it.

No relevant studies were found.

There was no evidence to support or refute the use of antiepileptic drugs for the primary or secondary prevention of seizures related to subarachnoid haemorrhage. Well-designed randomised controlled trials are urgently needed to guide clinical practice 9).

2011

An electronic literature search was conducted for English language articles describing the incidence and treatment of seizures after aneurysmal subarachnoid hemorrhage from 1980 to October 2010. A total of 56 articles were included in this review. Seizures often occur at the time of initial presentation or aneurysmal rebleeding before aneurysm treatment. Seizures occur in about 2% of patients after invasive aneurysm treatment, with a higher incidence after surgical clipping compared with endovascular repair. Non-convulsive seizures should be considered in patients with poor neurological status or deterioration. Seizure prophylaxis with antiepileptic drugs is controversial, with limited data available for developing recommendations. While antiepileptic drug use has been linked to worse prognosis, studies have evaluated treatment with almost exclusively phenytoin. When prophylaxis is used, 3-day treatment seems to provide similar seizure prevention with better outcome compared with longer-term treatment 10).

2010

The objective was addressed through the development of a critically appraised topic that included a clinical scenario, structured question, search strategy, critical appraisal, assessment of results, evidence summary, commentary, and bottom line conclusions. Neurology consultants and residents, a medical librarian, clinical epidemiologists, and content experts in the fields of epilepsy, neurosurgery, and critical care contributed to the review and placed the evidence in clinical context.

There were no relevant randomized, controlled trials that addressed the question. A post hoc analysis of data from 4 trials of tirilazad for aSAH showed that prophylactic AED therapy was associated with worse Glasgow Outcome Scale scores at 3 months (odds ratio 1.56, 95% confidence interval 1.16-2.10; P = 0.003) but numerous confounders limit data interpretation.

There are insufficient data to support or refute the prophylactic use of AED therapy after aSAH. Randomized, controlled trials are needed to address the efficacy and risks of AEDs in this setting and should take into account factors such as aneurysmal factors (location, hemorrhage grade, degree of parenchymal injury), type of aneurysm surgery (clip vs. coil), and evaluate the timing and duration of AED use 11).

Case series

2017

Human et al. performed a prospective, single-center, randomized, open-label trial of a brief (3-day) course of levetiracetam (LEV) versus extended treatment (until hospital discharge). The primary outcome was in-hospital seizure. Secondary outcomes included drug discontinuation and functional outcome.

Eighty-four SAH patients had been randomized when the trial was terminated due to slow enrollment. In-hospital seizures occurred in three (9%) of 35 in the brief LEV group versus one (2%) of 49 in the extended group (p = 0.2). Ten (20%) of the extended group discontinued LEV prematurely, primarily due to sedation. Four of five seizures (including one pre-randomization) occurred in patients with early brain injury (EBI) on computed tomography (CT) scans (adjusted OR 12.5, 95% CI 1.2-122, p = 0.03). Good functional outcome (mRS 0-2) was more likely in the brief LEV group (83 vs. 61%, p = 0.04).

This study was underpowered to demonstrate superiority of extended LEV for seizure prophylaxis, although a trend to benefit was seen. Seizures primarily occurred in those with radiographic EBI, suggesting targeted prophylaxis may be preferable. Larger trials are required to evaluate optimal chemoprophylaxis in SAH, especially in light of worse outcomes in those receiving extended treatment 12).

2016

Panczykowski et al.retrospectively analyzed a prospectively collected database of subarachnoid hemorrhage patients admitted to the Department of Neurological Surgery, University of Pittsburgh Medical Center,

Between 2005 and 2007, all patients received prophylactic AEDs upon admission. After 2007, no patients received prophylactic AEDs or had AEDs immediately discontinued if initiated at an outside hospital. A propensity score-matched analysis was then performed to compare the development of clinical and electrographic seizures in these 2 populations.

Three hundred and fifty three patients with spontaneous subarachnoid hemorrhage were analyzed, 43% of whom were treated with prophylactic AEDs upon admission. Overall, 10% of patients suffered clinical and electrographic seizures, most frequently occurring within 24 hours of ictus (47%). The incidence of seizures did not vary significantly based on the use of prophylactic AEDs (11 versus 8%; P=0.33). Propensity score-matched analyses suggest that patients receiving prophylactic AEDs had a similar likelihood of suffering seizures as those who did not (P=0.49).

