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Ri, S. Management of Poststroke Thalamic Pain. Encyclopedia. Available online: https://encyclopedia.pub/entry/24050 (accessed on 06 August 2024).
Ri S. Management of Poststroke Thalamic Pain. Encyclopedia. Available at: https://encyclopedia.pub/entry/24050. Accessed August 06, 2024.
Ri, Songjin. "Management of Poststroke Thalamic Pain" Encyclopedia, https://encyclopedia.pub/entry/24050 (accessed August 06, 2024).
Ri, S. (2022, June 15). Management of Poststroke Thalamic Pain. In Encyclopedia. https://encyclopedia.pub/entry/24050
Ri, Songjin. "Management of Poststroke Thalamic Pain." Encyclopedia. Web. 15 June, 2022.
Management of Poststroke Thalamic Pain
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This entry is adapted from the peer-reviewed paper 10.3390/diagnostics12061439

Poststroke thalamic pain (PS-TP), a type of central poststroke pain, has been challenged to improve the rehabilitation outcomes and quality of life after a stroke. It has been shown in 2.7–25% of stroke survivors; however, the treatment of PS-TP remains difficult, and in majority of them it often failed to manage the pain and hypersensitivity effectively, despite the different pharmacotherapies as well as invasive interventions. Central imbalance, central disinhibition, central sensitization, other thalamic adaptative changes, and local inflammatory responses have been considered as its possible pathogenesis. Allodynia and hyperalgesia, as well as the chronic sensitization of pain, are mainly targeted in the management of PS-TP. Commonly recommended first- and second-lines of pharmacological therapies, including traditional medications, e.g., antidepressants, anticonvulsants, opioid analgesics, and lamotrigine, were more effective than others. Nonpharmacological interventions, such as transcranial magnetic or direct current brain stimulations, vestibular caloric stimulation, epidural motor cortex stimulation, and deep brain stimulation, were effective in some cases/small-sized studies and can be recommended in the management of therapy-resistant PS-TP.

thalamic pain central pain stroke pain poststroke thalamic pain central poststroke pain thalamus

1. Poststroke Thalamic Pain

Poststroke thalamic pain (PS-TP), or broadly central poststroke pain (CPSP), is centralized, neuropathic, often characterized with hyperalgesia and allodynia, and is a complaint in 2.7 to 25% of stroke survivors [1][2][3][4][5]. The prevalence of PS-TP was highly variable because of the different study durations as well as the clinical characteristics of the stroke population included in the clinical studies, e.g., stroke etiology, distribution of stroke lesions, and clinical management [1][2][3][4]. PS-TP may develop immediately after a stroke; however, apparent PS-TP often comes later in the postacute phase or the recovery phase following the stroke, e.g., months to years [1][3][4][6], and thalamic stroke may be recalled again later because of the development of PS-TP, which has also been called the Dejerine–Roussy syndrome [1][6][7].
Thalamic pain syndrome commonly follows an ischemic stroke or hemorrhagic stroke in the thalamic and lateral medullary areas [3][8][9]. PS-TP occurs after thalamic stroke with sensory deficits, and it often comes up to 40% in the acute phase following the stroke, e.g., within a month of the stroke [10][11][12]. Over 40% of patients with PS-TP have symptoms between one and 12 months after the stroke, and sometimes PS-TP develops between one and six years poststroke [10][12].
Up to 74% of stroke survivors with PS-TP showed gradually increased pain rather than rapid worsening following the stroke, in no relation with the general demographic data and the existence of sensory deficits. Younger age was shown as a risk factor of PS-TP [13].
Right-sided stroke lesions were more commonly associated with the development of PS-TP than left-sided ones. The affected right hemisphere of the brain is better reactive for pain medication [6].

1.1. The Pathogenesis of PS-TP

The underlying mechanisms of PS-TP are poorly understood, contributing to challenges in its management. The thalamus, as a relay station for all sensory tracts in the brain, works to decode sensory information and process it, which goes to the somatosensory cortex where it is interpreted [14][15][16]. Actually, several parts of thalamus, especially the ventrocaudal regions of the thalamus such as the ventral posterior nuclei or the ventral lateral nuclei, the lateral posterior nuclei, as well as the thalamic sensory tracts, e.g., the simultaneously affected spinothalamic tract and the anterior pulvinar nucleus, have been known as the high-risk areas of the development of PS-TP [14][17].
The damage to the thalamus or thalamic sensory tracts due to stroke can cause thalamic pain syndrome [14][17][18]. The damage-related changes of the processing and interpretation of peripheral sensory information, e.g., tactile, temperature, pressure, including the loss of them, as well as their malfunction in the afferent pathway from the thalamus to the cortex in central poststroke pain, e.g., tactile or temperature stimuli to the thalamus, can be interpreted as painful (allodynia) or amplifying of painful stimuli, which make it worse (hyperalgesia) [18][19][20][21]. On the other hand, the central sensitization of pain follows due to persistent overactivity [18][20][21].
The pathogenesis of PS-TP has been considered and discussed by several possible theories, such as central imbalance, central disinhibition, central sensitization, other thalamic changes, and inflammatory responses on the affected neural pathway due to stroke [14][17][18][22].

