The CSF is secreted mainly by the choroid plexuses located on the roofs of the lateral, third and fourth ventricles. After leaving the fourth ventricle, CSF flows around the brain stem, the cerebellum, the hemispheres, and down in the subarachnoid space then back up to the basal cisterns. Note that the vector of the CSF flow is outward from the ventricles as the gradient of pressure is highest in the ventricles and diminishes successively along the subarachnoid pathways. Absorption of the CSF occurs mainly through the arachnoid villi which project into the parasagittal venous sinuses and to a much lesser extent through the epidural veins of the vertebral column (5).
Cisternography is performed by introducing a radiolabeled pharmaceutical (usually Indium-111-DTPA) intrathecally by lumbar puncture and following its flow by taking sequential pictures over a period of hours and days. In a normal subject the tracer will rise to the basal cisterns in 1 to 3 h and then proceed to flow over the convexities collecting in the sagittal area in 12 to 24 h. Frequently there is greater flow over the anterior aspects of the hemispheres than over the posterior. The ventricles are normally not visualized at any time during this series and the cisterns are usually clear of activity by 24 h.
In patients with normal pressure hydrocephalus, there is impairment of the reabsorption of the CSF by the arachnoid granulations. Reversal of flow leads to early ventricular visualization (ventricular reflux), which persists for 24-48 h or more with little or no flow of the tracer over the convexities to the sagittal area. In isolated cerebral atrophy with normal CSF reabsorption, there may be ventricular reflux but it will be not as marked or persistent as in NPH (6).
A typical clinical scenario is the one of a patient with recent onset of intellectual deterioration who undergoes a " dementia work-up" and is found to have dilated cerebral ventricles out of proportion from the cortical atrophy on the head CT. At that point, the possibility of NPH is raised.
The classical clinical findings of NPH ( intellectual deterioration with gait disturbances and urinary incontinence) are non specific and are often encountered in patients with other degenerative brain conditions. Some features on the head CT (marked ventricular enlargement, periventricular hypodensity, absent/slight cortical atrophy, absent cortical infarcts) (7), and on MRI (upward bowing of the corpus callosum, flattening of the cortical gyri against the inner table of the calvarium, increased CSF flow void (8) enhance suspicion of NPH but can only be used as indicators of the disease. The intrathecal lumbar spinal infusion test (9) and 24 hour intracranial pressure monitoring has not been found to add significant diagnostic information to the clinical and radiological features (10). The most widely accepted test presently seems to be the measurement of conductance to outflow of CSF (11) with a reported positive predictive value of 96%% for favorable outcome after shunting procedure. This technique requires special expertise (12) and it is often not well tolerated by patients (13,14).
As late as the seventies, cisternography in combination with pneumoencephalography was considered jointly as the gold standard test for the diagnosis of NPH (1,2,15). Some authors still advocate cisternography for evaluation of patients with suspected NPH (16,17,18), or at least, they acknowledge its favorable positive predictive value (12). However, recent studies of outcome after ventricular shunting have found that the predictive accuracy of cisternography is low (3,4) and it appears many centers no longer use the test (14).
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10. Gjerris F, Borgesen S, Sorensen P, eds. Outflow of cerebrospinal fluid. Alfred Benson Symposium 27. Copenhagen: Munksgaard, 1989.
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13. Albeck M, Borgesen S, Gjerris F, Schmidt J, Sorensen PS. Intracranial pressure and cerebrospinal fluid outflow conductance in healthy subject. J Neurosurg. 1991; 74: 597-600.
14. Graff-Radford N, Godresky J, Jones M. Variables predicting surgical outcome in symptomatic hydrocephalus in the elderly. Neurology 1989; 39: 1601-1604.
15. Huckman M. Normal pressure Hydrocephalus: Evaluation of diagnostic tests. AJNR 1991; 2: 385-395.
16. Larson A, Moonen M, Bergh AC,Lindberg S, Wikkelso C. Predictive value of quantitative cisternography in normal pressure hydrocephalus. Acta Neurol Scand 1990; 81: 327-332.
17. Jacobs M, Mantil J, Peiglin D, Andrews J. Radionuclide cisternography and MRI in the evaluation of normal pressure hydrocephalus.J Nucl Med 1989; 14: 819-884.
18. Shih WJ, Tibbs P. Normal-pressure hydrocephalus. JAMA 1990.264:336-7.
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