Eric Wexler, M.D., Ph.D., Modern Brains PsychiatryEric Wexler, M.D., Ph.D.Diplomate, American Board of Psychiatry & Neurology

Provider Resource

The Neuropsychiatry of Normal Pressure Hydrocephalus

Psychiatric and behavioral disturbance is a core, under-recognized dimension of idiopathic normal pressure hydrocephalus (iNPH), not an incidental comorbidity. A 2026 systematic review and meta-analysis of 22 studies found that 73.4% of iNPH patients have at least one neuropsychiatric symptom on the Neuropsychiatric Inventory, and roughly 46% carry at least one formal psychiatric diagnosis, yet the same task force concluded psychiatric morbidity in iNPH is likely underidentified and undertreated (Belessiotis-Richards et al., 2026).

This review covers the phenomenology and prevalence of psychiatric symptoms in NPH, the misdiagnosis problem in both directions, the diagnostic workup that separates NPH from primary psychiatric illness and dementia, and psychotropic management. The evidence base is dominated by observational studies and case reports; only one small pilot RCT has examined shunting's effect on psychiatric symptoms, so most conclusions are low-to-moderate certainty (Belessiotis-Richards et al., 2026).

Psychiatric and behavioral symptoms as manifestations of NPH

The psychiatric syndrome of iNPH is fundamentally a frontal-subcortical circuit disorder, driven by ventricular expansion compressing frontal cortical and subcortical structures, stretching white matter tracts (corona radiata, corpus callosum, anterior thalamic radiation), and reducing volume and perfusion of the caudate, putamen, and nucleus accumbens (Del Giovane et al., 2026; Pearce et al., 2024; Peterson et al., 2019). This explains why apathy and psychomotor slowing dominate the picture, and why some symptoms reverse quickly after CSF drainage: functional network abnormalities can partially normalize within 24 hours of a tap test (Griffa et al., 2020, 2021).

Pooled prevalence estimates from the 2026 meta-analysis, all with substantial heterogeneity, are summarized below.

Symptom domainPooled prevalence (95% CI)Notes
Apathy69.2% (63.1–74.6)Most common feature; often mistaken for depression
Depression30.1% (20.1–42.3)Severity markedly greater than controls (Hedge's g 1.31)
Agitation22.6% (11.8–39.1)Few studies, wide confidence interval
Anxiety21.9% (13.2–34.2)Frequently co-occurs with depression and apathy
Disinhibition21.0% (11.8–34.7)NPI-based, small samples
Psychotic syndromes8.0% (3.3–18.3)Hallucinations, delusions, schizophrenia; all low-quality studies
OCD symptomsNot meta-analyzedProminent on SCL-90; case reports
ManiaNot meta-analyzedCase reports of “secondary mania” only

Source: Belessiotis-Richards et al., 2026; OCD and mania estimates from case reports (Kwentus & Hart, 1987; Leung et al., 2016; Markianos et al., 2009; Mishra et al., 2011; Reisch et al., 2005).

Apathy

Apathy is the signature psychiatric feature (~69%) and is clinically distinct from depression: it presents as reduced motivation, diminished goal-directed behavior, and emotional indifference without dysphoria, guilt, or rumination (Belessiotis-Richards et al., 2026; Steffens et al., 2022). It maps onto specific circuitry: right caudate hypoperfusion on SPECT, reduced postsynaptic D2-receptor binding in the nucleus accumbens on PET, and right precuneus compression on VBM. Improvement after shunting tracks with caudate reperfusion and Frontal Assessment Battery gains (Chadani et al., 2022; Kanemoto et al., 2019; Ouchi et al., 2007). Apathy also flags reversibility: apathetic patients show better gait improvement after tapping (Allali et al., 2018).

Depression

Depression (~30%, but up to 46\u201356% in some series) shows a frontal-subcortical phenotype: psychomotor retardation, lack of spontaneity, and cognitive slowing that overlaps heavily with iNPH's own cognitive profile and with late-life "vascular depression," since cardiovascular risk factors are overrepresented in iNPH (Andersson et al., 2024; Israelsson et al., 2016). In the INPH-CRasH study, suspected depression occurred in 46% of iNPH patients versus 13% of controls (adjusted OR 6.4, 95% CI 3.8\u201310.9) and was the strongest predictor of poor quality of life (Israelsson et al., 2016, 2020).

