Posterior fossa hematoma: CT perfusion as a tool to reveal occult intracranial hypertension and support surgical decision-making – a case report

Abstract

Background

Spontaneous posterior fossa hematoma is a neurological emergency associated with rapid deterioration from brainstem compression and localized intracranial hypertension. The resulting mass effect can reduce regional perfusion, but these changes are often not fully appreciable on non-contrast CT, and MRI is not always feasible in unstable patients. Invasive intracranial pressure (ICP) monitoring in the posterior fossa could provide direct information on compartmental pressure; however, catheter placement is technically challenging and carries risks including cerebellar hemorrhage, cerebrospinal fluid (CSF) leak, cranial nerve palsy, and brainstem contusion. Consequently, infratentorial ICP monitoring is rarely used, and treatment decisions are based on clinical examination, supratentorial ICP values, and conventional imaging, which may underestimate pressure effects. CT perfusion (CTP) offers a rapid, noninvasive method to assess regional perfusion, detect indirect signatures of occult intracranial hypertension, and identify cerebellar tissue at risk of reversible ischemia.

Case presentation

A 50-year-old woman with arterial hypertension was found comatose with a Glasgow Coma Scale (GCS) score of 3, mid-mydriatic non-reactive pupils, and absent airway protective reflexes. Non-contrast CT revealed a large right cerebellar hematoma. CT perfusion demonstrated hypoperfusion at the hematoma site, with prolonged time-to-maximum (TMAX) in the surrounding cerebellar parenchyma and reduced cerebral blood flow (CBF) despite preserved cerebral blood volume (CBV), suggesting salvageable tissue. In the absence of large-vessel stenosis, prolonged TMAX was interpreted as most consistent with reduced effective cerebral perfusion pressure, plausibly related to compartmental intracranial hypertension in the posterior fossa. Prolonged TMAX with low CBV was also observed in the ipsilateral cerebral peduncle, indicating localized ischemia likely related to upward transtentorial herniation. The patient underwent emergency external ventricular drain placement and posterior fossa decompression with hematoma evacuation. Follow-up CTP on postoperative day seven showed normalization of perfusion parameters, with improved CBV and CBF and reduced TMAX.

Conclusions

This case illustrates how CTP can complement conventional imaging in posterior fossa hematomas by providing physiological information that is otherwise difficult to obtain invasively. By revealing perfusion patterns consistent with occult compartmental intracranial hypertension and demonstrating viable tissue at risk, CTP may counterbalance prognostic nihilism and support timely surgical decision-making in patients with posterior fossa hematoma.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12883-026-04852-2.

Background

The main neurological emergencies include ischemic stroke, spontaneous intraparenchymal hemorrhage (ICH), traumatic brain injury (TBI), and subarachnoid hemorrhage (SAH) [1, 2]. In the early phases of a neurological emergency, the key questions are whether there is a mass effect with raised intracranial pressure (ICP) and whether there is a risk of macrovascular (mainly in ischemic stroke and SAH) or microvascular (mainly in TBI and ICH) malperfusion. In both situations, the common final pathway is regional cerebral ischemia [2–5].

In TBI, CT scanning and early ICP monitoring provide a reasonable approximation of the risk of ischemia and/or transtentorial herniation and help guide treatment, which is often surgical [2]. In contrast, in the management of ICH, both ICP monitoring and perfusion assessment are less standardized and are often considered of limited relevance in routine care, despite emerging data on their potential utility [5–7].

Beyond the type of emergency (stroke, ICH, SAH, TBI), the primary location of the lesion is also crucial for both diagnosis and treatment. When the pathology is primarily supratentorial, ICP monitoring is straightforward, and quantification of the volume and midline shift of a mass lesion, as well as assessment of basal cisterns, is relatively standardized [2, 5]. Conversely, when there is an infratentorial lesion with ischemic (stroke) or mass effect (ICH or TBI), MRI is usually required, either to detect early diffusion restriction or to identify descending herniation through the foramen magnum or ascending herniation through the tentorium. However, MRI is not always readily available and, in any case, requires time in a clinical setting where “time is brain” [1, 6, 8, 10]. Similarly, ICP monitoring in the posterior fossa is impractical and largely anecdotal [6, 9].

