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Craig Evinger

Publications and source records attributed to Craig Evinger.

9 recordsLinked to original sources
PubMed2007

The three-neuron corneal reflex circuit and modulation of second-order corneal responsive neurons.

Neurons located in the border region between the interpolaris and caudalis subdivisions of the spinal trigeminal nucleus (Vi/Vc) are second order neurons of the corneal reflex, receiving corneal afferents and projecting to the lid closing, orbicularis oculi (OO) motoneurons. Recordings of Vi/Vc neurons identified by antidromic activation from stimulation of the facial nucleus and non-identified Vi/Vc neurons reveal two neuron types, phasic and tonic. Corneal stimulation elicits Adelta latency action potentials that occur early enough to initiate OO contraction and C-fiber latency action potentials that can modulate the end of the blink in phasic Vi/Vc neurons. Tonic Vi/Vc neurons exhibit a constant irregular, low frequency discharge as well as the cornea-evoked activity exhibited by phasic neurons. For both phasic and tonic neurons, blink amplitude increases with the total number of spikes evoked by the corneal stimulus. Peak firing frequency predicts peak orbicularis oculi EMG activity. Paradigms that suppress cornea-evoked blinks differentially affect Vi/Vc neurons. Microstimulation of the border region between the spinal trigeminal caudalis subdivision and the C1 spinal cord (Vc/C1) significantly reduces the number of spikes evoked by corneal stimulation and suppresses blink amplitude. In the paired stimulus paradigm, a blink evoked by a corneal stimulus 150 ms after an identical corneal stimulus is significantly smaller than the blink elicited by the first stimulus. Vi/Vc neuron discharge, however, is slightly larger for the second blink. Our data indicate that second-order Vi/Vc neurons do not determine the specific pattern of OO muscle activity; rather Vi/Vc neurons initiate OO motoneuron discharge and program the activity of another circuit that generates the late phase of the blink. The Vc/C1 suppression of Vi/Vc neurons suggests that the Vc/C1 region provides an "internal model" of the intended blink.

Action Potentials↗
PubMed2006

Cerebellar modulation of trigeminal reflex blinks: interpositus neurons.

Because of its simplicity, blinking is a prominent model system in analysis of adaptation and conditioning with the cerebellum. Nevertheless, data on the role of the cerebellum in modulation of normal reflex blinks are limited. We correlated the discharge of interpositus (IP) neurons with normal trigeminal reflex blinks and blink adaptation in urethane-anesthetized rats. Two groups of IP neurons responded to cornea stimulation. One group, pause neurons, showed a long cessation of their tonic discharge beginning 6 ms before the end of lid closure. The second group, burst neurons, exhibited a transient increase in firing frequency at a constant interval after the cornea stimulus. The cessation of pause neuron activity appeared to contribute to the termination of blinks. The tonic discharge rate increased and the cessation of pause neuron activity was delayed coincident with increased amplitude and duration of reflex blinks produced by blink adaptation. There was a coincident increase in the amplitude and duration of reflex blinks with increased tonic activity and delayed pause in pause neurons treated with the GABA(A) antagonist, gabazine. Burst neurons did not appear to modulate reflex blinks. Burst neuron discharge correlated neither with blink characteristics normally nor with blink adaptation. These findings indicated that pause neurons affect reflex blinks by providing a tonic excitatory input to facial motoneurons during lid closure and then disfacilitating those motoneurons to adjust the termination of lid closure. Burst neurons may play a role in eyelid conditioning.

Action Potentials↗
PubMed2006

Eyelid movements during blinking in patients with Parkinson's disease.

We examined eyelid movements during spontaneous, voluntary, and trigeminal reflex blinks in 16 patients with mild to moderate Parkinson's disease (PD) off medication and 14 controls. Voluntary and reflex blink amplitudes tended to be smaller than normal for PD patients, whereas eyelid kinematics (amplitude-maximum velocity relationship) for all three blink types were normal. Spontaneous blink rate was less than normal for 10 patients and abnormally high for 6 patients. A significant positive correlation between spontaneous blink amplitude and blink rate was found. These observations suggest that PD modifies the gain of a premotor blink circuit shared by spontaneous, voluntary, and reflex blinks.

Adult↗
PubMed2006

Asymmetry of blinking.

PURPOSE: Too investigate asymmetry in eyelid movements with blinking, the stability of the asymmetry, and its modifiability in normal humans. METHODS: Differences in the start time and amplitude between the two eyelids were assessed for voluntary blinks and reflex blinks evoked by supraorbital trigeminal nerve stimulation. These variables were also measured before and up to 18 months after 2 hours of unilateral upper lid restraint. RESULTS: With voluntary blinks, one eyelid consistently began to close earlier and made a larger eyelid movement than the other eyelid. Stimulation of the supraorbital branch of the trigeminal nerve evoked relatively larger amplitude blinks in one eyelid that correlated with the asymmetries of voluntary blinks. There was a continuum of eyelid asymmetry across all subjects that was stable and independent of other biological asymmetries, such as handedness. Briefly reducing eyelid mobility created a long-lasting change in eyelid asymmetry with blinking. CONCLUSIONS: Eyelid asymmetry results from differences in the excitability of motoneurons in the left and right facial motor nuclei and does not appear to involve asymmetries in cortical inputs to the brain stem. Because adaptive processes modify the motoneuron excitability that creates eyelid asymmetry, these processes may underlie changes in blinking associated with facial palsy and may play a role in the development of disorders that affect one side of the face, such as hemifacial spasm.