Propensity score-matched analysis suggests that prophylactic AEDs do not significantly reduce the risk of seizure occurrence in patients with spontaneous subarachnoid hemorrhage 13).

2014

Current guidelines recommend against the use of phenytoin following aneurysmal subarachnoid hemorrhage (aSAH) but consider other anticonvulsants, such as levetiracetam, acceptable. The objective of Karamchandani was to evaluate the risk of poor functional outcomes, delayed cerebral ischemia (DCI) and delayed seizures in aSAH patients treated with levetiracetam versus phenytoin. Medical records of patients with aSAH admitted between 2005-2012 receiving anticonvulsant prophylaxis with phenytoin or levetiracetam for >72 hours were reviewed. The primary outcome measure was poor functional outcome, defined as modified Rankin Scale (mRS) score >3 at first recorded follow-up. Secondary outcomes measures included DCI and the incidence of delayed seizures. The association between the use of levetiracetam and phenytoin and the outcomes of interest was studied using logistic regression. Medical records of 564 aSAH patients were reviewed and 259 included in the analysis after application of inclusion/exclusion criteria. Phenytoin was used exclusively in 43 (17%), levetiracetam exclusively in 132 (51%) while 84 (32%) patients were switched from phenytoin to levetiracetam. Six (2%) patients had delayed seizures, 94 (36%) developed DCI and 63 (24%) had mRS score >3 at follow-up. On multivariate analysis, only modified Fisher grade and seizure before anticonvulsant administration were associated with DCI while age, Hunt-Hess grade and presence of intraparenchymal hematoma were associated with mRS score >3. Choice of anticonvulsant was not associated with any of the outcomes of interest. There was no difference in the rate of delayed seizures, DCI or poor functional outcome in patients receiving phenytoin versus levetiracetam after aSAH. The high rate of crossover from phenytoin suggests that levetiracetam may be better tolerated 14).

2013

Exploratory analysis was performed on 413 patients enrolled in CONSCIOUS-1 (Clazosentan to Overcome Neurological Ischemia and Infarction Occurring after Subarachnoid Hemorrhage), a prospective randomized trial of clazosentan for the prevention of angiographic vasospasm. The association among clinical, laboratory, and radiographic covariates and the occurrence of seizures following SAH were determined. Covariates with a significance level of p < 0.20 on univariate analysis were entered into a multivariate logistic regression model. Receiver operating characteristic (ROC) curve analysis was used to define optimal predictive thresholds.

Of the 413 patients enrolled in the study, 57 (13.8%) had at least 1 seizure following SAH. On univariate analysis, a World Federation of Neurosurgical Societies grade of IV-V, a greater subarachnoid clot burden, and the presence of midline shift and subdural hematomas were associated with seizure activity. On multivariate analysis, only a subarachnoid clot burden (OR 2.76, 95% CI 1.39-5.49) and subdural hematoma (OR 5.67, 95% CI 1.56-20.57) were associated with seizures following SAH. Using ROC curve analysis, the optimal predictive cutoff for subarachnoid clot burden was determined to be 21 (of a possible 30) on the Hijdra scale (area under the curve 0.63).

A greater subarachnoid clot burden and subdural hematoma are associated with the occurrence of seizures after aneurysm rupture. These findings may help to identify patients at greatest risk for seizures and guide informed decisions regarding the prescription of prophylactic anticonvulsive therapy. Clinical trial registration no.: NCT00111085 (ClinicalTrials.gov) 15).

2008

A total of 137 adult patients were enrolled in this two-year retrospective study. Baseline prognostic variables were analyzed based on Cox’s proportional hazards model after a minimum of one-year follow-up.

Seizures occurred in 21 patients who had SAH, including acute symptomatic seizures in 11.7% (16/137) and unprovoked seizures in 3.6% (5/137). None progressed to status epilepticus during hospitalization. After a minimum of one-year follow-up, the mean Glasgow Outcome Score was 3.5 +/- 1.4 for patients with seizures and 3.1 +/- 1.1 for those without.

