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Blink-induced saccadic oscillations.

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Blink-Induced
Saccadic Oscillations
T. C. Hain, MD, D. S. Zee, MD, and M. Mordes, M D
A patient with a neurodegenerative disease had abnormal saccades only when he blinked. These saccades were
hypermetric and were followed immediately, without
any intersaccadic interval, by a large, oppositely directed saccade (dynamic overshoot). To explain these
findings, we hypothesize that a blink-related neural signal can modulate the activity of pause cells that normally inhibit saccadic burst neurons during fixation. In
pathological circumstances, abnormal function of pause
cells could lead to large-amplitude saccadic oscillations.
In normal subjects, blinks could induce short bursts of
low-amplitude flutter.
Hain TC, Zee DS, Mordes M: Blink-induced saccadic
oscillations. Ann Neurol 19:299-301, 1986
Some patients cannot produce normal saccades unless
they blink simultaneously. The saccades are then faster
and larger and are initiated more quickly [4]. Here we
describe a patient who produced relatively normal saccades without a blink, but when saccades were accompanied by a blink, a large, oppositely directed saccade
without any apparent intersaccadic interval (dynamic
overshoot) immediately followed.
Case Report
A 3 7-year-old man had had a progressive neurological disorder of unknown cause for over 15 years that was characterized by dysarthria, gait ataxia, and abnormal eye movements.
The major ocular motor abnormality was that horizontal saccades, when associated with a blink but not otherwise, had
large dynamic overshoots (Fig 1B). Quick phases of optokinetic and vestibular nystagmus that occurred in association with a blink also showed these dynamic overshoots.
Saccades made without blinks either had no dynamic overshoot (Fig IA), or in rare instances had a small dynamic
overshoot (less than 0.5 degree). The peak velocityamplitude relationship (main sequence) was the same for
all saccades whether they were associated with blinks or
whether they were the primary saccade or a dynamic overshoot (Fig 2).
Blinks during fixation always produced two or more toand-fro saccades of 1 to 2 degrees in amplitude, without an
intersaccadic interval (Fig 1C). Only rarely were such bursts
From the Department of Neurology, Johns Hopkins Hospital, Baltimore, MD.
Received Mar 18, 1985, and in revised form July 17. Accepted for
publication Aug 5, 1985.
Address reprint requests to Dr Hain, Department of Neurology,
Meyer 2-147, Johns Hopkins Hospital, 600 N Wolfe Street, Baltimore, MD 21205.
of flutter observed without a blink. All types of saccadic
oscillations observed during fixation, including those associated with a blink, were also present in darkness. Saccades,
both with and without blinks, were initiated promptly, as the
average latencies for saccades with a blink (281 -+ 81; n =
94) and without (294 Ifr 45; n = 26) were not significantly
different from each other or from normal (275 k 75) El].
Discussion
The major observations that need explanation in this
patient are that ( 1 ) saccades with blinks had large dynamic overshoots and (2) blinks alone induced ocular
flutter. The question arises: How might blinks be expected to alter saccadic eye movements o r produce
saccadic oscillations? One possibility is through the influence of pause cells in the brainstem. These neurons
(located in the midline of the caudal pons) cease dacharging (pause) immediately before, and time-locked
to, the saccade; otherwise they discharge at a constant
rate. Experimental findings suggest that the pause cells
tonically inhibit the burst cells of the brainstem (which
lie in the paramedian reticular formation) that generate
the immediate premotor commands for saccadic eye
movements [2]. In this way, pause cells may prevent
extraneous burst cell activity that might lead to saccadic oscillations [53. If blinks inhibit pause cells of the
brainstem, this would explain the observation that
blinks, in this patient, could induce saccadic instability.
What physiological data are available to support this
hypothesis? Unfortunately, our knowledge of the effect of blinks on the neural circuitry that generates
saccades and on pause cells in particular is sparse. In
monkeys, all pause cells pause and most burst cells
burst weakly during blinks unaccompanied by a saccade {V. Henn, personal communication, 19841.
Although the pause cells pause during blinks, and a
decrease in pause cell activity might explain emergence
of burst cell activity during blinks, the primary effect
of blinks need not necessarily be on the pause cells. A
direct blink-induced increase in burst cell discharge
could feed back on the pause cells and in turn decrease
their discharge. Not enough is known yet about normal anatomical connections to allow a distinction to be
made between the two possibilities. In either case,
blinks could lead to saccadic oscillations.
