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Congenital heart disease consists of cardiac anomalies that originated before or during the truncus arteriosus stage. The central nervous system, serving all organs, is the first to develop. It is the only organ possessing a third circulation. Immediately after the neural tube closes at the fourth week, its lining of immature ependymal cells secretes a proteinaceous neural tube fluid (NTF) at a pressure higher than the amniotic pressure. The resulting distention helps to shape not only the embryonic brain and spinal cord but also the bordering mesodermal cells that later will form vertebrae. The choroid plexus does not begin to secrete true cerebrospinal fluid until two weeks later. Should hypersecretion occur during this critical two week interval, the neural tube will overdistend and allow NTF to infiltrate into mesoderm (Fig. 1). Here, this fluid with its extraneous protein, may damage cells that are destined to form the anlagen of mesodermal organs such as the heart. It may also damage the primitive gut resulting in pulmonary, gastrointestinal and genitourinary anomalies. The most convincing evidence that the neural tube had been overdistended is the combination of anterior and posterior spina bifida that constitutes bilateral hemivertebrae. Vertebral anomalies are present in congenital heart disease though scarcely recognizable on the chest film of the newborn.

Some years ago, it came to my attention that a small tumor in the subarachnoid space may so elevate the protein content of spinal fluid that its mechanical interference with fluid removal will increase intracranial pressure. Leakage ofplasma from vessels in the tumor causes the high protein content and represents a breakdown of the blood-cerebrospinal fluid barrier (i). Tumors buried within the brain or cord are less apt to increase cerebrospinal fluid protein but do tend to become cystic. I suspected that this retained protein-rich fluid did not result from liquefaction necrosis but from leakage of blood plasma, i.e., a breakdown ofthe blood-brain barrier. Preliminary studies showed that the Tiselius pattern of cyst fluid resembled that of the patient's serum, offering support to the leakage theory (2). This investigation ofcyst fluids initiated a review ofthe subject of the blood-brain barrier, which proved so interesting that it has sidetracked the original problem.

IN ADDITION to the nerves of ordinary sensation, the mucous membranes of the nose and paranasal sinuses are innervated by both sympathetic and parasympathetic fibers. In the past several years, the department of neurosurgery at the Cleveland Clinic Hospital has been carrying out operative procedures which in some cases interrupt the sympathetic nerve supply to the head and in other cases the parasympathetic nerve supply. 1 These procedures have afforded us an opportunity of observing the effect on the nasal mucosa of sympathetic denervation on the one hand and parasympathetic denervation on the other. The parasympathetic fibers leave the brain stem as the nervus intermedius, which constitutes a portion of the facial nerve. At the geniculate ganglion some of the parasympathetic fibers leave the facial nerve to form the greater superficial petrosal nerve, which passes to the sphenopalatine ganglion; from there, postganglionic fibers go with the deep branches of the maxillary

Traumatic subdural hematoma is a definite clinical entity that has been given considerable attention in the medical literature since Virchow's classic description1of "hematomas of the dura mater" in 1857. The lesion consists of an encysted collection of blood, situated between the dura and the arachnoid membranes, usually over the convexity of the cerebral hemisphere. It is my aim to sketch briefly the clinical and pathologic aspects of this interesting lesion and to dwell particularly on the reason for its delayed clinical manifestations. The majority of published reports of cases of traumatic subdural hematoma are similar in one respect, that is, in the occurrence of a latent interval between the reception of trauma and the onset of pressure symptoms. The cranial trauma that was responsible may have been severe or so trivial as to be readily forgotten. In many instances a history of trauma that had been denied previously

In this presentation an explanation is sought for the syndrome of increased intracranial pressure which occasionally accompanies an attack of otitis media and which is not due to meningitis, encephalitis or abscess of the brain. Quincke1in 1896 described a syndrome in which the signs of increased intracranial pressure were associated with the finding of clear cerebrospinal fluid on lumbar puncture. He stated the belief that in such cases an excess of cerebrospinal fluid results from hypersecretion of the choroid plexus. He referred to the condition as "serous meningitis" and described otitis as one of the predisposing factors. Various terms have since been coined to describe and label conditions of this type, such as "cerebral pseudoabscess," "meningismus," "serous meningitis," "serous ependymitis," "arachnoiditis," "hypertensive meningeal hydrops," "toxic hydrocephalus," and "otitic hydrocephalus." Recent articles by Symonds,2Frazier,3Dandy,4Davidoff and Dyke,5McAlpine,6Williams,7and Ersner and Myers6described and authors' experiences with

Excision of aneurysms of the hepatic artery involving or distal to the gastroduodenal artery requires restoration of blood flow to the distal hepatic arteries. Successful excision of such an aneurysm utilizing a splenic artery to distal hepatic artery anastomosis is reported.

AFTER evacuation of a subdural hematoma the compressed hemisphere may fail to expand spontaneously. This may be a grave prognostic sign. Trotter,1 Coleman,2 Coblentz3 and Voris4 have discussed this aspect of subdural hematoma. We agree with Coleman and Coblentz that failure of the compressed hemisphere to expand is more likely than cerebral edema to cause serious symptoms. Coleman found that the compressed hemisphere may not expand for several days after evacuation of the clot. It has been shown that the hemisphere may still be in a compressed state at autopsy even though the hematoma has been adequately evacuated.5 We have . . .

