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Biomedical subjects

O J Andy

Publications and source records attributed to O J Andy.

87 records · Page 5Linked to original sources
PubMedDate not supplied

Mesothalamic discharge in a chronic pain, allergy and fluid retention syndrome (case report).

A 32-year-old woman was bedridden for a year because of chronic pain and headaches. She had insomnia, depression, suicidal thoughts and a severe chemical allergy. She had been on steroid therapy for two years and became Cushingoid with striae in the arm pits, groins and abdomen. However, she had no hypertension, nor the buffalo fat and hirsutism. She was very edematous, with a weight gain from 112 to 180 lbs. The fluid retention did not conform to the syndrome of inappropriate antidiuretic hormone. Studies revealed abnormal scalp EEG discharges and high-voltage seizure discharges in the posterior thalamus. Electrothalamic stimulation suppressed the thalamic discharges and relieved the patient's pelvic pain and headaches. After one month of several thalamic stimulations per day, she was able to get out of bed and ambulate. In addition, the patient no longer was edematous and was tolerating perfumes and floor detergents. Steroids were progressively reduced without complications of withdrawal. She went from a completely steroid dependent state to independent during the first 1-1/2 yrs of thalamic stimulation. With continued thalamic stimulation she has done well for 8-1/2 yrs, weighs 112 lbs, keeps house and drives a car. It's speculated the illness is a chronic pain multiple syndrome predominantly due to mesothalamic discharges and body infirmities. The mesothalamic discharge implicated neural networks, which represent biologic systems, i.e. pain, sleep, fluid retention, etc. Therapeutic stimulation attenuates the discharges and the neural networks return to their normal set points of homeostasis.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

Cocaine-induced brainstem seizures and behavior.

A variety of abnormal sensory/motor behaviors associated with electrical discharges recorded from the bilateral brainstem were induced in adult WKY rats by mechanical (electrode implants) and DC electrical current stimulations and by acute and chronic administration of cocaine. The electrode implant implicated one side or the other of the reticular system of the brainstem but subjects were not incapacitated by the stimulations. Cocaine (40 mg/kg) was injected subcutaneously for an acute experiment and subsequent 20 mg/kg doses twice daily for 3 days in a chronic study. Cocaine generated more abnormal behaviors in the brainstem perturbation group, especially the electrically perturbated subjects. The abnormal behaviors were yawning, retrocollis, hyperactivity, hypersensitivity, "beating drum" behavior, squealing, head bobbing, circling, sniffing, abnormal posturing, and facial twitching. Shifts in the power frequency spectra of the discharge patterns were noted between quiet and pacing behavioral states. Hypersensitivity to various auditory, tactile, and visual stimulation was present and shifts in the brainstem ambient power spectral frequency occurred in response to tactile stimulation. These findings suggest that the brainstem generates and propagates pathological discharges that can be elicited by mechanical and DC electrical perturbation. Cocaine was found to activate the discharge system and thus induce abnormal behaviors that are generated at the discharge site and at distant sites to which the discharge propagates. Cognitive functions may also be involved since dopaminergic and serotonergic cellular elements at the brainstem level are also implicated.

Animals↗
PubMedDate not supplied

Chronic pain as a reticular formation syndrome.

Evidence was previously presented to support the thesis that chronic pain is activated by neuronal elements that make up the multisynaptic short axon core of the reticular system (Andy and Peeler 1985). The present thesis, that chronic pain is a reticular formation syndrome, is based on a retrospective analysis of four patients with chronic pain who were successfully treated with a lesion in the anterior thalamus and stimulation electrode implants in the posterior thalamus and pontomesencephalic brain stem. The reticular formation was the common underlying anatomic substrate at those three sites. In addition to chronic pain, all the patients had other symptoms attributable to other body organs and systems. The number and type of symptoms that made up the syndrome differed between patients. Symptoms making up the core of the syndrome were pain, anxiety, nervousness, insomnia, and depression. Experimental and clinical findings are briefly presented to demonstrate the various reticular formation sites, pragmatically considered "reticular functional systems," from which symptoms may arise. It is hypothesized that the symptoms are recruited by a low threshold "pain oscillator" that is generated at one reticular site and subsequently permeates the rest of the reticular system. Therapeutic stimulation inactivates the low threshold system by "jamming" it.

Adult↗
PubMedDate not supplied

Tonotypic cortical representation in man (case report).

Cortical stimulation--evoked perception of tones differing in pitch suggests that the perception of pitch may be discretely organized in the human auditory parakoniocortex. Findings, obtained from a neurosurgical patient undergoing temporal lobectomy, are discussed with reference to anatomical and functional considerations of the auditory parakoniocortex in humans. These tonotypic findings are potentially significant since, as previously reported, auditory sensations have not been analyzed in relation to perceptual categories of pitch.

