Acta Neurochirurgica
https://doi.org/10.1007/s00701-018-3606-9

CASE REPORT - FUNCTIONAL NEUROSURGERY - EPILEPSY

Diffuse vasospasm after transcortical temporal lobectomy for intractable
epilepsy
James Charles Dickerson 1

1

1

& Joaquin Andres Hidalgo & Zachary Stidham Smalley & James Mason Shiflett

1

Received: 15 February 2018 / Accepted: 25 June 2018
# Springer-Verlag GmbH Austria, part of Springer Nature 2018

Abstract
Cerebral delayed ischemia due to arterial vasospasm is a rare complication following epilepsy surgery. Here we report the third
known case and first of diffuse vasospasm. A 48-year-old woman underwent a transcortical anterior left temporal lobectomy.
Eleven days later, she had new-onset expressive aphasia with narrowing of the anterior, middle, and posterior cerebral arteries,
and increased velocities via transcranial Doppler. She was treated with fluids, nimodipine, and permissive hypertension. At
6 months, her speech was near baseline. Cerebral vasospasm may represent a rare cause of morbidity after anterior temporal
lobectomy; a literature review on the subject is presented.
Keywords Epilepsy . Neurosurgery . Epilepsy surgery . Vasospasm . Diffuse . Triple H . Amygdalohippocampectomy . Temporal
lobe resection . Transsylvian . Transcortical

Abbreviations
SAH
Subarachnoid hemorrhage
MRI
Magnetic resonance imaging
PET
Positron emission tomography
NSICU Neuroscience intensive care unit
CT
Computed tomography
POD
Post-operative day
MCA
Middle cerebral artery
CTA
Computed tomography angiography
ICA
Internal carotid artery
This work has not been previously presented at any conference or
published elsewhere.
There was no clinical trial registration number for this work.
This article is part of the Topical Collection on Functional Neurosurgery–
Epilepsy
* James Charles Dickerson
jcdickerson@umc.edu

ACA
IV
CSF

Anterior cerebral artery
Intravenous
Cerebrospinal fluid

Introduction
Cerebral artery vasospasm is a known complication following
subarachnoid hemorrhage (SAH), but has also been reported
following a variety of neurosurgical procedures, including
surgical resection for intractable epilepsy [1, 9, 10, 15, 19].
Presently, there are only two reported cases of clinically apparent vasospasm following epilepsy surgery, and both were
limited to the ipsilateral vasculature [3, 12]. Here we report
what we believe to be the first case of symptomatic diffuse
vasospasm following an anterior temporal lobectomy. We discuss the clinical course, management, and relevant literature.

Joaquin Andres Hidalgo
jhidalgo@umc.edu
Zachary Stidham Smalley
zsmalley@umc.edu
James Mason Shiflett
jshiflett@umc.edu
1

Department of Neurosurgery, University of Mississippi Medical
Center, 2500 North State Street, Jackson, MS 39216, USA

Case presentation
A 48-year-old right-handed African-American female suffering
from complex partial seizures with secondary generalization
was referred to our institution for cortical mapping and staged
resection of epileptogenic foci. At the time of admission, she
was experiencing manual and oromandibular automatisms with

Acta Neurochir

speech arrest approximately twice a week refractory to treatment with divalproex, lacosamide, and topiramate.
Pre-operative Wada testing demonstrated language representation in the left hemisphere, and magnetic resonance imaging (MRI) without the administration of intravenous contrast showed left hippocampal sclerosis. Positron emission
tomography (PET) scan did not reveal any abnormal hypermetabolic foci. Neuropsychological testing demonstrated no
receptive or expressive language difficulties.
She underwent a craniotomy for subdural electrode placement on hospital day 1, and video electrocorticography delineated an irritative zone in the lateral and proximal aspects of
the left posterior temporal electrode corresponding to the left
mesial temporal lobe. On hospital day 7, she was taken to the
operating room for electrode removal and left temporal lobectomy using an anterior transcortical approach. Resection included the left temporal lobe, hippocampus, amygdala, and
uncus; final pathology was consistent with type 1b cortical
dysplasia. There were no intraoperative complications, and
she was transferred to the neuroscience intensive care unit
(NSICU) for 24-h post-operative observation. A routine
post-operative MRI revealed bilateral temporal-occipital junction restricted diffusion, as well as right occipital horn and
fourth ventricle interventricular hemorrhage (Fig. 1a, b).
On post-operative day (POD) 1 following the lobectomy,
the patient developed a fever and leukocytosis. Blood and
urine cultures were drawn and then empiric broad spectrum
antibiotics started; lower extremity ultrasonography was negative for thrombosis. On POD 4, a lumbar puncture was performed: the gram stain was negative but the white blood cell
count was 12,792 with 90% neutrophils; the glucose, 12; and
protein, 390. There were 46,727 red blood cells in the third
tube. After 6 days, none of the cultures demonstrated growth,
her fever and leukocytosis resolved, and the antibiotics were
discontinued.
Fig. 1 a Post-resection axial
diffusion weighted MRI sequence
showing parieto-occipital infarct.
b Axial susceptibility weighted
MRI sequence revealing right
parieto-occipital cortical
contusion and hemorrhage tract
from deep subdural grid
placement with subsequent
interventricular hemorrhage in
left occipital horn