1.2. The Diagnosis of PS-TP

The first diagnostic step is to suspect the history of thalamic stroke and centralized chronic neuropathic pain [6][21]. Any stroke lesion of the thalamus or the spinothalamic tract should be checked firstly, which has a high risk for the development of PS-TP [14][17].
The diagnosis of poststroke thalamic pain (PS-TP) begins with and is based on the anamnesis, e.g., sensory disorder, tactile and thermal hypersensitivities, and later pain on the entire contralateral half after a thalamic stroke [1][2][23], and on clinical examination, e.g., cold/warm-interpreting errors, severe, constant, or intermittent pain made worse by touching, cold-stimulating, or palpating on the affected side [21].
The ventrocaudal regions of the thalamus have been known as the high-risk areas of PS-TP development and include the ventral posterior nuclei or the ventral lateral nuclei, and the lateral posterior nuclei [14][17]. The lesions of the thalamus or the thalamic sensory tracts affected by stroke, which was approved by brain imaging such as MRI or CT, is the most important checkpoint in the diagnosis of PS-TP [14][17][18].
The clinical findings and their timely changes following stroke can be also helpful for its diagnosis. The thermal as well as pinprick sensation impairment due to the spinothalamic tract dysfunction is a predictor of the development of PS-TP or CPSP. Neurophysiological tests such as electroencephalogram (EEG) and somatosensory-evoked potential (SEP) examination can be individually performed in the diagnosis of PS-TP [24].

2. Pharmacologic Treatments of PS-TP

Because of lacking direct causal therapies and the limitation of symptomatic therapies, its management remains still one of the large difficulties in stroke rehabilitation. The PS-TP has been known for many years, but the evidence of its symptomatic management is mostly low or very low, with the difficulties and the outcomes of these treatments often unsatisfactory [25][26].
The main therapeutic approaches are to improve tactile and thermal hypersensitivity as well as neuropathic pain and quality of life in patients with PS-TP by using traditional pharmacological treatments and nonpharmacological interventions available for patients with PS-TP. Therefore, the evaluation and treatment of PS-TP often require an interdisciplinary team including a neurologist and pain medicine specialist, and occasionally a neurosurgeon [20][25][26].
One double-blinded, placebo-controlled trial with oral amitriptyline and carbamazepine for PS-TP showed that only amitriptyline had a significant reduction of pain when compared to placebo [5]. Amitriptyline and imipramine reduced thermal and mechanical hypersensitivity and pain in another study [13][27][28][29].
In an open-label, observational study with PS-TP, fluvoxamine had a significant pain relief in visual analogue scale (VAS) after the treatment of 4 weeks. Interestingly, the significant pain reduction was only in the patients who were treated within 1 year from stroke [30].
Duloxetine, a serotonin–norepinephrine reuptake inhibitor, is known to be effective against centralized neuropathic pain in multiple sclerosis [31].
Pregabalin is the most tested agent for the management of centralized neuropathic pain, but the evidence for its effectiveness is mixed. The safety, efficacy, and tolerability of pregabalin were also approved in a cohort study including 219 patients with PS-TP [32].
In a prospective observational study, gabapentin, another anticonvulsant, at 300 mg twice daily, was effective in the management of PS-TP in 84 patients with thalamic stroke [33]. Additionally, the use of gabapentin has been reported individually in a few patients with PS-TP [26].
The third-line or other medications of PS-TP have not been well-assessed, but they could be individually used. Opioid or opioid antagonist, medical cannabinoids, mexiletine, clonidine, and beta-blockers can be recommended as the third line treatment in individual cases with PS-TP. Intravenous infusions of lidocaine, often together propofol or ketamine, steroid, naloxone, as well as intrathecal baclofen or ketamine also showed their effectiveness in a few reports with acute severe pain of PS-TP [28][29][34][35][36].

3. Nonpharmacological Interventions of PS-TP

In the cases with intractable PS-TP, nonpharmacological interventions can be recommended as an important option, and appear to be effective in the treatment of PS-TP, but the evidence is relatively low, especially due to the limited numbers of participants. Additionally, invasive electrical brain stimulation can be followed by serious adverse events, which were recovered in most patients [37].