Psychosis, mania, and OCD

Psychosis (~8%) is real but atypical; the NEJM review notes that hallucinations and marked personality change are not typical of iNPH and should prompt consideration of comorbidity (Johnson & Williams, 2025). Notably, there is an epidemiologic and genetic link with schizophrenia: schizophrenia prevalence is elevated in iNPH (~3.1% vs 0.9%), and Mendelian randomization suggests shared genetic predisposition (OR 1.03, 95% CI 1.01\u20131.05) (Belessiotis-Richards et al., 2026; Vanhala et al., 2019). Mania and OCD in NPH rest on case reports only; a distinctive neurochemical finding is that CSF serotonin metabolite (5-HIAA) is normal while dopamine metabolite (HVA) is elevated, which the authors used to explain the observed lack of SSRI benefit for OCD symptoms in NPH (Markianos et al., 2009).

NPH misdiagnosed as psychiatric illness, and vice versa

The dominant misdiagnosis pathway is apathy and psychomotor slowing read as major depression, delaying recognition of a structural, potentially reversible condition (Marouf et al., 2021). People with iNPH have 2.48-fold higher odds of a recorded psychiatric diagnosis, and the adjusted odds of depression are strikingly elevated (mild OR 8.5; moderate OR 12.3; severe OR 27.8) (Belessiotis-Richards et al., 2026). The classic case literature illustrates both the trap and the payoff of correct diagnosis:

Presenting as depression
Rosen & Swigar and Price & Tucker described NPH presenting as agitated or retarded depression, with apathy, inattention, and poverty of thought mimicking depressive illness (Price & Tucker, 1977; Rosen & Swigar, 1976).
Psychosis before neurology
Pinner et al. reported a 68-year-old with paranoid psychosis and mild cognitive impairment before any neurological signs; gait disturbance and incontinence developed later, and psychosis fully remitted after lumboperitoneal shunt (Pinner et al., 1997).
Decades of misdiagnosis
Lying-Tunell described two patients with roughly 20-year psychiatric histories (one having received over 120 ECT treatments) whose psychotic symptoms ceased entirely after shunting (Lying-Tunell, 1979).
The reverse error
The 2021 NEJM case (a 70-year-old with pre-existing bipolar disorder) shows the opposite trap: attributing new gait, cognitive, and urinary decline to the known psychiatric illness. Most of his chronic mood symptoms were bipolar, while the new triad was NPH (Marouf et al., 2021).

Red flags for NPH masquerading as psychiatric disease

  • New-onset apathy, affective, or psychotic symptoms in an older adult without a prior psychiatric history
  • Gait disturbance, the usual earliest and most prevalent sign (>90%)
  • Urinary urgency
  • Insidious progression over months
  • Cognition that does not respond to psychotropic adjustment
  • MRI showing ventriculomegaly out of proportion to atrophy

(Marouf et al., 2021; Maroufi et al., 2026; Price & Tucker, 1977; Rosen & Swigar, 1976)

Differentiating NPH from primary psychiatric illness and dementia

Distinguishing apathy from depression is the central bedside task: apathy features emotional indifference, passivity, and absence of rumination, whereas depression features dysphoria, hopelessness, guilt, and often anxiety, though the two co-occur in 14\u201338% of neurocognitive disorders (Lanct\u00F4t et al., 2023; Steffens et al., 2022). Against neurodegenerative dementia, iNPH is a subcortical dementia (slowed processing, executive dysfunction, memory that benefits from cueing, preserved naming and remote memory), contrasting with Alzheimer's cortical pattern of prominent amnesia, aphasia, and agnosia (Johnson & Williams, 2025; Skalick\u00FD et al., 2020). The complication is that iNPH and Alzheimer's disease co-exist in 20\u201357% of cases, and comorbid AD reduces shunt response and blunts neuropsychiatric improvement (Belessiotis-Richards et al., 2026; Soderlund et al., 2025).

