Microgravity environment and compensatory: Decompensatory phases for intracranial hypertension form new perspectives to explain mechanism underlying communicating hydrocephalus and its related disorders

Abstract

The pathogenesis underlying communicating hydrocephalus has been centered on impaired cerebrospinal fluid (CSF) outflow secondary to abnormal CSF pulsation and venous hypertension. Hydrodynamic theory of hydrocephalus fares better than traditional theory in explaining the possible mechanisms underlying communicating hydrocephalus. Nonetheless, hydrodynamic theory alone could not fully explain some conditions that have ventriculomegaly but without hydrocephalus. By revisiting brain buoyancy from a fresher perspective, called microgravity environment of the brain, introducing wider concepts of anatomical and physiological compensatory-decompensatory phases for a persistent raise in intracranial pressure, and along with combining these two concepts with the previously well-accepted concepts of Monro-Kellie doctrine, intracranial hypertension, cerebral blood flow, cerebral perfusion pressure, brain compliance and elasticity, cerebral autoregulation, blood-brain and blood-CSF barriers, venous and cardiopulmonary hypertension, Windkessel phenomenon, and cerebral pulsation, we provide plausible explanations to the pathogenesis for communicating hydrocephalus and its related disorders.

Keywords: Brain compliance; Monro – Kellie doctrine; Windkessel effect; brain pulsation; buoyancy; communicating hydrocephalus; microgravity.

Figure 1

The Archimedes's principle: Any submerged object is in equilibrium and remains motionless whenever weight of the object (F¹) equals to object lower surface fluid pressure (F²)

Figure 2

Sinking skin flap syndrome after right frontotemporoparietal decompressive craniectomy

Figure 3

During “compensatory phase,” the macrocirculatory arterial (Macro-cir) pulsation is increased to augment cerebral blood flow, more cerebrospinal fluid in the arachnoid spaces is absorbed to the venous sinuses; and at microcirculatory arterioles (Micro-cir) and in intact autoregulation, the vasoconstrictive response may occur toward the end of the compensatory phase. Cases with impaired autoregulation, hyperemia, and brain edema can cause brain swelling during this phase. During this compensatory phase, the intracranial pressure waveform shows peak P1 wave

Figure 4

During “decompensatory phase,” presence of loss of Windkessel effect or pulsation in macrocirculation (Macro-cir) secondary to a persistent rise in intracranial pressure that would result in stagnation of blood in both macro- and microcirculation (Micro-cir) causing hyperemia and venous hypertension. Venous hypertension (raise V jugular wave or peak P2 intracranial pressure wave) is also aggravated by secondary pulmonary hypertension and all these may contribute toward brain swelling and low brain compliance or stiff brain. Cerebrospinal fluid outflow to venous sinuses is reduced by lack of pulsation, venous hypertension, and swollen brain