Rostral Lesions Research Articles

The basilar pontine gray of the opossum (Didelphis virginiana). II. Experimental determination of neocortical input.

AbstractThe pattern of neocortical input into the basilar pons of the opossum was determined by employing the Nauta‐Gygax technique ('54) on the brains of animals previously subjected to neocortical lesions. The results indicate that every neocortical area projects to some portion of the basilar pons in this form. Degenerating fibers resulting from more rostral cortical lesions (frontal and preorbital areas) terminated profusely within the medial and ventral nuclei and, to a lesser extent, in the smaller dorsal nucleus. Fascicles from more caudal areas (striate and peristriate cortices) ended abundantly in the lateral nuclear group, and in the lateral part of the ventral nucleus. Every neocortical region studied projected to some portion of the ventral pontine nucleus. Degenerating fibers terminated to some extent within each nucleus of the basilar pons as a result of lesions in midcortical regions (paramarginal, postorbital and parietal cortices). A few fibers of frontal, orbital and parietal origin terminated in the contralateral basilar pontine gray.

Combined effects of hypothalamic lesioning and light in the advancement of puberty.

Anterior-basal hypothalamic lesions were produced in alternate rat pups of a given litter at age 3–4 days; the remaining pups were sham-operated. The litters were then placed in either constant light or absolute darkness and the female young removed from the environment on the day of vaginal opening and sacrificed. Both the light-lesioned (LL) and dark-lesioned (DL) groups matured at essentially the same time and significantly earlier than the corresponding light-sham-operated (LS) and dark-sham-operated (DS) groups, the onset of maturation in the latter 2 being virtually identical. All 4 groups matured earlier than sham-operated controls reared in diurnal lighting. The results demonstrate that rostral hypothalamic lesions can produce precocious puberty regardless of lighting conditions. (Endocrinology 82: 865, 1968)

Thyroid activity following administration of morphine in rats with hypothalamic lesions

The inhibitory effect of morphine on pituitary-thyroid activity in the rat is abolished by bilateral electrolytic lesions involving the region of the medial mammillary nuclei of the hypothalamus whereas rostral hypothalamic lesions do not alter the response to morphine. It is suggested that the action of morphine may be due to activation of areas inhibiting the release of TSH from the pituitary gland.

Food intake and activity of rats with rostral hypothalamic lesions.

SummaryRats with lesions placed bilaterally in the region of the anterior hypothala-mus, when compared with control rats, eat more food in the heat, eat less food at cool and cold temperatures, and run less in response to cold stress. In addition, it was demonstrated that abnormalities in temperature regulation following the lesions are not transitory, but are clearly evident 9 months after the operations.

Effects of lesions upon thalamically induced electrocortical desynchronization and recruiting

1. (1) Unilateral lesions rostral to thalamic recruiting sites altered, attenuated, or abolished cortical recruiting, bilaterally. Lesions involving n. reticularis and n. ventralis anterior were most effective in abolishing recruiting responses, while more rostral lesions including n. caudatus and n. prothalamicus either raised the threshold or delayed the development of recruiting. 2. (2) Desynchronization produced by high frequency stimulation of the same sites in the thalamus was not affected by such rostrally placed lesions, but was abolished by lesions caudal to the site of stimulation, at the level of the posterior commissure. 3. (3) The results indicate that pathways mediating recruiting responses (low frequency stimulation) and those subserving desynchronization (high frequency stimulation) are different; the former course rostrally, and the latter caudally, apparently via the mesencephalic reticular formation.

Effects of brain stem lesions on aldosterone and cortisol secretion.

Brain stem lesions were made by high frequency coagulation in cats that had been maintained on regular or low sodium diets. Four hours after placing the lesion, adrenal venous blood was collected for determination of the secretion rates of aldosterone and cortisol. Discrete lesions placed in the dorsal central region of the rostral midbrain, involving primarily the posterior commissure, the periaqueductal gray substance and structures immediately adjacent to it, resulted in significant reductions in aldosterone output both types of animals. Cortisol output was somewhat depressed in cats on the regular diet following discrete lesions of the rostral midbrain, while in the low sodium group the output of this steroid was unaffected. Larger lesions which involved the habenulae, the stria medullaris and/or the pineal gland, in addition to the central rostral midbrain, modified or obscured the effects of the discrete rostral midbrain lesions on steroid secretion. In animals on either diet these larger lesions re...

Effects of lesions of the rostral thalamus on brain waves and behavior in cats

The EEG and behavioral effects following rostral thalamic lesions were studied in 14 cats; 3 with complete transection, 5 with complete electrolytic lesions, and 6 with partial destruction. Behavioral effects following either complete transection or complete destruction of the rostral thalamus were similar in quality, but different in the degree of severity. The signs and symptoms were: spasticity, difficulty in walking and swallowing, reduced motility and reactivity, catatonic reaction, tendency to stick the head in a corner, and so on. These changes could last from 2 to 8 weeks. The only residual effects were some spasticity of the legs and a slight increase of docility. Cats with rostral thalamic destruction could learn a visual form discrimination. EEG effects following either complete transection or complete destruction of the rostral thalamus were again similar in quality but different in the degree of severity. ( a) The arousal pattern could be elicited within from 3 to 25 days after surgery. As shown by 3 cats with massive lesions, EEG arousal could be absent during behavioral arousal. ( b) The sleep spindles were either absent throughout the postoperative survival period or might have recovered to some slight extent within 3 (transection lesion) or 5 (electrolytic lesion) months. ( c) Both barbiturate burst and recruiting responses were seen to be affected at the terminal experiment, i.e. restricted to localized cortical areas and poorly organized in form. Partial damage to the rostral thalamus caused only transient and slight behavioral and EEG changes in the immediate post-operative period. The results are discussed in relation to the thalamic role in behavior and the functional significance of the final common path from the thalamic diffuse projection system to the cortex.

