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Biomedical subjects

C Dearman

Publications and source records attributed to C Dearman.

7 recordsLinked to original sources

Competencies of novice nurse educators.

Appropriate preparation for the nurse faculty role has been debated for many years. Currently, the master of science in nursing (MSN) is considered to be the minimal acceptable preparation. The focus of most MSN programs, however, is advanced knowledge and skill in clinical nursing. The purpose of this study is to identify the perceptions of novice nurse faculty concerning nurse faculty competencies, to ascertain the extent to which novice nurse faculty demonstrate the competencies, and to determine mechanisms through which competencies are obtained. The findings indicate that many novice nurse faculty are not educationally prepared for the faculty role.

Attitude↗

Adjunctive brainstem behaviors in the rat.

UNLABELLED: Adjunctive behaviors refers to behaviors that are "out of context" and/or excessive in amount. The terminology was first used for unexplained behaviors associated with food pellet ratio contingencies in food deprived rats (Falk, 1971). Clinically, unrelated and complex excessive behaviors were also noted with brainstem and diencephalic discharges (Andy, 1986, 1989 and 1995; Andy and Jurko, 1986). The objective of this study was to develop a model of brainstem generated adjunctive behaviors in the rat. METHOD: Sixty-one adult rats were used. Kindling was induced by mechanical and DC electrical perturbations in the midbrain. Nine different treatment groups were established in which lesions and drugs were used separately and in different combinations. Cocaine was used to accentuate, and dextrorphan to attenuate the kindling process. Behaviors were visually analyzed and recorded by video camera; they were not quantified. DC stimulation and EEGs were doen with Grass instruments. Recording and stimulation sights were verified histologically. RESULTS: A total of 45 different behaviors were elicited. DC stimulation kindled subjects had significantly more behaviors than did electrode insertion alone and cocaine alone. However, cocaine combined with DC stimulation increased the number and intensity of the kindled behaviors. Dextrorphan tended to facilitate catatonic and sleep states. Behaviors occurred randomly and were unrelated, even when they occurred in clusters. The behaviors were associated with four abnormal EEG discharge patterns. CONCLUSION: We speculate that brainstem behaviors are innate adjunctive drives that are generated in the brainstem reticular formation. They are monitored by the cortex and partially modified by environmental and cortical inputs.

Animals↗

Dextrorphan effects on cocaine and brainstem perturbation.

UNLABELLED: Dextrorphan is a noncompetitive blocker of N-methyl-D-aspartate (NMDA) receptors. Since NMDA blockers are known to reduce the locomotor stimulatory and toxic effects of cocaine, it was speculated that dextrorphan would attenuate cocaine-induced behavioral excitatory motor activity associated with and without mechanical perturbation of the brainstem. TECHNIQUE: Motor activity was recorded following dextrorphan and/or cocaine challenge in 25 SHR rats. Ten were naive subjects. Mini-osmotic pumps delivering cocaine (2.5 mg/0.49 ul/hr) were placed in 15 subjects, and infusion was halted after the third infusion day. On the fifth day either a dextrorphan (25 mg/kg, subcutaneous) or a dextrorphan and cocaine (40 mg/kg, intraperitoneal) challenge was done. Ten rats had bipolar electrode implants in the bilateral brainstem. Five were treated with DC current lesions in each of 12 days over a 3-week period. The effects of brainstem lesions on escape behavior were also evaluated in those five subjects. RESULTS: In the naive subjects, dextrorphan reduced motor activity (P = .0001), whereas combined cocaine and dextrorphan increased motor activity (P = 0.04). In lesioned subjects, dextrorphan decreased motor activity (P = 0.0001). In electrode implant subjects, combined dextrorphan and cocaine challenge decreased the motor activity (P = 0.04). Hyperactivity in the electrode implant group was greater than in the lesioned subjects. Midbrain electrolytic lesions attenuated escape behavior. A variety of behaviors were produced by brainstem lesions. CONCLUSIONS: Dextrorphan and brainstem lesions reduced motor hyperactivity and escape behavior. In electrode implant subjects dextrorphan counteracted the expected cocaine excitatory motor effects. Dextrorphan did not activate nor facilitate seizures.

Animals↗

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↗

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↗