Clinical Neurology and Neurosurgery 196 (2020) 105980

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Clinical Neurology and Neurosurgery
journal homepage: www.elsevier.com/locate/clineuro

Case Report

Asymmetric SIRPIDs in a vertebrobasilar stroke: Implications for
understanding its origin

T

José L. Fernández-Torrea,d,e,*, María Martín-Garcíaa,e, Enrique Marco de Lucab,e,
Miguel A. Hernández-Hernándezc,e
a

Department of Clinical Neurophysiology, Marqués de Valdecilla University Hospital, Santander, Cantabria, Spain
Departments of Radiology Marqués de Valdecilla University Hospital, Santander, Cantabria, Spain
c
Departments of Intensive Medicine, Marqués de Valdecilla University Hospital, Santander, Cantabria, Spain
d
Department of Physiology and Pharmacology, University of Cantabria (UNICAN), Santander, Cantabria, Spain
e
Biomedical Research Institute (IDIVAL), Santander, Spain
b

A R T I C LE I N FO
Keywords:
Stimulus-induced rhythmic
Periodic, or ictal discharges
Vertebrobasilar stroke
Thalamus
Midbrain
Pathophysiology

1. Introduction
Stimulus-induced rhythmic, periodic, or ictal discharges (SIRPIDs)
are abnormal discharges occurring after alerting stimuli, including auditory, tactile or nociceptive stimulation in comatose or stuporous patients. In recent years, several studies have described the incidence and
clinical significance of SIRPIDs [1,2], but the pathophysiology remains
incompletely understood.
The aim of this report is to describe the case of a patient who had a
vertebrobasilar ischemic event in whom asymmetric SIRPIDs due to an
extensive right thalamic and mesencephalic infarction, were noted. This
case provides data that allows us to understand the mechanisms that
might underlie SIRPIDs.
2. Case report
A 72-year-old woman was admitted to our emergency unit because
of an acute decrease in the level of consciousness. She had history of
atrial fibrillation on treatment with oral acenocoumarol and bisoprolol.
A computed tomography (CT) scan of the brain revealed an acute ischemic stroke involving the right thalamus and midbrain from a top of
the basilar thrombosis. No signs of acute bleeding were observed. She

was transferred to the intensive care unit (ICU), where neurological
examination showed her to be comatose with the right pupil larger and
with an absent pupil reaction. At 72 h, a second cranial CT scan disclosed a significant increase in infarction of the right thalamus and
midbrain, and the appearance of new acute ischemic lesions in the right
occipital lobe and right hemicerebellum (Fig. 1), along with a small
ischemic lesion in the left thalamus. Despite 4 days without sedation,
the patients ‘s clinical state worsened to a Glasgow Coma Scale 4 and
extensor posturing to noxious stimuli. Video-electroencephalogram (vEEG) showed slowing of the background activity consistent with a
diffuse encephalopathy. Pain and auditory stimulation produced
asymmetric bilateral rhythmic, negative-positive sharp waves involving
both frontal regions notably more prominent on the left (Fig. 2), corresponding to SIRPIDs. Two days later, v-EEG remained unchanged.
Given the neurological situation and the poor prognosis, the clinical
team and family decided to limit therapeutic support and the patient
died on day 5.
3. Discussion
At present, the exact pathophysiology of SIRPIDs is unknown.
SIRPIDs lie on an electroencephalographic spectrum now known as the

⁎
Corresponding author at: Department of Clinical Neurophysiology, Marqués de Valdecilla University Hospital, Avda. Valdecilla 25, 39008, Santander, Cantabria,
Spain.
E-mail address: joseluis.fernandezt@scsalud.es (J.L. Fernández-Torre).

https://doi.org/10.1016/j.clineuro.2020.105980
Received 28 April 2020; Received in revised form 24 May 2020; Accepted 29 May 2020
Available online 02 June 2020
0303-8467/ © 2020 Elsevier B.V. All rights reserved.

Clinical Neurology and Neurosurgery 196 (2020) 105980

J.L. Fernández-Torre, et al.

Fig. 1. A Brain CT scan revealing ischemic lesions involving he right thalamus, midbrain and occipital lobe (white arrows). Note the presence also of a small infarct in
the left thalamus (black arrow).

Fig. 2. A, B and C) Observe the occurrence of bilateral but asymmetric rhythmic, frontal sharp waves notably more prominent on the left side elicited by auditory and
painful stimulation compatible with SIRPIDS. Note the significant asymmetry of SIRPIDs on the right side. Low filter: 0.53 Hz; High filter: 70 Hz; Notch filter: 50 Hz.
Vertical bar: 200 μV; horizontal bar: 1 s (30 mm/s) in A and B, and 2 s (15 mm/s) in C.

