Ann
ou«
84: 1975
VISUAL SUPPRESSION OF VESTIBULAR NYSTAGMUS AFTER CEREBELLAR LESIONS SETSUKO TAKEMOffi,
M.D.
TOKYO, JAPAN
SUMMARY - Visual suppression of calorically induced vestibular nystagmus was observed following discrete lesions of various structures in the cerebellum. Unilateral lesions of the flocculus resulted in a complete loss or a significant reduction in visual suppression when the quick phase of the nystagmus was directed to the ipsilateral side of the lesions, and bilateral flocculus lesions caused a bilateral loss of suppression. Nodulus lesions resulted in a loss of suppression, and this loss tended to recover in time. Lesions of the dentate nucleus resulted in a very short term loss of suppression. Extirpation or lesions of the uvula, vermis, paraflocculus, cerebellar cortex, or the fastigial or interpositus nuclei had no observed effect on the visual suppression of vestibular nystagmus. The results of this study suggest that the flocculus and nodulus function as intermediators through which the visual system can modify or alter vestibular reflexes. Also, this phenomenon, that is, loss of visual suppression after the flocculus and nodulus lesion, is very useful to diagnose the localized lesion in the cerebellum.
It has been repeatedly documented that nystagmus of vestibular origin is influenced by conditions which effect the visual fixation mechanism.t-" Spontaneous labyrinthine nystagmus is much more prominent with the eyes closed or covered than it is with eyes open," Also, nystagmus provoked by caloric stimulation or by rotation is more prominent in darkness than in light," In normal subjects, calorically provoked nystagmus is suppressed in light by 50% of the slow phase velocity observed in darkness.'
Sixty juvenile rhesus monkeys (macoca mulatta), weighing between 2 and 4 kg, and fifteen cats, weighing between 2 and 3 kg, were used for this study. The monkeys were restrained in a primate chair and their heads were fixed with a sponge-covered clamp. The cats were placed in a restraining box, and their heads were fixed by applying dental bars to the jaws. Alertness was maintained by injections of amphetamine sulfate (0.5 mg/kg ).
Nystagmus of vestibular origin is also influenced by the cerebellum, and it has been shown that lesions in the flocculus reduce or abolish the ability to suppress vestibular nystagmus." This study is an attempt to further localize the mechanisms in the cerebellum which effect the visual suppression of vestibular nystagmus. Discrete lesions were created in various locations of the rhesus monkeys and cat cerebellum and changes in visual suppression of calorically induced nystagmus were observed.
Eye movements were recorded in light and in darkness using the techniques of electronystagmography ( ENG). Platinum needle electrodes were fixed to the outer canthi of each eye, and a reference electrode was placed at the midline of the forehead. All of the eye movement recordings were direct current coupled, differentiated to yield velocity in both directions and finally clipped to display the slow phase velocity only. Conventional recording polarity was used wherein an upward pen deflection indicates an eye
METHODS AND MATERIALS
From the Department of Otolaryngology, Teikyo University School of Medicine, Tokyo, Japan. Supported by NIH Research Grant NS 10412-03. 318
Downloaded from aor.sagepub.com at PRINCETON UNIV LIBRARY on July 27, 2015
319
VESTIBULAR NYSTAGMUS
/
/
B
Fig. 1. Visual suppression in normal animals. A) The top trace is the time base at 1 mark/sec. The middle trace is the bitemporal horizontal ENG, and the bottom trace shows slow phase velocity. The bottom trace is a photocell recording showing the period of stimulation ( a ), followed by a period in darkness (b). The animal was then in light (c), followed by a succeeding period in darkness (d). Normal visual suppression was shown (period c) . Vertical bars at the right shows the calibration, 10 for eye movement and 100 for eye velocity. B) The mean visual suppression in twenty monkeys at 27C and 47C are shown. The open circles show the visual suppression of stimulating right ear and the closed circles show the left ear. The mean visual suppression was 53%±3 at 27C and 51%±2 at 47C.
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movement to the right. Calibration of the ENG was accomplished by measuring the slope of the slow phase of optokinetic nystagmus ( OKN). Maximum mean values of the slopes of the slow phase induced in both directions by stimulus velocities of 45 j sec on five separate test occasions were taken to represent 45 jsec. 0
0
Caloric stimuli, using 20 cc of water generally at 27C or 47C over a 20 second period, were applied to provoke vestibular nystagmus. A three to five minute recovery period was allowed between irrigations. The slow phase
velocity responses curve from both the monkeys and the cats was very similar to the standard Hallpike curve. After each irrigation, the amount of visual suppression of the slow phase of caloric nystagmus was tested by using the following paradigm. As illustrated in Figure lA, the stimulus was given, in light, during the initial 20 seconds of the trial (period a). The animal was then immediately placed in darkness for 15 seconds (period b), and during this time the slow phase velocity reached a plateau. The lights were then turned on for a 10 second period (period c) causing an immediate suppression of
Downloaded from aor.sagepub.com at PRINCETON UNIV LIBRARY on July 27, 2015
320
SETSUKO TAKEMORl
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ou«
84: 1975
VISUAL SUPPRESSION OF VESTIBULAR NYSTAGMUS AFTER CEREBELLAR LESIONS SETSUKO TAKEMOffi,
M.D.
