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In the book "neuroanatomy through clinical cases" by blumenfield, it says
"Sensory pathways and the brainstem reticular activating systems are spared"
in patients with locked in syndrome.
If basilar artery infarcts cause locked in syndrome, how come the DCML and spinothalamic tracts are not affected. The basilar artery supplies blood to almost of the pons and the DCML/spinothalamic tracts run through there
TL;DR: based on the neuroanatomy, why does Locked-in syndrome spare sensation?
"Sensory pathways and the brainstem reticular activating systems are spared"
in patients with locked in syndrome.
If basilar artery infarcts cause locked in syndrome, how come the DCML and spinothalamic tracts are not affected. The basilar artery supplies blood to almost of the pons and the DCML/spinothalamic tracts run through there
TL;DR: based on the neuroanatomy, why does Locked-in syndrome spare sensation?