an organized topographic manner to the middle layers of specific cortical areas; and of neurons that receive less clear subcortical inputs
which project more diffusely to the cerebral cortex [3]. Moreover, the
thalamus has reciprocal connections with the cerebral cortex, representing the thalamo-cortico-thalamic network (Fig. 3). Cortico-thalamic projections provide excitatory signals to both neuronal populations and to the thalamic reticular nucleus (TRN). The TRN contains
GABAergic interneurons which provide feedback inhibition to the
thalamocortical neurons.
SIRPIDs occur mainly in patients with severe impairment of the
level of consciousness. It is reasonable to think that the structures

"ictal-interictal continuum" [2]. SIRPIDs occur when a sensory stimulus
of a different nature (tactile, auditory, nociceptive) facilitates the appearance of rhythmic or periodic discharges from a injured cortex. The
process likely involves dysregulation of subcortical–cortical projections,
particularly thalamocortical in a markedly abnormal brain with a hyperexcitable cortex. Of note, there does not appear to be a specific cause
of SIRPIDs, and they have been associated with anoxic brain injury and
cardiac arrest, cerebral hemorrhage, traumatic brain injury, drug toxicity, and metabolic disturbances [1,2].
The thalamus contains excitatory thalamocortical projections from
neurons that transmit modality-specific inputs (sensory relay nuclei) in
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Clinical Neurology and Neurosurgery 196 (2020) 105980

J.L. Fernández-Torre, et al.

Fig. 2. (continued)

Fig. 2. (continued)

the presence of SIRPIDS between 36 and 72 h in comatose patients after
cardiac arrest has been recently reported with a favorable outcome. The
investigators suggested that SIRPIDS might be considered as a type of
reactivity in the context of a viable hyperexcitable cortex [4]. However,
it is possible that in specific clinical situations, the source of SIRPIDS is
via a different pathophysiological mechanism and, therefore, may be
associated with a different prognosis. Of note, a recent case exhibiting
corneal reflex-induced SIRPIDs suggests more extensive damage that
includes the brainstem [5].
In conclusion, while the exact pathophysiology of SIRPIDs has not
been determined, our clinical case provides some evidence of the role of
the thalamus and midbrain in the generation of this intriguing electroencephalographic phenomenon.

involved in the arousal system could have a role in its pathophysiology.
Thus, an abnormal state of arousal has been implicated in the source of
stimulus-induced seizures and SIRPIDs. It seems reasonable to speculate
that there is cortical hyperexcitability in which sudden activation of
sensory pathways can trigger epileptiform-induced EEG patterns.
Conversely, the TRN might also play a critical role in enabling the
conscious appreciation of stimuli and events by synchronizing activity
in the thalamus with cortical activity. Hence, the TRN can be considered the "gatekeeper of the gatekeeper (thalamus)". In the presence
of a disruption of the excitatory cortico-thalamic axons, the absence of
inhibition mediated by the TRN, might facilitate the occurrence of
SIRPIDs.
In our case, there was an extensive right thalamic and mesencephalic infarction apparently closely related to the abolition of the
SIRPIDs in the right hemisphere. There was no evidence suggesting the
coexistence of diffuse cortical damage. The involvement of the TRNmediated inhibition by the thalamic infarct might lead to an excess of
cortical stimulation, facilitating the occurrence of reflex epileptiform
discharges. Another hypothesis is that the thalamic lesions caused a
decrease in the activity of the excitatory thalamocortical projections
resulting in the asymmetry of the right SIRPIDs (Fig. 3). Interestingly,

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“We confirm that we have read the Journal’s position on issues involved in ethical publication and affirm that this report is consistent
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Clinical Neurology and Neurosurgery 196 (2020) 105980

J.L. Fernández-Torre, et al.

Fig. 3. A) Thalamocortico- thalamic network that could be implicated in the origin of SIRPIDS; B) Note that the lesion of the right thalamus and decrease of the
function of the right thalamo-cortical projections could explain the presence of asymmetric SIRPIDs.

Declaration of Competing Interest

rhythmic, periodic, or ictal patterns and spontaneous electrographic seizures, Clin.
Neurophysiol. 128 (2017) 2279–2285, https://doi.org/10.1016/j.clinph.2017.09.
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[3] E.E. Benarroch, The midline and intralaminar thalamic nuclei. Anatomic and functional specificity and implications in neurologic disease, Neurology 71 (2008)
944–949, https://doi.org/10.1212/01.wnl.0000326066.57313.13.
[4] G. Barbella, J.W. Lee, V. Alvarez, et al., Prediction of regaining consciousness despite
an early epileptiform EEG after cardiac arrest, Neurology 94 (2020) e1675–e1683,
https://doi.org/10.1212/WNL.0000000000009283.
[5] H.-J.-J. Lin, T.-Y.-Y. Hung, Y.-J.-J. Hsieh, J.-J.-J. Tsai, C.-W.-W. Huang, Spontaneous
and stimulus-induced rhythmic periodic or ictal discharges (SIRPIDs) with rhythmic
eye blinking and ocular dipping in a post-anoxic comatose patient: a case report,
Neurol. Sci. 37 (2016) 2027–2030, https://doi.org/10.1007/s10072-016-2677-8.

The authors declare that they have no conflicts of interests.
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