In the emergency management of patients with posterior fossa ICH, current diagnostic tools therefore appear limited [6, 7]. Spontaneous ICH is frequently associated with degenerative arterial disease and advanced age, and when it is located in the posterior fossa, diagnostic uncertainty may foster therapeutic nihilism, contributing to self-fulfilling negative prognoses [9, 11].

Prognostic grading systems such as the ICH Score include infratentorial location as a severity component; however, they do not directly reflect regional perfusion or brainstem vulnerability [12, 13].

We present a case of posterior fossa ICH in which CT perfusion (CTP) was perceived as useful both to infer the mass effect due to high ICP, supporting the decision for prompt surgical intervention, and to identify an area of viable penumbral tissue, encouraging an aggressive rather than nihilistic approach.

Case presentation

A 50-year-old woman with a history of arterial hypertension was last seen well at 7:00 PM. Before going to bed she had complained of general malaise and vomiting. At 9:19 PM, she was found unresponsive and comatose. Emergency Medical Services arrived at 9:32 PM. On initial assessment, her Glasgow Coma Scale (GCS) score was 6 (E4V1M1), with sphincter incontinence and systemic hypertension. She was intubated on the scene for airway protection.

Upon arrival at the Emergency Department, her GCS had deteriorated to 3. The pupils were isocoric, mid-mydriatic and non-reactive to light, with leftward gaze deviation and absent airway protective reflexes.

Non-contrast CT (NCCT) performed at 10:41 PM revealed a large right cerebellar and vermian hematoma with early mass effect on posterior fossa structures and displacement toward the tentorium. CT angiography excluded vascular abnormalities. CTP showed hypoperfusion in the hemorrhagic core of the right cerebellar hematoma (Fig 1, Panel 1), associated with prolonged time-to-maximum (TMAX) in the apparently normal surrounding cerebellar parenchyma. This apparently preserved tissue, despite maintained cerebral blood volume (CBV), exhibited reduced cerebral blood flow (CBF). Given the hemorrhagic nature of the lesion and the exclusion of major arterial stenosis, the prolonged TMAX in the surrounding cerebellar parenchyma was interpreted as compatible with delayed microvascular transit and reduced effective cerebral perfusion pressure (CPP). In the setting of systemic hypertension and absent large-vessel disease, compartmental intracranial hypertension within the posterior fossa was considered a plausible contributing mechanism.

Fig 1.

Panel 1 CT perfusion maps with corresponding NCCT slices in a patient with spontaneous cerebellar hematoma. CT perfusion maps show markedly prolonged TMAX in the perilesional cerebellar tissue, consistent with local HICP effects. A hemorrhagic core with a reduced CBV suggests microvascular disruption. The corresponding CBF and NCCT images confirm the hemorrhagic lesion and mass effect on the surrounding cerebellar parenchyma. Panel 2 CT perfusion maps with corresponding NCCT slices illustrating supratentorial perfusion changes in a patient with a spontaneous cerebellar hematoma. CT perfusion reveals a markedly prolonged TMAX with a low CBV in the right cerebral peduncle, consistent with localized HICP and transtentorial herniation (TTH). Perihematomal tissue shows prolonged TMAX with compensatory CBV increase, suggestive of potentially salvageable tissue. A focal area of reduced CBV is evident at the hematoma vertex. Panel 3 CT perfusion maps with corresponding NCCT slices after posterior fossa decompression in a patient with spontaneous cerebellar hematoma. CT perfusion maps show improvement of the previously described perfusion abnormality in the right cerebellar region, with reduction of TMAX prolongation and improved CBV/CBF patterns around the surgical site. The corresponding NCCT confirms expected postoperative changes after evacuation of the hematoma. Panel 4 CT perfusion maps with corresponding NCCT slices illustrating postoperative supratentorial perfusion changes in a patient with spontaneous cerebellar hematoma. CT perfusion reveals improvement of the previously described abnormality at the level of the right cerebral peduncle, consistent with relief of the local compressive effect. The corresponding perfusion maps show a more symmetric supratentorial pattern compared with the pre-operative study

The mass effect, difficult to quantify in the small volume of the posterior cranial fossa, was further illustrated by significantly prolonged TMAX in the right cerebral peduncle (Fig.1, Panel 2), likely due to compression of basilar artery perforators. As these are terminal vessels, the combination of low CBV and prolonged TMAX suggested exhausted compensatory capacity and an urgent need for surgery to prevent severe motor sequelae (left-sided hemiplegia).

