Makindo Medical Notes

Related Subjects: |Acute Stroke Assessment (ROSIER&NIHSS) |Atrial Fibrillation |Atrial Myxoma |Causes of Stroke |Ischaemic Stroke |Cancer and Stroke |Cardioembolic stroke |CT Basics for Stroke |Endocarditis and Stroke |Haemorrhagic Stroke |Stroke Thrombolysis |Hyperacute Stroke Care

Introduction

Thalamic Pain Syndrome, also known as Dejerine–Roussy Syndrome, is a chronic and debilitating neuropathic pain condition that arises following damage to the thalamus, most commonly due to a stroke. The syndrome is characterized by persistent, often severe, pain contralateral to the side of the thalamic lesion. This condition can significantly impact a patient's quality of life and presents challenges in management.

Etiology: Damage to the thalamic sensory nuclei

• Ischemic Stroke: Infarction in the thalamic region due to occlusion of small penetrating arteries.
• Hemorrhagic Stroke: Intracerebral hemorrhage involving the thalamus.
• Tumors: Neoplastic lesions affecting the thalamus.
• Trauma: Traumatic brain injury involving the thalamic area.
• Multiple Sclerosis: Demyelinating lesions in the thalamus.

Arteries commonly involved in thalamic strokes include

• Posterior Cerebral Artery (PCA): Particularly the thalamogeniculate branches.
• Posterior Choroidal Arteries: Supply the posterior thalamus.
• Paramedian Thalamic-Mesencephalic Arteries: Branches of the basilar artery.

Pathophysiology

The thalamus acts as a relay center for sensory signals to the cerebral cortex. Damage to the ventroposterolateral (VPL) and ventroposteromedial (VPM) nuclei disrupts the normal processing of somatosensory information. This leads to altered pain perception, resulting in neuropathic pain. Mechanisms proposed include:

• Deafferentation: Loss of inhibitory input leads to hyperexcitability of thalamic neurons.
• Central Sensitization: Enhanced responsiveness of central neurons to stimulation.
• Altered Neurotransmitter Levels: Imbalances in glutamate, GABA, and other neurotransmitters.

Clinical Features

• Contralateral Hemisensory Loss: Initial numbness and decreased sensation on the side opposite the lesion.
• Development of Pain: Onset of severe, persistent pain in the affected area weeks to months after the initial injury.
• Nature of Pain: Described as burning, aching, stabbing, or throbbing. Pain may be spontaneous or triggered by stimuli that are not normally painful (allodynia).
• Dysesthesia: Unpleasant abnormal sensations.
• Hyperalgesia: Increased sensitivity to painful stimuli.
• Emotional Distress: Depression and anxiety due to chronic pain.
• Possible Hemiparesis: Weakness on the contralateral side if motor pathways are involved.

Differential Diagnosis

Conditions that may mimic Thalamic Pain Syndrome include:

• Central Post-Stroke Pain (CPSP): Neuropathic pain following stroke in other central nervous system regions.
• Complex Regional Pain Syndrome (CRPS): Painful condition affecting a limb after injury.
• Peripheral Neuropathies: Diabetic neuropathy, post-herpetic neuralgia.
• Musculoskeletal Pain: Shoulder pathologies or joint diseases.
• Psychogenic Pain Disorders: Pain without identifiable physical cause.

Investigations

• Neuroimaging:
  • Magnetic Resonance Imaging (MRI): Preferred modality to identify thalamic lesions, infarcts, or hemorrhages.
  • Computed Tomography (CT) Scan: Useful in acute settings to detect hemorrhagic strokes.
• Neurological Examination: Assessment of sensory deficits, motor function, reflexes, and coordination.
• Somatosensory Evoked Potentials (SSEPs): May help assess sensory pathway integrity.
• Laboratory Tests: To exclude metabolic or systemic causes if indicated.

Management is challenging and often unsatisfactory

Pharmacological Treatment

• Antidepressants:
  • Tricyclic Antidepressants (TCAs): Amitriptyline, nortriptyline.
  • Selective Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs): Duloxetine, venlafaxine.
• Anticonvulsants:
  • Gabapentin: Modulates calcium channels to reduce neuronal excitability.
  • Pregabalin: Similar mechanism to gabapentin with possibly faster onset.
  • Carbamazepine: Sodium channel blocker; useful in neuropathic pain.
  • Lamotrigine: May be beneficial in some patients.
• Analgesics:
  • Opioids: Tramadol or stronger opioids may be considered, but risk of dependence exists.
  • Nonsteroidal Anti-Inflammatory Drugs (NSAIDs): Often ineffective for neuropathic pain.
• Other Medications:
  • Topical Agents: Lidocaine patches, capsaicin cream.
  • NMDA Receptor Antagonists: Such as ketamine in refractory cases.

Non-Pharmacological Treatment

• Physical Therapy: To improve function and reduce discomfort.
• Psychological Support: Cognitive-behavioral therapy to help cope with chronic pain.
• Occupational Therapy: Assistance with activities of daily living.

Interventional Procedures

• Deep Brain Stimulation (DBS):
  • Targeting the ventral posterolateral (VPL) or ventral posteromedial (VPM) nucleus of the thalamus.
  • Considered in refractory cases not responding to medical therapy.
• Motor Cortex Stimulation: Epidural stimulation of the motor cortex may alleviate pain.
• Intrathecal Drug Delivery: Administration of medications directly into the cerebrospinal fluid.
• Repetitive Transcranial Magnetic Stimulation (rTMS): Non-invasive technique that may reduce pain intensity.

Prognosis

Thalamic Pain Syndrome is often chronic and can be debilitating. Early recognition and a comprehensive treatment plan can improve quality of life. However, response to therapy varies, and complete pain relief is difficult to achieve. Support from healthcare professionals, family, and support groups is essential.

References

• Klit H, Finnerup NB, Jensen TS. Central post-stroke pain: clinical characteristics, pathophysiology, and management. Lancet Neurol. 2009;8(9):857-868.
• Kim JS. Post-stroke pain. Expert Rev Neurother. 2009;9(5):711-721.
• Canavero S, Bonicalzi V. Central pain syndrome: elucidation of genesis and treatment. Expert Rev Neurother. 2007;7(11):1485-1497.
• Leung A, Fallah A, Cai Y, et al. The use of motor cortex stimulation (MCS) in the treatment of neuropathic pain. Brain Sci. 2018;8(7):132.