Electrophysiological assessment of the cranial reflexes

Electrophysiological assessment methods play a key role in the diagnosis of various neurological disorders. Electrophysiological evaluation of cranial reflexes is particularly valuable for neurologists. This article provides an overview of electrophysiological evaluation methods for cranial reflexes, which are most commonly used in clinical practice. They provide objective assessment of the functional integrity of nervous system structures that make up the cranial reflex arc, identify the level and, in some cases, the nature of disease, as well as pathophysiological mechanisms of central and peripheral nervous system disorders. We describe the instruments and main approaches to analysing the results for the standard blink reflex, blink reflex with prepulse inhibition, blink reflex with paired stimuli and recovery curve evaluation, reflex inhibition of the levator palpebrae superioris, jaw jerk reflex, and reflex inhibition (cutaneous silent period) of the masseter muscle.

Sex, blinking, and dry eye

Blinking sustains the corneal tear film generated by sexually dimorphic lacrimal and meibomian glands. Our study examines whether trigeminal control of blinking is also sexually dimorphic by investigating trigeminal reflex blinking, associative blink modification, and spontaneous blinking in male and female rats before and after unilateral dry eye caused by exorbital gland removal. Before gland removal, female rats exhibited a lower threshold for evoking trigeminal reflex blinks, a weaker effect of associative blink modification, and longer-duration spontaneous blinks than males. Spontaneous blink rate, reflex blink excitability, and occurrence of blink oscillations did not differ between the sexes. Reanalysis of previous data showed that humans showed the same blink sexual dimorphisms as rats. During the first 2 wk of dry eye, trigeminal blink circuit excitability and blink oscillations steadily rose in male rats, whereas excitability and blink oscillations did not change in females. Following dry eye, spontaneous blink duration increased for both males and females, whereas spontaneous blink rate remained constant for males but decreased for females. The associative modification treatment to depress trigeminal blink amplitude initially produced blink depression in males that converted to blink potentiation as trigeminal excitability rose, whereas females exhibited progressively more blink depression. These data indicated that dry eye increased excitability in male trigeminal reflex blink circuits at the expense of circuit modifiability, whereas trigeminal modifiability increased in females. This increased modifiability of female trigeminal blink circuits with dry eye may contribute to the preponderance of females developing the focal dystonia, benign essential blepharospasm. NEW & NOTEWORTHY All the elements controlling the corneal tear film are sexually dimorphic. Blinking, which smooths and maintains the tear film, also exhibits sex differences. Dry eye increases the sexual dimorphisms of blinking, including increased exaggeration of excitability in males and enhanced modifiability of the female trigeminal complex. This increased modifiability may explain female predominance in the development of the focal dystonia, benign essential blepharospasm.

Effects of subthalamic deep brain stimulation on blink abnormalities of 6-OHDA lesioned rats

Parkinson's disease (PD) patients and the 6-hydroxydopamine (6-OHDA) lesioned rat model share blink abnormalities. In view of the evolutionarily conserved organization of blinking, characterization of blink reflex circuits in rodents may elucidate the neural mechanisms of PD reflex abnormalities. We examine the extent of this shared pattern of blink abnormalities by measuring blink reflex excitability, blink reflex plasticity, and spontaneous blinking in 6-OHDA lesioned rats. We also investigate whether 130-Hz subthalamic nucleus deep brain stimulation (STN DBS) affects blink abnormalities, as it does in PD patients. Like PD patients, 6-OHDA-lesioned rats exhibit reflex blink hyperexcitability, impaired blink plasticity, and a reduced spontaneous blink rate. At 130 Hz, but not 16 Hz, STN DBS eliminates reflex blink hyperexcitability and restores both short- and long-term blink plasticity. Replicating its lack of effect in PD patients, 130-Hz STN DBS does not reinstate a normal temporal pattern or rate to spontaneous blinking in 6-OHDA lesioned rats. These data show that the 6-OHDA lesioned rat is an ideal model system for investigating the neural bases of reflex abnormalities in PD and highlight the complexity of PD's effects on motor control, by showing that dopamine depletion does not affect all blink systems via the same neural mechanisms.

