A hidden mesencephalic variant of central pain.


Journal

European journal of pain (London, England)
ISSN: 1532-2149
Titre abrégé: Eur J Pain
Pays: England
ID NLM: 9801774

Informations de publication

Date de publication:
08 2020
Historique:
received: 28 09 2019
revised: 20 04 2020
accepted: 09 05 2020
pubmed: 19 5 2020
medline: 26 1 2021
entrez: 19 5 2020
Statut: ppublish

Résumé

Central post-stroke pain (CPSP) can arise after lesions anywhere in the central somatosensory pathways, essentially within the spinothalamic system (STS). Although the STS can be selectively injured in the mesencephalon, CPSP has not been described in pure midbrain infarcts. Of more than 300 CPSP consecutive cases, we describe five patients who developed definite neuropathic pain following lesions circumscribed to the postero-lateral mesencephalon. The mesencephalic lesion responsible for pain was always haemorrhagic and always involved the spinothalamic tract (STT), as demonstrated by suppressed laser-evoked potentials in every case, with or without preserved lemniscal function. In three cases the midbrain injury could be ascribed to trauma, presumably from the cerebellar tentorium. As a result of the paucity of sensory symptoms, the pain was considered as 'psychogenic' in two of the patients until electrophysiological testing confirmed STT involvement. Postero-lateral midbrain lesions should be added to potential causes of CPSP. Because pain and spinothalamic deficits may be the only clinical sign, and because small lateral midbrain lesions may be difficult to trail with MRI, mesencephalic CPSP can be misdiagnosed as malingering or psychogenic pain for years. Selective spinothalamic injury caused by small lateral midbrain lesions is a very rare cause of central post-stroke pain that can remain undiagnosed for years. It appears to obey to haemorrhagic, sometimes post-traumatic lesions. Sudden development of contralateral burning pain with isolated spinothalamic deficits may be the only localizing sign, which can be easily objectively detected with electrophysiological testing.

Sections du résumé

BACKGROUND
Central post-stroke pain (CPSP) can arise after lesions anywhere in the central somatosensory pathways, essentially within the spinothalamic system (STS). Although the STS can be selectively injured in the mesencephalon, CPSP has not been described in pure midbrain infarcts.
METHODS
Of more than 300 CPSP consecutive cases, we describe five patients who developed definite neuropathic pain following lesions circumscribed to the postero-lateral mesencephalon.
RESULTS
The mesencephalic lesion responsible for pain was always haemorrhagic and always involved the spinothalamic tract (STT), as demonstrated by suppressed laser-evoked potentials in every case, with or without preserved lemniscal function. In three cases the midbrain injury could be ascribed to trauma, presumably from the cerebellar tentorium. As a result of the paucity of sensory symptoms, the pain was considered as 'psychogenic' in two of the patients until electrophysiological testing confirmed STT involvement.
CONCLUSION
Postero-lateral midbrain lesions should be added to potential causes of CPSP. Because pain and spinothalamic deficits may be the only clinical sign, and because small lateral midbrain lesions may be difficult to trail with MRI, mesencephalic CPSP can be misdiagnosed as malingering or psychogenic pain for years.
SIGNIFICANCE
Selective spinothalamic injury caused by small lateral midbrain lesions is a very rare cause of central post-stroke pain that can remain undiagnosed for years. It appears to obey to haemorrhagic, sometimes post-traumatic lesions. Sudden development of contralateral burning pain with isolated spinothalamic deficits may be the only localizing sign, which can be easily objectively detected with electrophysiological testing.

Identifiants

pubmed: 32419231
doi: 10.1002/ejp.1588
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1393-1399

Informations de copyright

© 2020 European Pain Federation - EFIC®.

Références

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Auteurs

Philippe Convers (P)

Central Integration of Pain Unit, Lyon Centre for Neurosciences (CRNL), INSERM U1028, UCB Lyon 1, UJM Saint Etienne, Saint Etienne, France.
Department of Neurology, CHU Saint Etienne, Saint Etienne, France.

Christelle Creac'h (C)

Central Integration of Pain Unit, Lyon Centre for Neurosciences (CRNL), INSERM U1028, UCB Lyon 1, UJM Saint Etienne, Saint Etienne, France.
Department of Neurology, CHU Saint Etienne, Saint Etienne, France.
Department of Pain Center, CHU Saint Etienne, Saint Etienne, France.

Albert Beschet (A)

Department of Neurology, CH, Valence, France.

Bernard Laurent (B)

Central Integration of Pain Unit, Lyon Centre for Neurosciences (CRNL), INSERM U1028, UCB Lyon 1, UJM Saint Etienne, Saint Etienne, France.
Department of Neurology, CHU Saint Etienne, Saint Etienne, France.
Department of Pain Center, CHU Saint Etienne, Saint Etienne, France.

Luis Garcia-Larrea (L)

Central Integration of Pain Unit, Lyon Centre for Neurosciences (CRNL), INSERM U1028, UCB Lyon 1, UJM Saint Etienne, Saint Etienne, France.
Department of Neurology, CH, Valence, France.

Roland Peyron (R)

Central Integration of Pain Unit, Lyon Centre for Neurosciences (CRNL), INSERM U1028, UCB Lyon 1, UJM Saint Etienne, Saint Etienne, France.
Department of Neurology, CHU Saint Etienne, Saint Etienne, France.
Department of Pain Center, CHU Saint Etienne, Saint Etienne, France.

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