FeatureNPHPrimary depressionAlzheimer's disease
GaitWide-based, shuffling, “magnetic”; >90%Usually normal (retardation possible)Late finding
Cognitive patternFrontal-subcortical; memory aided by cuesEffort-dependent, inconsistentCortical amnesia, aphasia, agnosia
Predominant affectApathy, emotional indifferenceDysphoria, guilt, anxietyApathy, anxiety
Urinary symptomsUrgency / detrusor overactivity (75–90%)Not typicalLate
ImagingVentriculomegaly (Evans ≥0.3), DESH, acute callosal angleNormal / age-appropriateCortical + hippocampal atrophy
Response to CSF drainageGait improves within hoursNoneNone
Hallucinations / delusionsNot typical (~8%)Possible if severeMore common

(Johnson & Williams, 2025; Marouf et al., 2021; Maroufi et al., 2026; Skalick\u00FD et al., 2020; Soderlund et al., 2025)

Diagnostic workup

Imaging (MRI first-line per ACR 2024): the Evans index (\u22650.3) is a required marker of ventriculomegaly but is nonspecific (AUC 0.87), whereas an acute callosal angle (\u226490\u00B0) is far more discriminating (AUC up to 0.97); the NEJM case had a callosal angle of 66\u00B0 (Marouf et al., 2021; Soderlund et al., 2025; Zi\u00F3\u0142kowski et al., 2023). DESH (disproportionately enlarged subarachnoid space hydrocephalus) has a positive predictive value ~77% for shunt response but poor negative predictive value (~25%), and is present in ~60% of patients (Al-Tarawni et al., 2024; Johnson & Williams, 2025). A newer CT-based splenial angle showed near-perfect separation of NPH from Alzheimer's and Parkinson's diseases and controls (AUC 0.999) in a single study and awaits replication (Kaya et al., 2026).

CSF drainage tests: the high-volume tap test (30\u201350 mL) has high positive predictive value (~90%) but poor sensitivity (~58%) and negative predictive value (~20%); a negative tap does not exclude iNPH (Johnson & Williams, 2025; Mihalj et al., 2016; Zi\u00F3\u0142kowski et al., 2023). Extended lumbar drainage (24\u201372 h) reaches ~90% sensitivity and specificity and is the next step when suspicion is high but the tap is negative; the main risk is meningitis (1\u20132%) (Johnson & Williams, 2025; Maroufi et al., 2026). The NEJM diagnostic-and-treatment algorithm captures this stepwise logic, with feedback loops to reconsider alternative (including psychiatric) diagnoses when expected improvement fails to appear.

Effect of CSF shunting on psychiatric symptoms

Shunting is the definitive treatment and improves gait in 75\u201380% of patients (gait velocity up ~30%, for example 0.67 to 0.96 m/sec), with less consistent cognitive benefit (2024 Cochrane review: "unclear," SMD 0.35, 95% CI \u22120.04 to 0.74) (Maroufi et al., 2026; Pearce et al., 2024; Williams et al., 2022). Psychiatric outcomes are favorable but less robustly proven:

Depression
The pooled effect of shunting on depression scores was small and non-significant (−0.30, 95% CI −0.62 to 0.01), though individual studies show large drops (for example, prevalence 36% to 5% at 3 months). Importantly, depression remained overrepresented (46% vs 13%) at 1–3 years post-shunt in INPH-CRasH, so it does not uniformly resolve (Andersson et al., 2024; Belessiotis-Richards et al., 2026; Israelsson et al., 2016).
Apathy
Improves after shunting (for example, 86% to 73%; significant Apathy Evaluation Scale gains at 1 month in a 2026 multicenter series), correlating with cognitive improvement (Belessiotis-Richards et al., 2026; Peterson et al., 2016; Scalia et al., 2026).
Psychosis
Case reports document full remission after shunting, including decades-long psychotic illness (Lying-Tunell, 1979; Pinner et al., 1997).

The corollary is clinical: psychiatric symptoms secondary to NPH may respond to CSF diversion rather than psychotropics, so recognizing and treating the hydrocephalus comes first.

Psychotropic management in NPH

No controlled trials of any psychotropic exist specifically in iNPH, and antidepressant efficacy in this population has explicitly not been established, so management is extrapolated from geriatric and dementia evidence with NPH-specific cautions (Andersson et al., 2024; Virhammar et al., 2026).

