Scand J Pain 2018; 18(1): 121–124

Educational case report
Harsha Shanthanna*

A case report of a thalamic stroke associated
with sudden disappearance of severe chronic low
back pain
https://doi.org/10.1515/sjpain-2017-0169
Received November 23, 2017; revised December 21, 2017; accepted
January 10, 2018; previously published online February 10, 2018

Abstract
Background: Chronic pain conditions are associated
with neuroplasticity within the central nervous system.
In most patients the maladaptive consequence of neuroplasticity supports prolonged course of chronic pain,
despite the absence of a commensurate etiology. From a
pain neuromatrix perspective it can involve three different circuits within the central nervous system; the classical sensory pathway, the limbic system pathway, and the
associative pathways involving the parietal cortical connections. Although this can be conceptualized as a fluid
system composed of several interacting networks, it can
be broadly separated into a nociceptive specific network
of spino-thalamic neurons and second order neurons
beyond thalamus that are not nociceptor specific. Thalamus acts as an important relay station that conveys nociceptive signaling to higher centres. Neuroplastic changes
can potentially involve any parts within this neuromatrix.
It is very uncommon to observe the sudden disappearance
of such a chronic pain condition.
Methods and results: In this case report, the author
describes the clinical course of a patient with severe
chronic low back pain (CLBP), whose pain suddenly disappeared after a stroke involving his left thalamus. Although
extremely rare, existing case reports of such disappearance of pain with a secondary stroke in patients suffering
from central post stroke pain (CPSP) are reviewed. The
author further postulates hypotheses that could potentially explain this phenomenon based on the existing
knowledge.

*Corresponding author: Harsha Shanthanna, Department of
Anesthesia, St. Joseph’s Healthcare, McMaster University,
50 Charlton Avenue East, Hamilton, L8N 4A6, Canada,
Tel.: +905-522-1155, Ext. 33853, E-mail: shanthh@mcmaster.ca

Conclusions and implications: Although extremely rare
and unpredictable, a thalamic stroke involving areas that
are involved in chronic pain signaling can potentially lead
to disappearence of an existing chronic pain condition.
This is the first case report of such sudden disappearence
of CLBP with well established nociceptive pathology supported by clinical and imaging findings. This unique case
report could potentially generate ideas for future research
and clinical treatment in the field of neuromodulation and
brain stimulation.
Keywords: neuromodulation; neuroplasticity; thalamic
pain; post-stroke pain; thalamic stroke; deep brain
stimulation.

1 Introduction
Pain is transmitted from peripheral nociceptors to
higher cortical areas, where it is perceived, localized and
emotionally experienced. The various neural networks
of the body-pain neuromatrix sub serve the sensorydiscriminative, affective-motivational, and evaluativecognitive dimensions of pain experience [1, 2]. Within
this network, thalamus acts as an important relay centre
to process peripheral signals before they are relayed to
higher cortical areas [3]. Thalamus is also prominently
involved in patients who suffer from central post stroke
pain (CPSP) syndrome [4], and is an important target for
deep brain stimulation for chronic pain [5, 6]. Through
this report, the author highlight a case of sudden disappearance of chronic low back pain (CLBP) in a patient
who had left thalamic stroke and review the relevant
literature.

2 Case report
A 66 year old gentleman with a 6 year history of CLBP was
referred to our pain clinic for management in November

© 2018 Scandinavian Association for the Study of Pain. Published by Walter de Gruyter GmbH, Berlin/Boston. All rights reserved.

