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. 2026 Feb 26;6(1):100334. doi: 10.1016/j.ynirp.2026.100334

Case report: Hemodynamic dynamics in central variant PRES via serial ASL/DTI

Xueping Lu a,b, Kai Tang c, Qiao Wang d, Wenyu Wang a,e, Xinling Xie a, Changqing Zhan a,⁎
PMCID: PMC12964009  PMID: 41799259

Abstract

Background

Central variant posterior reversible encephalopathy syndrome (PRES) is a rare subtype (4% of cases) affecting brainstem and deep structures, presenting with severe hypertension but minimal neurological deficits, creating diagnostic challenges.

Case presentation

A 34-year-old man presented with a two-month history of severe, refractory headache and malignant hypertension (256/150 mmHg). Brain MRI revealed diffuse T2-weighted and FLAIR hyperintensity in the pons and right middle cerebellar peduncle (MCP). Using serial arterial spin labeling (ASL) and diffusion tensor imaging (DTI), we provide the first longitudinal evidence of acute-phase biphasic hemodynamics in central variant PRES: concurrent pontine CBF of 27.1 mL/100 g/min (contralateral reference: 25.2 ± 1.8 mL/100 g/min) and right MCP CBF of 29.3 mL/100 g/min (contralateral reference: 39.1 ± 2.1 mL/100 g/min). This regional perfusion imbalance is consistent with autoregulatory failure and blood-brain barrier (BBB) compromise, leading to vasogenic edema. Critically, the coexistence of these opposing patterns reveals complementary hemodynamic phenotypes of cerebrovascular dysregulation. Post-treatment, pontine CBF was 25.3 mL/100 g/min (contralateral reference: 25.3 ± 1.8 mL/100 g/min) and right MCP CBF was 38.6 mL/100 g/min (contralateral reference: 39.2 ± 2.2 mL/100 g/min), both within the reference range of the contralateral regions, accompanied by progressive increase of fractional anisotropy (FA) on DTI at both the 6-day and 90-day follow-up imaging time points.

Conclusion

This case demonstrates biphasic hemodynamic changes in central variant PRES, supporting autoregulatory failure as the mechanism. Serial ASL/DTI provide valuable biomarkers for monitoring recovery in this rare phenotype.

Keywords: Arterial spin labeling, Central variant, Diffusion tensor imaging, Posterior reversible encephalopathy syndrome

1. Background

Posterior reversible encephalopathy syndrome (PRES) is a clinico-radiological entity characterized by acute neurological symptoms – including headache, altered mental status, seizures, and visual disturbances – accompanied by reversible vasogenic edema predominantly affecting posterior cerebral regions (Triplett et al., 2022; Hugonnet et al., 2013). Initially termed reversible posterior leukoencephalopathy syndrome (RPLS) due to symptom reversibility with treatment (Hinchey et al., 1996), PRES is now recognized to involve regions beyond the classic parieto-occipital areas. McKinney et al. (2007) identified a distinct “central variant PRES” subtype affecting the brainstem, basal ganglia, thalamus, cerebellum, and posterior limb of the internal capsule (McKinney et al., 2007). The pathophysiology centers on cerebrovascular autoregulatory failure, though the initiating mechanism remains debated (Fugate and Rabinstein, 2015; Sheikh-Bahaei et al., 2020). Advanced neuroimaging techniques, such as arterial spin labeling (ASL) and diffusion tensor imaging (DTI), are particularly suited to investigate the hemodynamic and microstructural underpinnings of PRES (Fazeli et al., 2022; Utsunomiya, 2011). ASL provides a non-invasive, quantitative measure of cerebral blood flow (CBF), enabling the evaluation of perfusion abnormalities central to autoregulatory dysfunction (Wang et al., 2023). DTI, by quantifying the directionality of water diffusion, offers insights into white matter microstructural integrity, which can be compromised by vasogenic edema (Keijzer et al., 2023). According to the hyperperfusion theory, severe hypertension exceeding autoregulatory capacity leads to vasodilation, endothelial injury, and blood-brain barrier (BBB) disruption (Fugate and Rabinstein, 2015; Fazeli et al., 2022). Conversely, the hypoperfusion theory proposes that cerebral vasospasm triggered by hypertension, neurotoxins, or systemic inflammation causes ischemia and subsequent vasogenic edema (Sheikh-Bahaei et al., 2020; Sarbu et al., 2014; Brubaker et al., 2005; Vanacker et al., 2015; Bartynski and Boardman, 2008). These mechanisms are not mutually exclusive.

