An Adult Case of Symptomatic Porencephalic Cyst Following Removal Massive Subcortical Hematoma
2025 Volume 47 Issue 1 Pages 21-25
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2025 Volume 47 Issue 1 Pages 21-25
The hematoma cavity typically remains collapsed after intracranial hematoma evacuation, but here we report an adult case in which the cavity expanded into a cystic form, developing into a porencephalic cyst, after the removal. A 73-year-old woman was admitted to our hospital presenting with a disturbance of consciousness. A CT scan showed a subcortical hemorrhage with a blend sign and brain herniation, prompting emergent hematoma evacuation. Although there was an improvement in her symptoms after the operation, her consciousness deteriorated on the 14th day post-operation. A CT scan revealed a porencephalic cyst. Reoperation was performed, and no further recurrence of the cyst was noted. Reports of hematoma cavities expanding into a cystic form after hematoma removal are rare, and the mechanisms of such cyst expansion are not well understood. In this case, we hypothesize two pathways: 1) Residual hematoma components moving through the ventricular wall due to osmotic pressure differences between the hypertonic fluid and cerebrospinal fluid (CSF), and 2) Protein-rich plasma components leaking out of cells due to blood-brain barrier (BBB) disruption caused by cerebral hemorrhage. We also consider the possibility of a check valve mechanism.
The hematoma cavity typically remains collapsed following hematoma evacuation. In this report, we describe a rare case of early postoperative expansion of the hematoma cavity into cystic form, developing into a porencephalic cyst, after craniotomy for subcortical hemorrhage in the frontal lobe. This case prompted a review of the literature concerning similar occurrences.
A 73-year-old woman with a history of hypertension and dementia, who was otherwise independent in daily activities, was found unconscious on the street during an early morning walk and was emergently transported to our hospital.
Her vital signs upon arrival were as follows: blood pressure 105/69 mmHg, pulse 86 beats per minute, and a Japan Coma Scale (JCS) score of II-10. She exhibited right-sided hemiplegia and motor aphasia. Laboratory tests, including complete blood count, general biochemistry, and coagulation studies, showed no significant abnormalities (platelet count 224,000/μl, prothrombin time-international normalized ratio (PT-INR) 1.16, activated partial thromboplastin time (APTT) 30.6 seconds).
A head CT performed two hours post-onset revealed a 5 cm high-density area in the left frontal lobe, diagnosed as a subcortical hemorrhage without ventricular perforation (Figure 1). One hour post-admission, the patient’s consciousness level worsened to JCS III-200, and her left pupil was dilated, prompting an emergency craniotomy to remove the hematoma.
During the procedure, a corticotomy was performed at the site where the hematoma was exposed on the brain surface, and the hematoma was accessed. The liquid component was aspirated, followed by the removal of the posterior superior part of the hematoma. Leakage of cerebrospinal fluid (CSF) from the medial side of the hematoma suggested a possible communication with the ventricles. No abnormal vessels were observed within the visible range. The procedure was concluded under external decompression without replacing the bone flap.
Postoperatively, the patient was managed in intensive care, showing improvements such as the ability to track with her eyes and mimic expressions, although right hemiplegia persisted. Approximately 14 days later, her responsiveness decreased, and a follow-up head CT revealed that the hematoma cavity had expanded into a cystic formation (Figure 2). A second surgery was undertaken, revealing a mixture of brownish liquid hematoma and a slightly firm hematoma at the previous surgical site. No internal CSF leakage was noted.
The hematoma cavity was extensively irrigated with artificial CSF to prevent reaccumulation, and the entry points on the brain surface were coagulated to establish a connection between the hematoma and the CSF cavities. Tissue from the posterior superior area, including the cyst wall and residual hematoma, was sent for pathological examination. The hematoma wall exhibited signs of microvascular amyloid angiopathy. The cavity fluid contained inflammatory and degenerative cells, but no malignant features were detected. Following surgery, the patient’s consciousness improved gradually, and she was transferred for rehabilitation post-cranioplasty.
Porencephalic cysts, characterized by the accumulation of cerebrospinal fluid within the brain parenchyma, are rare and often associated with perinatal vascular events such as cerebral ischemia or hemorrhage [1–2]. Reports of such cysts expanding into a cystic shape in the hematoma cavity shortly after craniotomy for hematoma removal in adults are scarce, with only three cases identified in our review (Table 1) [3–5]. The mechanisms behind cyst formation following craniotomy remain largely unclear.
|
Author (year, Reference) |
Age/Sex |
Presentation | CT finding of ICH | 1st treatment | 2nd treatment | Cyst recurrence | |||
|---|---|---|---|---|---|---|---|---|---|
| Location | Fluid-blood level | IVH | Method | Method | Timing of surgery | ||||
| Miyata (2000, 1) | 62/ M | vomiting,/ lethargic state | Rt-subcortical (temporoparietal) | + | – | Craniotomy | Drainage | day 17 | – |
| Lt-hemiparesis, visual field defect | |||||||||
|
Asayama (2015, 2) |
82/ F | disturbance of consciousness | Rt-subcortical (parietal) | – | – | Craniotomy | Drainage | day 8 | – |
| Lt-hemiparesis | |||||||||
|
Shinagawa (2020, 3) |
69/ F | disturbance of consciousness | Rt-subcortical (parietal) | + | – | Craniotomy | Craniotomy | day 10 | – |
| Lt-hemiparesis & hemispatial neglect | |||||||||
| Present case | 73/ F | disturbance of consciousness | Lt-subcortical (frontotemporal) | + | – | Craniotomy | Craniotomy | day 14 | – |
| Rt-hemiparesis, motor aphasia | |||||||||
IVH: intraventricular hemorrhage
Case 1 reported that the ventricle and hematoma cavity were separated by a thin layer of ventricular wall after hematoma removal, and a unidirectional influx of CSF into the hematoma cavity occurred due to an osmotic gradient between the CSF and residual blood components within the hematoma cavity [3].