Antipsychotics
Use with particular caution. Drug-induced parkinsonism worsens the already-impaired gait and raises fall and institutionalization risk; first-generation agents and risperidone carry the highest extrapyramidal risk, while quetiapine, aripiprazole, and olanzapine are lower-risk options. Antipsychotic sensitivity (intolerance to low doses) has been reported in NPH. Anticholinergic agents for extrapyramidal symptoms (for example, benztropine) should be avoided given cognitive risk. Comorbid schizophrenia does not preclude shunting: 75% of such patients still had a verified shunt response (Divac et al., 2014; Factor et al., 2019; Mishra et al., 2011; Rogowska et al., 2023; Vanhala et al., 2019).
Antidepressants
Avoid anticholinergic agents (tricyclics); anticholinergic antidepressants are associated with increased dementia risk (adjusted odds ratio up to 1.29) and with falls and cognitive decline in older adults. In dementia broadly, antidepressant efficacy for depression is weak, and they are ineffective (possibly harmful) for apathy. The normal CSF serotonin turnover in NPH offers a mechanistic rationale for observed SSRI ineffectiveness against OCD symptoms (Belessiotis-Richards et al., 2025; Büyükgök et al., 2026; Coupland et al., 2019; Markianos et al., 2009; Reuben et al., 2024).
Apathy
Methylphenidate has the best (albeit indirect) evidence: a double-blind single-patient study in a shunted NPH patient showed dose-dependent improvement, and multiple Alzheimer's disease RCTs support modest benefit (start 5 mg AM/noon, titrate to 10 mg BID, monitor BP/HR) (Azhar et al., 2022; Cummings et al., 2024; Keenan et al., 2005).
ECT
Appears safe and effective in NPH, including with VP shunts: a systematic review found no shunt malfunctions across 12 studies, and case reports describe marked, sustained response in both shunted and non-shunted NPH. Two caveats: ECT can transiently raise intracranial pressure (evidence is mixed), and programmable shunt valves can change setting after ECT (or MRI) and should be verified and reprogrammed; decisions should be multidisciplinary (psychiatry, anesthesia, neurosurgery) (Aksoy et al., 2025; Benn et al., 2026; Hanretta & Malek-Ahmadi, 2001; Johnson & Williams, 2025; Parker et al., 2026).
Anticholinergic burden generally
NPH patients are especially vulnerable given baseline cognitive and gait impairment. Bladder antimuscarinics (for example, oxybutynin) commonly prescribed for the urinary symptoms in 75–90% of patients add anticholinergic dementia risk (adjusted odds ratio ~1.65 at high exposure), so prefer lower-risk agents or non-pharmacologic strategies (Coupland et al., 2019; Hook et al., 2022; Maroufi et al., 2026).

Evidence gaps and emerging data

The field's central weakness is the absence of controlled psychotropic trials in NPH and reliance on low-quality, heterogeneous observational data for shunting's psychiatric benefit (Belessiotis-Richards et al., 2026). Psychosis remission after shunting and methylphenidate for apathy rest on case-level evidence needing replication (Keenan et al., 2005; Pinner et al., 1997). Screening for depression should be built into the iNPH workup, and the effect of antidepressant treatment in this population is a stated research priority (Israelsson et al., 2016, 2020). Emerging genetic (shared schizophrenia/iNPH liability), CSF proteomic, and dopaminergic-imaging work may eventually clarify whether psychiatric symptoms are caused by, comorbid with, or mechanistically shared with the hydrocephalus (Belessiotis-Richards et al., 2026; de Geus et al., 2025; Lee et al., 2020).

