Richard S. Kramer

Traumatic Anterior Atlanto-occipital Dislocation

The five cases of atlanto-occipital dislocation reported in the world literature are reviewed, and four additional cases are presented, including two survivors. The pathological anatomy of this potentially catastrophic injury and its management are briefly discussed. Because immediate recognition of the atlanto-occipital dislocation is critical to proper treatment and because the neurological findings are extremely varied, a new radiographic criterion for its identification has been developed.

Brain Adenosine Triphosphate: Decreased Concentration Precedes Convulsions

The concentration of adenosine triphosphate in the brain decreased before the onset of generalized convulsions in unanesthetized rats subjected to acute hypoxia or treated with hydroxylamine or pentylenetetrazole (Metrazol). As the convulsive episode continued, adenosine triphosphate decreased further. Stimulation of adenosine triphosphate production forestalled its disappearance from the brain and delayed the development of seizure activity.

Spontaneous regression of prolactin-producing pituitary adenomas

Two women evaluated for amenorrhea, galactorrhea, and hyperprolactinemia had radiographic changes of the sella turcica (localized erosion on trispiral tomography) suggestive of a pituitary tumor. Both patients experienced spontaneous regression of apparent prolactin-secreting adenomas with a marked decrease in the quantity of galactorrhea and a reduction of serum prolactin concentrations to the normal range. One patient noted a marked improvement of headaches and spontaneous menses resumed in the other patient.

Effects of Hyperbaric Oxygenation on Metabolism VII. Succinate Protection Against Oxygen Toxicity in Large Animals

Significant protection was demonstrated against the development of convulsive activity in small animals using 0.4 M sodium succinate (1-4) injected intraperitoneally in a dosage of 12 mM/kg of body weight, Succinate protection against hyperbaric oxygen (HPO) at 5, 7, 9, and 11 ATA of 100% oxygen (5) was shown not to be due to the hyperosmolarity of the solution infused and led to our proposal that maintenance of normal ATP concentrations in brain and other tissues is of prime importance in protecting animals subjected to HPO. No significant delay of onset of convulsive activity was observed with hyperosmolar solutions of NaCl, sodium malate, an NAD-linked TCA cycle intermediate, or glucose. These results are consonant with the observation of Chance et al. (6) that HPO adversely affects NAD-linked substrates of oxidative phosphorylation, and have stimulated further studies using the FAD-linked substrates, succinate and alpha-glycerophosphate. We report here the results of experiments using sodium succinate as a protective agent against the toxic effects of HPO in large animals. These studies were carried out to determine the feasibility of using succinate in humans as a protective agent when HPO is used in the treatment of certain clinical conditions such as gas gangrene. Dogs (12-18 kg) were infused intravenously with 0.4 M sodium succinate, pH 6.4, in a dosage of 8 mM/kg of body weight/hr, for 50 min prior to and during exposure to 100% oxygen at a pressure of 40 psig. Control experiments were conducted by subjecting the same animals, either untreated or infused with equivalent doses of saline or sodium malate, to identical conditions of HPO 48-72 hr prior to the succinate experiments. Thus, each dog served as its own control, and time to convulsions could be compared directly (Table I).