Higher mean World Federation of Neurological Societies grade on presentation was predictive of seizure, but seizure itself was not a significant prognostic predictor after a minimum of one-year follow-up. Regarding potential side effects of anti-epileptic drugs, anti-epileptic therapy should be carefully administered to patients with seizures after aneurysmal SAH 16).

2007

Rosengart et al. examined data collected in 3552 patients with SAH who were entered into four prospective, randomized, double-blind, placebo-controlled trials conducted in 162 neurosurgical centers and 21 countries between 1991 and 1997. The prevalence of AED use was assessed by study country and center. The impact of AEDs on in-hospital complications and outcome was evaluated using conditional logistic regressions comparing treated and untreated patients within the same study center.

Antiepileptic drugs were used in 65.1% of patients and the prescribing pattern was mainly dependent on the treating physicians: the prevalence of AED use varied dramatically across study country and center (intraclass correlation coefficients 0.22 and 0.66, respectively [p < 0.001]). Other predictors included younger age, worse neurological grade, and lower systolic blood pressure on admission. After adjustment, patients treated with AEDs had odds ratios of 1.56 (95% confidence interval [CI] 1.16-2.10; p = 0.003) for worse outcome based on the Glasgow Outcome Scale; 1.87 (95% CI 1.43-2.44; p < 0.001) for cerebral vasospasm; 1.61 (95% CI 1.25-2.06; p < 0.001) for neurological deterioration; 1.33 (95% CI 1.01-1.74; p = 0.04) for cerebral infarction; and 1.36 (95% CI 1.03-1.80; p = 0.03) for elevated temperature during hospitalization.

Prophylactic AED treatment in patients with aneurysmal SAH is common, follows an arbitrary prescribing pattern, and is associated with increased in-hospital complications and worse outcome 17).


From July 1998 to June 2002, 453 patients with spontaneous subarachnoid hemorrhage were treated. In the first 9 months, 79 patients were administered PHT until discharged from the hospital, unless a drug reaction occurred first. In the last 39 months, PHT was discontinued 3 days after admission (370 patients), unless there was a history of epilepsy (four patients). This study represents a retrospective analysis of prospectively collected data, with follow-up periods of 3 to 12 months after discharge. RESULTS: The 3-day PHT regimen produced a statistically significant reduction (P = 0.002) in the rate of PHT complications. In the first period, seven (8.8%) out of 79 patients experienced a hypersensitivity reaction, compared with two (0.5%) out of 370 patients in the second period. The percentage of patients having seizures, both short- and long-term, did not change significantly. In the first period, the seizure rate during hospitalization was 1.3%; in the second period, it was 1.9% (P = 0.603). At an average follow-up period of 6.7 months, three (5.7%) out of 53 survivors in the first period experienced a seizure (including those who had a seizure during hospitalization). In the second period, 12 (4.6%) out of 261 survivors experienced a seizure at an average follow-up period of 5.4 months (P = 0.573).

A 3-day regimen of PHT prophylaxis is adequate to prevent seizures in subarachnoid hemorrhage patients. Drug reactions are significantly reduced, but seizure rates do not change. Short-term PHT administration may be a superior treatment paradigm 18).

2005

Naidech et al. studied 527 SAH patients and calculated a “PHT burden” for each by multiplying the average serum level of PHT by the time in days between the first and last measurements, up to a maximum of 14 days from ictus. Functional outcome at 14 days and 3 months was measured with the modified Rankin scale, with poor functional outcome defined as dependence or worse (modified Rankin Scale > or =4). We assessed cognitive outcomes at 14 days and 3 months with the telephone interview for cognitive status. RESULTS: PHT burden was associated with poor functional outcome at 14 days (OR, 1.5 per quartile; 95% CI, 1.3 to 1.8; P<0.001), although not at 3 months (P=0.09); the effect remained (OR, 1.6 per quartile; 95% CI, 1.2 to 2.1; P<0.001) after correction for admission Glasgow Coma Scale, fever, stroke, age, National Institutes of Health Stroke Scale > or =10, hydrocephalus, clinical vasospasm, and aneurysm rebleeding. Seizure in hospital (OR, 4.1; 95% CI, 1.5 to 11.1; P=0.002) was associated with functional disability in a univariate model only. Higher quartiles of PHT burden were associated with worse telephone interview for cognitive status scores at hospital discharge (P<0.001) and at 3 months (P=0.003). CONCLUSIONS: Among patients treated with PHT, burden of exposure to PHT predicts poor neurologic and cognitive outcome after SAH 19).