TOKYO, JAPAN
SUMMARY - Visual suppression of calorically induced vestibular nystagmus was observed following discrete lesions of various structures in the cerebellum. Unilateral lesions of the flocculus resulted in a complete loss or a significant reduction in visual suppression when the quick phase of the nystagmus was directed to the ipsilateral side of the lesions, and bilateral flocculus lesions caused a bilateral loss of suppression. Nodulus lesions resulted in a loss of suppression, and this loss tended to recover in time. Lesions of the dentate nucleus resulted in a very short term loss of suppression. Extirpation or lesions of the uvula, vermis, paraflocculus, cerebellar cortex, or the fastigial or interpositus nuclei had no observed effect on the visual suppression of vestibular nystagmus. The results of this study suggest that the flocculus and nodulus function as intermediators through which the visual system can modify or alter vestibular reflexes. Also, this phenomenon, that is, loss of visual suppression after the flocculus and nodulus lesion, is very useful to diagnose the localized lesion in the cerebellum.
It has been repeatedly documented that nystagmus of vestibular origin is influenced by conditions which effect the visual fixation mechanism.t-" Spontaneous labyrinthine nystagmus is much more prominent with the eyes closed or covered than it is with eyes open," Also, nystagmus provoked by caloric stimulation or by rotation is more prominent in darkness than in light," In normal subjects, calorically provoked nystagmus is suppressed in light by 50% of the slow phase velocity observed in darkness.'
Sixty juvenile rhesus monkeys (macoca mulatta), weighing between 2 and 4 kg, and fifteen cats, weighing between 2 and 3 kg, were used for this study. The monkeys were restrained in a primate chair and their heads were fixed with a sponge-covered clamp. The cats were placed in a restraining box, and their heads were fixed by applying dental bars to the jaws. Alertness was maintained by injections of amphetamine sulfate (0.5 mg/kg ).
Nystagmus of vestibular origin is also influenced by the cerebellum, and it has been shown that lesions in the flocculus reduce or abolish the ability to suppress vestibular nystagmus." This study is an attempt to further localize the mechanisms in the cerebellum which effect the visual suppression of vestibular nystagmus. Discrete lesions were created in various locations of the rhesus monkeys and cat cerebellum and changes in visual suppression of calorically induced nystagmus were observed.
Eye movements were recorded in light and in darkness using the techniques of electronystagmography ( ENG). Platinum needle electrodes were fixed to the outer canthi of each eye, and a reference electrode was placed at the midline of the forehead. All of the eye movement recordings were direct current coupled, differentiated to yield velocity in both directions and finally clipped to display the slow phase velocity only. Conventional recording polarity was used wherein an upward pen deflection indicates an eye
METHODS AND MATERIALS
From the Department of Otolaryngology, Teikyo University School of Medicine, Tokyo, Japan. Supported by NIH Research Grant NS 10412-03. 318
Downloaded from aor.sagepub.com at PRINCETON UNIV LIBRARY on July 27, 2015
319
VESTIBULAR NYSTAGMUS
/
/
B
Fig. 1. Visual suppression in normal animals. A) The top trace is the time base at 1 mark/sec. The middle trace is the bitemporal horizontal ENG, and the bottom trace shows slow phase velocity. The bottom trace is a photocell recording showing the period of stimulation ( a ), followed by a period in darkness (b). The animal was then in light (c), followed by a succeeding period in darkness (d). Normal visual suppression was shown (period c) . Vertical bars at the right shows the calibration, 10 for eye movement and 100 for eye velocity. B) The mean visual suppression in twenty monkeys at 27C and 47C are shown. The open circles show the visual suppression of stimulating right ear and the closed circles show the left ear. The mean visual suppression was 53%±3 at 27C and 51%±2 at 47C.
100
-° ~
~ (/)
T
50
~I
»
0
0/sec
o
L...---'-_ _" - - _
27
47
TEMP. OF WATER (Oe)
movement to the right. Calibration of the ENG was accomplished by measuring the slope of the slow phase of optokinetic nystagmus ( OKN). Maximum mean values of the slopes of the slow phase induced in both directions by stimulus velocities of 45 j sec on five separate test occasions were taken to represent 45 jsec. 0
0
Caloric stimuli, using 20 cc of water generally at 27C or 47C over a 20 second period, were applied to provoke vestibular nystagmus. A three to five minute recovery period was allowed between irrigations. The slow phase
velocity responses curve from both the monkeys and the cats was very similar to the standard Hallpike curve. After each irrigation, the amount of visual suppression of the slow phase of caloric nystagmus was tested by using the following paradigm. As illustrated in Figure lA, the stimulus was given, in light, during the initial 20 seconds of the trial (period a). The animal was then immediately placed in darkness for 15 seconds (period b), and during this time the slow phase velocity reached a plateau. The lights were then turned on for a 10 second period (period c) causing an immediate suppression of
Downloaded from aor.sagepub.com at PRINCETON UNIV LIBRARY on July 27, 2015
320
SETSUKO TAKEMORl
A
U
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n.", U","'","t".",
t
l'"
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11
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