After CTP assessment, the patient underwent emergent external ventricular drain (EVD) placement followed by surgical hematoma evacuation. The supratentorial ICP recorded via the EVD before craniotomy was 18 mmHg. Peri-operatively, CPP optimization focused on MAP targeting. Norepinephrine was initiated together with intravascular volume. After discontinuation of sedative agents, systemic arterial pressures increased spontaneously and MAP values remained sufficient, when considered alongside the recorded supratentorial ICP, to support an estimated CPP ≥ 70–75 mmHg during the early postoperative course. These hemodynamic targets were maintained as part of routine neurocritical care. Postoperatively, supratentorial ICP monitored via the EVD remained within a non-pathological range (peak: 16 mmHg; typical values: 8–12 mmHg), without the need for escalation of ICP-directed therapy.

An immediate postoperative NCCT showed expected postsurgical changes after EVD placement and posterior fossa decompression, with evacuation of the right cerebellar hematoma and a small residual hyperdense component at the surgical site (Fig 1, Panel 3). Postoperative CTP showed improvement of the previously described perfusion abnormality at the level of the right cerebral peduncle, consistent with relief of the local compressive effect (Fig. 1, Panel 4). A follow-up CTP repeated on postoperative day seven before ICU discharge confirmed normalization of perfusion parameters, with improved CBV and CBF and reduced TMAX compared with the pre-operative study, consistent with improved perfusion dynamics.

At intensive care unit (ICU) discharge, after seven days, the patient exhibited spontaneous eye opening, fluent and appropriate speech, and mild left-sided hemiparesis. At the one-month follow-up, the patient was alert and oriented, with fluent speech and no cranial nerve deficits. Motor examination showed mild left-sided weakness (MRC: upper limb 3/5; lower limb 4/5). She was able to ambulate with assistance, and functional status was [mRS 4].

CTP acquisition and analysis

CTP was performed at presentation, repeated in the immediate postoperative period, and again on postoperative day seven at ICU discharge. Acquisition was obtained on a Siemens CT scanner and post-processing was performed with Syngo.via. Analysis was primarily qualitative and comparative across studies, focusing on the spatial distribution of perfusion abnormalities and their evolution after decompression and MAP-targeted hemodynamic optimization, without formal ROI-based quantitative measurements.

Discussion

Spontaneous cerebellar hematoma is a life-threatening condition frequently associated with rapid neurological deterioration, primarily due to local intracranial hypertension within a confined anatomical compartment with minimal compensatory capacity [6, 11].

Surgical evacuation is generally considered in patients with neurological deterioration/coma, brainstem compression and/or obstructive hydrocephalus, and a large hematoma burden (e.g., ≥ 15 mL), particularly when no primary intra-axial bleeding is present [5]. However, similar to supratentorial ICH, surgical indication and timing remain highly variable across centers, reflecting limited high-grade evidence and therefore an heterogeneous practice patterns [14]. In infratentorial hemorrhage, beyond age and comorbidity burden, the risk of secondary brainstem ischemia related to impaired posterior fossa perfusion is the potentially avoidable critical determinant of outcome. At present, these physiological considerations are rarely supported by direct bedside measurements, because infratentorial compartment pressure is seldom monitored and regional intraparenchymal CBF is not routinely measurable in standard care [5].

Direct ICP monitoring in the posterior fossa is rarely performed by neurosurgeons because potential complications, including cerebellar bleeding, cerebrospinal fluid leakage, cranial nerve palsies, and brainstem contusion, are major deterrents. Differences in pressure between supratentorial and infratentorial compartments have been described, suggesting that normal supratentorial ICP may mask secondary injury related to elevated pressure in the posterior fossa [6].

Moreover, patients with posterior fossa ICH may present with very poor neurological status, but the clinical picture can also be unreliable, influenced by sedation, acute hydrocephalus, or seizures. Previous studies have identified predictors of poor outcome in spontaneous cerebellar hematoma, including low GCS score, hematoma volume (≈ 15 mL), and radiological indicators such as brainstem compression, tonsillar herniation through the foramen magnum, or upward cerebellar vermis herniation [15]. These features may discourage surgical intervention, particularly in patients with severely compromised neurological status. Excessive prognostic pessimism in such cases exposes decisions to the risk of self-fulfilling prophecy [9, 11].

