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UNLABELLED: Traumatic brain injury (TBI) is a leading cause of disability in young people in the United States. Disorders of arousal and attention are common in closed head injury (CHI). Daytime drowsiness impairs participation in rehabilitation, whereas nighttime wakefulness leads to falls and behavioral disturbances. Sleep disturbances in TBI reported in the literature have included excessive daytime somnolence, sleep phase cycle disturbance, narcolepsy, and sleep apnea. Although well known to the clinician treating these patients, the extent and prevalence of disrupted sleep in patients in an acute inpatient rehabilitation unit has not been described. OBJECTIVE: To determine the prevalence of sleep wake cycle disturbance (SWCD) in patients with CHI in a TBI rehabilitation unit. DESIGN: Prospective observational. SETTING: Inpatient specialized brain injury rehabilitation unit. Patients. Thirty-one consecutive admissions to a brain injury rehabilitation unit with the diagnosis of CHI. RESULTS: Twenty-one patients (68%) had aberrations of nighttime sleep. There was no significant difference in Glasgow Coma Score on admission to trauma nor was there any significant difference in age between the affected and unaffected groups. Patients with SWCD had longer stays in both the trauma center (P < .003) and the rehabilitation center (P < .03). CONCLUSIONS: There is a high prevalence of SWCD in CHI patients admitted to a brain injury rehabilitation unit. Patients with SWCD have longer stays in both acute and rehabilitation settings and may be a marker for more severe injury.

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The inhibitory role of the medial amygdala (MA) in maternal behavior control was explored. Injections of N-methyl-D,L-aspartic acid (NMA), an excitotoxic amino acid, into the MA resulted in a dramatic facilitation of maternal behavior in virgin female rats when pups were presented to them 12 days following the injections. This effect was specific to MA in that NMA injections into the basolateral amygdala were ineffective. The facilitatory effect of NMA injections into MA was found to be hormone dependent in that ovariectomies abolished the effect. Subsequent experiments provided evidence that NMA injections into MA induced a pseudopregnant state lasting about 13 days, and that maternal behavior was greatly facilitated only when pups were presented to such females coincident with pseudopregnancy termination. When pups were presented 24 days following injections of NMA into MA, rather than 12 days, only a modest facilitation of maternal behavior was observed. It was concluded that NMA injections into MA influence maternal behavior in two ways: By inducing an hormonal state stimulatory for maternal behavior and by removing neural inhibition over maternal behavior.

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Cardiovascular responses to increasing (20, 40, and 60%) concentrations of nitrous oxide or nitrogen in oxygen for 15 minutes as well as responses to 2 hours of exposure to 60% nitrous oxide or nitrogen in oxygen were determined and compared in 30 healthy, supine, untrained volunteers who received no other drugs or medications. No concentration of nitrogen produced a significant change in any cardiovascular variable measured, nor did 20 and 40% N2O. Sixty percent nitrous oxide for 15 minutes significantly increased PaCO2, heart rate, stroke volume, cardiac output, mean arterial blood pressure, and central venous pressure. Inhalation of 60% nitrogen also produced no significant change in any cardiovascular variable. In contrast, inhalation of nitrous oxide for 2 hours transiently increased arterial blood pressure (at 15 minutes), heart rate (at 15 and 30 minutes), stroke volume (at 15, 30, and 45 minutes) and decreased systemic vascular resistance (at 15 minutes). Cardiac output significantly increased for the 1st hour of exposure to 60% nitrous oxide but returned to values similar to control (room air) during the 2nd hour. Prolonged inhalation of nitrous oxide resulted in a constant increase in PaCO2 and progressive but mild decreases in arterial pH and calculated base deficit but no change in dead space/tidal volume ratios. These findings demonstrate that nitrous oxide stimulates the cardiovascular system in supine, healthy, untrained volunteers but that the stimulation is transient. The data suggest that early stimulation of the cardiovascular system during nitrous oxide breathing may be related to central nervous system excitation secondary to incomplete anesthesia and/or an increase in PaCO2.

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Inhalation of 60% nitrous oxide in oxygen by seven adult male volunteers for 60 min was found to increase significantly polymorphonuclear leuocyte (PMN) chemotaxis, but not to influence total white or PMN blood cell counts. Also, the addition or morphine 0.2 mg kg-1 i.v. during the breathing of nitrous oxide did not alter any variable. These results indicate that nitrous oxide and nitrous oxide incombination with morphine do not depress PMN chemotaxis.

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Peripheral vascular and myocardial effects of increasing concentrations of nitrous oxide (0 to 70 per cent) in oxygen were determined in 15 unanaesthetized calves before and after replacement in their natural heart (NH) with a pneumatically driven artificial heart (AH). Nitrous oxide produced concentration-related decreases in arterial and mixed venous pH and increases in minute ventilation and arterial and mixed venous carbon dioxide tensions in both NH and AH calves. Nitrous oxide resulted in significant increases in cardiac output, stroke volume and mean aortic, pulmonary artery and right atrial pressures in NH and AH calves, but did not significantly change systemic vascular resistance in either group of animals. Heart rate was increased in NH calves but was fixed in AH calves. Elevations in heart rate and cardiac output at nitrous oxide concentrations greater than 30 per cent and aortic pressure at 70 per cent nitrous oxide were significantly greater in NH than AH animals (P less than 0.05). These data demonstrate that nitrous oxide stimulates the cardiovascular system in spontaneously breathing mammals and that the changes result from improved venous return and an increase in myocardial chronotropy. Our findings also suggest that cardiovascular stimulation during nitrous oxide breathing may be related to increased concentrations of arterial and/or venous carbon dioxide.

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