2000

Rhoney et al. reviewed 95 SAH patient charts using standardized forms. Variables included prophylaxis duration, seizure incidence and timing, CT findings, AED adverse events, and 1-year patient follow-up.

Prehospital seizures occurred in 17.9% (17/95) of patients; another 7.4% (7/95) had a questionable prehospital seizure. In-hospital seizures occurred in 4.1% (4/95) of patients, a mean of 14.5 +/- 13.7 days from ictus; three of these four patients were receiving an AED at the time of seizure. Inpatient AED were prescribed to 99% of the cohort for a median of 12 (range 1 to 68) days. Approximately 8% of the cohort had posthospital discharge seizures; this included the patients who had prehospital or in-hospital seizures, 50% of whom were receiving AED therapy at the time of the seizure. Adverse effects occurred in 4. 1%; none were serious. The thickness of cisternal clot was associated with having a seizure; no other clinical predictors were identified. Having a seizure at any time did not adversely affect outcome.

In this SAH population, the majority of seizures happened before medical presentation. In-hospital seizures were rare and occurred more than 7 days postictus for patients receiving AED prophylaxis. The vast majority of putative clinical predictors did not help predict the occurrence of seizures; only the thickness of the cisternal clot was of value in predicting seizures. Patient selection for and the efficacy and timing of AED prophylaxis after SAH deserve prospective evaluation 20).

Experimental Studies

A study demonstrated that Valproic Acid (VPA) improves neurological outcome and decreases brain injury in a mouse model of SAH 21).

Recommendations

Dana G. Boeck, PharmD Department of Pharmacy, University Health System, San Antonio, Texas Division of Pharmacotherapy, The University of Texas at Austin College of Pharmacy Pharmacotherapy Education and Research Center University of Texas Health Science Center at San Antonio November 20, 2015 boeck11-20-15.pdf

1) , 18)

Chumnanvej S, Dunn IF, Kim DH. Three-day phenytoin prophylaxis is adequate after subarachnoid hemorrhage. Neurosurgery. 2007 Jan;60(1):99-102; discussion 102-3. PubMed PMID: 17228257.

2) , 8)

Raper DM, Starke RM, Komotar RJ, Allan R, Connolly ES Jr. Seizures after aneurysmal subarachnoid hemorrhage: a systematic review of outcomes. World Neurosurg. 2013 May-Jun;79(5-6):682-90. doi: 10.1016/j.wneu.2012.08.006. Epub 2012 Sep 25. Review. PubMed PMID: 23022642.

3)

Rowe AS, Goodwin H, Brophy GM, Bushwitz J, Castle A, Deen D, Johnson D, Lesch C, Liang N, Potter E, Roels C, Samaan K, Rhoney DH; Neurocritical Care Society Pharmacy Section. Seizure prophylaxis in neurocritical care: a review of evidence-based support. Pharmacotherapy. 2014;34(4):396-409. doi: 10.1002/phar.1374. Epub 2013 Nov 26. Review. PubMed PMID: 24277723.

4) , 12)

Human T, Diringer MN, Allen M, Zipfel GJ, Chicoine M, Dacey R, Dhar R. A Randomized Trial of Brief Versus Extended Seizure Prophylaxis After Aneurysmal Subarachnoid Hemorrhage. Neurocrit Care. 2017 Aug 22. doi: 10.1007/s12028-017-0440-5. [Epub ahead of print] PubMed PMID: 28831717.

5)

Dewan MC, Mocco J. Current practice regarding seizure prophylaxis in aneurysmal subarachnoid hemorrhage across academic centers. J Neurointerv Surg. 2015 Feb;7(2):146-9. doi: 10.1136/neurintsurg-2013-011075. Epub 2014 Jan 28. PubMed PMID: 24474163.

