Ingestive behavior evoked by hypothalamic stimulation and schedule-induced polydipsia are related.

Some, but not all, rats eat or drink in response to electrical stimulation of the lateral hypothalamus. Similarly, some, but not all, rats given food intermittently display schedule-induced polydipsia. In this experiment, animals that ate or drank during electrical stimulation tended also to be those displaying polydipsia. Thus, individual differences in predisposition to engage in ingestive behavior are consistent under two very different conditions.

Sexual receptivity: facilitation by medial preoptic lesions in female rats.

Lesions in the medial preoptic area of ovariectomized female rats reduced the quantity of estrogen needed to induce sexual receptivity in these animals. In addition, the number of days over which receptive behavior could be elicited after a single initial estrogen injection and with subsequent daily progesterone treatment was significantly increased by lesions in the medial preoptic area. These findings support the view that estrogen acts to reduce an inhibitory action that is tonically exerted by the medial preoptic area on pathways mediating estrous behavior.

Sex differences in taste preference for glucose and saccharin solutions.

Taste preferences of mature male and female rats for caloric and noncaloric sweet solutions have been found to differ. Although females do not drink more water than males, they consume significantly greater quantities of a slightly sweet 3 percent glucose and a very sweet 0.25 percent saccharin solution. When given a choice, males switch their initial preference for a saccharin solution to a preference for a glucose solution after several days, while females maintain a preference for the saccharin solution. Females also prefer significantly higher concentrations of saccharin than males do.

Polydipsia elicited by the synergistic action of a saccharin and glucose solution.

Rats consume significantly more of a solution combining saccharin and glucose than equivalent solutions of these substances presented in separate bottles. Fluid consumption may exceed body weight. Experiments helping to delineate the basis of this synergistic action are presented.

Modification of motivated behavior elicited by electrical stimulation of the hypothalamus.

Previous reports demonstrated that hypothalamic stimulation may elicit either eating, drinking, or gnawing and emphasized both the specificity of the neural circuits mediating these behaviors and the similarity to behavior during natural-drive states such as hunger and thirst. We find that, after a period of very consistent elicitation of one of these behaviors, the animal may exhibit an equally consistent alternate behavior. A learning component is implicated in the association of hypothalamic stimulation with a particular behavior pattern.

Short-latency antidiuresis following the initation of food ingestion.

A factor associated with the ingestion of food is shown to produce a short-latency antidiuresis. Animals consuming large quantities of a highly palatable solution during a period of food deprivation exhibit an antidiuresis immediately following the initiation of eating. The rapidity of the response raises the possibility of a signaling factor separate from postingestional influences.

Object-carrying by rats: an approach to the behavior produced by brain stimulation.

Rats were provided with opportunity to turn reinforcing hypothalamic stimulation on and off by traversing back and forth across a chamber. When provided with edible and inedible objects, all animals that self-stimulated carried them from the stimulation to the nonstimulation side. Neither food deprivation nor a history of stimulus-bound eating produced a preference for the edible objects. Equivalent stimulation provided without regard to the animals' location in the chamber did not elicit object-carrying. Results are interpreted in terms of the natural conditions which normally elicit this species-specific unit of behavior. Implications for understanding other behavior patterns elicited by hypothalamic stimulation are suggested.

Apraxic agraphia with neglect-induced paragraphia.

Agraphia may result from the loss or unavailability of the memory of movements necessary to form written letters. For this mechanism to be invoked, it must first be demonstrated that there is no language deficit and that there is no disconnection between language and motor areas. A left-handed patient demonstrated bilateral agraphia and apraxia, but not aphasia, following a right parietal infarction. Preservation of the ability to type with the left hand demonstrated that the right hemisphere was not disconnected from language input. In addition, paragraphic errors while typing were shown to be secondary to left hemispatial neglect.

Thalamic neglect. Possible role of the medial thalamus and nucleus reticularis in behavior.

A patient had an ischemic infarction of the right medial thalamus, with a resultant contralateral neglect syndrome. We propose that the medial thalamic nuclei, particularly centromedian and parafascicularis (CMPF), are normally involved in the arousal-activation process by which an organism can be aroused by and respond to novel or important stimuli. Specifically, we propose that (1) the mesencephalic reticular formation subserves tonic arousal to novel or painful stimuli by inhibiting the nucleus reticularis thalami (NR) and (2) that selective attention is mediated by cortical input to NR. The CMPF is closely associated with motor systems (basal ganglia, ventrolateral nucleus of the thalamus [VL], and frontal lobes). A pathway involving CMPF, the frontal cortex, and the portion of NR associated with VL may be important in preparing the tonically aroused organism for action. Unilateral lesions of CMPF therefore induce an asymmetric hypokinesia, and bilateral lesions may induce akinetic mutism.