Given the extreme rarity of central variant PRES and the absence of longitudinal data regarding its imaging characteristics and hemodynamic changes, reporting such cases is essential to advance understanding of this condition and its potential pathogenesis.

2. Case presentation

A 34-year-old man presented with a two-month history of persistent, severe headache refractory to analgesics. Neurological examination revealed no focal deficits, cerebellar signs, or meningeal irritation. On admission, his blood pressure was 256/150 mmHg measured in the supine position, consistent with malignant hypertension. Brain MRI was performed on a 3.0 T Philips scanner (Philips Healthcare) using an 8-channel brain phased-array coil. The imaging protocol included T1-weighted, T2-weighted, fluid-attenuated inversion recovery (FLAIR), and diffusion-weighted imaging (DWI) sequences. ASL was performed using a pseudo-continuous labeling (pCASL) sequence with a single post-labeling delay (PLD) of 1800 ms and a labeling duration of 1800 ms, employing a 2D Echo Planar Imaging (EPI) readout. An M0 image was acquired as a reference for CBF quantification to improve reproducibility. Diffusion tensor imaging (DTI) was acquired using a single-shot spin-echo echo-planar imaging sequence with a maximum b-value of 1000 s/mm2 along 30 non-collinear directions, plus one non-diffusion-weighted volume (b = 0 s/mm2).

Brain MRI (Fig. 1) showed diffuse T2-weighted and FLAIR hyperintensity in the pons, with prominent involvement of the right middle cerebellar peduncle (MCP). To ensure accurate anatomical correspondence across time points, a dedicated image processing and co-registration pipeline was employed. First, the regions of interest (ROIs) delineating the lesions in the pons and right MCP were manually drawn on the acute-phase FLAIR images using ITK-SNAP software (version 3.8.0). Subsequently, all follow-up FLAIR, ASL CBF, and DTI FA maps were rigidly co-registered to the acute-phase FLAIR space using SPM12 (Statistical Parametric Mapping) with normalized mutual information as the cost function. ASL revealed altered CBF in the affected regions: 29.3 mL/100 g/min in the right MCP and 27.1 mL/100 g/min in the central pons. Quantitative region-of-interest (ROI) analysis was performed on the contralateral normal-appearing cerebellar peduncle and pons. All ROIs were manually delineated on the acute-phase FLAIR images. To ensure anatomical consistency across time points, the same ROI masks were then coregistered and applied to the corresponding follow-up images, as described in the co-registration pipeline above. Mean CBF values were 39.1 ± 2.1 mL/100 g/min for the cerebellar peduncle and 25.2 ± 1.8 mL/100 g/min for the pons. These values, obtained from the contralateral homologous regions in the same patient, are consistent with established normative CBF ranges for brainstem and cerebellar peduncle structures (Approximate normative ranges for brainstem: 24.5 ± 0.6 mL/100 g/min; for cerebellar peduncles: 59 ± 17 mL/100 g/min) (Biagi et al., 2007; Zhang et al., 2010). DTI demonstrated fractional anisotropy (FA) within the lesions of 0.29 in the right middle cerebellar peduncle and 0.36 in the central pons. These values were outside those in the reference ROIs in the contralateral regions (0.52 ± 0.03 and 0.53 ± 0.04, respectively), suggesting potential microstructural alterations within the affected pontocerebellar white matter pathways. Intracranial MRA showed no vasospasm, stenosis, or occlusion. Cerebrospinal fluid obtained via lumbar puncture revealed mildly elevated protein (747.5 mg/L; reference <450 mg/L) with normal cell count and glucose, arguing against an infectious process. Extensive serological testing for infectious (HIV, syphilis, common viral encephalitides) and autoimmune/paraneoplastic etiologies (ANA, ANCA, anti-NMDA receptor, anti-AQP4 antibodies) was negative. Following intensive antihypertensive therapy, his blood pressure gradually normalized and the headache completely resolved.

