Spinal cord seizures in transverse myelopathy: Report of two cases

Cherrick, Abraham; Ellenberg, Maury

doi:10.1016/0003-9993(86)90125-5

Cited by 9 publications

(17 citation statements)

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“…Van Den Pol et al (1996) have also demonstrated seizure activity in the spinal cord following the relief of chronic glutamate receptor blockade. Interestingly, this neuronal hyperactivity (i.e., spinal seizures) at the level of the spinal cord has been reported in humans with transverse myelopathy (Cherrick and Ellenberg, 1986). Of note, in humans these paroxysmal phenomena are responsive to anticonvulsants such as carbamazepine (Cherrick and Ellenberg, 1986).…”

Section: Discussionmentioning

confidence: 95%

“…Spinal cord seizures have been reported both in humans and animals (Kao and Crill, 1972;Bordbar and Behishti, 1975;Lothman and Somjen, 1976;Ryan et al, 1984;Yu et al, 1984;Cherrick and Ellenberg, 1986;Schlag et al, 2000). In animals this seizure activity has many of the features similar to seizures induced in the cerebral cortex (Cherrick and Ellenberg, 1986). In humans this activity presents as tonic spasm with variable association of clonic activity and dysesthesia.…”

Section: Discussionmentioning

confidence: 96%

“…It is therefore possible, as has been done by others (Davenport et al, 1977), to use spinal paroxysms as a less complicated model for paroxysmal events characteristic of epileptic foci in supraspinal central nervous system structures. Spinal cord seizures have been reported both in humans and animals (Kao and Crill, 1972;Bordbar and Behishti, 1975;Lothman and Somjen, 1976;Ryan et al, 1984;Yu et al, 1984;Cherrick and Ellenberg, 1986;Schlag et al, 2000). In animals this seizure activity has many of the features similar to seizures induced in the cerebral cortex (Cherrick and Ellenberg, 1986).…”

Section: Discussionmentioning

confidence: 96%

“…Kao and Crill (1972) were the first to demonstrate that topical application of penicillin to the spinal cord results in prolonged depolarizations with high-frequency repetitive firing in spinal motor neurons, manifested by segmental myoclonus in the unparalyzed animal. Spinal seizures are induced by the same agents that cause seizures when applied to rostral central nervous system areas and do not involve simultaneous cortical involvement (Cherrick and Ellenberg, 1986). It is therefore possible, as has been done by others (Davenport et al, 1977), to use spinal paroxysms as a less complicated model for paroxysmal events characteristic of epileptic foci in supraspinal central nervous system structures.…”

Section: Discussionmentioning

confidence: 98%

“…Sensory complaints include bouts of burning, itching, numbness, and tingling that are usually self-limited and brief in nature. Factors that have precipitated these bursts include hyperventilation, tactile stimulation, movement, exercise, and hot baths (Cherrick and Ellenberg, 1986). Spinal cord seizure can be induced with electrical current or via numerous drugs such as strychnine or tranexamic acid (Lothman and Somjen, 1976).…”

Section: Discussionmentioning

confidence: 99%

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Right‐sided vagus nerve stimulation inhibits induced spinal cord seizures

Tubbs¹,

Salter²,

Killingsworth³

et al. 2005

Clinical Anatomy

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We have previously shown that left-sided vagus nerve stimulation results in cessation of induced spinal cord seizures. To test our hypothesis that rightsided vagus nerve stimulation will also abort seizure activity, we have initiated seizures in the spinal cord and then performed right-sided vagus nerve stimulation in an animal model. Four pigs were anesthetized and placed in the lateral position and a small laminectomy performed in the lumbar region. Topical penicillin, a known epileptogenic drug to the cerebral cortex and spinal cord, was next applied to the dorsal surface of the exposed cord. With the exception of the control animal, once seizure activity was discernible via motor convulsion or increased electrical activity, the right vagus nerve previously isolated in the neck was stimulated. Following multiple stimulations of the vagus nerve and with seizure activity confirmed, the cord was transected in the midthoracic region and vagus nerve stimulation performed. Right-sided vagus nerve stimulation resulted in cessation of spinal cord seizure activity in all animals. Transection of the spinal cord superior to the site of seizure induction resulted in the ineffectiveness of vagus nerve stimulation in causing cessation of seizure activity in all study animals. As with left-sided vagus nerve stimulation, right-sided vagus nerve stimulation results in cessation of induced spinal cord seizures. Additionally, the effects of right-sided vagus nerve stimulation on induced spinal cord seizures involve descending spinal pathways. These data may aid in the development of alternative mechanisms for electrical stimulation for patients with medically intractable seizures and add to our knowledge regarding the mechanism for seizure cessation following peripheral nerve stimulation. Clin. Anat. 20:23-26, 2007. V V C 2005 Wiley-Liss, Inc.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

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Right‐sided vagus nerve stimulation inhibits induced spinal cord seizures

Tubbs¹,

Salter²,

Killingsworth³

et al. 2005

Clinical Anatomy

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Spinal Movement Disorders in Neuromyelitis Optica: An Under‐recognized Phenomenon

Abboud

Fernández

Mealy

et al. 2016

Movement Disord Clin Pract

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Background: Spinal cord demyelination can cause several movement disorders. Although these abnormal movements could be the presenting symptom of the disease and, at times, the major source of disability, they are often overlooked, mislabeled, or undertreated. The aims of this study were to clearly define and establish common terminology for spinal movement disorders (SMDs) and characterize their full spectrum in patients with neuromyelitis optica (NMO). Methods: We chart reviewed 37 patients with NMO or NMO spectrum disorder. We classified spinal movement disorders under five categories: tonic spasms; focal dystonia; spinal myoclonus; spontaneous clonus; and tremors of spinal origin. We examined clinical, MRI, and medication data of symptomatic patients. Results: Of the 37 patients (86.4% female; mean age: 51 AE 17 years; mean disease duration: 9.4 AE 5.3 years), 16 (43.2%) had one or more form of SMDs. Compared to those without SMDs, patients with SMDs were generally older at presentation and were less likely to be African Americans. An abnormal movement was the main complaint in at least one posthospitalization visit in all symptomatic patients. Thirteen (35.1%) patients had paroxysmal tonic spasms, 2 (5.4%) had focal dystonia, 3 (8%) had postural/ action tremors, and no patient had spinal myoclonus or spontaneous clonus. In 9 patients, spasms were painful. There was no signal abnormality in the basal ganglia or the brainstem/cerebellum in any of the symptomatic patients. Conclusions: SMDs are common in NMO and are often a major source of disability. Using clear, unified terminology to describe SMDs is crucial for both clinical and research purposes.The prototype pathological substrates for movement disorders are the basal ganglia, other deep subcortical nuclei, the cerebellum, and their connections in the brainstem.

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