Acoustic Stimulation↗
PubMedDate not supplied

Thalamic modulation of aggression.

This experiment extends Pavlov's method of contrasts for 8 components of aggression were quantitatively evaluated in 11 freely moving adult cats. Aggression was elicited from the perifornix septohypothalamic areas by a series of progressively increasing and decreasing stimulation parameters. Three levels of thalamic stimulation (low, medium, and high) were combined with the perifornix stimulations. High level thalamic stimulation tended to facilitate the aggressive response elicited by low level perifornix stimulation. Thalamic lesions attenuated the aggression response, especially those elicited during high level perifornix stimulation. It was suggested that within the hypothalamic induced aggression circuitry the center median nucleus modulates the excitatory state of the system. The discussion concerns anatomic and physiologic pathways through which the center median nucleus may modulate the sensory, motor, and affective-autonomic subsystems into a well integrated aggressive state. These experimental findings are supported by the clinically established treatment of aggression by stereotaxic lesions placed in the center median nucleus.

Aggression↗
PubMedDate not supplied

The hippocampus and stress induced 17-OHCS elevations.

The physiologic contribution of the limbic brain to emotionally induced stress is still poorly understood. The present study is designed to more specifically evaluate the role of the hippocampus in stress induced plasma 17-OHCS elevations. The conditional reflex to a sequential presentation of tone and shock was used as the stress agent in adult mongrel dogs. Plasma 17-OHCS levels were determined by the Porter-Silber method. Control and stress levels of 17-OHCS were determined before and after unilateral (left) hippocampectomy, and subsequent contralateral (right) hippocampectomy. A unilateral posterior hippocampal lesion partially attenuated (20%) the normal 17-OHCS stress response. In contrast to unilateral lesions, equivalent bilateral posterior hippocampal lesions abolished the normal 17-OHCS stress response. These observations support the thesis that the elevated 17-OHCS levels in response to the conditioning paradigm is dependent on the hippocampus. Furthermore, it is dependent upon the continuity of the hippocampal circuit and not upon the volumetric steroid binding capacity of the hippocampus. These studies also suggest that a unilaterally functioning hippocampus may be adequate to meet the physiologic needs of stress, as reflected by the 17-OHCS response.

11-Hydroxycorticosteroids↗
PubMedDate not supplied

Limbic hypertension induced by stress and septal stimulation. Stress-locked-in hypertension.

For this study, it was postulated that hypertension of emotional origin is generated within the limbic system. To validate this thesis, septal induced blood pressure elevations were combined with a stressful experience in adult rats (spontaneously hypertensive and Wistar Kyoto rats). Stress consisted of intermittent confinement in a plexiglass tube. The results revealed that hypertension induced by electric stimulation of the septum during the stressful state could subsequently be elicited by the stressful state alone, without electric stimulation of the septum. It was postulated that the cortically modulated stress circuit converged with the electrically activated limbic pressor circuit at the level of the septum. This convergence resulted in the formation of one cortico-limbic circuitry which could be activated by stress alone. This underlying mechanism may be considered as a model of neural sensitization in the production of stress-induced limbic hypertension.

Animals↗
PubMedDate not supplied

Limbic system seizures and aggressive behavior (superkindling effects).

This study was done to further analyze the neural mechanisms underlying aggressive behavior associated with psychomotor or temporal lobe seizures. The studies revealed that superkindling the aggressive system by sequential stimulations at seizure-inducing thresholds, of two or more sites in the limbic, hypothalamic, and basal ganglia structures facilitated the production of aggressive seizures. Aggressive behavior in the freely moving cat was evaluated in relation to the occurrence of hissing and growling during stimulation, after-discharge and postictal period. The behavior was correlated with the frequency of the elicited seizures and the seizure durations. Aggression did develop as a component behavioral manifestation of the limbic (psychomotor) seizure. Development of aggressive seizures was facilitated by "priming" the aggressive system. Optimum levels of aggressive behavior occurred with seizures of medium duration. Catecholamine blockers tended to attentuate the occurrence of aggression, whereas the agonist tended to facilitate it. Once the aggressive system was rendered hyperexcitable, exteroceptive stimuli also evoked aggressive attack behavior. It was concluded that repeatedly recurring limbic system seizures through superkindling mechanisms can eventually render the limbic-basal ganglia-preoptico-hypothalamic aggressive system hyper-responsive to both recurring seizures and to exteroceptive stimuli with resulting aggressive behavior with or without an accompanying seizure.

