G Sangiovanni — Page 2

PubMedDate not supplied

Alteration of complex IV and acetylcholine-related enzymes in experimental spinal cord injury.

Acute, severe injury of the rabbit spinal cord, induced by the weight-drop method, causes alterations of the enzyme activities related to cholinergic and energy metabolism. Morphological examinations at the trauma site show degenerative processes in neurons 0.5 hr posttrauma and a marked decrease in the number of living cells 24 hrs later. Both biochemical and cytochemical findings show that the tissue metabolic and morphologic derangement, caused by severe spinal cord injury, is mostly confined to the gray matter at an early stage (0.5 hr), whereas 24 hrs later the white matter is also involved. The decrease in choline acetyl-transferase and acetylcholinesterase activities in the gray matter parallels the impairment of complex IV (cytochrome c oxidase) of the respiratory chain and the presence of morphological alteration in neurons. The dramatic drop in the enzyme activities, observed 24 hrs after the induction of the severe trauma is clearly associated with the loss of cells.

Acetylcholinesterase↗

PubMedDate not supplied

[Benign intracranial hypertension and thrombosis of the venous sinuses during contraceptive treatment: anatomo-clinical and neuroradiological observations (author's transl)].

The side-effects of oral contraceptives on the nervous system have been studied in 2 patients. The first case, a young woman who, after several years, of cyclic consumption of 4 mg of norethylsterone acetate and 0.05 mg of ethynilestradiol, died from a transtentorial temporal hernia due to severe intracranial hypertension. Angiography, and later autopsy, showed thrombosis of the dural venous sinuses and also of the majority of the emissary veins with C.S.F. blockage. The second case, a patient who took 1 mg of norethyndrone and 0.05 mg of mestranol for 20 months, developed a focal symptomatology (Grand Mal, global aphasia without lowering of the level of conscionsness) which cleared up rapidly. The CAT performed during the clinical illness showed mild signs of intracranial hypertension while cerebral angiography normal. It seems possible that the hormonal treatment may disturb the mechanisms of C.S.F. production-reabsorbtion and the filtration dynamics of the blood-brain barrier and perhaps, cause alteration of hypothalamic-hypophysial function. This would explain a transitory symptomatology, such as benign intracranial hypertension. However, the thrombosis of the venous sinuses (sometimes, as in our first case, massive) may be due to the venous stasis, that accompanies intracranial hypertension and to the altered blood coagulation.

Adult↗