Summary

Psychiatric symptoms, led by apathy (~69%) and depression (~30%), with less common psychosis (~8%) and rare mania/OCD, are intrinsic to iNPH and reflect frontal-subcortical circuit disruption (Belessiotis-Richards et al., 2026; Peterson et al., 2019). Because NPH readily mimics depression and dementia and can be misread as primary psychiatric illness (and vice versa), an older adult with new apathy, affective, or psychotic symptoms plus gait disturbance, urinary urgency, and disproportionate ventriculomegaly warrants an NPH workup (MRI with callosal angle and DESH assessment, then tap test or extended lumbar drainage) (Johnson & Williams, 2025; Maroufi et al., 2026; Zi\u00F3\u0142kowski et al., 2023). Shunting is first-line and can improve, and sometimes remit, psychiatric symptoms, though depression may persist (Belessiotis-Richards et al., 2026; Israelsson et al., 2016). Psychotropics have no NPH-specific trial base; when used, minimize anticholinergic and extrapyramidal risk, consider methylphenidate for apathy, and regard ECT as safe with attention to programmable-valve settings (Keenan et al., 2005; Mishra et al., 2011; Parker et al., 2026).

References

  1. Aksoy, I., Lafli Tunay, D., & Aksoy, M. (2025). Monitoring intracranial pressure change through optic nerve sheath ultrasound during electroconvulsive therapy. The Journal of ECT. doi.org/10.1097/YCT.0000000000001187
  2. Al-Tarawni, F., Abdulbaki, A., Polemikos, M., et al. (2024). Idiopathic normal pressure hydrocephalus: survey on current diagnostic and therapeutic procedures in clinical practice in Germany. Acta Neurochirurgica, 166(1), 477. doi.org/10.1007/s00701-024-06354-x
  3. Allali, G., Laidet, M., Armand, S., et al. (2018). Apathy in idiopathic normal pressure hydrocephalus: A marker of reversible gait disorders. International Journal of Geriatric Psychiatry, 33(5), 735-742. doi.org/10.1002/gps.4847
  4. Andersson, J., Maripuu, M., Sjövill, M., Lindam, A., & Laurell, K. (2024). Depressive symptoms, functional impairment, and health-related quality of life in idiopathic normal pressure hydrocephalus: A population-based study. PLoS One, 19(7), e0308079. doi.org/10.1371/journal.pone.0308079
  5. Azhar, L., Kusumo, R. W., Marotta, G., Lanctôt, K. L., & Herrmann, N. (2022). Pharmacological management of apathy in dementia. CNS Drugs, 36(2), 143-165. doi.org/10.1007/s40263-021-00883-0
  6. Belessiotis-Richards, C., Brady, E., Abrol, E., et al. (2026). Neuropsychiatric features in patients with idiopathic normal pressure hydrocephalus: A systematic review and meta-analysis. Neurology: Clinical Practice, 16(2), e200586. doi.org/10.1212/CPJ.000000000000200586
  7. Belessiotis-Richards, C., Hayes, J., Feng Yap, Y., et al. (2025). Systemic medications and dementia risk: a systematic umbrella review. Molecular Psychiatry, 30(11), 5578-5599. doi.org/10.1038/s41380-025-03129-3
  8. Benn, K. W., Wong, R., Bevan, M., & Chong, T. W. H. (2026). Electroconvulsive therapy ameliorates neuropsychiatric symptoms in an older adult patient with nonshunted normal pressure hydrocephalus. The Journal of ECT. doi.org/10.1097/YCT.0000000000001227
  9. Büyükgök, D., Ince Guliyev, E., & Bilgiç, B. (2026). Apathy in dementia: Pharmacological and nonpharmacological treatment strategies. Current Opinion in Psychiatry, 39(2), 160-167. doi.org/10.1097/YCO.0000000000001054
  10. Chadani, Y., Kashibayashi, T., Yamamoto, T., et al. (2022). Association of right precuneus compression with apathy in idiopathic normal pressure hydrocephalus: a pilot study. Scientific Reports, 12(1), 20428. doi.org/10.1038/s41598-022-23800-x