Fig. 1.

Fig. 1

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Brain MRI on admission. (A–G) Right middle cerebellar peduncle: The lesion appeared hypointense on T1-weighted imaging (A) and hyperintense on T2-weighted (B) and FLAIR (C) sequences. On diffusion imaging, the lesion showed corresponding isointensity on diffusion-weighted imaging (DWI) (D) and hyperintensity on the apparent diffusion coefficient (ADC) map derived from diffusion tensor imaging (DTI) (E), findings consistent with vasogenic edema. Arterial spin labeling (ASL) (F) showed cerebral blood flow (CBF) of 29.3 ± 5.6 mL/100 g/min. Diffusion tensor imaging (DTI) (G) showed fractional anisotropy (FA) of 0.29 ± 0.15, indicating potential microstructural alteration in the pontocerebellar white matter tracts. (H–N) Central pons: The lesion was hypointense on T1-weighted imaging (H) and hyperintense on T2-weighted (I) and FLAIR (J) sequences, displaying longitudinal striations. On diffusion imaging, corresponding isointensity on DWI (K) and hyperintensity on the ADC map from DTI (L) were observed. ASL (M) showed CBF of 27.1 ± 4.5 mL/100 g/min. DTI (N) showed FA of 0.36 ± 0.11.

Day 6 follow-up MRI (Fig. 2) revealed a marked reduction in both the extent and signal intensity of the pontine T2/FLAIR hyperintensity. ASL showed right MCP CBF was 33.3 mL/100 g/min (admission: 29.3 mL/100 g/min) and pontine CBF was 25.4 mL/100 g/min (admission: 27.1 mL/100 g/min). Reference CBF values in contralateral normal-appearing regions remained largely unchanged (39.1 ± 2.0 mL/100 g/min and 25.2 ± 1.7 mL/100 g/min). DTI showed FA of 0.48 in the right MCP and 0.52 in the central pons. Reference FA in the contralateral normal regions also showed no significant change (0.52 ± 0.02 and 0.53 ± 0.03, respectively).

Fig. 2.

Fig. 2

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Brain MRI at the 6-day follow-up. A reduction in lesion size and signal intensity was observed on both T2-weighted and FLAIR sequences. (A–G) Right middle cerebellar peduncle: ASL (F) showed CBF of 33.3 ± 3.6 mL/100 g/min. DTI (G) showed FA of 0.48 ± 0.19. (H–N) Central pons: ASL (M) showed CBF of 25.4 ± 5.8 mL/100 g/min. DTI (N) showed FA of 0.52 ± 0.13.

The 90-day follow-up MRI (Fig. 3) showed complete radiological resolution of the pontine lesion on T2-weighted and FLAIR sequences. ASL revealed right MCP CBF of 38.6 mL/100 g/min and pontine CBF of 25.3 mL/100 g/min, both within the reference range of the contralateral regions (39.2 ± 2.2 and 25.3 ± 1.8 mL/100 g/min, respectively). DTI showed FA of 0.51 in the right MCP and 0.54 in the central pons, values within the reference range of the contralateral regions (0.52 ± 0.03 and 0.53 ± 0.02, respectively).

Fig. 3.