6) , 19)

Naidech AM, Kreiter KT, Janjua N, Ostapkovich N, Parra A, Commichau C, Connolly ES, Mayer SA, Fitzsimmons BF. Phenytoin exposure is associated with functional and cognitive disability after subarachnoid hemorrhage. Stroke. 2005 Mar;36(3):583-7. Epub 2005 Jan 20. PubMed PMID: 15662039.

7) , 16)

Lin YJ, Chang WN, Chang HW, Ho JT, Lee TC, Wang HC, Tsai NW, Tsai MH, Lu CH. Risk factors and outcome of seizures after spontaneous aneurysmal subarachnoid hemorrhage. Eur J Neurol. 2008 May;15(5):451-7. doi: 10.1111/j.1468-1331.2008.02096.x. Epub 2008 Mar 5. PubMed PMID: 18325027.

9)

Marigold R, Günther A, Tiwari D, Kwan J. Antiepileptic drugs for the primary and secondary prevention of seizures after subarachnoid haemorrhage. Cochrane Database Syst Rev. 2013 Jun 5;(6):CD008710. doi: 10.1002/14651858.CD008710.pub2. Review. PubMed PMID: 23740537.

10)

Lanzino G, D’Urso PI, Suarez J; Participants in the International Multi-Disciplinary Consensus Conference on the Critical Care Management of Subarachnoid Hemorrhage. Seizures and anticonvulsants after aneurysmal subarachnoid hemorrhage. Neurocrit Care. 2011 Sep;15(2):247-56. doi: 10.1007/s12028-011-9584-x. Review. PubMed PMID: 21751102.

11)

Riordan KC, Wingerchuk DM, Wellik KE, Zimmerman RS, Sirven JI, Noe KH, Patel BM, Demaerschalk BM. Anticonvulsant drug therapy after aneurysmal subarachnoid hemorrhage: a critically appraised topic. Neurologist. 2010 Nov;16(6):397-9. doi: 10.1097/NRL.0b013e3181efc92f. PubMed PMID: 21150393.

13)

Panczykowski D, Pease M, Zhao Y, Weiner G, Ares W, Crago E, Jankowitz B, Ducruet AF. Prophylactic Antiepileptics and Seizure Incidence Following Subarachnoid Hemorrhage: A Propensity Score-Matched Analysis. Stroke. 2016 Jul;47(7):1754-60. doi: 10.1161/STROKEAHA.116.013766. Epub 2016 Jun 14. PubMed PMID: 27301932; PubMed Central PMCID: PMC4927347.

14)

Karamchandani RR, Fletcher JJ, Pandey AS, Rajajee V. Incidence of delayed seizures, delayed cerebral ischemia and poor outcome with the use of levetiracetam versus phenytoin after aneurysmal subarachnoid hemorrhage. J Clin Neurosci. 2014 Sep;21(9):1507-13. doi: 10.1016/j.jocn.2014.03.009. Epub 2014 Jun 3. PubMed PMID: 24919470.

15)

Ibrahim GM, Fallah A, Macdonald RL. Clinical, laboratory, and radiographic predictors of the occurrence of seizures following aneurysmal subarachnoid hemorrhage. J Neurosurg. 2013 Aug;119(2):347-52. doi: 10.3171/2013.3.JNS122097. Epub 2013 Apr 12. PubMed PMID: 23581590.

17)

Rosengart AJ, Huo JD, Tolentino J, Novakovic RL, Frank JI, Goldenberg FD, Macdonald RL. Outcome in patients with subarachnoid hemorrhage treated with antiepileptic drugs. J Neurosurg. 2007 Aug;107(2):253-60. PubMed PMID: 17695377.

20)

Rhoney DH, Tipps LB, Murry KR, Basham MC, Michael DB, Coplin WM. Anticonvulsant prophylaxis and timing of seizures after aneurysmal subarachnoid hemorrhage. Neurology. 2000 Jul 25;55(2):258-65. PubMed PMID: 10908901.

