Roger Bannister

Preservation of autoregulation of cerebral blood flow in autonomic failure

Cerebral blood flow (CBF) measurements have been made at systolic pressures between 40 and 170 mm Hg in 8 patients with chronic autonomic failure and widespread sympathetic efferent defects. Hypotension was produced by head up tilt. Cerebral autoregulation was preserved over a wide range and only failed at a systolic pressure close to 60 mm Hg, which is below the level at which it fails in normal subjects. Therefore, although autoregulation is probably mediated largely by local myogenic factors, its lower limit appears to be reduced by defective sympathetic function. These findings help to explain the remarkable tolerance of severe postural hypotension in autonomic failure.

Immunoglobulin synthesis within the central nervous system in disseminated sclerosis.

Abstract In a patient with disseminated sclerosis, lymphocytic cells of the cerebrospinal fluid maintained in vitro synthesised immunoglobulins G and A, but not IgM. This provides a direct demonstration that IgG and IgA, present in the cebrospinal fluid, were derived at least in part from cells within the central nervous system.

Pressor amines and monoamine-oxidase inhibitors for treatment of postural hypotension in autonomic failure. Limitations and hazards.

The short-term effects of pressor amines were investigated in four patients with postural hypotension caused by autonomic failure. In supine patients p-tyramine alone or with a monoamine-oxidase inhibitor produced pronounced supine hypertension without abolishing the symptoms associated with a postural fall in blood-pressure. Phenylephrine or ephedrine maintained a normal blood-pressure on standing but caused supine hypertension. Thus the effects of p-tyramine with or without a monoamine-oxidase inhibitor were unpredictable and did not include relief of postural hypotension. Phenylephrine or ephedrine had some beneficial effect, but since all these drugs influence standing pressure only at the expense of pronounced supine hypertension, alternative therapy must be sought.

Parkinsonism, system degenerations and autonomic failure

Publisher Summary This chapter discusses progressive autonomic failure that occurs as an additional feature in two distinct, well-recognized types of primary degenerative disease, namely, Parkinsons disease and multiple-system atrophy. Whatever their clinical resemblances, Parkinsons disease and striatonigral degeneration differ in their histopathology. As with Parkinsonism, autonomic failure may occur in a number of unrelated conditions. The neurological, as opposed to the cardiovascular, features are equally insidious. In progressive autonomic failure, the homeostatic control of blood pressure is disturbed by lesions at several levels from the hypothalamus to the periphery. Cardiovascular reflexes, like somatic reflexes, have afferent, central, and efferent connections, and the next stage in the investigation of postural hypotension and a blocked Valsalva manoeuvre is to try to show whether the lesion is afferent or efferent.

Clinical studies of autonomic function and dysfunction

A discussion of progressive autonomic failure in man. This is one of the few neurological diseases disrupting cardiovascular function. Both central and peripheral pathways are involved. Means of diagnosing defects in autonomic reactions are described. Abnormalities in responses due to multiple system atrophy (MSA) are discussed most extensively.