Contributions of the left intralaminar and medial thalamic nuclei to memory. Comparisons and report of a case.

A patient complained of memory disturbance after a small left thalamic infarction. Neuropsychological testing revealed her memory to be normal provided that she was allowed to rehearse or use semantic encoding strategies. When these strategies were prevented, her performance was impaired. Mapping of the lesion demonstrated involvement of the caudal intralaminar nuclei (centre médian and parafascicular nuclei), and portions of the medial nuclei (medioventral [reuniens], centromedial, and the most inferior aspect of the mediodorsal nucleus). The majority of mediodorsal nucleus, the mammillary bodies, the mammillothalamic tract, and the anterior thalamic nuclei, were spared. A comparison among our patient's performances and those of alcoholic Korsakoff patients, patient NA, and amnestic patients with circumscribed diencephalic lesions suggests that there are two distinct behavioral and anatomic types of memory impairment associated with diencephalic lesions. The severe amnesia associated with damage to the mammillary bodies, midline nuclei, mammillothalamic tract, and/or dorsomedial nucleus of the thalamus (eg, Korsakoff and NA) is characterized by encoding deficits that never approximate normal performance. The memory disturbance associated with damage to the intralaminar and medial nuclei of the thalamus is milder and is characterized by severe distractibility.

Posterior neocortical systems subserving awareness and neglect. Neglect associated with superior temporal sulcus but not area 7 lesions.

OBJECTIVE: In humans and monkeys, the intraparietal sulcus separates the superior parietal lobule from the inferior parietal lobule (IPL). Whereas in humans Brodmann's area 7 is above this sulcus, in monkeys it is below and therefore part of the IPL. In humans, the IPL consists of Brodmann's areas 39 and 40. Some investigators contend that the monkey homologue of the human IPL (areas 39 and 40) is the monkey's IPL (area 7). Others contend that it is, at least in part, in the monkey's superior temporal sulcus (STS). In humans, IPL lesions induce neglect. Although IPL lesions in monkeys also have been reported to induce neglect, the STS was involved in these lesions. We sought to learn which of these two areas, when ablated, produces neglect. DESIGN: Study of five adult stump-tailed macaque monkeys by making five isolated STS and six IPL lesions. RESULTS: Inferior parietal lobule lesions were associated with misreaching but not with unilateral neglect. Neglect was observed in association with five of the six STS lesions. CONCLUSIONS: With regard to neglect, STS may be the monkey homologue of the human IPL. Animals with STS lesions and humans with IPL lesions may manifest unilateral neglect because these areas are necessary for normal awareness of external stimuli. This awareness may result from the integration of the areas important in stimulus localization (the "where is it?" system) and stimulus identification (the "what is it?" system), as well as the areas important in defining the biologic importance of stimuli, such as the frontal lobes and limbic areas.

Response time in monkeys with unilateral neglect.

Four monkeys were trained to open a door with either the right or left hand in response to a tactile stimulus to either leg. After unilateral frontal arcuate ablation inducing unilateral neglect, the response time on this task increased most when the monkey responded with the hand contralateral to the lesion, but also increased when the monkey used the hand ipsilateral to the lesion. The side of stimulation had no effect on response time. Control (anterior superior temporal) lesions did not cause neglect and only affected response time slightly in one monkey (using the limb contralateral to the lesion). We conclude that response time is increased in animals with unilateral neglect and that the increase results from a defect in intention to act (motor neglect) rather than from sensory neglect.

Unilateral hypokinesia and motor extinction.

A patient with a right caudate hemorrhage demonstrated left limb hypokinesia but did not have sensory inattention or sensory extinction. The left-sided hypokinesia was increased by bilateral simultaneous movements (motor extinction).

Myokymia, muscle hypertrophy and percussion "myotonia" in chronic recurrent polyneuropathy.

Three unusual features were observed in a patient with chronic relapsing polyneuropathy: myokymia, muscle hypertrophy, and prolonged contraction in response to muscle percussion. Low nerve conduction velocity and conduction block were demonstrated in all motor nerves tested, indicating a demyelinating peripheral neuropathy. Myokymia was caused by spontaneous motor unit activity which was shown to originate in peripheral nerves, since it persisted after nerve block and was abolished by regional curarization. Muscle hypertrophy was attributed to increased peripheral nerve activity, and the prolonged contraction of muscle in response to direct percussion was attributed to irritability of intramuscular nerve terminals.

Two forms of ideomotor apraxia.