21)

Tso MK, Lass E, Ai J, Loch Macdonald R. Valproic Acid treatment after experimental subarachnoid hemorrhage. Acta Neurochir Suppl. 2015;120:81-5. doi: 10.1007/978-3-319-04981-6_14. PubMed PMID: 25366604.

4th Annual EANS Vascular Section Meeting and Joint EANS/ESMINT Meeting

4th Annual EANS Vascular Section Meeting and Joint EANS/ESMINT Meeting

September 7 — September 8

Nice, France

 

Topics for abstracts can include (but are not limited to):
Vascular malformations
Vascular rare diseases
Experimental vascular neurosurgery
Treatment and prevention of ischemia
Aneurysms
Management of Subarachnoid Haemorrhage

Please visit the meeting website here.

Update: Middle cerebral artery M4 segment aneurysm

Middle cerebral artery M4 segment aneurysm

Middle cerebral artery aneurysms, are mainly found in the proximal and bifurcation tracts and only in the 1.1-1.7% of cases they are located in the M4 segment of the middle cerebral artery 1) 2) 3).

Etiology

Generally, these aneurysms are secondary to traumatic brain injury and inflammatory or infectious diseases and only rarely they have idiopathic origin 4). At present, only nine cases of ruptured cortical middle cerebral artery aneurysms have been described in literature 5) 6) 7) 8) 9) 10). The patients are all males, except the case of Ricci et al. 11). The average age of the reported patients is 40 years. The size of the aneurysms is between 1 mm and 10 mm and, in most cases, they are saccular intracranial aneurysms or fusiform morphology. In five patients, the aneurysms present infectious etiology. Usually, they occur with ICH, sometimes associated with subarachnoid hemorrhage (SAH).

Treatment

The endovascular treatment (EVT) has been performed in four cases, while the surgical treatment has been performed in three cases (two of trapping and one of clipping). In one patient, the infectious aneurysm has resolved spontaneously after antibiotic therapy. In all treatments performed, the patients have improved the neurologic symptoms and no residual aneurysms have been observed in the subsequent neuroradiology follow-up 12). Although surgery remains the main choice in the M4 aneurysms, because of the extremely distal location of them over the motor/somatosensory cortices, 13) Lv et al. 14) propose the use of the EVT in all types of the M4 aneurysms, especially after the surgery, when it is impossible to locate the small ruptured aneurysm. The main difficulty of the surgery is the precise surgical localization of the small M4 aneurysms 15). An inaccurate localization of these vascular lesions may result in larger craniotomies and unnecessary arachnoid and pial dissections with possible resultant permanent neurological injuries 16). In cases of aneurysms or arteriovenous malformations located at the sylvian point or at the posterior superior aspect of the insula, especially in dominant hemisphere, to reduce the dissection and open easily sylvian fissure, a logical path would follow the angular artery in the sylvian fissure cutting the arachnoid fibers and retracting only the tissues which are necessary to gain more exposure of the lesion 17).

Case reports

2017

A 53-year-old female was admitted with a sudden severe headache, nausea, vomiting, and a slight left hemiparesis. The computed tomography (CT) scan showed subarachnoid hemorrhage (SAH) in the left sylvian fissure and intracerebral hemorrhage (ICH) in the left posterior parietal area. The CT angiography (CTA) reconstructed with 3D imaging showed a small saccular aneurysm in the M4 segment in proximity of the angular area. A left parieto-temporal craniotomy was performed, the aneurysm was clipped and the ICH evacuated. The motor deficit was progressively recovered. At 3-month follow-up examination, the patient was asymptomatic and feeling well. Surgery is the best choice for the treatment of ruptured M4 aneurysms with ICH in the opinion of Ricci et al., because it allows to evacuate the hematoma and to exclude the aneurysm from the intracranial circulation. In addition, we suggest both the use of the neuronavigation technique and of the indocyanine green videoangiography (ICGV) for the aneurismal surgery 18).