Adult↗
PubMed2005

Modification of cornea-evoked reflex blinks in rats.

Although maintaining the tear film on the cornea is the most important role of blinking, information about the organization and modification of cornea-evoked blinks is sparse. This study characterizes cornea-evoked blinks and their modification in urethane-anesthetized rats. Cornea-evoked blinks typically begin 16.2 ms after an electrical stimulus to the cornea and last an average of 50.2 ms. In anesthetized rats, the blink only occurs ipsilateral to the stimulus. In response to cornea stimulation, the orbicularis oculi EMG activity typically exhibits two bursts that correlate with the arrival of A delta and C-fiber inputs to the spinal trigeminal complex. In the paired-stimulus paradigm, suppression of the blink evoked by the second cornea stimulus occurs for interstimulus intervals less than 300 ms and is exclusively unilateral. Stimulation of the contralateral cornea does not affect subsequent blinks evoked from stimulation of the ipsilateral cornea. To determine whether activation of cornea-related neurons in the border region between the spinal trigeminal caudalis subdivision and the C1 spinal cord (Vc/C1) inhibits the second blink in the paired-stimulus paradigm, we examine the suppression of cornea-evoked blinks caused by microstimulation in this region. This suppression of orbicularis oculi EMG activity begins 8.3 ms after Vc/C1 stimulation. Activation of this region, however, is unlike suppression in the paired-stimulus paradigm because Vc/C1 activation bilaterally inhibits cornea-evoked blinks. Thus, activation of Vc/C1 is a previously unidentified mechanism for modulating cornea-evoked blinks.

Afferent Pathways↗
PubMed2005

Animal models of focal dystonia.

Animal models indicate that the abnormal movements of focal dystonia result from disordered sensorimotor integration. Sensorimotor integration involves a comparison of sensory information resulting from a movement with the sensory information expected from the movement. Unanticipated sensory signals identified by sensorimotor processing serve as signals to modify the ongoing movement or the planning for subsequent movements. Normally, this process is an effective mechanism to modify neural commands for ongoing movement or for movement planning. Animal models of the focal dystonias spasmodic torticollis, writer's cramp, and benign essential blepharospasm reveal different dysfunctions of sensorimotor integration through which dystonia can arise. Animal models of spasmodic torticollis demonstrate that modifications in a variety of regions are capable of creating abnormal head postures. These data indicate that disruption of neural signals in one structure may mutate the activity pattern of other elements of the neural circuits for movement. The animal model of writer's cramp demonstrates the importance of abnormal sensory processing in generating dystonic movements. Animal models of blepharospasm illustrate how disrupting motor adaptation can produce dystonia. Together, these models show mechanisms by which disruptions in sensorimotor integration can create dystonic movements.

Animals↗
PubMed2002

Lid restraint evokes two types of motor adaptation.

Unilateral reduction in eyelid motility produced two modes of blink adaptation in humans. The first adaptive modification affected both eyelids. Stimulation of the supraorbital branch of the trigeminal nerve (SO) ipsilateral to the upper eyelid with reduced motility evoked bilateral, hyperexcitable reflex blinks, whereas contralateral SO stimulation elicited normally excitable blinks bilaterally. The probability of blink oscillations evoked by stimulation of the ipsilateral SO also increased with a reduction in lid motility. The increased probability of blink oscillations correlated with the enhanced trigeminal reflex blink excitability. Thus, the trigeminal complex ipsilateral to the restrained eyelid coordinated an increase in excitability and blink oscillations independent of the eyelid experiencing reduced motility. The second type of modification appeared only in the eyelid experiencing reduced motility. When tested immediately after removing lid restraint, blink amplitude increased in this eyelid relative to the normal eyelid regardless of the stimulated SO. A patient with seventh nerve palsy exhibited the same two patterns of blink adaptation. These results were consistent with two forms of adaptation, presumably because unilateral lid restraint produced two error signals. The corneal irritation caused by reduced blink amplitude generated abnormal corneal inputs. The difference between proprioceptive feedback from the blink and expected blink magnitude signaled an error in blink amplitude. The corneal irritation appeared to drive an adaptive process organized through the trigeminal complex, whereas the proprioceptive error signal drove an adaptive process involving just the motoneurons controlling the restrained eyelid.

Adaptation, Physiological↗