Three-Dimensional Eye–Head Coordination After Injection of Muscimol Into the Interstitial Nucleus of Cajal (INC)

Abstract

. The interstitial nucleus of Cajal (INC) is thought to be the "neural integrator" for torsional/vertical eye position and head posture. Here, we investigated the coordination of eye and head movements after reversible INC inactivation. Three-dimensional (3-D) eye-head movements were recorded in three head-unrestrained monkeys using search coils. INC sites were identified by unit recording/electrical stimulation and then reversibly inactivated by 0.3 l of 0.05% muscimol injection into 26 INC sites. After muscimol injection, the eye and head 1) began to drift (an inability to maintain stable fixation) torsionally: clockwise (CW)/ counterclockwise (CCW) after left/right INC inactivation respectively.2) The eye and head tilted torsionally CW/CCW after left/right INC inactivation, respectively. Horizontal gaze/head drifts were inconsistently present and did not result in considerable position offsets. Vertical eye drift was dependent on both vertical eye position and the magnitude of the previous vertical saccade, as in head-fixed condition. This correlation was smaller for gaze and head drift, suggesting that the gaze and head deficits could not be explained by a first-order integrator model. Ocular counterroll (OC) was completely disrupted. The gain of torsional vestibuloocular reflex (VOR) during spontaneous eye and head movements was reduced by 22% in both CW/CCW directions after either left or right INC inactivation. Our results suggest a complex interdependence of eye and head deficits after INC inactivation during fixation, gaze shifts, and VOR. Some of our results resemble the symptoms of spasmodic torticollis (ST).

Keeping Your Head On Target

“…This repetitive cycle of head movements is similar to the abnormal head movements provoked in monkeys by experimental perturbation of the proposed neural integrator for head control (Klier et al, 2002Farshadmanesh et al, 2007Farshadmanesh et al, , 2008. The repetitive head movements observed in normal subjects also resembled movements seen in patients with CD, prompting further exploration of the hypothesis that dysfunction of a neural integrator for head control underlies this disorder (Klier et al, 2002Farshadmanesh et al, 2007Farshadmanesh et al, , 2008. .…”

“…The proposal that jerky OHM in CD are a form of head nystagmus is consistent with recent concepts of the pathogenesis of CD. Studies in animals have suggested that a circuit involving the interstitial nucleus of Cajal (INC) and the nucleus of Darkschewitsch serves as a neural integrator for holding the head steady (Hassler and Hess, 1954;Malouin and Bédard, 1982;Klier et al, 2002;Farshadmanesh et al, 2007;Klier et al, 2007). Experimental perturbations of these regions cause abnormal head postures along with OHM similar to those seen in CD.…”

“…The central mechanisms controlling head movements are less well understood than those of the eyes, but studies in animals have implied that the brain has evolved mechanisms for head control that are similar to those of the eyes (Freedman and Sparks, 1997a, b;Ceylan et al, 2000;Corneil et al, 2002;Klier et al, 2002;Peterson, 2004;Liao et al, 2005;Farshadmanesh et al, 2007;Gandhi and Sparks, 2007;Klier et al, 2007;Gandhi et al, 2008). More specifically, neural circuits in the interstitial nucleus of Cajal and the nearby nucleus of Darkschewitsch appear to serve as a neural integrator responsible for keeping the head steady when it is turned toward an eccentric target (Hassler and Hess, 1954;Malouin and Bédard, 1982;Klier et al, 2002Klier et al, , 2007Farshadmanesh et al, 2007). Dysfunction of these circuits may underlie abnormal head movements in certain human diseases.…”

Palatal tremor and facial dyskinesia in a patient with POLG1 mutation

“…[26][27][28][29] Unilateral iC lesion leads to ipsilesional TN and unilateral stimulation of the iC evokes ipsilateral eye torsion and head tilt in nonhuman. 30,31 In humans, iC lesion sparing riMLF may induce ipsilesional TN 28 and contraversive 32,33 or ipsiversive 28 ocular tilt reaction. Here, the dysfunction of vertical saccades is consistent with an inhibition of the riMLF but modulation of OTR can also suggest a stimulation of the iC.…”

Dissociated Palsy of Vertical Saccades: Loss of Voluntary and Visually Guided Saccades With Preservation of Reflexive Vestibular Quick Phases

“…The INC is an element of the indirect VOR pathway between the vestibular nuclei and ocular motor nuclei (31,32), comprising the vertical eye velocity-to-position integrator. Unilateral chemical inactivation of the simian INC has little or no effect on the vertical VOR (27,33), but the torsional gain is reduced (33). Bilateral INC lesions cause low VOR gain and a phase lead (27).…”