2007

A 41-year-old man presented with an infarction manifesting as left-sided weakness and dysarthria. Magnetic resonance angiography revealed a subacute stage infarction in the right MCA territory and complete occlusion of the right ICA. Angiography demonstrated aneurysmal dilatation of the M4 segment of the right MCA. Surgery was performed to prevent hemorrhage from the aneurysm. The aneurysm was proximally clipped guided by Navigation-CT angiography and flow to the distal MCA was restored by superficial temporal artery-middle cerebral artery (STA-MCA) anastomosis 19).

2005

A 20-year-old man with an intracerebral haemorrhage due to a ruptured aneurysm, which arose from a penetrating artery of the distal middle cerebral artery (MCA; M4 segment). Excision of the aneurysm was successfully achieved via a right pterional approach. The follow-up angiogram demonstrated filling of the parent vessel and no residual aneurysm. This report illustrates the angiographical finding of a penetrating artery aneurysm of the distal MCA and summarizes the previous reports to discuss their pathological and clinical characteristics 20).
 
1) , 4) , 5) , 20)

Ahn JY, Han IB, Joo JY. Aneurysm in the penetrating artery of the distal middle cerebral artery presenting as intracerebral haemorrhage. Acta Neurochir (Wien). 2005 Dec;147(12):1287-90; discussion 1290. Epub 2005 Aug 29. PubMed PMID: 16133768.
2) , 8) , 14)

Lv N, Zhou Y, Yang P, Li Q, Zhao R, Fang Y, Xu Y, Hong B, Zhao W, Liu J, Huang Q. Endovascular treatment of distal middle cerebral artery aneurysms: Report of eight cases and literature review. Interv Neuroradiol. 2016 Feb;22(1):12-7. doi: 10.1177/1591019915617317. Epub 2015 Dec 3. Review. PubMed PMID: 26637241; PubMed Central PMCID: PMC4757379.
3)

Elsharkawy A, Lehečka M, Niemelä M, Billon-Grand R, Lehto H, Kivisaari R, Hernesniemi J. A new, more accurate classification of middle cerebral artery aneurysms: computed tomography angiographic study of 1,009 consecutive cases with 1,309 middle cerebral artery aneurysms. Neurosurgery. 2013 Jul;73(1):94-102; discussion 102. doi: 10.1227/01.neu.0000429842.61213.d5. PubMed PMID: 23615110.
6)

Horiuchi T, Tanaka Y, Takasawa H, Murata T, Yako T, Hongo K. Ruptured distal middle cerebral artery aneurysm. J Neurosurg. 2004;100:384–8.
7)

Lee SM, Park HS, Choi JH, Huh JT. Ruptured mycotic aneurysm of the distal middle cerebral artery manifesting as subacute subduralhematoma. J Cerebrovasc Endovasc Neurosurg. 2013;15:235–40.
9) , 13) , 15) , 16)

Raza SM, Papadimitriou K, Gandhi D, Radvany M, Olivi A, Huang J. Intra-arterial intraoperative computed tomography angiography guided navigation: a new technique for localization of vascular pathology. Neurosurgery. 2012 Dec;71(2 Suppl Operative):ons240-52; discussion ons252. doi: 10.1227/NEU.0b013e3182647a73. PubMed PMID: 22858682.
10) , 11) , 12) , 18)

Ricci A, Di Vitantonio H, De Paulis D, Del Maestro M, Raysi SD, Murrone D, Luzzi S, Galzio RJ. Cortical aneurysms of the middle cerebral artery: A review of the literature. Surg Neurol Int. 2017 Jun 13;8:117. doi: 10.4103/sni.sni_50_17. eCollection 2017. PubMed PMID: 28680736; PubMed Central PMCID: PMC5482160.
17)

Ausman JI, Diaz FG, Malik GM, Tomecek F. A new microsurgical approach to cerebrovascular lesions of the sylvian point: report of two cases. Surg Neurol. 1990 Jul;34(1):48-51. PubMed PMID: 2360163.
19)

Lee SH, Bang JS. Distal Middle Cerebral Artery M4 Aneurysm Surgery Using Navigation-CT Angiography. J Korean Neurosurg Soc. 2007 Dec;42(6):478-80. doi: 10.3340/jkns.2007.42.6.478. Epub 2007 Dec 20. PubMed PMID: 19096593; PubMed Central PMCID: PMC2588183.