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Allodynia in the flank after thalamic stroke
Mitsuhiro Yoshita1, Masahito Yamada
1Department of Neurology & Neurobiology of Aging, Kanazawa University Graduate School of Medical Science, Takara-machi 13-1, Kanazawa 920-8641, Japan. myoshita@ucdavis.edu
Summary
Thalamic pain, often linked to specific thalamic nuclei, can also result from lesions in the posteroventral thalamus. This finding suggests the ventral posteroinferior nucleus may cause unique post-stroke pain syndromes like allodynia.
Area of Science:
- Neurology
- Neuroscience
- Pain Medicine
Background:
- Thalamic pain syndrome is a debilitating neurological condition.
- Lesions in the ventral posteromedial (VPM) and ventral posterolateral (VPL) nuclei are traditionally implicated.
- Understanding the precise neuroanatomical correlates of thalamic pain is crucial for effective treatment.
Observation:
- Two patients presented with allodynia and hyperpathia in the flank contralateral to a thalamic lesion.
- Imaging revealed small lesions specifically in the posteroventral region of the thalamus.
- These symptoms represent a unique presentation of post-stroke pain.
Findings:
- The observed clinical presentation suggests that lesions in the ventral posteroinferior (VPI) nucleus may be responsible for this specific type of thalamic pain.
- This contrasts with the commonly assumed involvement of VPM and VPL nuclei.
- The VPI nucleus's role in processing somatosensory information warrants further investigation.
Implications:
- This research expands the understanding of the neuroanatomical basis of thalamic pain.
- It highlights the potential role of the VPI nucleus in somatosensory processing and pain pathways.
- Further studies are needed to confirm the VPI nucleus's involvement and explore therapeutic targets for this unique pain syndrome.
