1f:T426,SINCE Osler first described focal neurological abnormalities associated with systemic lupus erythematosus (SLE) in 1903,¹there have been many similar reports. Most commonly described have been acute organic mental syndromes,²cerebrovascular disorders,³and seizures.⁴Chorea,⁵Guillain-Barré Syndrome,^6,7subarachnoid hemorrhage,⁸peripheral neuropathy,^9,10and cranial nerve palsies¹¹are not infrequent. Since the advent of the LE cell preparation in 1948, the diagnosis of SLE has been made with increasing frequency and the presenting picture has indeed proved to be varied. Neurological abnormality may be the initial or only manifestation of the disease.^7,12Myelopathy, however, has rarely been reported as a complication of SLE; there are thus far only seven definite cases. It is the purpose of this paper to report four additional cases of myelopathy including two in which it was the initial and major manifestation of SLE.

Report of Cases

20:T53e,The administration of 1.5 mg of progesterone to ovariectomized estrogen-primed rats induced a surge in plasma norepinephrine (NE) preceding the pituitary LH release. The injection of reserpine (2 mg/kg) 2 h prior to progesterone completely blocked the progesterone effects on both NE and LH plasma surges. On the other hand, the adminitration of phenoxybenzamine prior to progesterone, blocked the steroid effect on LH without inhibiting the plasma NE rise. Contrarily, the alpha-blocker was able to induce a rapid increase in the amine levels 2 h after its injection. The determination of NE in the anterior hypothalamus of these rats revealed that simultaneously with the plasma NE rise induced by progesterone there was a fall in the hypothalamic amine levels. Both reserpine and phenoxybenzamine caused a depletion in the amine content of the anterior hypothalamus. In experiments measuring the arteriovenous difference in the concentration of NE across the brain following progesterone-induced LH release, it was found that most NE comes from the brain. The amine rise was evident in the jugular vein while the arterial NE concentration showed a slight increase. These findings raise the possibility that the changes in circulating NE may reflect an enhanced noradrenergic activity occurring in the brain from which the LH surge results.

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