Rate of recovery of functioning in cats with rostral reticular lesions; an experimental study.

Recent studies, experimental and clinical, emphasize that damage to the rostral brain stem leads to derangement of consciousness, the site of emphasis being the mesial tegmentum of the midbrain. Earlier Bremer 2 stressed the similarity between sleeping cats and those with cerveau isol~ (midbrain transection) and attributed the former to interruption of the tonic drive propagated rostrally over the great afferent paths. The cerveau isol~ preparation also showed the spontaneous spindling of the sleep electroencephalogram . Lindsley, Bowden and Magoun s added selective sections of the lemniscus to enc~phale isol5 (acute C1 transection) preparations. This did not convert the activation tracing characteristic of the enc~phale isol5 to the cerveau isol~ type. However, lesions that instead destroyed sub- and hypothalamus from optic chiasm to mammillary bodies or anterior midbrain did produce a sleep tracing. Additionally, Lindsley et al2 studied the effects of chronic lesions. In animals with lesions in the ponto-midbrain tegmentum, midbrain tegmentum, hypothalamus, and junction between hypothalamus and thalamus, the common behavioral result (variable in degree depending upon site and extent of the lesion) was a postoperative somnolence or lethargy in which the animal displayed little or no spontaneous activity of a purposive sort, and seemed unaware of ordinary environmental stimuli. The animal with a midbrain tegmental lesion blocking much or all of the rostral end of the reticular activating system lay on its side with eyes closed as if deeply asleep during its ~l-day survival period. By contrast, in ~ anireals in which the periaqueductal gray was injured an approximation of normal sleeping-waking behavior was regained. Two others, with lateral mesencephalic lesions which spared the mesial tegmentum, became able to stand and walk again and showed activation of the electroencephalo graphic tracing. Experiments on 9 monkeys reported by French and Magoun 6 appeared generally to confirm these results so far as destruction of the reticular activating system and the associated behavioral deficits are concerned.

Hemiballismus Relieved by Ventral Quadrant Section of the Cervical Spinal Cord without Paralysis

Hemlballismus, as you know, is a rare disorder in which violent, uncontrollable movements of one arm and leg occur. The term hemiballismus, credited to Kussmaul by Oppenheim, is reserved for those cases in which the movements are massive, violent, flinging movements of one extremity or one half of the body. Walker 17 stated that hemiballismus probably should be considered a variety of choreo-athetosis. These involuntary actions may begin at times with little more than flinging of an article from the hand, but soon reach such dramatic violence that the patient may be thrown from the bed by them. The flingings and hurlings of the extremities usually persist through every waking moment. Although the movements disappear with sleep, sleep is usually impossible even with heavy sedation. The patient becomes distraught and eventually exhausted 9 by the violent constant movements and usually dies of pneumonia or cardiac failure in a few days to 5 weeks. Greiff 5 in 1883 was the first to localize the lesion to the contralateral corpus subthalamicum. This was forgotten until Bonhocffer t in 1897, Jakob in 19~3 and Martin 1~ in 19~7 revcrified the pathology to be in the contralateral subthalamic nucleus of Luys. Moersch and Kernohan 13 in 1939 reported a case. Whittier 18 in 1947 was able to find 30 cases with adequate pathological studies of the subthalamic nucleus. In 6 of these the subthalamic nucleus was intact, but it was presumed that its connections were interrupted. In 4 cases no change was noted in the nucleus or its connections. Meyers et al. 12 believed that the lesion may arise in different areas of a neural circuit rather than be confined to the nucleus of Luys. In the majority of instances, the lesion is vascular, either hemorrhage or thrombosis, although occasional cases of neoplastic involvement have been reported. Hampel 6 stated that the blood supply of the subthalamic nucleus is derived from three arterics--a branch of posterior cerebral, a choroidal artery and a branch of the posterior communicating. Carpenter 4 felt that the primary blood supply is from branches of the posterior cerebral artery. The Vogts had expressed the belief that a topical relationship existed in the subthalamic nucleus. In the cases reviewed by Whittier 18 the oral pole was destroyed in 17, with the face being involved. Meyers et al. 1~ have felt that there is a somatotopic localization in the nucleus with rostral lesions causing movement of the head and neck, lesions of the middle portion affecting the upper extremity and the caudal portion involving the lower extremity. Herz and Meyers ~ proposed a theory for the pathogenesis of hemiballismus in which impulses of the kinetic circuit flow from the periphery to the thalamus and are passed on to the postcentral areas 1, ~, 3--then by U-fibers to the motor area 4 and 4Y and premotor area 6 (Fig. 1).

Hyperactivity and pulmonary edema from rostral hypothalamic lesions in rats.

Hyperactivity and pulmonary edema from rostral hypothalamic lesions in rats.