LOW-PRESSURE HYDROCEPHALIC STATE AND VISCOELASTIC ALTERATIONS IN THE BRAIN

MOST SHUNT-DEPENDENT HYDROCEPHALIC patients present with predictable s ymptoms of headache and mental status changes when their cerebrospinal fluid shunts malfunction. Their intracranial pressure (ICP) is usuall y high, and they usually respond to routine shunt revision. This repor t describes 12 shunted patients who were admitted with the full-blown hydrocephalic syndrome but with low to low-normal ICP. All 12 patients had been maintained previously on medium-pressure shunts. Their sympt oms included headache, lethargy, obtundation, and cranial neuropathies . At peak symptoms, their ventricular sizes were large (ventricular/bi parietal ratio of 0.35 to 0.45) in six and massive (ventricular/bipari etal ratio >0.45) in six and their ICPs ranged from 2.2 to 6.6 mm Hg, with a mean of 4.4 +/- 1.3 mm Hg (+/-standard deviation), i.e., below or well within the pressure range of their shunts. The pressure volume index of three patients at peak symptoms ranged from 39.2 to 48.5 ml, with a mean of 43.9 +/- 4.6 ml, which represents a 190% increase from the predicted normal value. Seven patients failed to improve with mul tiple shunt revisions, including the use of low-pressure valves. In 11 patients, symptoms and ventriculomegaly were not reversed except with prolonged external ventricular drainage at subzero pressures (mean ex ternal ventricular drainage nadir pressure of -5.7 +/- 3.6 mm Hg, for a mean period of 22.2 days). During external ventricular drainage trea tment, symptoms correlated only with ventricular size and not with ICP . AH 11 were subsequently treated successfully with a new medium- or l ow-pressure shunt. One patient was treated successfully with prolonged shunt pumping. We postulate that: 1) the development of this low-pres sure hydrocephalic state is related to alteration of the viscoelastic modulus of the brain, secondary to expulsion of extracellular water fr om the brain parenchyma, and to structural changes in brain tissues du e to prolonged overstretching; 2) certain patients are susceptible to developing low-pressure hydrocepha!ic state because of an innate low b rain elasticity due to bioatrophic changes; 3) low-pressure hydrocepha lic state symptoms are due not to pressure changes but to brain tissue distortion and cortical ischemia secondary to severe ventricular dist ortion and elevated radial compressive stresses within the brain; and 4) treatment must be directed toward allowing the entry of water into the brain parenchyma and the restoration of baseline brain viscoelasti city.