  11. Coupland, C. A. C., Hill, T., Dening, T., et al. (2019). Anticholinergic drug exposure and the risk of dementia: A nested case-control study. JAMA Internal Medicine, 179(8), 1084-1093. doi.org/10.1001/jamainternmed.2019.0677
  12. Cummings, J., Lanctot, K., Grossberg, G., & Ballard, C. (2024). Progress in pharmacologic management of neuropsychiatric syndromes in neurodegenerative disorders: A review. JAMA Neurology, 81(6), 645-653. doi.org/10.1001/jamaneurol.2024.0586
  13. de Geus, M. B., Wu, C. Y., Dodge, H., et al. (2025). Unbiased CSF proteomics in patients with idiopathic normal pressure hydrocephalus to identify molecular signatures and candidate biomarkers. Neurology, 104(5), e213375. doi.org/10.1212/WNL.00000000000213375
  14. Del Giovane, M., Darvishi, V., David, M. C. B., et al. (2026). Modelling the effect of ventricular expansion on white matter in normal pressure hydrocephalus. Brain, awag312. doi.org/10.1093/brain/awag312
  15. Divac, N., Prostran, M., Jakovcevski, I., & Cerovac, N. (2014). Second-generation antipsychotics and extrapyramidal adverse effects. BioMed Research International, 2014, 656370. doi.org/10.1155/2014/656370
  16. Factor, S. A., Burkhard, P. R., Caroff, S., et al. (2019). Recent developments in drug-induced movement disorders: A mixed picture. The Lancet Neurology, 18(9), 880-890. doi.org/10.1016/S1474-4422(19)30152-8
  17. Griffa, A., Bommarito, G., Assal, F., et al. (2021). Dynamic functional networks in idiopathic normal pressure hydrocephalus: Alterations and reversibility by CSF tap test. Human Brain Mapping, 42(5), 1485-1502. doi.org/10.1002/hbm.25308
  18. Griffa, A., Van De Ville, D., Herrmann, F. R., & Allali, G. (2020). Neural circuits of idiopathic normal pressure hydrocephalus: A perspective review of brain connectivity and symptoms meta-analysis. Neuroscience and Biobehavioral Reviews, 112, 452-471. doi.org/10.1016/j.neubiorev.2020.02.023
  19. Hanretta, A. T., & Malek-Ahmadi, P. (2001). Successful ECT in a patient with hydrocephalus, shunt, hypopituitarism, and paraplegia. The Journal of ECT, 17(1), 71-4. doi.org/10.1097/00124509-200103000-00016
  20. Hook, A., Randall, J. L., Grubb, C. M., et al. (2022). Anti-cholinergic drug burden in patients with dementia increases after hospital admission: a multicentre cross-sectional study. BMC Geriatrics, 22(1), 783. doi.org/10.1186/s12877-022-03235-9
  21. Israelsson, H., Allard, P., Eklund, A., & Malm, J. (2016). Symptoms of depression are common in patients with idiopathic normal pressure hydrocephalus: The INPH-CRasH study. Neurosurgery, 78(2), 161-8. doi.org/10.1227/NEU.0000000000001093
  22. Israelsson, H., Larsson, J., Eklund, A., & Malm, J. (2020). Risk factors, comorbidities, quality of life, and complications after surgery in idiopathic normal pressure hydrocephalus: Review of the INPH-CRasH study. Neurosurgical Focus, 49(4), E8. doi.org/10.3171/2020.7.FOCUS20466
  23. Johnson, M. D., & Williams, M. A. (2025). Idiopathic normal-pressure hydrocephalus. The New England Journal of Medicine, 393(22), 2243-2253. doi.org/10.1056/NEJMra2306506
  24. Kanemoto, H., Kazui, H., Suehiro, T., et al. (2019). Apathy and right caudate perfusion in idiopathic normal pressure hydrocephalus: A case-control study. International Journal of Geriatric Psychiatry, 34(3), 453-462. doi.org/10.1002/gps.5038
  25. Kaya, M., Konukoglu, O., Genç, H., Cindemir, E., & Onay, M. (2026). Differentiation of normal pressure hydrocephalus from Alzheimer's and Parkinson's diseases using the splenial angle measured on brain CT: diagnostic performance and reliability study. Neuroradiology, 68(7), 1787-1797. doi.org/10.1007/s00234-026-04018-4
