A case report of a thalamic stroke associated with sudden disappearance of severe chronic low back pain

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 sensory-discriminative, affective-motivational, and evaluative-cognitive 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 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 multilevel 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 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.

Figure 1:

T1 weighted MRI image demonstrating stroke in the left thalamus.

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.

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 taken into account in future research and neuromodulatory treatments, including deep brain stimulation.