In Case 2, the cystic content was characterized as a hypertonic fluid filled with cells and proteins due to residual hematoma components and inflammatory changes. It was hypothesized that a concentration gradient facilitated CSF flow from the ventricular side to the hematoma side, and a check valve mechanism contributed to the cyst enlargement [4].
Case 3 described CSF influx driven by ventricular pulsations through a narrow gap between the lateral ventricle and the hematoma cavity, with the choroid plexus also playing a role, activating a check valve mechanism [5]. It is well known that CSF can flow from the ventricles to the periventricular white matter under high osmotic pressure [6–7], but, according to Shinagawa et al, osmotic pressure differences alone are unlikely to cause cysts to enlarge rapidly enough to produce a mass effect [5].
In the initial CT of our case, the hematoma showed a low-density area anteriorly and a high-density area posteriorly, presenting a blend sign, which was also seen in the three cases described above [3–5]. The blend sign has been reported as a risk factor for hematoma expansion in plain CT scans [8], but, when adjacent to the ventricles or subarachnoid space, it is more likely to reflect accumulated CSF rather than active bleeding [9].
Furthermore, when the blood-brain barrier (BBB) is disrupted, protein-rich plasma components can leak from the blood into the extracellular space, contributing to vasogenic edema and leading to water inflow into the hematoma side due to the higher colloid osmotic pressure [10–11].
In Case 2, a low-density area inside the hematoma may have indicated vasogenic edema due to BBB disruption [4]. Thus, strong cases of blend sign and vasogenic edema might suggest that pathways through the ventricular wall and disrupted BBB could contribute to the enlargement of the cyst formed in the hematoma cavity from the onset of bleeding.
Although no intraventricular hemorrhage was observed in the initial CT of the present case, a small amount of CSF leakage was noted inside the hematoma during the first surgery, and the immediate postoperative CT showed a mixture of air and hematoma in the ventricles, suggesting communication between the ventricles and the hematoma cavity. No CSF leakage from the ventricular side was observed during the second surgery, and the cyst content was filled with a hypertonic fluid rich in cells due to residual hematoma components and inflammatory changes. This suggests that there was direct communication between the ventricles and the hematoma cavity, and osmotic and concentration gradients facilitated CSF influx into the hematoma cavity, possibly activating a check valve mechanism leading to cyst enlargement.
Yamaguchi et al reported subacute hematoma enlargement due to CSF accumulation, where a small hole formed in the ventricular wall near the hematoma did not extend to the intraventricular hematoma but was covered by it. Over time, part of it dissolved, weakening the adhesion to the ventricular wall and functioning like a check valve [9]. Although it is difficult to prove this directly, the rapid increase in the liquid component led to craniotomy being performed based on follow-up CTs conducted 3–15 hours after admission. The four cases, including this one, that developed a porencephalic cyst after craniotomy showed a clear difference in the timing of the second surgery, which occurred 8–17 days post-admission. This suggests that the presence or absence of hematoma removal surgery, and the differences in residual hematoma volume, could have facilitated CSF influx due to higher concentration gradients.
As far as we could ascertain, there are no studies that evaluate the check valve mechanism as a cause of cyst enlargement in porencephalic cysts using MRI. It may be possible, however, to elucidate the check valve mechanism by using 3D-SPACE (three-dimensional sampling perfection with application optimized contrasts using different flip angle evolutions) and PC-MRI (phase-contrast cine MRI), as these methods can verify the flow and communication of CSF within the cyst [12]. Additionally, methods such as intraoperative Valsalva maneuver [13] and the calculation of HU (Hounsfield Unit) values in the cyst and subarachnoid space using CT myelography have been reported as useful for confirming the presence of a check valve mechanism [14].
In the second surgery of this case, the hematoma cavity was thoroughly irrigated with artificial CSF to eliminate the concentration gradient, and the entry holes on the brain surface were adequately coagulated, concluding the surgery. Subsequently, the patient progressed without recurrence, although some cases reported in the past have been cured with drainage alone, suggesting that further accumulation of cases is necessary.
Moreover, in cases of subcortical hemorrhage near the ventricles without evident ventricular perforation, especially those with a blend sign, there is a possibility of developing a porencephalic cyst post-hematoma removal, necessitating careful follow-up. Additionally, preventive measures during the initial surgery, such as ventriculoplasty to block CSF inflow, might have been possible.
We experienced a case in which a hematoma cavity expanded into a cystic porencephalic cyst shortly after craniotomy for hematoma removal in an adult. Previous cases have also suggested CSF influx into the hematoma cavity, and strong instances of blend sign and vasogenic edema indicate the potential for CSF accumulation, warranting caution. Additionally, there are reports of cure with drainage alone, underscoring the need for accumulation of more cases to inform treatment strategies.
None
The datasets generated during and/or analyzed during the current study are available from the corresponding author on reasonable request.