  26. Keenan, S., Mavaddat, N., Iddon, J., Pickard, J. D., & Sahakian, B. J. (2005). Effects of methylphenidate on cognition and apathy in normal pressure hydrocephalus: A case study and review. British Journal of Neurosurgery, 19(1), 46-50. doi.org/10.1080/02688690500080893
  27. Kwentus, J. A., & Hart, R. P. (1987). Normal pressure hydrocephalus presenting as mania. The Journal of Nervous and Mental Disease, 175(8), 500-2. doi.org/10.1097/00005053-198708000-00010
  28. Lanctôt, K. L., Ismail, Z., Bawa, K. K., et al. (2023). Distinguishing apathy from depression: A review differentiating the behavioral, neuroanatomic, and treatment-related aspects of apathy from depression in neurocognitive disorders. International Journal of Geriatric Psychiatry, 38(2), e5882. doi.org/10.1002/gps.5882
  29. Lee, J. Y., Park, S. B., Lee, M., et al. (2020). Detailed visual assessment of striatal dopaminergic depletion in patients with idiopathic normal pressure hydrocephalus: unremarkable or not? BMC Neurology, 20(1), 277. doi.org/10.1186/s12883-020-01861-7
  30. Leung, A., Bleakley, C., Loh, A., Saran, K., & Stewart, S. E. (2016). Pediatric obsessive-compulsive disorder exacerbation and obstructive hydrocephalus: A case report. Pediatrics, 138(4), e20160558. doi.org/10.1542/peds.2016-0558
  31. Lying-Tunell, U. (1979). Psychotic symptoms in normal-pressure hydrocephalus. Acta Psychiatrica Scandinavica, 59(4), 415-9. doi.org/10.1111/j.1600-0447.1979.tb04483.x
  32. Markianos, M., Lafazanos, S., Koutsis, G., Sfagos, C., & Seretis, A. (2009). CSF neurotransmitter metabolites and neuropsychiatric symptomatology in patients with normal pressure hydrocephalus. Clinical Neurology and Neurosurgery, 111(3), 231-4. doi.org/10.1016/j.clineuro.2008.10.001
  33. Marouf, F., Glover, M., Wininger, B., & Curry, W. T. (2021). Case 10-2021: A 70-year-old man with depressed mood, unsteady gait, and urinary incontinence. The New England Journal of Medicine, 384(14), 1350-1358. doi.org/10.1056/NEJMcpc2027090
  34. Maroufi, S. F., Yasar, S., Moghekar, A., & Luciano, M. G. (2026). Idiopathic normal pressure hydrocephalus: A review. JAMA. doi.org/10.1001/jama.2026.15519
  35. Mihalj, M., Dolić, K., Kolić, K., & Ledenko, V. (2016). CSF tap test – obsolete or appropriate test for predicting shunt responsiveness? A systematic review. Journal of the Neurological Sciences, 362, 78-84. doi.org/10.1016/j.jns.2016.01.028
  36. Mishra, B. R., Sarkar, S., Mishra, S., et al. (2011). Antipsychotic sensitivity in normal pressure hydrocephalus. General Hospital Psychiatry, 33(1), 83.e11-3. doi.org/10.1016/j.genhosppsych.2010.09.014
  37. Ouchi, Y., Nakayama, T., Kanno, T., et al. (2007). In vivo presynaptic and postsynaptic striatal dopamine functions in idiopathic normal pressure hydrocephalus. Journal of Cerebral Blood Flow and Metabolism, 27(4), 803-10. doi.org/10.1038/sj.jcbfm.9600389
  38. Parker, T., Mensah, E., St Brice, K., et al. (2026). Safety of electroconvulsive therapy with implanted ventricular shunts: A systematic review and case series. The Journal of ECT. doi.org/10.1097/YCT.0000000000001171
  39. Pearce, R. K. B., Gontsarova, A., Richardson, D., et al. (2024). Shunting for idiopathic normal pressure hydrocephalus. The Cochrane Database of Systematic Reviews, 8, CD014923. doi.org/10.1002/14651858.CD014923.pub2
  40. Peterson, K. A., Housden, C. R., Killikelly, C., et al. (2016). Apathy, ventriculomegaly and neurocognitive improvement following shunt surgery in normal pressure hydrocephalus. British Journal of Neurosurgery, 30(1), 38-42. doi.org/10.3109/02688697.2015.1029429