We were able to simulate qualitatively the effects of
blinks on our patient’s saccades using a model of the
normal saccadic premotor circuitry described previously IS]. The main assumptions were that blinks directly lower pause cell tone and that there was an increased delay in an internal feedback loop used to
prevent pause cells from discharging during saccades.
Applying the idea that blinks reduce the rate of
discharge from pause cells has other interesting implications for both normal and abnormal ocular motor
behavior. In patients with ocular flutter or opsoclonus,
the hypothesis suggests that blinks could increase the
299
1"
1
BLINK
0
TARGET
L
7
L l
201
Fig I. Eflects of blinks on saccades. The top tracing shows horizontal position (search coil technique). The middle tracing shows
the blink trace (electrooculogram),and the bottom tracing shows
target displacement. Time impulses shown along the top are at
1-second intervals. (A) Saccades made without a blink show little or no dynamic overshoot. (B) Saccade made with a blink
shows a large dynamic overshoot. (C) A blink alone causes several back-to-back, to-and-fro saccades (ocularputter). (R =
rightward; L = leftward; U = up; D = down.)
/
RIGHT
EYE
LEFT
EYE
I
100 m?,
Fig 3. Blink-induced ocular putter in a normal subject (search
cod technique).A blink (upper tracing)fell upon a small corrective saccade and was asjociated with a short bunt of nearly conjugate ocularputter. This pattern was consiJtent and common in
this subject. (R = rightward; L = leftward.)
.
.. . .. . ....
.
O r . . .
PEAK
VELOCITY
20.0
0.0
40.0
60.0
PRIMARY SACCADE AMPLITUDE
F i g 2. Peak velocity-amplitude relationship (in degrees) for saccades. Saccades without an accompanying blink are plotted as
triangles, those with blinks as dots, and dynamic overshoots as
open circles. All points fall on the same peak velocity-amplztude
relationship curve.
number of cycles of flutter or trigger inappropriate
saccades. Also, in normal subjects, an appropriately
timed blink during a saccade might produce lowamplitude (0.25-degree) flutter or increase the fraction
of saccades with dynamic overshoots. Short blinkassociated bursts of conjugate ocular flutter have, in
fact, been consistently observed in one of our normal
subjects (Fig 3).
In patients who have difficulty triggering saccades
without blinks (e.g., patients with Huntington's disease
[ 3 ] or with ocular motor apraxia), a blink might enable
300 Annals of Neurology
Vol 19 No 3 March 1986
them to make a saccade by reducing the discharge rate
of pause cells and allowing a saccade to proceed. In
patients who have difficulty generating saccades of normal amplitude and velocity without a blink [47, the
blink signal may ensure that the pause cells turn off
promptly and are not allowed to resume discharging
before the saccade is over. An inappropriate resumption of pause cell discharge might cause hypometric
saccades.
Finally, this hypothesis could explain how blinks
might increase the velocity of pathologically slow saccades. If saccades were slow because only a fraction of
the pause cells were inhibited, only a fraction of the
burst cells would be allowed to discharge. Slow saccades would then result. However, by inhibiting all
pause cells, blinks would allow the entire population of
burst cells to discharge and thereby increase saccadic
velocity to normal.
Supported in part by NIHgrants R O l EY05505 and RO1 EY01849.
References
1. Abel LA, Troost BT, Dell'Osso LF: The effects of age o n normal
saccadic characteristics and their variability. Vision Res 23:3337, 1983
2. Keller EL: Control of saccadic eye movements by midline brain
stem neurons. In Baker R, Berthoz A (eds): Control of Gaze by
Brain Stem Neurons. New York: ElsevieriNorth Holland, 1977
Starr A: A disorder of rapid eye movements in Huntington’s
chorea. Brain 90:545-564, 1967
Zee DS, Chu FC, Leigh J, et al: Blink-saccade synkinesis. Neurology (Cleveland) 33:1233-1236, 1983
Zee DS, Robinson DA: A hypothetical explanation of saccadic
oscillations. Ann Neurol 5:405-414, 1979
Benign Versive
or Circling Epilepsy
with Bilateral 3-cps
Spike-and-Wave Discharges
in Late Childhood
Henri Gastaut, MD,+ Umberto Aguglia, MD,P
and Paolo Tinuper, MDS
Twenty-eight of 920 patients seen between the ages of 8
and 20 years for a first seizure manifested versive or
circling events associated with bilateral rhythmic 3-cps
spike-and-wave discharges. In 21 (75%), the seizures appeared between the ages of 10 and 14 years. Paroxysmal
adversion or gyration was always toward the same side
in a given patient. “Break of contact” during the ictus
was found in 70% of the seizures, and secondary
generalization occurred in half. Ictal electroencephalographic recordings failed to show a focal hemispheric
origin. Additional features were: absence of prior
major diseases; normal results of neurological and
neuroradiological examinations; excellent response to
anticonvulsant treatment with sodium valproate andlor
phenobarbital; frequent family history of epileptic seizures (25% of patients); and association with generalized
seizures (57.2% of patients). We conclude that versive or
circling epilepsy with bilateral rhythmic 3-cps spikeand-wave discharges represents a benign form of primary generalized epilepsy in late childhood.