3.1. Noninvasive Brain Stimulation

3.1.1. Repetitive Transcranial Magnetic Stimulation (rTMS)

Repetitive transcranial magnetic stimulation (rTMS) as a noninvasive brain stimulation therapy has been often recommended in the treatment of PS-TP [25][38][39]. The rTMS is a safe and well-tolerated intervention [39]. In an interesting study using diffusion tensor imaging fiber tracking, it was shown that the corticospinal tract as well as the thalamocortical tract plays a role in pain reduction by rTMS [40]. Moreover, the antalgic effect of rTMS in patients with PS-TP was more prominent in patients without depression [41]. Five daily sessions of rTMS over the motor cortex area in patients with refractory PS-TP resulted in pain relief lasting 2 weeks [42]. 

3.1.2. Transcranial Direct Current Stimulation (tDCS)

An emerging treatment for intractable PS-TP is transcranial direct current stimulation (tDCS), a noninvasive brain stimulation, together with repetitive transcranial magnetic stimulation (rTMS) in clinical practice [43]. The safety and effectiveness of tDCS has been reported in many clinical studies for different neuropathic pain syndromes [44].

3.1.3. Vestibular Caloric Stimulation (VCS)

In some patients with PS-TP, the pain decreased after VCS, which may rebalance the imbalance in the bilateral integration of thermal sensation, so called as the thermosensory disinhibition hypothesis, and this effect was due to the temporary activation of the parieto-insular vestibular cortex of VCS [22][45]. Vestibular caloric irrigation of the ear can lead to the activation of several areas in the contralateral hemisphere, including the insular cortex. The posterior insula is responsible for painful stimuli. Because of the phylogenetically and anatomical proximity of both the pain and vestibular area, VCS may improve the symptoms of PS-TP, which represents a pathological amplification of the thalamic posterior insular response to pain [23].

3.2. Invasive Therapeutic Interventions of Brain Stimulation

3.2.1. Epidural Motor Cortex Stimulation (EMCS)

Compared with other invasive brain stimulations, e.g., deep brain stimulation (DBS), epidural motor cortex stimulation (EMCS) is more frequently used because this intervention is safer and easier, and it has more indications, including PS-TP [46][47]. Based on the progress of neurosurgical techniques, it is a safe surgical intervention to implant a EMCS neurostimulator for the long-term electrical brain stimulation over the primary motor cortex [46][47] Additionally, the positive response of 10 Hz - rTMS in the preoperative test can predict the analgetic effect of EMCS [48].

3.2.2. Deep Brain Stimulation (DBS) in PS-TP

DBS has been well-known as a safe and effective therapy in the management of many neurological diseases, especially essential tremors, other tremors, obsessive-compulsive disorder, neuropathic pain, traumatic brain injury, Tourette’s syndrome, and drug-resistant epilepsy [49].
Deep brain stimulation has also shown to be effective in over 50% of patients with PS-TP, and the stimulation to the thalamus alone showed less effect than other area stimulations in combination, e.g., periventricular/periaqueductal gray matter (PVG/PAG) or periventricular/periaqueductal gray matter (PVG/PAG) plus thalamus/internal capsule [50][51][52]. However, DBS, an invasive brain stimulation, was less effective or ineffective to PS-TP than other diseases or neuropathic pain syndromes in one cohort study [53].

3.2.3. Spinal Cord Stimulation

Spinal cord stimulation (SCS) was rarely recommended in PS-TP; however, in one cohort study, SCS improved with over 50% of pain reduction in 30% of patients with PS-TP [54].
The SCS therapy for PS-TP has been studied in a few cohort studies, which suggested that SCS can improve the long-term pain relief effect in some participants, but it was often ineffective in most patients with PS-TP [54][55][56].

3.3. Other Nonpharmacological Therapies

One therapy–comparative study with an acupuncture group (n = 32) and a pregabalin (75 mg, twice a day) group (n = 32) showed that acupuncture could effectively relieve the symptoms of PS-TP with long-term effect, and it is better than pregabalin [57].
Bee venom injection at acupuncture points reduced significantly the pain symptoms of PS-TP in visual analogue scores after three weeks compared with baseline and the control group [58].
However, a recent systematic review concluded that the included studies were with poor or fair quality and the outcomes were mixed with low evidence [25]. Perhaps acupuncture therapy can be recommended as an adjunctive treatment for PS-TP.
Cognitive-behavioral therapy was useful in the prevention of depression in patients with PS-TP [59]. Psychologic relaxation therapy should also be a part of adjunctive treatment [13].

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