THE term hydrocephalus refers to distention of the cerebral ventricles, usually as the result of obstruction somewhere along the pathway of the cerebrospinal-fluid circulation. Occult indicates that enlargement of the ventricles has occurred after union of the cranial sutures, and hence the head remains of normal size. Hydrocephalus is said to be noncommunicating or obstructive if the blockade of circulation is in the ventricular system and communicating or nonobstructive if there is a normal patency of the pathways from the ventricular system to the lumbar subarachnoid space. Its causes are numerous and include tumors encroaching on the ventricles, carcinomatosis of . . .

Symptomatic occult hydrocephalus with "normal" cerebrospinal-fluid pressure.a treatable syndrome.

The special clinical problem of symptomatic hydrocephalus with normal cerebrospinal fluid pressure: Observations on cerebrospinal fluid hydrodynamics

✓ The distribution of compliance and outflow resistance between cerebral and spinal compartments was measured in anesthetized, ventilated cats by analysis of the cerebrospinal fluid (CSF) pressure response to changes in CSF volume. Cerebral and spinal compartments were isolated by inflating a balloon positioned epidurally at the level of C-6. The change of CSF volume per unit change in pressure (compliance) and change of CSF volume per unit of time (absorption) were evaluated by inserting pressure data from the experimental responses into a series of equations developed from a mathematical model. It was found that 68% of total compliance is contributed by the cerebral compartment while the remaining 32% is contained within the spinal axis. The cerebral compartment accounted for 84% of total CSF absorption. The mechanism for spinal absorption appears to be similar in that no differences were obvious on the basis of pressure dynamics.

Compartmental analysis of compliance and outflow resistance of the cerebrospinal fluid system

A mathematical model of the cerebrospinal fluid (CSF) system was developed to help clarify the kinetics of the intracranial pressure (ICP). A general equation predicting the time course of pressure was derived in terms of four parameters: the intracranial compliance, dural sinus pressure, resistance to absorption, and CSF formation. These parameters were measured in the adult cat, and the equation was tested by comparing experimental and calculated values of the time course of pressure in response to volume changes. The theoretical and experimental results were in close agreement, and the role of each parameter in governing the dynamic equilibrium of the ICP was determined. From this analysis, dynamic tests were developed for rapid measurement of CSF formation, absorption resistance, and the bulk intracranial compliance. These techniques are applicable to clinical settings, providing data that are useful in characterizing the physiological mechanisms responsible for raised ICP and assessing changes induced by therapy.

A nonlinear analysis of the cerebrospinal fluid system and intracranial pressure dynamics.

THE SIGNS and symptoms of increased intracranial pressure and cerebral compression have occupied the interest of numerous investigators since earliest times. Although changes in vital signs in response to alterations in intracranial dynamics have long been recognized, the importance of these changes in the diagnosis and management of patients with expanding intracranial lesions has been questioned. In particular, the arterial hypertension which is readily produced experimentally by increased intracranial pressure has been considered to be of limited clinical significance because it has been assumed that blood pressure does not increase until the intracranial pressure approaches the diastolic pressure and that this rarely occurs. This conclusion was based primarily on periodic recording of the lumbar subarachnoid pressnre and thus requires the additional assumption that the spinal fluid pressure at all times approximates the intracranial pressure. In a previous report we presented experimental evidence that obstruction at the tentorial incisura during expansion of a supratentorial mass prevents communication of pressure to the posterior fossa and spinal cana1.l Also, as the pressure gradient across the incisura increases, the vasopressor threshold decreases, and arterial hypertension may then occur, with absolute intracranial pressures far below the diastolic pressure.? The first purpose of the present experiments was to extend these observations in an attempt to determine the sequence of events which ultimately lead to neurological deterioration and death during gradual expansion of an intracranial mass lesion. The history of the investigation of cerebral compression before 1900 was reviewed by

Cerebral vasomotor paralysis produced by intracranial hypertension.

The mechanism of the change in cerebrospinal fluid pressure following an induced change in the volume of the fluid space.

Observations on the interrelationships of intracranial pressure and cerebral blood flow.

CUSHING in 1901 stated: "The fact that cerebral compression occasions a rise in blood pressure is universally known but it does not seem to have been recognized that the degree of this elevation occurspari passuwith the degree of compression to which medullary centers are subjected."1He later elaborated clinically on this concept.2Although his experimental work demonstrated clearly that blood pressure elevation did not occur until high degrees of compression had developed, the application of the experimental concept to clinical problems inexplicably lost sight of this fact. In the next four decades it became widely accepted teaching that the clinical state produced by expanding intracranial lesions is characterized by a concomitant association among increased intracranial pressure, vascular hypertension and bradycardia, a triad of responses that has been termed the Cushing phenomenon. These changes in the vital signs are seen together so rarely in subjects with high

Experimental and clinical observations on rising intracranial pressure.

WE HAVE previously reported that changes in cerebral blood flow may have a profound effect in the same direction on the cerebrospinal fluid pressure of rhesus monkeys. 1 The present communication deals with this relationship in man. MATERIAL AND METHODS The types of patients studied and the methods of continuously recording the several pressures of interest have been described. 2 Included in this study are patients who were sufficiently cooperative to hyperventilate and lie quietly. OBSERVATIONS The administration of carbon dioxide in air increases the cerebral blood flow 3 and the cerebrospinal fluid pressure. 4 Hyperventilation decreases the flow 5 and the fluid pressure. 4 The cerebrospinal fluid pulse pressure varies concomitantly with the irregular arterial pulses of auricular fibrillation and extrasystoles. These procedures and conditions usually cause concomitant changes in the arterial pressure in the same direction, which have been assumed by other investigators to be the causative mechanism,

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Influence of changes in cerebral blood flow on the cerebrospinal fluid pressure.

THE CLINICAL and experimental association of high cerebrospinal fluid pressures with disorders of the central nervous system has influenced the diagnostic and therapeutic thinking of investigators and clinicians for over half a century. Meyers' 1 critical evaluation of the physiologic experimentation designed to study this relation using experimental animals casts grave doubts on the assumption that there was a necessary association between moderate elevations in pressure and symptomatology. Previously, Browder and Meyers 2 had presented convincing clinical evidence that the orthodox mechanistic thinking in this regard was unsound and unsafe. Nevertheless, studies have since appeared attributing reactions to low pressure 3 as well as to high pressure, 4 and the assumption of a causative relation between high and low pressures and disorders of the central nervous system, at least under certain circumstances, remains widespread among informed experts.

Henry W. Ryder

Papers

The mechanism of the change in cerebrospinal fluid pressure following an induced change in the volume of the fluid space.

Observations on the interrelationships of intracranial pressure and cerebral blood flow.

Experimental and clinical observations on rising intracranial pressure.

Influence of changes in cerebral blood flow on the cerebrospinal fluid pressure.

Failure of abnormal cerebrospinal fluid pressure to influence cerebral function.