Preservation of voluntary saccades after intracarotid injection of barbiturate

Lesser, Ronald P.; Leigh, R. John; Lüders, Hans; Morris, Harold H.; Tomsak, Robert L.; Lockwood, Kirk

doi:10.1212/wnl.35.8.1108

Cited by 7 publications

(4 citation statements)

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“…As noted previously, the ipsilateral conjugate eye deviation associated with unilateral cerebral hemisphere dysfunction reflects an input deficit of the ipsilateral supranuclear gaze mechanisms to the control of gaze direction. To some extent, the intact cerebral hemisphere can direct gaze in both directions as evidenced by the preservation of horizontal saccades following unilateral cerebral lesions (Lesser et al, 1985). In the present study, input from the intact left cerebral hemisphere did not overcome the effects of right ISA on gaze as well as the intact right brain compensated during left ISA.…”

Section: Discussioncontrasting

confidence: 74%

Hemisphere Asymmetry for Eye Gaze Mechanisms

Meador

Loring

Lee

et al. 1989

Brain

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To investigate left/right asymmetries in cerebral gaze mechanisms, eye deviation was evaluated in 90 patients following intracarotid sodium amylobarbitone injections. For right-handed subjects with left cerebral language dominance, the occurrence and severity of eye deviation were greater for right versus left hemisphere injections. In contrast, subjects with mixed cerebral dominance for language/handedness exhibited no left/right difference in the incidence of eye deviation. The results are consistent with right cerebral dominance for attentional/intentional mechanisms directed at external space. Further analysis suggests that the cerebral asymmetry for gaze may be due to an evolutionary loss of attentional/intentional mechanisms by the left cerebral hemisphere as language function developed.

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Section: Discussioncontrasting

confidence: 74%

Hemisphere Asymmetry for Eye Gaze Mechanisms

Meador

Loring

Lee

et al. 1989

Brain

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“…In humans, even voluntary saccadic movements have been observed after inactivation of frontal areas by intracarotid injection of barbiturates. This is undoubtedly due to the fact that the posterior cortical areas that control saccadic movements are irrigated by the vertebrobasilar system [17]. Recent brain mapping studies in animals have demonstrated that there are also cortical centers and pathways that trigger saccadic eye movements in the occipital and inferior parietal cortex [6,7,18].…”

Section: Discussionmentioning

confidence: 99%

Epileptic nystagmus: A case study video‐EEG correlation

García‐Pastor,

López‐Esteban,

Peraita‐Adrados

2002

Epileptic Disorders

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Epileptic nystagmus (EN) is an uncommon phenomenon characterized by repetitive and rapid saccades, in association with epileptic discharges. We present a critical video‐EEG recording in a patient with occipital seizures that appeared clinically as EN. The subject, male, 70 years‐old, was examined because of generalized tonic‐clonic seizures, preceded by left cephalic version. These were controlled using i.v. PHT, but partial seizures persisted, which we recorded using video‐EEG. Clinically, we observed episodes of left conjugate deviation of the eyes, accompanied by horizontal nystagmoid movements, with a rapid leftward component and visual hallucinations. The patient did not lose consciousness. Ictal EEG: spike rhythm in the posterior right occipito‐temporal region extending to adjacent and contralateral regions, followed by post‐discharge of slow waves. The video‐EEG was interpreted as partial oculo‐clonic status epilepticus of right temporo‐occipital origin. Cranial MRI: old, bilateral hemorrhaging occipital contusions associated with previous cranial injury. The picture persisted for two days, and disappeared with administration of CBZ 600 mg/d. Our patient's nystagmus seemed to be related to the critical activity recorded in the right occipito‐temporal region. The co‐existence of visual hallucinations and the video‐EEG correlation support this possibility. This phenomenon is probably due to epileptic activation of the cortical center of saccadic movements, with a rapid phase of nystagmus, contralateral to the focus, and a slow ipsilateral phase in association with a defect in the gaze‐fixing system (“leaky neural integrator”) [published with videosequences].

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“…Although much attention has been paid to the role of the frontal eye fields in producing ictal eye deviation (Lesser et al, 1985;Godoy et al, 1990), in only 3 reported patients with EN did the EEG seizures involve the frontal areas unilaterally (Trevisan and Dettori, 1967) or bilaterally (Pritchard and Tucker, 1982;Kaplan and Lesser, 1989). Moreover, bilateral frontal ictal activity was associated with upbeat nystagmus.…”

Section: Localization Of Focal Eeg Seizures Associated With Enmentioning

confidence: 99%

Epileptic Nystagmus

Stolz¹,

Chatrian²,

Spence³

1991

Epilepsia

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Two cases of epileptic nystagmus (EN) are described. The first patient had no history of seizures and experienced attacks of EN associated with oscillopsia and followed by horizontal diplopia and esotropia. These episodes could be triggered by certain visual stimuli and ocular pressure. The second patient had a history of generalized tonic-clonic seizures. He displayed episodes of EN that changed direction in the course of the attacks simultaneously with a shift of the EEG discharge from one occipital region to the other. Cortical blindness followed postictally. On recovery from the postictal state, both patients were neurologically normal. With standard electrodes, the EEG seizures associated with EN involved the occipital, posterotemporal, and parietal areas of the scalp contralateral to the fast phase of the nystagmus. In the first patient, use of supplementary scalp electrodes further localized the seizures to an anterior occipital site intermediate between standard occipital and posterotemporal electrodes. Thirty-six previously reported cases of EN were associated with partial seizures. Horizontal EN most commonly results from seizure activity involving the occipital cortex, although participation of adjoining portions of the parietal and temporal cortexes is possible.

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Preservation of voluntary saccades after intracarotid injection of barbiturate

Cited by 7 publications

References 0 publications

Hemisphere Asymmetry for Eye Gaze Mechanisms

Hemisphere Asymmetry for Eye Gaze Mechanisms

Epileptic nystagmus: A case study video‐EEG correlation

Epileptic Nystagmus

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