Gastaut H, Aguglia U, Tinuper P: Benign versive
or circling epilepsy with bilateral 3-cps
spike-and-wave discharges in adolescents.
Ann Neurol 17:301-303, 1786
It is well known that generalized or focal seizures occurring in late childhood or adolescence are frequently
From the “Institute of Neurologic Research, WHO Collaborating
Centre for Research and Teaching in Neurosciences, Medical Faculty, University of Marseille, Marseille, France, the ?Department of
Neurology, Medical Faculty, University of Catanzaro, Catanzaro,
and the $Department of Neurology, Medical Faculty, University of
Bologna, Bologna, Italy.
Received Dec 11, 1984, and in revised form May 20, 1985. Accepted for publication Aug 12, 1985.
Address reprint requests to Dr Aguglia, Via E. Cuzzocrea 13,89100
Reggio Calabria, Italy.
benign or functional 14, 93. The association of bilateral
synchronous 3-cps spike-and-wave (SW) discharges
with versive or rotatory seizures is reported in the
literature, and one of us (H. G.) proposed, in a preliminary report 171, that such an association may represent a variety of primary generalized epilepsy.
Patients and Methods
In a retrospective survey of 720 patients seen during the past
7 years by one of us (H. G.) for their first seizure, which
occurred between the ages of 8 and 20 years, 28 patients (15
boys, 13 girls) were identified using the following criteria:
presence of versive or rotatory seizures with or without secondary generalization or presence of bilateral rhythmic 3-cps
SW discharges on interictal electroencephalogram. A detailed description from patients and their relatives provided
us with the clinical pattern of the seizures. In 7 patients, we
were able to record at least one electroencephalographicversive seizure. Neuropsychiatric examination was performed in
all patients. A Wechsler-Bellevue test was performed in patients with clinically suspected mental impairment.
These 28 patients have been followed up for a mean of 9.0
I+_ 5.0 years (range, 4 to 24 years). Their last electroencephalographic examination was done between the ages of 12 and
35 years (mean, 17.5 I+_ 5.3 years).
Results
The first versive or circling seizure occurred in these
patients between 8.5 and 17.8 years of age (mean, 12.7
2 2.3 years). In 75% of the patients the seizures appeared between 10 and 14 years of age. No patient
had a history of major prior disease (slight perinatal
asphyxia in 8 and simple febrile convulsions in 4 patients). In 25% of patients there was a family history of
epileptic seizures (febrile convulsions, 10.7%; absences, 10.7%; tonic-clonic seizures, 3.6%). Results of
neuropsychiatric examination were normal in all patients but 3 , who showed slight mental impairment (IQ
90 by the Wechsler-Bellevue test). Brain computed
tomographic scanning was performed in 16 patients
and all results were normal.
The epileptic seizures were characterized by con jugate eye and head turning, by complete adversion of
one half of the body, or by one to three complete turns
(rotatory or circling fits). Paroxysmal adversion or gyration was always toward the same side in a given patient. Ictal “break of contact” was found in 70% and
secondary generalization followed in 50% of the versive or circling fits. Seizures typically lasted 5 to 15
seconds and their frequency ranged from three per
week to one per year (mean, 1.2 per month). Seizure
onset frequently occurred upon awakening, after sleep
deprivation or alcohol abuse, or during menses. Nonversive seizures occurred in 57.2% of patients and
were always generalized (absences, 50%; bilateral myoclonic jerks on awakening, 7.2%).
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