CHAPTER I PAIN (Part 2)

and the surrounding tissues may appear almost or quite normal postmortem. It is natural, therefore, to assume some functional change, such as spasm, to account for the pain, paralysis, and other functional changes recognized at the bedside. In favor of the hypothe- sis of vascular spasm, or Gefasskrise, are two considerations: (@ A rise of blood-pressure has many times been demonstrated by Pal before, as well as during, the crisis. This hypertension cannot be accounted for as a result of pain, since in many of Pal’s cases it pre- ceded the pain. He has found it in the gastric crises of tabes, as well as in the uremic, saturnine, and arteriosclerotic cases. (0) During an attack of transient blindness occurring in a patient who had been subject to various other “crises,” ophthalmoscopic ex- aminations showed a high-grade spasm or contraction of the retinal arteries. So much for the theory and the evidence on which it is based. It seems to me a good working hypothesis as an explanation of many of the transient amauroses, aphasias, monoplegias, hemiplegias, and headaches associated with chronic nephritis. Like other theories, it is to be tested partly by what it enables us to discover. Like the atomic theory, it may lead us to perceive and so to fill in certain gaps, such as appear in the following table: are the most CRISES Abdominal. | Peripheral, Pulmonary 1. Arteriosclerosis......| Foy oF = 2. Nephritic hyperten- | | | sion (“uremia”)... +? = = 3. Tabes dorsalis. . Es + = + 4. Plumbism. + = - -_ I may here acknowledge my deep indebtedness to Rudolf Schmidt's book on Pain,! which has guided and confirmed my own observa- tions on many points. 1 pain—its Causation and Diagnostic Significance, by Rudolf Schmidt; translated by Karl M. Vogel and Hans Zinsser, J. B. Lippincott Company, 1908.