Both hyperammonemia and blood-brain barrier (BBB) breakdown have been implicated in the evolution of hepatic encephalopathy. To define a possible relationship, Swiss Albino mice were subjected to sublethal encephalopathic doses of ammonium acetate; the integrity of the BBB was determined grossly with Evans blue and quantitatively with [14C]-alpha-aminoisobutyrate (AIB). Some animals were injected with a dose of ammonium acetate sufficient to maintain coma for 1 hr (AC group). One group, termed stuporous (AS), received only enough ammonium acetate to interfere with grooming and exploratory activity; this dosage was insufficient to completely block the righting response, which was absent in the AC group. When compared to that of controls (CON) receiving normal saline instead of ammonium acetate, cerebral tissue from the AC group was stained blue and contained nearly double the amount of AIB; AS group brain tissue was unstained and the AIB content did not differ significantly from normal. Some of the AC group were pretreated with drugs known to retard BBB breakdown; one set received dexamethasone (AC-DXMN), another the ornithine decarboxylase inhibitor difluoromethyl ornithine (AC-DFMO), and a third L-ornithine (AC-ORN). Brain tissue from the AC-ORN group stained blue and AIB content did not differ significantly from that of the untreated AC group. Cerebral tissue of the AC-DXMN pretreatment group stained light blue; AIB content was significantly lower than in the AC group and greater than the CON group. The AC-DFMO brains were unstained and AIB content was significantly lower than in the AC group but did not differ significantly from CON. These results indicate that hyperammonemia may induce BBB breakdown but that the disruption of barrier integrity is not antecedent to the development of coma, although it seems to coincide with coma in time.(ABSTRACT TRUNCATED AT 250 WORDS)

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Paradoxical cerebral air embolism is an unusual complication following insertion of a subclavian intravenous catheter. We report an ultimately fatal case in a 75-year-old man in whom the diagnosis was confirmed by computerized tomographic (CT) scanning. W e postulate that air passed through a physiologically closed but anatomically patent foramen ovale.A 75-year-old black man with an ileocutaneous fistula had an alimentation catheter inserted into the right subclavian vein while in the Trendelenburg position. After completion of the maneuver and assumption of a sitting position, the patient became unresponsive in midsentence. Neurological evaluation revealed right conjugate gaze preference with full conjugate excursion to the left upon left caloric stimulation with cold water. The patient was not responsive to verbal stimulation; noxious stimulation caused decerebrate posturing on the right. All extremities were rigid. Deep tendon reflexes were symmetrically hyperactive and plantar responses were bilaterally extensor.A chest radiograph showed neither pneumothorax nor hemothorax, and the tip of the central venous catheter lay in the region of the superior vena cava. An unenhanced brain CT scan performed o n a GE 8800 unit, employing a 1 cm collimator, reveaied multiple small, well-defined collections of markedly decreased attenuation within both cerebral hemispheres. Attenuation coefficients of the lesions were equivalent to that of air in the left frontal sinus. Presumably, the abnormalities represented intrahemispheric collections of air, probably within and around small-caliber arteries (Figure).Three hours later the patient was placed on 10056 oxygen and transferred to a monoplace hyperbaric recompression (HBR) chamber. One hundred percent oxygen given at 3 atm absolute pressure for 45 minutes elicited no improvement. H e was then transferred to a multiplace H B R chamber where the treatment protocol of the US Navy Diving Manual, Table GA, was followed [ 5 ] . N o improvement occurred, and the patient remained in a vegetative state until his death eight weeks later. CT scans performed four and six weeks postictus revealed poorly defined areas of infarction density scattered throughout both cerebral hemispheres. Investigation for the mechanism of paradoxical embolization by the indocyanine green test and the technetium 99m-labeled macroaggregated albumin test failed to show major right-to-left shunts in either the heart or lungs.Systemic air embolism is almost invariably iatrogenic ex-

Transient contrast enhancing lesions can be seen with CT in patients with MS, particularly during acute exacerbations. Conventional 40 gm iodine enhancement technique followed by immediate postinfusion scanning was compared with high dose (80 gm iodine) enhancement technique followed by a 1-hour delayed CT scan; delayed high dose technique (DHD) in nine exacerbations. New lesions, totaling 36 in all, were observed in each case with the DHD technique. With time, the borders expanded in 98% of lesions, thus confirming in vivo that a defective blood-brain barrier (BBB) underlies this phenomenon.

Glycerol, an effective cerebral dehydrating agent, also has gluconeogenic properties, and can thereby elevate serum glucose to dangerously high levels in predisposed patients treated for cerebral edema. The nonketotic hyperosmolar hyperglycemic state usually occurs in cases of maturity onset diabetes or prediabetes, as in the two elderly patients discussed in this paper. The pathogenesis usually evolves through a constant diabetogenic stress that causes persistent hyperglycemia resulting in the exhaustion of ordinarily adequate insulin stores, ultimately allowing hyperglycemia to progress unchecked to metabolic coma. Precautions to recognize this development should be taken in appropriate patients.