  41. Peterson, K. A., Mole, T. B., Keong, N. C. H., et al. (2019). Structural correlates of cognitive impairment in normal pressure hydrocephalus. Acta Neurologica Scandinavica, 139(3), 305-312. doi.org/10.1111/ane.13052
  42. Pinner, G., Johnson, H., Bouman, W. P., & Isaacs, J. (1997). Psychiatric manifestations of normal-pressure hydrocephalus: A short review and unusual case. International Psychogeriatrics, 9(4), 465-70. doi.org/10.1017/s1041610297004602
  43. Price, T. R., & Tucker, G. J. (1977). Psychiatric and behavioral manifestations of normal pressure hydrocephalus. A case report and brief review. The Journal of Nervous and Mental Disease, 164(1), 51-5. doi.org/10.1097/00005053-197701000-00009
  44. Reisch, T., Brekenfeld, C., & Barth, A. (2005). A case of hydrocephalus occlusus presenting as bipolar disorder. Acta Psychiatrica Scandinavica, 112(2), 159-62. doi.org/10.1111/j.1600-0447.2004.00480.x
  45. Reuben, D. B., Kremen, S., & Maust, D. T. (2024). Dementia prevention and treatment: A narrative review. JAMA Internal Medicine, 184(5), 563-572. doi.org/10.1001/jamainternmed.2023.8522
  46. Rogowska, M., Thornton, M., Creese, B., et al. (2023). Implications of adverse outcomes associated with antipsychotics in older patients with dementia: A 2011-2022 update. Drugs & Aging, 40(1), 21-32. doi.org/10.1007/s40266-022-00992-5
  47. Rosen, H., & Swigar, M. E. (1976). Depression and normal pressure hydrocephalus. A dilemma in neuropsychiatric differential diagnosis. The Journal of Nervous and Mental Disease, 163(1), 35-40. doi.org/10.1097/00005053-197607000-00005
  48. Scalia, G., Pitoia, R., Passarello, L., et al. (2026). Early cognitive, functional, and behavioral changes after ventriculoperitoneal shunt surgery in idiopathic normal pressure hydrocephalus: A multicenter prospective study. World Neurosurgery, 213, 125181. doi.org/10.1016/j.wneu.2026.125181
  49. Skalický, P., Mládek, A., Vlasák, A., et al. (2020). Normal pressure hydrocephalus: an overview of pathophysiological mechanisms and diagnostic procedures. Neurosurgical Review, 43(6), 1451-1464. doi.org/10.1007/s10143-019-01201-5
  50. Soderlund, K. A., Austin, M. J., Ben-Haim, S., et al. (2025). ACR Appropriateness Criteria® Dementia: 2024 update. Journal of the American College of Radiology, 22(5S), S202-S233. doi.org/10.1016/j.jacr.2025.02.031
  51. Steffens, D. C., Fahed, M., Manning, K. J., & Wang, L. (2022). The neurobiology of apathy in depression and neurocognitive impairment in older adults: a review of epidemiological, clinical, neuropsychological and biological research. Translational Psychiatry, 12(1), 525. doi.org/10.1038/s41398-022-02292-3
  52. Vanhala, V., Junkkari, A., Korhonen, V. E., et al. (2019). Prevalence of schizophrenia in idiopathic normal pressure hydrocephalus. Neurosurgery, 84(4), 883-889. doi.org/10.1093/neuros/nyy147
  53. Virhammar, J., Fasth, O., Ekblom, M., et al. (2026). Safety, tolerability, and efficacy of acetazolamide in idiopathic normal pressure hydrocephalus (DRAIN) in Sweden: A randomised, double-blind, placebo-controlled, phase 2 trial. The Lancet Neurology, 25(6), 550-559. doi.org/10.1016/S1474-4422(26)00126-2
  54. Williams, M. A., Nagel, S. J., Golomb, J., et al. (2022). Safety and effectiveness of the assessment and treatment of idiopathic normal pressure hydrocephalus in the adult hydrocephalus clinical research network. Journal of Neurosurgery, 137(5), 1289-1301. doi.org/10.3171/2022.1.JNS212782
  55. Ziółkowski, A., Kasprowicz, M., Czosnyka, M., & Czosnyka, Z. (2023). Brain blood flow pulse analysis may help to recognize individuals who suffer from hydrocephalus. Acta Neurochirurgica, 165(12), 4045-4054. doi.org/10.1007/s00701-023-05839-5