Fig. 3

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Brain MRI at the 90-day follow-up. T2-weighted and FLAIR sequences showed complete resolution of the pontine lesion. (A–G) Right middle cerebellar peduncle: ASL (F) showed CBF of 38.6 ± 6.9 mL/100 g/min. DTI (G) showed FA of 0.51 ± 0.23. (H–N) Central pons: ASL (M) showed CBF of 25.3 ± 5.5 mL/100 g/min. DTI (N) showed FA of 0.54 ± 0.16.

3. Discussion

Central variant PRES, representing roughly 4% of cases (McKinney et al., 2013), predominantly involves the brainstem and/or basal ganglia, with possible extension to the thalamus, cerebellum, or internal capsule (McKinney et al., 2007; Perera et al., 2025). Patients with the central variant of PRES typically present with marked acute hypertension (mean blood pressure, 196/121 mmHg) — a level substantially higher than that in classic PRES with parieto-occipital involvement (mean, 157/100 mmHg) — yet they exhibit minimal focal neurological deficits (Moon et al., 2013). This clinicoradiological dissociation increases the risk of misdiagnosis as encephalitis, demyelinating disease, or vasculitis (Zhang et al., 2016). Although parieto-occipital involvement predominates overall (∼98%), the central variant PRES is distinguished by brainstem and deep gray matter edema (McKinney et al., 2007; Bartynski and Boardman, 2007; Chaudhari et al., 2022).

This report represents the first case utilizing ASL to longitudinally document the dynamic evolution of cerebral perfusion within the culprit lesions of central variant PRES. It demonstrates that, compared to contralateral homologous regions, relatively low CBF in the right MCP and relatively high CBF in the pons coexisted during the acute phase, suggesting spatially heterogeneous autoregulatory failure. Most previous studies suggest that cerebrovascular autoregulatory dysfunction plays a central role in the pathogenesis of PRES, although the initial triggering event remains controversial (Fazeli et al., 2022; Hawkes et al., 2023).

The predominant theory posits that severe hypertension, which exceeds the upper limit of cerebral autoregulation, leads to hyperperfusion, endothelial dysfunction, and ultimately the disruption of the blood-brain barrier (Bogdanov and Khasanov, 2020; Seemiller and Malik, 2021). This disruption allows for the extravasation of plasma and macromolecules. This theory is supported by the high prevalence of hypertension among PRES patients, the rapid resolution of clinical and imaging abnormalities following blood pressure reduction (Temel et al., 2024) (Mizuma et al., 2016; Srichawla et al., 2025), and findings of cerebral hyperperfusion, evidenced by increased CBF and cerebral blood volume (CBV) within lesions in some studies (Vanacker et al., 2015; Bazhu et al., 2022; Katsuki et al., 2021).

An alternative hypothesis proposes that cerebrovascular vasoconstriction and hypoperfusion are the primary events, leading to cerebral ischemia and subsequent vasogenic edema (Vanacker et al., 2015; Singhal, 2021; Alberte-Woodward et al., 2021). In this context, the observed cerebral hypoperfusion may reflect an exaggerated compensatory vasoconstrictive response to endothelial dysfunction induced by hypertension, nephrotoxic agents (e.g., tacrolimus), or circulating inflammatory factors (e.g., during sepsis) (Alberte-Woodward et al., 2021; Marra et al., 2014; Bartynski, 2008; Chaudhuri et al., 2023).

However, existing studies universally lack direct longitudinal data on the evolution of cerebral blood perfusion within the culprit lesions of PRES. By employing ASL and DTI, this case report provides detailed longitudinal data that document the dynamic changes in cerebral perfusion and white matter microstructural integrity within the culprit lesions of a PRES patient during the acute phase and following clinical improvement.

This case reveals an acute biphasic hemodynamic pattern characterized by, on ASL, pontine CBF slightly above contralateral reference and right MCP CBF clearly below contralateral reference, with subsequent convergence toward physiological perfusion levels and progressive recovery of FA on DTI. The observed regional perfusion dichotomy supports the presence of spatially heterogeneous cerebrovascular autoregulatory failure, wherein transient blood–brain barrier disruption drives vasogenic edema. The parallel normalization of both perfusion and microstructural metrics aligns with a phased restoration of autoregulatory function.

