Using squirrel monkeys as experimental subjects, we reexamined the disputed role of the area postrema (AP) in motion‐induced vomiting. After anesthetization, the obex and rhomboid fossa were exposed surgically, and the AP was ablated by thermal coagulation using either a battery cautery or a CO2 microsurgical laser. Sham operations were performed on another sample of monkeys. Two or more weeks after surgery, all animals were given 10 daily 2‐hour horizontal rotations at 30 rpm. Every monkey in both the lesions and sham samples vomited on two or more test days. While the vomiting characteristics were modified following ablation of AP, its function is not indispensible for the development of motion sickness in horizontally‐rotated squirrel monkeys.
Following bilateral simple mastoidectomy, eight adult squirrel monkeys were subjected to argon laser irradiation (output wavelength of 488 nanometers) of the horizontal or posterior semicircular canals. Penetration of the bony canal wall and damage to the membranous labyrinth was achieved if multiple or superimposed burns were made (one watt bursts with durations from 0.2 to 1 second). The major morphologic effect of the penetrating lesions was a mild to prolific growth of fibrous tissue restricted to the immediate site of irradiation. Endolymphatic ducts were blocked by collapse of one membranous wall against the other, by filling in of the lumen with fibrous growth of the duct walls or by constriction caused by overgrowth of surrounding fibrous tissue filling the perilymphatic space. Blocking of the duct, however, can not account fully for functional vestibular changes following irradiation, because some dysfunction occurred in the absence of any discernible structural abnormality. On the other hand, some function remained when ducts were completely occluded. Except for the control ear animal, all others exhibited slight to moderate ataxia and loss of acrobatic ability for several days after irradiation. No spontaneous nystagmus was detected in any monkey. All animals of our series, even those with no apparent morphological changes, were characterized by at least temporary reduction of caloric‐induced nystagmus, but only two showed complete absence of responses. All monkeys showed a change in the direction of caloric responses from horizontal to rotary or mixed, and vigor of the responses lessened considerably. Monkeys having penetrating lesions of the posterior canal exhibited subnormal postrotatory nystagmus when rotated in a forward direction with vertical canalsplaced in the horizontal plane. Two of the monkeys were trained to track their pure tone detection thresholds by means of an automated, single‐lever conditioned‐avoidance procedure. Bone conduction hearing was normal after irradiation except for a 16 db threshold shift at 2,000 Hz in one animal. On the basis of our experience with squirrel monkeys, there would appear to be no hazardous or life‐threatening side effects of laser surgery of otic structures when done in this manner. Serious consideration should be given by otologists to the experimental application of lasers for human microsurgical purposes.
It has been suggested by numerous researchers that the development of conditioned food aversion (CFA) in experimental animals represents the presence of a subjective state of illness. Squirrel monkeys with proven susceptibility to rotation-induced vomiting were given surgical bilateral labyrinthectomies, a procedure known to abolish signs and symptoms of motion sickness in human beings. Postoperatively, labyrinthectomized monkeys neither vomited nor revealed any reduction in food consumption when exposed to provocative rotation. Other samples of monkeys known to be refractory to horizontal rotation and to sinusoidal vertical motion also exhibited little tendency to acquire a conditioned aversion to banana. But monkeys who had sham operations and those who revealed weak-to-strong signs of motion sickness exhibited a marked CFA (significant reduction in food intake). The strength of CFA was much greater when elicited in the test vehicle when compared with response in the home cage. The findings are interpreted as support for a limited application of CFA procedures for inferring the presence of motion-induced nausea and malaise.
Twelve adult squirrel monkeys were subjected to chronic lead exposure for a period of five to 24 weeks. Poisoning was confirmed by elevated blood lead levels, a consistent drop in body weight and by neurological signs of paresis and convulsions. Five animals died as a direct result of lead poisoning, and the remaining seven were sacrificed either when death seemed imminent (two animals) or at critical times during the experimental schedule. Bilateral cold and warm water irrigations as well as body rotational tests (upright, right side down and left side down, clockwise and counterclockwise), were given prior to lead poisoning and at various times during the experimental period. Positional and induced nystagmus (horizontal for caloric stimulation and both horizontal and vertical for rotatory stimulation) were recorded with eyes closed, by electronystagmography. Auditory detection thresholds for bone‐conducted pure tones were measured in two monkeys by a conditioned avoidance response technique. There was great intra‐ and inter‐subject variability in nystagmus duration and intensity (total number of eye beats and beat rate) for pre‐lead and lead intoxication conditions. Analysis of records was made difficult by the occurrence of positional and provocation nystagmus. Four of the 12 monkeys exhibited some positional nystagmus (mostly vertical when placed on either side) during the pre‐lead phase. Six of the group showed enhanced positional nystagmus or developed it during the lead intake phase. In general, both caloric‐ and rotational‐induced nystagmus decreased slightly in median duration and intensity under lead poisoned conditions, but the differences were not statistically reliable. Control measures of right‐left labyrinthine sensitivity and directional preponderance did not differ significantly from measures obtained under chronic lead intake conditions. After 20 weeks of lead intoxication, three animals showed a directional preponderance opposite that seen at the beginning of the study. Examination of the temporal bones of three monkeys revealed neither hair cell damage nor demyelination of VIIIth nerve fibers. Bone conduction detection thresholds remained within normal limits. A generalized state of muscular weakness due to chronic lead absorption could explain the unsteadiness which may have been mistaken for vestibular ataxia, reported by others in the literature.
The horizontal semicircular canal of squirrel monkeys was irradiated unilaterally with either an argon or carbon dioxide laser. Postoperatively, there was a small but significant reduction in caloric-induced ENG responses to 45 degrees thermal stimulation. The principal morphologic effect of laser irradiation was a plug of fibrous tissue or new bone within the lumen of the lesioned semicircular canal.
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