NPH can be reversible after cerebrospinal fluid (CSF) diversion. In the past no reliable criteria could be defined to predict the successful outcome of CSF shunting. Several authors demonstrated an increased cerebral blood flow after lumbar puncture in patients with NPH, indicating an underlying impairment of cerebral circulation autoregulation. 123I-AMP brain tomoscintigraphy was applied to 23 individuals with NPH before and after CSF drainage. Of these 23 patients, 10 underwent surgical shunting. The frontal and parietal hypoactive cortical pattern was present in NPH but not pathognomonic. Under stimulation of CSF pressure lowering, seven patients with improved outcome after shunting demonstrated an increase of cerebral perfusion in these areas, whereas a decrease of activity was found in three patients whose clinical status was unchanged after CSF diversion. This tomoscintigraphic test may be an interesting additional criterion for surgical admission.

After portacaval shunt in the rat, the transport of tryptophan and other neutral amino acids across the blood-brain barrier is enhanced. To determine the role of NH3 in the intracerebral transfer of tryptophan and serotonin metabolism, solutions containing either saline or NH3 or tryptophan or NH3 + tryptophan together were infused, respectively, into the internal carotid artery of rats in order to achieve blood levels similar to those observed after liver ischemia. After tryptophan infusion, a significant increase in the hypothalamic levels of tryptophan and 5-hydroxyindoleacetic acid was observed. A similar increment was found after NH3 infusion. NH3 + tryptophan infusion induced a significant increment in hypothalamic tryptophan and 5-hydroxyindoleacetic acid levels which were 2-fold greater than after tryptophan infusion. There was no significant change in 5-hydroxytryptamine levels in any of these experiments. Glutamine levels increased significantly after NH3 infusion. When tryptophan and NH3 were infused simultaneously, a significant reduction in glutamine levels occurred. These results cannot be explained by any modification of cerebral blood flow nor of the cerebral intercellular pH. Our data suggest that NH3 enhances the transfer of tryptophan across the blood-brain barrier and thus stimulates serotonin metabolism. The mechanism by which tryptophan transfer across the blood-brain barrier is facilitated is unknown. The reduction in glutamine levels in the hypothalamus when NH3 and tryptophan are infused together may be explained either by an inhibition of synthesis or by an intercellular influx of neutral amino acids and an efflux of glutamine as suggested by James et al.