Fred Plum

The neurologic basis of Cheyne-Stokes respiration☆

Abstract 1.1. Clinical and physiologic studies were performed in twenty-eight patients with Cheyne-Stokes respiration (CSR). Five of the twenty-eight were examined postmortem. Control studies were performed in the following groups showing regular respiration: normal subjects, patients with congestive heart failure, and patients with unilateral and bilateral cerebral vascular disease. 2.2. Neurologically, every subject with CSR exhibited signs of bilateral descending motor system dysfunction at supramedullary levels. Cardiac abnormalities and circulatory congestion, although frequent, were undetectable in five cases. 3.3. Every subject with CSR had hyperventilation and respiratory alkalosis. Peak ventilation coincided with maximal PaCO 2 , and apnea coincided with PaCO 2 levels considerably below the ventilatory threshold. 4.4. Every subject with CSR had an increased respiratory sensitivity to CO 2 , the mean ventilatory CO 2 response being approximately three times the normal. This increased sensitivity, which resulted from bilateral supramedullary brain dysfunction, was the principal cause of hyperpnea. Ventilation in CSR was also augmented by reduced oxygen tensions, resulting from moderate arterial oxygen desaturation. As a result, during late respiratory decrescendo, anoxemia continued to drive ventilation despite PaCO 2 levels considerably below the respiratory-stimulating threshold. 5.5. Periodic breathing is a pattern of neurogenic hyperpnea in which intense hyperventilation alternates with posthyperventilation apnea. Extracerebral abnormalities, although they may augment ventilatory periodicity, are not the primary cause of Cheyne-Stokes respiration.

THE EFFECT ON RESPIRATION OF CENTRAL NERVOUS SYSTEM DISEASE

Respiration is frequently disturbed during brain disease or dysfunction. However, i t is surprising that forebrain or upper brainstem abnormalities produce clinical disorders in breathing regulation almost as frequently as do lower pontine and medullary diseases. The present study emphasizes the commoner forms of neurologic respiratory abnormalities. The alterations are considered as they appear to the clinical observer and in a general order which reflects whether they develop with more rostra1 or more caudal neuraxis impairment. Whenever possible, the pathological physiology of the particular disorders and the associated neuroanatomic defects are outlined or inferred. Some of these inferences are tentative, since it can be difficult to separate neurologic and nonneurologic factors influencing respiration. I n many cases, autopsies fail to reveal chemical or circulatory abnormalities and, in others, they show a plethora of brain lesions, a t least some of which are irrelevant to the respiratory abnormality.

FOCAL PERIODIC SLOW TRANSIENTS IN EPILEPSIA PARTIALIS CONTINUA: CLINICAL AND PATHOLOGICAL CORRELATIONS IN TWO CASES.

Abstract Two cases of epilepsia partialis continua with pathological documentation are described. Periodic focal negative or negative-positive potential changes occurred in the EEG of these patients. These slow transients are interpreted as local shifts of the steady potential of the cerebral cortex recorded transcranially. Their relationships to the focal epileptic discharge are discussed.

Potassium depletion by enemas

Abstract Repeated prolonged enemas, often preceded by administration of cathartics, resulted in profound hypokalemia and weakness in an adult male suffering extensive muscle paralysis and a cauda equina nerve root lesion. Dietary potassium had been restricted to approximately 40 mEq. daily during the period that deficiency developed. Returns from experimental enemas given to this patient had potassium contents as high as 256 mEq. Potassium loss seemed to be greater when contact between infused enema fluid and the dilated atonic bowel was prolonged. Similar depletion might be expected in patients with Hirschsprungs disease and neurogenic atony of the bowel who require repeated enemas.

Partial brown-séquard syndrome associated with coarctation of the aorta: Review of literature and report of a surgically treated case

Abstract A review of the literature has revealed three instances of neurological disease presumed to be secondary to the collateral circulation associated with coarctation of the aorta. None of these patients were subjected to surgical correction of the coarctation; therefore a causal relationship can only be assumed. A case of partial Brown-Sequard syndrome with associated coarctation of the aorta has been reported. Although the resolution of the neurological defects is not yet complete, sufficient change has occurred over a period of 2 years to suggest that a causal relationship exists. Although the threat of neurological complications appears to be uncommon, it serves as an additional indication for surgical correction of coarctation.

Disorders of the Cervical Spinal Cord in Older Patients

Cervical spondylosis with compression of the spinal cord is the most common producer of spastic paraparesis of the lower extremities in middle-aged and elderly persons. Other conditions which are likely to produce this picture, often combined with impaired function of the arms, are subacute combined degeneration, amyotrophic lateral sclerosis, and multiple sclerosis. Features which are important in differential diagnosis are listed.Intermittent cervical traction produces at least temporary clinical improvement in most cases of cervical spondylosis, and sometimes the degree of improvement is remarkable in view of the underlying abnormality of bone and cartilage.