Trigeminal high-frequency stimulation produces short- and long-term modification of reflex blink gain

Reflex blinks provide a model system for investigating motor learning in normal and pathological states. We investigated whether high-frequency stimulation (HFS) of the supraorbital branch of the trigeminal nerve before the R2 blink component (HFS-B) decreases reflex blink gain in alert rats. As with humans (Mao JB, Evinger C. J Neurosci 21: RC151, 2001), HFS-B significantly reduced blink size in the first hour after treatment for rats. Repeated days of HFS-B treatment produced long-term depression of blink circuits. Blink gain decreased exponentially across days, indicating a long-term depression of blink circuits. Additionally, the HFS-B protocol became more effective at depressing blink amplitude across days of treatment. This depression was not habituation, because neither long- nor short-term blink changes occurred when HFS was presented after the R2. To investigate whether gain modifications produced by HFS-B involved cerebellar networks, we trained rats in a delay eyelid conditioning paradigm using HFS-B as the unconditioned stimulus and a tone as the conditioned stimulus. As HFS-B depresses blink circuits and delay conditioning enhances blink circuit activity, occlusion should occur if they share neural networks. Rats acquiring robust eyelid conditioning did not exhibit decreases in blink gain, whereas rats developing low levels of eyelid conditioning exhibited weak, short-term reductions in blink gain. These results suggested that delay eyelid conditioning and long-term HFS-B utilize some of the same cerebellar circuits. The ability of repeated HFS-B treatment to depress trigeminal blink circuit activity long term implied that it may be a useful protocol to reduce hyperexcitable blink circuits that underlie diseases like benign essential blepharospasm.

Conditioned Eyelid Movement Is not a Blink

Based on kinematic properties and distinct substrates, there are different classes of eyelid movement described as eyeblinks. We investigate whether the eyelid movements made in response to a conditioned stimulus (CS) are a category of eyelid movements distinct from blinks. Human subjects received 60 trials of classical eyelid conditioning with a tone as the CS and electrical stimulation of the supraorbital branch of the trigeminal nerve as the unconditioned stimulus (UCS). Before and after training, reflex blinks were elicited with the UCS. The kinematics of conditioned responses (CRs) differed significantly from those of reflex blinks. The slope of the amplitude-maximum velocity function was steeper for reflex blinks than for CRs, and reflex blink duration was significantly shorter than CR duration. Unlike reflex blinks, for which maximum velocity was independent of blink duration, the maximum velocity of CRs depended on CR duration. These quantitative and qualitative differences indicated that CRs were a unique class of eyelid movements distinct from blinks and eyelid movements with vertical saccadic gaze shifts.

Threshold of permanent cornea thermal damage due to incidental continuous wave CO2 laser irradiation

Cornea thermal damage due to incidental continuous wave CO2 laser irradiation is studied numerically based on bio-heat equation. The interaction of laser with tissue leads to a rapid temperature increased in target and the nearby tissue. As the temperature of the eye surface reaches 44?C, a sensation of pain will cause aversion response of the reflex blink and/or shifting away from the source of pain. The aim of the work is to predict numerically the threshold limit of incidental laser power that causes damage to the anterior part of the cornea, which can be healed within 2-5 days as long as damage is not exceeding the outer part of the eye (epithelium). A finite element analysis is used to predict temperature distribution through the cornea where the necroses region can be obtained using thermal dose equation. The thermal dose that required for damaging the cornea is predicted from previously published experimental data on rhesus monkeys and used later as a limit for shrinkage to human cornea. The result of this work is compared by international standard of safety and a good nearby result is obtained which verified the result of this work.

Activity of Primate V1 Cortical Neurons During Blinks

Every time we blink our eyes, the image on the retina goes almost completely dark. And yet we hardly notice these interruptions, even though an external darkening is startling. Intuitively it would seem that if our perception is continuous, then the neuronal activity on which our perceptions are based should also be continuous. To explore this issue, we compared the responses of 63 supragranular V1 neurons recorded from two awake monkeys for four conditions: 1) constant stimulus, 2) during a reflex blink, 3) during a gap in the visual stimulus, and 4) during an external darkening when an electrooptical shutter occluded the entire scene. We show here that the activity of neurons in visual cortical area V1 is essentially shut off during a blink. In the 100-ms epoch starting 70 ms after the stimulus was interrupted, the firing rate was 27.2 ± 2.7 spikes/s (SE) for a constant stimulus, 8.2 ± 0.9 spikes/s for a reflex blink, 17.3 ± 1.9 spikes/s for a gap, and 12.7 ± 1.4 spikes/s for an external darkening. The responses during a blink are less than during an external darkening ( P < 0.05, t-test). However, many of these neurons responded with a transient burst of activity to the onset of an external darkening and not to a blink, suggesting that it is the suppression of this transient which causes us to ignore blinks. This is consistent with other studies where the presence of transient bursts of activity correlates with the perceived visibility of a stimulus.