Paroxysmal sensory-motor attacks due to a spinal cord lesion identified by MRI.

Tonic spasms are a common clinical manifestation in patients with neuromyelitis optica

“…The remarkable response observed in patients who received carbamazepine and acetazolamide is consistent with previous reports 4,17 and with the hypothesis that a dysfunction of ion channels is involved in the pathogenesis of the spasms probably facilitating ephaptic transmission 4,16,17 . Despite abundant evidence linking TS and MS, only few reports have suggested their association with NMO 8,[18][19][20] .…”

“…Matthews proposed an alternative explanation, that during a voluntary movement, when activation along the corticospinal tract reaches the demyelinated plaques, impulses are wholly or partially blocked, thus spreading to the neighboring axons 14 . The proximity of the demyelinated axons, without the intervening glial tissue, has been claimed to support the lateral spread of activation 15,16 . On the other hand, TS have been widely been recognized to be related to a localized inflamatory reaction rather than to chronic established areas of demyelination 17 .…”

Current symptomatology in multiple sclerosis and neuromyelitis optica

“…It was proposed that, when activation along the corticospinal tract reaches demyelinated plaques, impulses are wholly or partially blocked; therefore there is spreading to the neighboring axons and consequently tonic seizures . Moreover, the proximity of these demyelinated axons is thought to support the lateral spread of activation . In addition, tonic seizures are widely recognized to be related to a localized inflammatory reaction rather than chronic established areas of demyelination .…”

Painful tonic/dystonic spasms in Sjogren's syndrome

“…Ekbom et al 12 described two patients with spinal cord pathology in whom unilateral "tonic spasms" were succeeded by a contralateral burning sensation. Sozzi et al 13 reported a patient with a large high cervical demyelinating plaque and a similar clinical presentation which they termed "motor-sensory spinal attacks." Both groups attributed this clinical picture to a transverse ephaptic transmission of neural activity from a motor to an adjacent sensory pathway.…”