To the Editor:— I am concerned about the article by Ginsberg et al ( JAMA 200 :180, 1967) emphasizing the risks inherent in the application of inflatable splints. These authors, however, employed a plastic boot, not an open-end splint. Their conclusions were based on theory and on the results of an indirect method of recording blood flow in five normal persons. There were no confirmatory laboratory studies. They overlooked the following articles demonstrating the usefulness and safety of circumferential pneumatic compression: JAMA 162 :274, 1956; JAMA 167 :985, 1958; Cleveland Clin Quart 32 :1, 1965; JAMA 196 :491, 1966; and Surg Gynec Obstet 123 :792, 1966. When in 1952 I first began to apply the pneumatic splint, I also thought it would be dangerous to employ pressures in excess of capillary pressure. However, subsequent angiographic studies on the forelimb of the dog showed that some blood flow was maintained even when

The cardinal symptom of intervertebral disk infection in 10 patients was sudden excruciating back pain that frequently radiated down one leg or both legs and usually was not relieved with opiates. These infections usually occurred after a diagnostic or therapeutic procedure on the spine or as a result of venous spread from an infection in the pelvis. Characteristic roentgenographic features did not appear for four or more weeks. The sedimentation rate was consistently high, but returned to normal after the infection subsided. For four patients treated conservatively with antibiotics, complete bed rest, and body casts, the average length of convalescence was 8 months; for six patients treated by laminectomy in addition to other therapeutic measures, it was 4.8 months.

Excerpt Graves' disease may be considered to be a thyroid-pituitary syndrome. The two chief manifestations of the disorder are exophthalmos and hyperplastic goiter with hyperthyroidism. They usuall...

To the Editor.— A recent letter, "Diphenylhydantoin in the Treatment of Duodenal Ulcer" ( 219 :511, 1972), has encouraged me to express a long held hypothesis that both pernicious anemia and polycythemia are primarily of neurologic origin. In pernicious anemia the gastric mucosa is thin, pale, and atrophic. There is anacidity, low hemoglobin, posterolateral sclerosis, and no peptic ulcer. In polycythemia the gastric mucosa is thick, turgid, and hypertrophic. There is hyperacidity, elevated hemoglobin, no posterolateral sclerosis, and often peptic ulcer. All of which suggest that pernicious anemia may be the end result of sympathicotonia, ie, local sympathetic over-function (as in Raynaud's disease) affecting gastric mucosa. Conversely, its antithesis, polycythemia, may be the expression of the end result of vagotonia, ie, parasympathetic over-function affecting gastric mucosa. If this thesis is correct, both are primary neurologic disorders. Since splanchnicectomy raises gastric acidity and vagotomy lowers it, pernicious anemia should respond to the

In a prior communication 1 we described our attempts to modify herpes simplex following the decompression operation 2 on the fifth cranial nerve by using hydrocortisone ointments and bacterial ointments locally. In 148 patients, approximately one-third developed herpes, and we could not modify the attack rate by the use of the above agents. Since that time, 76 more patients have been operated on for tic douloureux using the same decompression or neurolysis type of procedure. Twenty-eight of these patients were painted with a 3% solution of an iodophor (Wescodyne) consisting of 7.75% polyethoxy polypropoxy ethanol-iodine complex; 3.75% nonylphenylether of propylene glycol-iodine complex; and 0.10% hydrogen chloride before and after operation twice daily. The use of this iodine complex did not modify the attack rate, as 12 of the 28 individuals developed florid herpes simplex. In addition, 4 patients were given poliomyelitis immune globulin (human), Merck Sharpe & Dohme, 10 cc.

In the past few years, decompression of [ill] sensory root of the fifth cranial nerve [ill]Taarnhoj operation) has largely replaced [ill]esection of the nerve root as the surgical treatment for trigeminal neuralgia used at the Cleveland Clinic Hospital. * The advantage of the decompression operation is that the sensation of the face is preserved. Herpes simplex often follows intracranial operative procedures on the fifth cranial nerve. The large number of decompression operations done provides a predictable source of patients with herpes simplex for scientific observation, and the additional incentive to find a preventive for this annoying complication in the patient's postoperative recovery period. Several years ago, the impression gained in informal conversations with dermatologists was that most of them believed that, while the course of the well-developed herpes simplex eruption was not influenced significantly by hydrocortisone, applied topically, the drug might be of some value if used early in the course

A kindred originally described 40 years ago now includes 97 individuals with definite or possible bilateral acoustic neuroma. The trait is autosomal dominant with high penetrance. Onset is at about 20 years of age and survival without surgery varies from 2 to 42 years. Severe accidents, including drowning, are common in the family, possibly due to neurological deficits. In screening such individuals, vestibular function is probably most sensitive, but complete audiometric studies, special roentgenologic examinations, and brain scan have proved useful. No single study can be relied upon to diagnose this disease or to exclude the diagnosis. Peripheral signs suggesting neurofibromatosis are rare but other central nervous system tumors, often asymptomatic, are common, which suggests that this trait represents a "central" form of neurofibromatosis. It is distinct from unilateral acoustic neuroma based on natural history and genetic etiology.

A most unusual survival of a gunshot wound of the head was apparently materially favored by an equally unusual treatment aimed at expansion of the area of cerebral defect.