While the patient was intermittently lethargic after surgery,
her mental status continued to improve following resolution of
the fever and leukocytosis. On POD 11, she was noted to have
new-onset expressive aphasia. She was transferred back to the
NSICU and underwent an MRI, which revealed restricted diffusion in the left middle cerebral artery (MCA) distribution
concerning for infarct. CT angiography (CTA) obtained the
following day demonstrated severe diffuse narrowing of the
distal internal carotid arteries (ICA), proximal anterior cerebral arteries (ACA), MCAs, and the entire posterior circulation (Fig. 2a). Transcranial Doppler showed peak flow velocities of 150 cm/s in the left ACA and 331 cm/s in the left
MCA. On the right, velocities were 273 cm/s in ACA and
187 cm/s in the MCA. Table 1 shows all recorded peak velocities. Overall, vasospasm was most severe in the left MCA and
right ACA territories based on transcranial Doppler (TCD).
Treatment for vasospasm was initiated with fluids,
nimodipine, and permissive hypertension. Eight days after
the initial CTA, on POD 20, a follow-up CTA was obtained
and demonstrated improvement in vasospasm (Fig. 2b). The
patient was discharged to a swing bed and completed a 21-day
course of nimodipine. At discharge, her aphasia was improving but was still present.
At the 6-month follow-up visit, her speech was significantly improved, and she was near her pre-operative baseline with
only mild dysnomia remaining. In addition, she remained seizure free on lacosamide and topiramate.

Discussion
Symptomatic vasospasm after epilepsy surgery is not an expected complication. This case represents only the third reported (Table 2), and as such our institution has no formalized
protocol to screen patients post-operatively. Given the rarity of

Acta Neurochir
Fig. 2 a Axial CTA image
showing diffuse narrowing of the
cerebral circulation, notably in
proximal left MCA territory. b
Follow-up CTA 8 days later
demonstrating increased diameter
of the anterior and middle
circulation compared to initial
CTA in a

the event, a low index of suspicion likely led to a delay in
diagnosis. This may also have occurred in the case presented
by Mandonett et al. (2009), where the patient’s aphasic symptoms worsened on POD 2, but the diagnosis did not occur until
POD 5. This group also employed intravenous (IV)
nimodipine and hydration and reported marked clinical improvement within 24 h, and symptom resolution within a
few months [12]. In Chakravarty et al. (2015), the onset of
symptoms occurred 38 h after the surgery, and the diagnosis
appears to have been prompt. This patient received intraarterial nimodipine, as well as blood pressure augmentation,
yielding symptom resolution within hours [3]. In the present
case, it is possible that the delay in treatment contributed to the
prolonged aphasia. While there was discussion of obtaining
digital subtraction angiography after the onset of the aphasia,
it was forgone as it was unlikely to change management.
Another plausible explanation for the vasospasm in our patient is meningitis [2]. While no organism was isolated, and
post-operative cerebrospinal fluid (CSF) studies must be
interpreted with caution, the patients were suggestive of bacterial infection [16, 20]. Bacterial meningitis has been shown to
lead to vasospasm, postulated to occur through cytokines such
as IL-1β and IL-6 [5]. However, these cytokine levels are also

Table 1

elevated in the CSF of rodents after trauma; simply undergoing
an operation may result in an increase in IL-1β and IL-6 [22].
While these three cases of clinically apparent vasospasm
following epilepsy surgery are the only examples known by
the authors, previous works estimate that the incidence of
radiographic vasospasm may be considerably higher.
Schaller et al. (1998) defined vasospasm as flow velocity increases of > 50% in comparison to pre-operative TCDs. They
found vasospasm in one or both of the MCAs in 14 of 20
patients (70%) undergoing amygdalohippocampectomy by
the transsylvian approach, but notably all were asymptomatic
[17]. In 2004, this same group demonstrated statistically significant increased flow velocities in the ipsilateral and contralateral MCAs relative to pre-operative baseline in the
transsylvian approach (n = 40), and in the ipsilateral MCA
alone in the transcortical approach (n = 40). For the ipsilateral
MCA, the transsylvian group’s pooled peak velocity represented a 79% increase over pre-operative TCDs, while the
transcortical group experienced a 49% increase. Therefore, it
is likely that a significant portion of these patients met their
previously used criteria for vasospasm. However, these increased velocities were not associated with neurologic deterioration [19].

