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BMC Neurology
Published in: BMC Neurology 1/2018

Open Access 01-12-2018 | Case report

A case report of delayed cortical infarction adjacent to sulcal clots after traumatic subarachnoid hemorrhage in the absence of proximal vasospasm

Authors: Christian Schinke, Viktor Horst, Ludwig Schlemm, Matthias Wawra, Michael Scheel, Jed A. Hartings, Jens P. Dreier

Published in: BMC Neurology | Issue 1/2018

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Abstract

Background

Cortical ischemic lesions represent the predominant pathomorphological pattern of focal lesions after aneurysmal subarachnoid hemorrhage (aSAH). Autopsy studies suggest that they occur adjacent to subarachnoid blood and are related to spasm of small cortical rather than proximal arteries. Recent clinical monitoring studies showed that cortical spreading depolarizations, which induce cortical arterial spasms, are involved in lesion development. If subarachnoid blood induces adjacent cortical lesions, it would be expected that (i) they also develop after traumatic subarachnoid hemorrhage (tSAH), and (ii) lesions after tSAH can occur in absence of angiographic vasospasm, as was found for aSAH.

Case presentation

An 86-year-old woman was admitted to our hospital with fluctuating consciousness after hitting her head during a fall. The initial computed tomography (CT) was significant for tSAH in cortical sulci. On day 8, the patient experienced a secondary neurological deterioration with reduced consciousness and global aphasia. Whereas the CT scan on day 9 was still unremarkable, magnetic resonance imaging (MRI) on day 10 revealed new cortical laminar infarcts adjacent to sulcal blood clots. Proximal vasospasm was ruled out using MR and CT angiography and Doppler sonography. CT on day 14 confirmed the delayed infarcts.

