Around half of patients with idiopathic normal-pressure hydrocephalus (iNPH) will develop dementia, despite responding to shunting, study findings suggest.
Many patients had other contributory factors to their dementia, but Ville Leinonen (Kuopio University Hospital, Finland) and colleagues say that about a quarter of the 146 patients in their study had dementia that was partly or wholly related to iNPH.
"There is clearly a need for systematic, prospective, and repeated long-term neuropsychological evaluation of shunted iNPH patients," they write in Neurosurgery. "This would enable the quantification of the potential cognitive improvement after shunt and help in recognition of the patients with risk of further cognitive deterioration."
The patients underwent shunting when they were about 70 years old, and the team followed them up a median of 4.8 years later. At this point, 80% of the patients had cognitive decline, with 46% having dementia. About two-thirds of the patients with dementia were dead at follow up, as were just over a third of those with mild or no cognitive decline.
Thirty patients had predominantly iNPH-related symptoms (progressive neuropsychologic symptoms plus motor impairment and incontinence), but 22 also had an alternative cause of dementia. Among all the demented patients, there were 18 with probable Alzheimer's disease and eight with vascular dementia.
Notably, eight patients had iNPH-related dementia with no evidence of Alzheimer's disease or vascular dementia.
The researchers note that physicians often referred patients with suspected shunt malfunction, and a third underwent shunt revision, with this being as frequent in patients who developed dementia as in those who did not. Thus, shunt malfunction did not likely contribute much to the high rate of dementia.
"Consequently, we suggest that iNPH, even after successful shunt treatment, may be an independent dementing disease or at least a risk factor for dementia," they say.
Patients' risk for dementia rose with increasing age and longer length of follow up, after accounting for confounders. It was also increased - more than 18-fold - if patients' first iNPH symptom was memory deficit, although the team cautions that the 95% confidence interval was very wide.
Leinonen et al comment that the diagnostic criteria for iNPH-related dementia currently "lack systematic description and standardization."
They conclude: "Thus, our results highlight the need for further clinical and neuropathological studies on potentially progressive iNPH-related memory disorder, as well as the need to test shunt function systematically in these cases."
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