Aggression↗
PubMedDate not supplied

A neurophysiologic model for aggressive behavior in the cat.

A neurophysiologic model for aggressive behavior in the cat is proposed. Stimulus-bound and seizure-bound aggression was evaluated in relation to limbic and basal ganglia induced seizures (after-discharges). Electrically induced limbic and basal ganglia after-discharges were used because they are known to implicate septohypothalamic sites from which aggression can be elicited by direct stimulation. The occurrence of behavioral aggression is correlated with the discharge characteristics of a single discharging system and with two interacting discharging systems. Aggression is composed of autonomic and somato-motor components which poses relatively low and high thresholds, respectively, for their activation. Aggression occurring during a combined septum and amygdala discharge was more intense and prolonged than with a septum discharge alone. Participation of a slow frequency discharging basal ganglia system activated seizure-bound aggression in an otherwise nonaggressive limbic seizure. The limbic and basal ganglia stimulations and after-discharges lowered the excitability threshold of the aggression system and made it more vulnerable to being activated by external stimuli, such as visual and auditory stimuli. These observations are reminiscent of patients with aggressive behavior associated with psychomotor seizures.

Aggression↗
PubMedDate not supplied

Regulation of aldosterone biosynthesis during sodium deficiency. Evidence for an essential role of the pituitary gland.

The aldosterone response to adrenocorticotropic hormone (ACTH) and angiotensin II (AII) was evaluated in patients with pituitary insufficiency before and after dietary sodium restriction (10 mEq Na+/day for 12 days). On normal sodium intake, plasma aldosterone concentration and plasma cortisol concentration failed to change from control levels in response to a single injection of ACTH or to a continuous 1-hour infusion of AII in patients with pituitary insufficiency. In response to dietary sodium restriction for 12 days, plasma renin activity (PRA) increased fivefold in patients with pituitary insufficiency, while plasma aldosterone concentration failed to increase significantly, averaging 11.0 +/- 3.1 before and 12.3 +/- 3.7 ng/dl (ns, p greater than 0.05) after sodium deficiency. Although aldosterone secretion failed to increase during sodium deficiency, the patients came into balance at 10 mEq without a significant change in arterial blood pressure (BP). In sharp contrast to the lack of aldosterone response to ACTH before sodium deficiency, plasma aldosterone concentration increased markedly from 12.9 +/- 3.3 to 156 +/- 17.3 ng/dl (p less than 0.001) in response to ACTH after sodium deficiency. Although the adrenal glomerulosa cells were markedly sensitive to ACTH during sodium deficiency, they remained almost totally refractory to AII since aldosterone secretion failed to increase significantly in response to continuous infusion of a pressor dose of AII for 1 hour. Replacement therapy with ACTH gel for 3 months in patients with pituitary insufficiency failed to restore a normal aldosterone response to either ACTH or AII. These data demonstrate that some non-ACTH pituitary factor(s) is essential for a normal aldosterone response to ACTH, AII, and sodium deficiency.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

A brainstem "mini-discharge" syndrome (anesthesia dolorosa).

Chronic pain consisting of anesthesia dolorosa secondary to bilateral interruption of the trigeminal nerves is presented as a brain stem reticular denervation syndrome. Electrothalamograms revealed fast frequency discharges in the mesothalamic prerubral and centermedian reticular formation. Mesothalamic electrical stimulation attenuated the discharges. Pain and other symptoms presumably of brainstem origin also were attenuated or abolished by therapeutic electrical stimulation twice daily. It is postulated that brain stem-represented behavioral generators are implicated by the reticular discharges in order to produce the complex symptomatology. Consequently the symptom complex is collectively identified as a brainstem "mini-discharge" syndrome. A theoretical discussion is presented to defend the thesis that reticular denervation-induced low threshold discharge system accounts for the episodic states of pain, dyskinesia, mood, and memory disturbances.

Brain Stem↗
PubMedDate not supplied

Limbic stimulation-induced hypersexuality. Levels of sexual drive.

Postictal sexual drive levels induced by limbic discharges were studied in eight adult male cats. Although sexual drive was exclusively dependent upon the presence or absence of testosterone, the level or degree of drive was dependent on the relative amounts of circulating testosterone and catecholamines in addition to the bioelectric state of the testosterone-binding cells. The limbic discharge was thought to induce postictal hypersexuality by its propagated discharge, suppressing the association neocortex and simultaneously activating the sexual hormone-binding cells of the diencephalon. The dissociation of the neocortex from the diencephalon was considered as a functional postictal diaschisis. These postictal physiologic changes were thought to account for the irrational automatic behavior and memory loss characteristic of patients with psychomotor seizures.

Aggression↗