Cysternography in Normal Pressure Hydrocephalus

Gabriel Soudry, M.D.

Charles Ahn M.D.

October 12, 1993

Case Presentation:

An 84 year old man was referred from the geriatric clinic for evaluation of gait abnormality, cognitive impairment and urinary incontinence. He was found to have severe short term memory loss but no other intellectual deficit and he exhibited postural instability with evidence of frontal release.

Findings:

A CT scan showed enlarged lateral ventricles. An MRI (transaxial and sagital) was performed to look for cerebral vascular disease and showed changes consistent with central atrophy. Cysternography showed early entry of tracer in the lateral ventricles at 6 hours (posterior view, arrows outline ventricular activity). Twenty-four and 48 hour images showed persistance of activity in the lateral ventricles (lateral view at 24 hours, arrows outline ventricular activity). These findings were compatible with normal pressure hydrocephalus (NPH). The consulting neurosurgeon advised against any shunting procedure.

Discussion:

Cysternography has been proposed in the past as a useful tool in evaluating patients with suspected NPH (1,2). Recently, its popularity seems to have been declining (3,4). This review will discuss the strengths and the weaknesses of the test as well as the controversies surrounding its usefulness.

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).

Conclusions:

All the tests presently available for the diagnostic of NPH have a suboptimal predictive accuracy.

A positive cysternogram may be helpful but a negative study has little prognostic value.

MRI assessment of CSF flow may be a promising technique for evaluation of patients with suspected NPH and is awaiting validation by prospective studies.

References:

1. Benson D, LeMay M, Patten D, Rubens A. Diagnosis of normal pressure hydrocephalus. New Eng J Med 1970;283:609-615.

2.James A Jr, DeLand F, Hodges F, Wagner H. Role of cisternography in diagnosis. JAMA 1970; 213:1615-1622.

3. Vanneste J, Augustijn P, Davies G, Dirven C, Fu Tan W. Normal-Pressure Hydrocephalus. Is cisternography still useful in selecting patients for a shunt? Arch Neurol. 1992;49:366-370.

4. Benzel E, Pelletier A, Levy P. Communicating Hydrocephalus in Adults : Prediction of Outcome after Ventricular Shunting Procedures. Neurosurgery 26:655-660,1990.

5. DeLand F, Wagner H. Atlas of Nuclear Medicine.Volume 1. W Saunders 1969.

6. Patten D, Benson D. Cisternography. Nuclear Medicine in Clinical practice. P.B. Schneider and S. Treves. Elsevier/North Holland Biomedical Press 1978.

7. Vassilouthis J. Syndrome of normal pressure hydrocephalus. J Neurosurg. 1984;61:501-509.

8. Bradley W, Whittemore A, Kortman K, Watanabe A, Hoomyak M, Terresi L, Davis S. Marked cerebrospinal fluid void: Indicator of successful shunt in patients with suspected normal-pressure hydrocephalus. Radiology 1991; 178: 459-466.

9. Katzman R, Hussey F. A simple constant infusion manometric test for measurement of CSF absorption. Rationale and method. Neurology (Minn) 1970;20:534-544.

10. Gjerris F, Borgesen S, Sorensen P, eds. Outflow of cerebrospinal fluid. Alfred Benson Symposium 27. Copenhagen: Munksgaard, 1989.

11. Borgesen S, Gjerris F. The predictive value of conductance to outflow of CSF in normal pressure hydrocephalus. Brain 1982 Mar; 105(Pt 1):65-86.

12. Black P, Ojemann R, Tzouras A. CSF Shunts for dementia, incontinence, and gait disturbance. Clin Neurosurg. 1985; 32: 632-51.

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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J. Anthony Parker, MD PhD, jap@nucmed.bih.harvard.edu