Beyond elucidating the pathophysiology of autoregulatory failure, advanced imaging holds promise for guiding clinical management. For example, assessing cerebrovascular reactivity (CVR) using ASL with a vasodilatory challenge (e.g., acetazolamide or CO2) in recovered patients could help quantify residual autoregulatory reserve and identify individuals at risk of recurrence. Furthermore, integrating quantitative ASL and DTI metrics into diagnostic protocols may enhance the specificity of MRI in atypical PRES presentations, potentially reducing dependence on invasive diagnostic procedures. Future studies should focus on validating these imaging biomarkers in larger cohorts and exploring their utility in monitoring treatment response and predicting long-term clinical outcomes.

Several limitations of this study should be acknowledged. Firstly, the interpretation of pontine CBF being slightly above the contralateral reference must be tempered by the inherent physiological variability of ASL-derived cerebral blood flow (typically 10–20% within subjects) (Berjón et al., 2025), which may constrain definitive conclusions regarding a relative hyperperfused state based on a single time point, although the serial imaging trend supports a dynamic hemodynamic shift. Secondly, as a single case report, the findings lack statistical validation and generalizability. Larger cohort studies are required to confirm the prevalence and significance of the observed biphasic perfusion pattern. Thirdly, the anterior pontine region of interest may be susceptible to field inhomogeneity artifacts inherent to 2D EPI-based ASL and DTI acquisitions, which could affect the absolute accuracy of CBF and FA measurements in this specific location. This technical limitation should be considered when interpreting the quantitative data from this region.

4. Conclusion

These findings refine current pathophysiological understanding of the central variant PRES and highlight the diagnostic utility of quantitative perfusion imaging in atypical presentations with subtle or non-specific clinical signs. Early recognition facilitates timely blood pressure optimization and may avert unnecessary investigations for inflammatory or demyelinating mimics. Larger prospective cohorts integrating longitudinal ASL, permeability biomarkers, and microstructural metrics are needed to validate biphasic perfusion signatures, establish prognostic thresholds, and refine imaging-based criteria for this under-recognized phenotype.

CRediT authorship contribution statement

Xueping Lu: Writing – original draft. Kai Tang: Visualization, Validation, Software, Methodology, Formal analysis. Qiao Wang: Visualization, Software, Project administration, Methodology. Wenyu Wang: Visualization, Software, Resources, Methodology. Xinling Xie: Software, Methodology. Changqing Zhan: Writing – review & editing, Investigation, Funding acquisition, Formal analysis, Data curation, Conceptualization.

Ethical approval and consent to participate

This study was reviewed and approved by the Ethics Committee of Wuhu No. 2 People's Hospital. Written informed consent was obtained from all participants. Additionally, written consent was acquired for the publication of any potentially identifiable images or data.

Consent for publication

Written informed consent for publication was obtained from the participant(s).

Availability of data and materials

The current study did not generate or analyze any primary data sets.

Funding

This work was supported by the Wuhu Municipal Health Commission Scientific Research Fund (Grant No. WHWJ2023y034) and the Health Research Project of Anhui Province (Grant No. AHWJ2024Aa30098).

Declaration of competing interest

We declare that we have no financial and personal relationships with other people or organizations that can inappropriately influence our work, there is no professional or other personal interest of any nature or kind in any product, service and/or company that could be construed as influencing the position presented in, or the review of, the manuscript entitled.

Acknowledgments

We extend our gratitude to Kai Tang, MD (Department of Medical Imaging, The Second People's Hospital of Wuhu), for his expert neuroradiological interpretation.

Data availability

Data will be made available on request.

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Data Availability Statement

The current study did not generate or analyze any primary data sets.

Data will be made available on request.

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