As cancer survival rates improve, there is a growing focus on the psychosocial and cognitive effects of long-term toxicity from cancer treatment. Consequently, cancer is increasingly being regarded as a chronic condition, with toxicity clinics established across Europe to address the rising demand for long-term psychosocial and cognitive support. This presentation will share the findings of a systematic review that examined symptoms of late radiation brain injury, while emphasising the importance of including neuropsychologists in existing psychosocial models of care and survivorship.

Idiopathic normal pressure hydrocephalus (iNPH) is a reversible neurological condition characterised by a classic clinical triad comprising progressive gait disturbance, cognitive impairment, and urinary incontinence, which may occur in varying combinations and degrees. These symptoms are associated with enlarged cerebral ventricles in the absence of raised intracranial pressure. The precise aetiology and underlying pathophysiological mechanisms are not well understood (Bubenikova et al., 2025). Timely and accurate diagnosis may lead to the reversal of symptoms through ventricular shunting.

Additional diagnostic testing is required to assist with selection of suitable patients who may benefit from shunt surgery. Graff-Radford & Jones (2019) suggest that the most important investigations are the MRI and a lumbar puncture (LP) with high volume removal of cerebrospinal fluid (i.e., ‘lumbar CSF tap-test’ or ‘tap-testing’). A ‘tap-test’, can facilitate the recognition of the subset of patients with iNPH who may benefit from shunt surgery. A structured clinical protocol is central to the uniform clinical management of this patient group.

In 2020, a hospital wide clinical guideline was developed at Austin Health to facilitate the clinical care, treatment and management of patients requiring tap-testing for suspected iNPH, and streamline the processes involved in tap-testing. This guideline was developed with input from colleagues in neurology, neurosurgery and physiotherapy, and incorporated the Epworth Idiopathic Normal Pressure Hydrocephalus (iNPH) Neuropsychology Test Protocol (Dridan, B., & Sloan, A. 2019).

Data collected over the past five years on 30 tap-test patients using the comprehensive clinical guideline will be presented. This will aim to answer questions regarding how often improvement occurs on cognitive and physical tap-test measures, level of concordance between cognitive and physical measures, which measures best predict whether or not a patient proceeds to ventricular shunting, and clinical outcomes for those patients who do proceed to shunt surgery. Differentiating iNPH from other neurodegenerative disorders and managing overlapping comorbidities will also be discussed.

Michelle J. Francis1, Ella Rowsthorn1,2, Ben Sinclair (PhD)1,3, Meng Law (MBBS FRANZCR MD FASFNR)1,3, Robert Whiriskey (MBBS)4, Matthew P. Pase (PhD)5, and Renerus J. Stolwyk (DPsych(Clin Neuro))5

Cerebral small vessel disease (SVD) is the leading cause of vascular cognitive impairment, yet its cognitive impact in community-dwelling older adults with mild, incidentally detected pathology remains poorly characterised. Most existing evidence derives from clinical cohorts with advanced disease, limiting understanding of the early disease spectrum.

This study examined associations between SVD severity and cognitive performance across seven domains in 241 community-dwelling adults aged 55–80 years (M = 67.1, SD = 5.15; 51% women) from the Brain and Cognitive Health (BACH) cohort. Participants underwent comprehensive neuropsychological assessment and 3T MRI on the same day. SVD was quantified using four markers (white matter hyperintensities, lacunes, cerebral microbleeds, enlarged perivascular spaces) and a composite burden score
Consistent with the community-based sample, SVD burden was predominantly low: 60% of participants scored 0 (none), 27% scored 1 (mild), and 10% scored 2 (moderate), with fewer than 3% reaching scores of 3–4 (severe). Due to the low prevalence of moderate-to-severe pathology, regression analyses were restricted to well-represented severity groups (n ≥ 30), meaning findings characterise the none-to-mild end of the SVD spectrum.

Cognitive performance was expressed using demographically-adjusted normative standardised scores. Across all SVD markers and burden levels, group means fell within the average to above-average normative range (i.e., performing comparably to or better than same-aged peers), with no systematic increase in below-normative performance as SVD burden increased. A priori, multiple linear regression models adjusted for age and sex revealed no statistically significant associations between SVD severity and cognitive performance after Bonferroni correction. In sensitivity analyses without correction, nominally significant effects (uncorrected p = .015–.035) were observed for overall SVD burden with executive function, and periventricular white matter hyperintensity severity with cognitive screener performance; in each case, higher SVD burden was associated with modestly lower scores, but none survived correction and effect sizes were small.

These findings support a staging model in which cognitive impairment emerges only beyond a critical burden threshold, and supports preserved cognitive function across a range of mild SVD pathologies.