This study characterizes trigeminal blinks in normal human subjects between 20 and 80 years of age, 60-year-old Parkinson's disease patients, and young and old guinea pigs. In normal humans over 60 years of age, lid-closing duration, and the excitability and latency of the trigeminal reflex blink increase significantly relative to younger subjects. Aged guinea pigs appear to display similar increases in reflex blink duration and latency. Reflex blink amplitude, however, does not change consistently with age. For subjects less than 70 years of age, a unilateral trigeminal stimulus evokes a 37% larger blink in the eyelid ipsilateral to the stimulus than in the contralateral eyelid, but 70-year-olds exhibit blinks of equal amplitude. In all cases, blink duration is identical for the two eyelids. If normal, age-related loss of dopamine neurons explains these trigeminal blink modifications, then Parkinson's disease should exaggerate age-related changes in these blink parameters. Preliminary data show that Parkinson's disease increases blink duration and excitability relative to age-matched control subjects. Thus, it seems likely that normal, age-related loss of dopamine neurons accounts for increases in trigeminal blink excitability and duration. A previously uncharacterized type of trigeminally evoked blink appears after age 40 in humans and in aged guinea pigs. In subjects less than 40 years old, a single trigeminal stimulus elicits a single reflex blink. In subjects over age 40, however, a single stimulus frequently evokes a reflex blink and additional blinks that occur at a fixed interval relative to the preceding blink. These "blink oscillations" may arise from oscillatory processes within trigeminal reflex blink circuits. The presence of exaggerated blink oscillations in subjects with dry eye and benign essential blepharospasm suggests that an alteration of blink oscillation mechanisms plays a critical role in these disorders.
Keywords dry eye; blinking; blepharospasm; eyelid movements; blink oscillations; brainstemThe primary purpose of the eyelids is to ensure corneal integrity. An important component of this protective function is maintaining the corneal tear film. Blink characteristics can determine tear film stability. Increasing blink amplitude thickens the lipid layer that overlies the aqueous layer of the tear film. This thickening reduces evaporation of the aqueous layer. Because each blink reforms the tear film, increasing blink frequency reduces tear film breakup. [1][2][3][4] Both innocuous stimuli such as air across the eyelashes, and noxious stimuli such as touching the cornea, elicit trigeminal reflex blinks. If abnormal corneal afferent activity caused by corneal irritation acts as an "error signal" that adjusts the amplitude and frequency of reflex blinks evoked by both innocuous and corneal stimuli, then corneal irritation creates an adaptive blink response regardless of whether a corneal or an innocuous trigeminal stimulus elicits the blink.An investigation of the effects of aging on trigeminal blinks 5 supports the hypothesis that corneal irritation modifies trigeminal reflex blinks evoked by innocuous stimuli. In people over age 40 years, a single innocuous, supraorbital (SO) nerve stimulus frequently evokes a reflex blink and additional blinks that occur at a nearly constant interval relative to the onset of the preceding blink, blink oscillations. Because blink oscillations are more frequent and larger than reflex blinks, this modification increases tear film stability. Peshori and colleagues 5 propose that the development of consistent blink oscillations in many individuals over age 40 years is a blink adaptation that compensates for the subclinical reduction in corneal wetting that accompanies aging. 6 This hypothesis predicts that innocuous SO stimuli should produce more blink oscillations in people with dry eye than in age-matched control subjects. We test this prediction by comparing the SO-evoked blinks of individuals with dry eye with those of age-matched controls. Given the frequent occurrence of dry eye at the onset of benign essential blepharospasm (BEB), 7 blink modifications associated with dry eye may play a role in the origin of BEB. We present a hypothesis that links the adaptive processes initiated by dry eye with the origin of BEB. METHODSMeasurements of eyelid movement and orbicularis oculi electromyographic (OOemg) activity were made on seven subjects, ranging in age from 44 to 72 years of age. Five female subjects had been diagnosed with dry eye at the SUNY Stony Brook Ophthalmology Clinic. The data from these subjects were compared with those from age-matched control subjects in another study. 5 Two normal subjects, a man and a woman, participated in an experimental paradigm described below. Apart from dry eye, no subject had any ocular disorders other than the need for corrective lenses. A previous study 8 detailed measurement of lid movements and OOemg used in the current study. Upper eye...
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.
The object of this study was to examine the relationship between excitatory postsynaptic potential (EPSP) amplitude, posttetanic potentiation, and EPSP amplitude modulation at synapses made by group Ia afferents on motoneurons in the rat. These relationships were evaluated in cells in untreated rats and in cells in rats treated with the gamma-aminobutyric acid-B (GABAB) receptor agonist baclofen and antagonist CGP-35348, which were used to manipulate Ca2+ entry into presynaptic terminals and consequently probability of transmitter release from them. There was no evidence for postsynaptic action of these drugs from measurement of their effects on motoneuron properties. During high-frequency stimulation (32 shock bursts at 167 Hz), EPSP amplitude either decreased (negative modulation) or increased (positive modulation) in response to successive stimuli at different connections. In untreated rats this frequency-dependent amplitude modulation behavior was inversely but weakly correlated with EPSP amplitude measured at low frequency. Intravenous (iv) administration of the GABAB agonist, baclofen, produced a marked and progressive decrease in EPSP amplitude measured at low frequency coincident with a change in frequency-dependent EPSP amplitude modulation toward more positive values (synaptic facilitation). In contrast, an increase in EPSP amplitude occurred after iv administration of the GABAB antagonist CGP-35348 that was accompanied by a negative shift in EPSP amplitude modulation during high-frequency stimulation. The negative shift in EPSP amplitude modulation (synaptic depression) after CGP-35348 application was much smaller than the positive shift induced by baclofen when normalized to the change in EPSP amplitude. Posttetanic potentiation decreased after baclofen but did not increase after CGP-35348. The relationship between modulation and EPSP amplitude was much steeper after GABAB receptor manipulation in either direction than that observed in the population of motoneurons in untreated preparations. This suggests that in the rat differences in probability of release play at most a small role in determining EPSP amplitude across the motoneuron pool.
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