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Shanthanna: Disappearance of chronic back pain after a stroke

2012. His comorbidities included obesity, hypertension,
type 2 diabetes mellitus, obstructive sleep apnea, hypothyroidism, and mild depression. Before being seen in
our clinic, he was being managed with hydromorphone
contin 12 mg (equivalent to 40 mg of morphine)-three
times a day, along with hydromorph 2 mg (equivalent to
10 mg of morphine) breakthrough tablets-taken as 3–4
times a day, in addition to pregabalin 150 mg twice a day.
He was referred to our clinic for consideration of spinal
interventions as his CLBP was moderate to severe in
intensity, despite his medical management. His clinical
examination did not reveal any red flags of neurological
pathology. Imaging findings suggested age related multi­
level degeneration of disc and facet elements, with significant arthropathy at lower three lumbar levels, along
with moderate foraminal narrowing. Based on his clinical and imaging findings, he was offered radiofrequency
(RF) ablation of medial branches of the affected facet
joints, after a positive diagnostic medial branch blockade. As the RF intervention was successful in controlling
his spinal pain for an average duration of 6–8 months,
he continued with repeat RF procedures with predictably
good success, without the need for other interventions
or increases to his medication. Over the course of 4 years
(2012–2015) he underwent seven RF sittings, and was due
for a repeat of the RF procedure during February 2016.
However, having missed his procedural appointment,
the patient and his wife visited our clinic during April
2016 to inform us of the following surprising developments. As per their report, during the month of January
2016, patient was observed to exhibit odd cognitive and
behavioral changes by his wife. He demonstrated forgetfulness, did not remember how to put on his positive pressure mask for sleep apnea, and was searching
for his deceased brother at home. He was taken to the
hospital, considering a diagnosis of early dementia or
vasculitis. However, further workup, including a CT
scan revealed that the patient had suffered an acute
left thalamic infarct. His MRI confirmed the location of
infarct to be posterior medial aspect of the left thalamus
(Figure 1). Because of the nonavailability of a 3D MRI, a
more precise location of the thalamic nucleus was not
possible.
Over the course of the next 1–2 weeks he was evaluated at the stroke prevention clinic. It was observed that
the patient recovered completely in his cognitive and
behavioral functions, as well as in his memory. Also,
fortunately enough, his CLBP completely disappeared
without the need to continue with any of his pain medications, including daily opioids, which he had been
on for more than 10 years. The following findings were

Figure 1: T1 weighted MRI image demonstrating stroke in the left
thalamus.

observed during the neurological examination in March
2016 (2 months after his thalamic stroke). His pupils were
equal and reactive to light. Visual fields were intact to
confrontation; however, he was not able to count fingers
in the upper quadrants in both eyes, but was able to
appreciate movement in these areas. Extraocular movements were full with no nystagmus. Facial sensation to
light touch and movements were normal. Hearing was
grossly normal. There was symmetrical palate elevation, normal trapezius strength and tongue was midline.
Muscle bulk, tone and power were normal in all four
extremities. Sensation was intact to light touch and vibration sense, observed in all dermatomes. Deep tendon
reflexes were 2 + throughout. Plantar response was flexor
bilaterally. Coordination was normal on finger-to-nose
testing and rapid alternating movements. There was no
bradykinesia. There were no extrapyramidal features.
Gait was normal. Tandem gait was slightly unsteady,
but within normal limits. Romberg was negative. Similar
neurological findings were observed during his examination in April 2016, as well as in his last follow up visit in
September 2017 (more than 18 months after his stroke).
With the sudden disappearance of CLBP, patient has not
felt the need for repeating his RF procedure. He continues
to be with minimal pain even 18 months after the stroke
without any need for opioid or other medications or spine
interventions.
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Shanthanna: Disappearance of chronic back pain after a stroke

3 Discussion
This is a unique case report of a thalamic stroke resulting in the disappearance of CLBP, with well established
nociceptive pathology supported by clinical and imaging
findings. To the author’s knowledge this is the only case,
besides the description by Head and Holmes of a case in
which a phantom limb pain disappeared after an infarct
of the opposite parietal lobe [7], of a peripheral source of
pain that has been positively affected as a result of stroke.
A few case reports of such occurrence in CPSP have been
described.