Destruction of parietal areas containing visuokinesthetic motor engrams, where motor acts may be programmed, should be distinguishable from apraxia induced by disconnection of these parietal areas from frontal motor areas. Destruction should result in inability to distinguish well-performed from poorly performed movements, whereas disconnection should not. We gave movement and act-discrimination tasks to apraxic and nonapraxic patients with anterior lesions or nonfluent aphasia, and to patients with posterior lesions or fluent aphasia. On both tasks, the performance of posterior/fluent patients was worse than that of all other patients. Our results suggest that there are two types of patients with ideomotor apraxia.

The effect of corpus callosum lesions on unilateral neglect in monkeys.

The cerebral hemispheres may be mutually inhibitory. An injured hemisphere may continue to be inhibited while the uninjured hemisphere is released from inhibition, inducing attentional bias. Patients with neglect might therefore benefit from transection of the corpus callosum. To test this hypothesis, we ablated the frontal arcuate gyrus alone or several months after corpus callosum transection in monkeys. Neglect was significantly worse in animals with a corpus callosum transection. Therefore, the hemispheres may be mutually excitatory or compensatory, and a callosal transection would not be therapeutic. Because the rate of recovery in the two groups was not different, recovery seemed to be an intrahemispheric phenomenon.

Dopamine agonist therapy for neglect in humans.

Lesions of ascending dopaminergic pathways induce neglect in animals. Apomorphine, a dopamine receptor agonist, decreases the magnitude of neglect in rats with cortical lesions. We treated two patients with 15 mg of bromocriptine daily for 3 to 4 weeks, one with chronic (longer than 6 months) and one with relatively more acute disabling neglect. Tests for neglect that significantly improved on therapy and worsened after its withdrawal included line, letter, and geometric figure cancellation tasks. Neither patient noted any untoward effects. Based on this open trial of dopamine agonist therapy in humans with neglect, larger controlled studies may be warranted.

Normal tactile threshold in monkeys with neglect.

To learn whether animals with parietotemporal lesions have sensory inattention or defective intention, we trained monkeys to respond with the contralateral limb to a threshold tactile stimulus. After parietotemporal lesions that induced neglect, the monkeys continued to respond normally to threshold stimuli on the side opposite the lesion (the neglected side), but made errors when stimulated on the normal side (ipsilateral to the lesion), often failing to use the contralateral extremity. On this learned task, there was no abnormality of sensory input or sensory attention. The problem was attributed to an impaired preparation to respond (intention).

Frontal lobe neglect in monkeys.

Using a crossed-response task, monkeys with neglect induced by frontal lesions appear to have motor rather than sensory neglect. However, the crossed-response task may not reveal sensory neglect (inattention) if no perceptual discrimination is required. We therefore trained two monkeys in a perceptually complex crossed-response task. Following unilateral frontal (arcuate gyrus) ablation, we found no contralateral perceptual disorders or sensory neglect in either monkey but did find a failure to respond with the contralateral arm (motor neglect) in both monkeys. We also found that the monkeys made more incorrect responses with the arm ipsilateral to the lesion than they did with the contralateral arm. The errors made by the ipsilateral arm could be a compensatory strategy or a disinhibition phenomenon. Because these incorrect responses were not rewarded and became more frequent as motor neglect improved, the incorrect responses of the ipsilateral arm are not a compensatory strategy, but rather a defect we term "disinhibition hyperkinesia" or "allokinesia."

Botulinum toxin-induced paralysis of frontotemporal muscles improves seizure focus localization.

BACKGROUND: Scalp EEG localization of epileptic foci may be obscured by electromyographic (EMG) artifact produced by ictal contraction of cranial muscles. Injection of botulinum toxin type A (BTX-A) into frontotemporal scalp muscles reduces EMG activity. Initial scalp video-EEG monitoring in three patients suggested partial seizures, but definitive lateralization or localization was precluded by EMG artifact. METHODS: EMG-guided BTX-A injection to bilateral frontotemporal muscles was performed. When artifact persisted, BTX-A administration was selectively repeated. Patients subsequently underwent scalp video-EEG monitoring 1 week later. RESULTS: All patients had reduction of EMG artifact during subsequent scalp video-EEG monitoring. No patient had adverse effects after BTX-A administration. All three patients had localization to either frontal or temporal lobes and definitive lateralization. Two of the three patients were able to proceed to invasive placement of frontotemporal subdural grid electrodes based on the BTX-A scalp video-EEG localization, and the third patient was determined to have a multifocal seizure disorder. CONCLUSIONS: Paralysis of frontotemporal scalp muscle after BTX-A administration reduces EMG artifact and may improve localization and lateralization of a seizure focus, providing a noninvasive technique for advancement toward epilepsy surgery.