Precisely in this context, preoperative CTP can complement conventional imaging by providing additional information on regional perfusion dynamics and revealing pathophysiological changes that are not detectable with standard modalities [7]. Once major vessel stenosis has been excluded by history and CT angiography, and when arterial pressure is normal or elevated, a prolonged TMAX is most plausibly explained by reduced CPP due to HICP [16]. By demonstrating preserved CBV in compressed but structurally normal brain surrounding the hematoma core, CTP can support the notion that aggressive intervention is not futile [5, 9, 10]. Importantly, the precise definition of focal perfusion damage that precedes overt neurological deficit, such as reduced CBV corresponding to partially reversible injury of the pyramidal tracts, helps clinicians link pathological mechanisms to symptoms, thereby increasing awareness and motivation to intervene early.

Nevertheless, posterior fossa CTP is technically challenging due to skull base beam-hardening, partial volume effects, and motion sensitivity, which may affect map reliability and inter-software comparability. In particular, beam-hardening and streak artifacts from the skull base/temporal bones may degrade the infratentorial source images and propagate into perfusion maps, potentially causing apparent transit-time prolongation or underestimation of perfusion, especially in the brainstem region [17, 18]. Although these limitations in the posterior fossa are real, their co-occurrence in an individual case to the point of rendering the examination unreliable can only be recognized after acquisition. In consecutive cohorts, the proportion of CTP examinations deemed non-diagnostic purely because of technical image-quality limitations is low [e.g., 2/116 (1.7%) excluded for poor image quality and 21/524 (4.0%) non-diagnostic due to motion artifacts], supporting that these constraints do not justify withholding CTP a priori [19, 20]. In the present case, perfusion assessment was qualitative and did not include standardized ROI-based quantification or predefined thresholds, which limits the precision of effect estimation. Moreover, CTP has inherent constraints in the reliability and cross-platform comparability of absolute perfusion values when benchmarked against gold-standard CBF measurement techniques; this is one reason why qualitative, pattern-based interpretation remains widely accepted in clinical practice [21–23]. Finally, CTP does not directly measure ICP or CPP; therefore, mechanistic conclusions regarding CPP-mediated changes must be interpreted cautiously and within the overall clinical context [24].

This report is subject to the limitations inherent to a single-case design, which restricts generalizability; nonetheless, it offers a rationale for further systematic studies of emergency functional imaging in this setting. Moreover, in patients with posterior fossa ICH, CT perfusion may provide adjunct physiological information by identifying potentially viable tissue and characterizing perfusion dynamics, which could help temper prognostic pessimism and support timely, proactive management in selected severe presentations.

Abbreviations

CSF

Cerebrospinal fluid

CBF

Cerebral blood flow

CBV

Cerebral blood volume

CPP

Cerebral perfusion pressure

CT

Computed tomography

CTA

CT angiography

CTP

CT perfusion

EVD

External ventricular drain

GCS

Glasgow Coma Scale

HICP

High intracranial pressure

ICH

Intracerebral hemorrhage

ICP

Intracranial pressure

ICU

Intensive care unit

NCCT

Non-contrast CT

SAH

Subarachnoid hemorrhage

TBI

Traumatic brain injury

TCD

Transcranial Doppler

TMAX

Time-to-maximum

TTH

Transtentorial herniation

Authors’ contributions

1.Giuseppina Irene Musca, MD: drafting and revising the manuscript, interpretation of imaging and clinical data, final approval of the version to be published.2.Fabrizio Zumbo, MD: interpretation of imaging and clinical data, final approval of the version to be published.3.Arturo Chieregato, MD: drafting and revising the manuscript, interpretation of imaging and clinical data, corresponding author, final approval of the version to be published.All authors had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Funding

No funding was received for this study.

Data availability

The data that support the findings of this study are available from the corresponding author upon reasonable request. Access to the data is subject to patient confidentiality, and the patient provided written informed consent for data sharing.

Declarations

Ethics approval and consent to participate

Not applicable. This article describes a single-patient case report based on routine clinical care. According to institutional and national regulations, formal ethics committee approval is not required for individual anonymized case reports.

Consent for publication

Written informed consent was obtained from the patient for publication of the case details and associated images. The completed consent form is held by the authors and is available for review by the Editor-in-Chief if requested.

Competing interests

The authors declare no competing interests.