Peak velocities by territory and laterality from all recorded transcranial Doppler examinations

Post-operative day

Left ACA (cm/s)

Left MCA (cm/s)

Lindegaard ratio
(left)

Right ACA (cm/s)

Right MCA (cm/s)

Lindegaard ratio
(right)

13
14
17
18
20
21

150
120
176
134
148
189

331
265
293
326
326
296

9.66
6.19
8.36
11.1
8.57
8.38

273
248
169
287
287
271

187
225
234
194
173
167

3.25
4.41
3.92
4.24
4.10
4.00

Acta Neurochir
Table 2

Comparison of reported cases of symptomatic vasospasm to date

Publication

Surgery

Presenting
symptoms

Time from
surgery to
symptoms

Treatment

Outcome

Mandonett et al.
(2009)

Antero-mesial temporal
lobectomy

Global aphasia

48 h

IV nimodipine and
hyperhydration

Improvement within 24 h
and complete resolution
by 2 months

Chakravarty et al. Selective
(2015)
amygdalohippocampectomy

Contralateral
weakness and
global aphasia

38 h

Intra-arterial nimodipine
and noradrenaline
infusion

Present Case

Expressive aphasia

12 days

Permissive hypertension,
IV fluids, and oral
nimodipine

Near-total return of power,
speech, and recognition
after 4 h
Improvement within
10 days and near
resolution by 6 months

Anterior temporal lobectomy

Lackner et al. (2012) defined vasospasm as velocities >
120 cm/s and found that 35 of 107 patients (33%) undergoing
either selective amygdalohippocampectomy or temporal lobe
resection had increased velocities. Eighteen had ipsilateral
MCA vasospasm alone, and 17 were found to have bilateral
MCA vasospasm [10]. The 35 patients with vasospasm had a
significantly higher incidence of unexpected post-operative
neurologic signs and symptoms, with the most common being
headache, aphasia, and cranial nerve and/or extremity paresis.
However, the study did not identify a timeline for these complications. It is unclear if they were the direct result of the
increased velocities or simply unexpected post-operative complications that correlated with vasospasm found at a later date.
Because of this, the clinical significance of the work remains
unclear [7, 14]. This paper did identify female gender and a
higher volume of post-operative blood as risk factors for
vasospasm.
The time from surgery to symptom onset in the three reported cases was remarkably different—38 h, 48 h, and 11 days. In
SAH secondary to aneurysm rupture, vasospasm has been
shown to occur over a wide range of 3–15 days, with a peak
incidence around days 6–8 [4, 21]. In studies of post-traumatic
vasospasm, there is also a large range (2–12 days), but with a
peak incidence 2–4 days after the insult [15]. Given the different peak incidences, it is unclear if these represent distinct pathways, or convergent ones. In both aneurysmal and traumatic
SAH, the volume of blood is predictive of vasospasm risk [4, 6,
13]. It is possible that the “micro-trauma” of surgery led to these
cases of post-operative vasospasm, or that they occurred via the
mechanism seen in aneurysmal SAH [18].
The pathophysiology of vasospasm after SAH is not well
understood, and at present it is thought to be a product of the
release of spasmogenic substances during blood clot lysis [8,
9]. Studies that have investigated vasospasm following surgery have speculated that it may be secondary to mechanical
manipulation of the vasculature or due to the spillage of blood
into the cisterns [1, 12, 18, 19]. In our transcortical approach,
there was no direct manipulation of the ipsilateral MCA, nor

would this alone account for the diffuse spasm. Given the
lumbar puncture demonstrating blood in the subarachnoid
space, we consider the degradation of blood products the more
plausible mechanism. In Mandonett et al. (2009), subarachnoid blood was visualized on the initial post-operative scan. In
Chakravarty et al. (2015), the post-operative scan was considered “unremarkable” and an image was not provided in the
manuscript. It is possible that the volume of subarachnoid
blood was larger in this case than in the other two, and this
may have led to diffuse rather than local vasospasm. There
was also intraventricular hemorrhage visualized on the postresection MRI, and vasospasm in association with intraventricular hemorrhage has been described [11]. It is possible that
the burden of subarachnoid blood and intraventricular blood,
and a possible meningitis, all contributed to an inflammatory
state leading to diffuse vasospasm.

Conclusion
Here we report the third known case of symptomatic vasospasm after surgery for epilepsy, and the first known instance
of diffuse vasospasm. Although rare, it is a documented and
treatable cause of post-operative morbidity. Therefore, in the
event of unexpected neurologic deficit post-resection, it is
reasonable to consider vasospasm, especially in the setting
of infection or the presence of subarachnoid or intraventricular
blood.

Compliance with ethical standards
Conflict of interest The authors declare that they have no conflict of
interest.
Ethical approval This article does not contain any studies with human or
animal participants performed by any of the authors.
Patient consent The patient consented for the use of their case in scholarly activities, such as education and research.

Acta Neurochir

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