3.1 Comparative literature
Soria and Fine described a report of disappearance of
thalamic pain after parietal cortical stroke and attributed
this to possible disruption of the thalamo-parietal radiations [8], while Hirato et al. [9] considered the possibility
of secondary cortical damage in a patient who had accidental putaminal lesion leading to pain disappearance. It
is interesting that the laterality of the subsequent stroke
lesion may not be crucial for the pain relieving effect, as
shown by the Daniele et al. [10] and Helmchen et al. [11],
both cases reporting resolution of thalamic pain following a second stroke in the contralateral hemisphere. They
postulated that the bilateral connections of the spinothalamic tract could partially explain this phenomenon,
and insisted that CPSP resulted from a bilateral disorder
of functional plasticity. Even in the present patient, bilateral pain was affected, despite the left sided lesion. There
is ample evidence to support that the pain processing
during noxious stimulation in normal subjects involves
bilaterally distributed networks [12].

3.2 R
 ole of thalamus and thalamo-cortical
projections in pain processing
It is well known that thalamus plays an integral part, and
acts as the major relay station between the spinothalamic
tracts (STT)-carrying the pain signals, and the cortical structures [2]. Further, the thalamus is also intricately involved
in processing pain memory [13]. The nociceptive inputs can
be transmitted directly through STT, or indirectly through
the spinoreticular, spinomesencephalic, or even dorsal
column pathways to the thalamus [2]. Although the pain
pathways beyond the thalamus have been hard to decipher
[14], a nociceptive-specific matrix comprising the cortical
regions receiving direct STT input has been described,

123

which includes the posterior operculum and insular areas
[2]. Following activation of this specific network, studies of
functional neuroimaging have consistently indicated that
there are many cortical areas that contribute to the pain
experience. However, none of them are specific to pain [2].
The cortical areas commonly activated by these thalamocortical projections include the areas of somato-sensory
cortex, the insula, anterior cingulate cortex (ACC), the prefrontal and posterior parietal areas.

3.3 P
 otential hypotheses to explain the
­disappearance of pain
In the present patient, disruption within the thalamocortical pathways could have led to selective loss of
afferent nociceptive signaling, leading to modulations
in the thalamo-parietal connections, and thereby abolishment of pain. Another hypothesis that can be considered is based on the specificity of nociceptive signaling,
as reported by Craig et al. [15]. Although not widely
accepted, Craig et al. reported that nociceptive signals
from lamina I are specifically projected via the posterior part of the ventral medial thalamic nucleus (VMpo)
and the ventral caudal part of the medial dorsal nucleus
(MDvc) [14, 15]. The present patient had a stroke that
involved the posterior medial aspect of the left thalamus,
which encompasses the above areas. However, he did not
develop central thalamic pain or contralateral loss of cold
sensation, which would be expected with Craig’s hypothesis. It is interesting to note that this thalamic stroke
did not result in CPSP, which can happen in 11%–55%
of patients, and is more common after lateral medullary
infarction or lesions in the ventroposterior part of the
thalamus [4]. It is suggested that thalamic pain develops
when there is impairment of spinothalamic transmission
with involvement of the anterior pulvinar nucleus [16].
From a therapeutic perspective, Rasche et al. [6] noted
that the best long-term results after deep brain stimulation were observed in patients with chronic low-back and
leg pain, compared to central pain syndromes such as
due to spinal cord injury and poststroke pain.

4 Conclusion and implications
While the consequence of a stroke is indeed poor on
health, it is intriguing that it carries the potential to eliminate a daily source of pain, anguish, and disability. It is
important that the potential for such neuroplasticity is
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Shanthanna: Disappearance of chronic back pain after a stroke

taken into account in future research and neuromodulatory treatments, including deep brain stimulation.
Acknowledgements: The author thanks Professor. Luis
Garcia-Larrea (Center for Neuroscience of Lyon) for his
insightful comments and valuable inputs, and Dr. Judith
Coret-Simon (Neuroradiology, McMaster University) for
reviewing patient’s imaging and reconfirming his findings. The author also acknowledges the support of the
patient and his wife towards writing this report.
Author’s statements
Research funding: None.
Conflict of interest: None.
Informed consent: Patient’s written informed consent has
been obtained for this report.
Ethical approval: Not applicable.
Author’s contributions: The author has been the patient’s
pain physician and attests to the veracity of this report. All
relevant literature search and writing of this report was
performed by the author.

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