Conclusions

We describe a case of delayed cortical infarcts around sulcal blood clots after tSAH in the absence of proximal vasospasm, similar to results found previously for aSAH. As for aSAH, this case suggests that assessment of angiographic vasospasm is not sufficient to screen for risk of delayed infarcts after tSAH. Electrocorticography is suggested as a complementary method to monitor the hypothesized mechanism of spreading depolarizations.
Literature
1.
Neil-Dwyer G, Lang DA, Doshi B, Gerber CJ, Smith PW. Delayed cerebral ischaemia: the pathological substrate. Acta Neurochir. 1994;131(1–2):137–45.CrossRef
2.
Stoltenburg-Didinger G, Schwarz K. Brain lesions secondary to subarachnoid hemorrhage due to ruptured aneurysms. In: Cervós-Navarro J, Ferszt R, editors. Stroke and microcirculation. New York: Raven Press; 1987. p. 471–80.
3.
Schatlo B, Dreier JP, Glasker S, Fathi AR, Moncrief T, Oldfield EH, et al. Report of selective cortical infarcts in the primate clot model of vasospasm after subarachnoid hemorrhage. Neurosurgery. 2010;67(3):721–8 discussion 8-9.CrossRef
4.
van Norden AG, van Dijk GW, van Huizen MD, Algra A, Rinkel GJ. Interobserver agreement and predictive value for outcome of two rating scales for the amount of extravasated blood after aneurysmal subarachnoid haemorrhage. J Neurol. 2006;253(9):1217–20.CrossRef
5.
Dreier JP, Sakowitz OW, Harder A, Zimmer C, Dirnagl U, Valdueza JM, et al. Focal laminar cortical MR signal abnormalities after subarachnoid hemorrhage. Ann Neurol. 2002;52(6):825–9.CrossRef
6.
Woitzik J, Dreier JP, Hecht N, Fiss I, Sandow N, Major S, et al. Delayed cerebral ischemia and spreading depolarization in absence of angiographic vasospasm after subarachnoid hemorrhage. J Cereb Blood Flow Metab. 2012;32(2):203–12.CrossRef
7.
Weidauer S, Vatter H, Beck J, Raabe A, Lanfermann H, Seifert V, et al. Focal laminar cortical infarcts following aneurysmal subarachnoid haemorrhage. Neuroradiology. 2008;50(1):1–8.CrossRef
8.
Brown RJ, Kumar A, Dhar R, Sampson TR, Diringer MN. The relationship between delayed infarcts and angiographic vasospasm after aneurysmal subarachnoid hemorrhage. Neurosurgery. 2013;72(5):702–7 discussion 7-8.CrossRef
9.
Perrein A, Petry L, Reis A, Baumann A, Mertes P, Audibert G. Cerebral vasospasm after traumatic brain injury: an update. Minerva Anestesiol. 2015;81(11):1219–28.PubMed
10.
Vora YY, Suarez-Almazor M, Steinke DE, Martin ML, Findlay JM. Role of transcranial Doppler monitoring in the diagnosis of cerebral vasospasm after subarachnoid hemorrhage. Neurosurgery. 1999;44(6):1237–47 discussion 47-8.PubMed
11.
Coyne TJ, Loch Macdonald R, Christopher WM. Angiographic vasospasm in a contemporary series of patients with aneurysmal subarachnoid haemorrhage. Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia. 1994;1(2):106–10.CrossRef
12.
Mills JN, Mehta V, Russin J, Amar AP, Rajamohan A, Mack WJ. Advanced imaging modalities in the detection of cerebral vasospasm. Neurol Res Int. 2013;2013:415960.CrossRef
13.
Kerkeni H, Schatlo B, Dan-Ura H, Remonda L, Muroi C, Diepers M, et al. Proximal arterial diameters on CT angiography and digital subtraction angiography correlate both at admission and in the vasospasm period after aneurysmal subarachnoid hemorrhage. Acta Neurochir Suppl. 2015;120:171–5.PubMed
14.
Ohkuma H, Manabe H, Tanaka M, Suzuki S. Impact of cerebral microcirculatory changes on cerebral blood flow during cerebral vasospasm after aneurysmal subarachnoid hemorrhage. Stroke. 2000;31(7):1621–7.CrossRef
15.
Dreier JP. The role of spreading depression, spreading depolarization and spreading ischemia in neurological disease. Nat Med. 2011;17(4):439–47.CrossRef
16.
Iwanowski L, Olszewski J. The effects of subarachnoid injections of iron-containing substances on the central nervous system. J Neuropathol Exp Neurol. 1960;19:433–48.CrossRef
17.
Hartings JA, York J, Carroll CP, Hinzman JM, Mahoney E, Krueger B, et al. Subarachnoid blood acutely induces spreading depolarizations and early cortical infarction. Brain. 2017;140(10):2673–90.CrossRef
18.
Dreier JP, Korner K, Ebert N, Gorner A, Rubin I, Back T, et al. Nitric oxide scavenging by hemoglobin or nitric oxide synthase inhibition by N-nitro-L-arginine induces cortical spreading ischemia when K+ is increased in the subarachnoid space. J Cereb Blood Flow Metab. 1998;18(9):978–90.CrossRef
19.
Dreier JP, Petzold G, Tille K, Lindauer U, Arnold G, Heinemann U, et al. Ischaemia triggered by spreading neuronal activation is inhibited by vasodilators in rats. J Physiol. 2001;531(Pt 2):515–26.CrossRef
20.
Dreier JP, Major S, Manning A, Woitzik J, Drenckhahn C, Steinbrink J, et al. Cortical spreading ischaemia is a novel process involved in ischaemic damage in patients with aneurysmal subarachnoid haemorrhage. Brain. 2009;132(Pt 7):1866–81.CrossRef
21.
Hinzman JM, Andaluz N, Shutter LA, Okonkwo DO, Pahl C, Strong AJ, et al. Inverse neurovascular coupling to cortical spreading depolarizations in severe brain trauma. Brain. 2014;137(Pt 11):2960–72.CrossRef
22.
Luckl J, Lemale CL, Kola V, Horst V, Khojasteh U, Oliveira-Ferreira AI, et al. The negative ultraslow potential, electrophysiological correlate of infarction in the human cortex. Brain. 2018;141(6):1734–52.CrossRef
23.
Vergouwen MD, Vermeulen M, van Gijn J, Rinkel GJ, Wijdicks EF, Muizelaar JP, et al. Definition of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage as an outcome event in clinical trials and observational studies: proposal of a multidisciplinary research group. Stroke. 2010;41(10):2391–5.CrossRef
24.
Balanca B, Meiller A, Bezin L, Dreier JP, Marinesco S, Lieutaud T. Altered hypermetabolic response to cortical spreading depolarizations after traumatic brain injury in rats. J Cereb Blood Flow Metab. 2017;37(5):1670–86.CrossRef
25.
Dreier JP, Fabricius M, Ayata C, Sakowitz OW, William Shuttleworth C, Dohmen C, et al. Recording, analysis, and interpretation of spreading depolarizations in neurointensive care: review and recommendations of the COSBID research group. J Cereb Blood Flow Metab. 2017;37(5):1595–625.CrossRef
Metadata
Title
A case report of delayed cortical infarction adjacent to sulcal clots after traumatic subarachnoid hemorrhage in the absence of proximal vasospasm
Authors
Christian Schinke
Viktor Horst
Ludwig Schlemm
Matthias Wawra
Michael Scheel
Jed A. Hartings
Jens P. Dreier
Publication date
01-12-2018
Publisher
BioMed Central
Published in
BMC Neurology / Issue 1/2018
Electronic ISSN: 1471-2377
DOI
https://doi.org/10.1186/s12883-018-1217-y

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