Acute obstructive hydrocephalus due to a third-ventricular lesion at the foramen of monro complicated by extensive cerebral and posterior circulation infarctions: A case report

Venkatesha1*, Gowdham Pannirselvam2

1 Nursing Officer, Kauvery Hospital, Marathahalli, Bangalore

2Sr. Nurse Educator, Kauvery Hospital, Marathahalli, Bangalore

*Correspondence

Abstract

Background

Acute obstructive hydrocephalus in adults is a potentially life-threatening neurological emergency. Although hydrocephalus may develop from several causes, lesions located near the foramen of Monro are particularly important because even a relatively small lesion can obstruct Cerebrospinal fluid (CSF) circulation and produce rapid ventricular enlargement and neurological deterioration. Colloid cysts are uncommon benign intraventricular lesions that characteristically occur near the foramen of Monro and may present with symptoms related to raised intracranial pressure or, rarely, sudden neurological deterioration. [1,2]

Case Presentation

We present the case of a man in his mid-thirties who presented with headache and vomiting and subsequently developed sudden loss of consciousness. On arrival at the emergency department, he had a markedly depressed level of consciousness, bilateral non-reactive pupils and abnormal vital signs. Emergency Computed Tomography (CT) of the brain demonstrated severe obstructive hydrocephalus secondary to a lesion at the foramen of Monro, with a radiological differential diagnosis of colloid cyst versus neoplasm. Bilateral External Ventricular Drainage (EVD) was performed for urgent CSF diversion. The initial clinical presentation and CT findings are documented in the clinical record.

Following initial ventricular decompression, serial neuroimaging demonstrated extensive ischemic infarctions involving the midbrain, bilateral thalami, gangliocapsular regions, right cerebellum, bilateral medial temporal and occipital regions in the posterior cerebral artery territories, hypothalamic regions, corpus callosum and cerebral cortices. Magnetic Resonance Imaging (MRI) demonstrated a well-defined intraventricular lesion at the foramen of Monro with internal haemorrhagic components, with differential diagnoses of atypical colloid cyst and astrocytoma with internal hemorrhage. As persistent CSF diversion was required, bilateral Ventriculoperitoneal (VP) shunts were subsequently placed. The patient also underwent tracheostomy and neuro-rehabilitation.

Conclusion

This case highlights the potentially rapid and severe neurological consequences of adult obstructive hydrocephalus caused by a lesion at the foramen of Monro. Early recognition, emergency ventricular decompression and close neurocritical care monitoring are essential. The case also demonstrates the complexity of management when acute hydrocephalus is accompanied by extensive cerebral and posterior circulation infarction. Because histopathological confirmation was not available, the intraventricular lesion should be regarded as a radiological differential diagnosis rather than a confirmed colloid cyst.

Keywords: Adult hydrocephalus; Obstructive hydrocephalus; Foramen of Monro; Colloid cyst; Third ventricle; External ventricular drain; Ventriculoperitoneal shunt; Cerebral infarction; Posterior cerebral artery infarction; Neurorehabilitation.

Introduction

Hydrocephalus is a pathological disturbance of cerebrospinal fluid dynamics resulting in abnormal accumulation of CSF within the ventricular system and/or subarachnoid spaces. In adults, hydrocephalus may be communicating or non-communicating, with obstructive or non-communicating hydrocephalus occurring when CSF flow is blocked within the ventricular system. [1,3]. The clinical significance of obstructive hydrocephalus depends not only on the size of the obstructing lesion but also on its anatomical location. The foramen of Monro is a narrow communication between the lateral ventricles and the third ventricle. A lesion at this site can interfere with CSF passage and result in rapid ventricular enlargement. Colloid cysts are classically situated close to the foramen of Monro and represent an important differential diagnosis for third-ventricular lesions producing obstructive hydrocephalus. [1,2]. Patients with acute obstruction may initially develop headache, nausea and vomiting. As intracranial pressure increases, neurological manifestations may progress to altered sensorium, pupillary abnormalities, brainstem dysfunction and, in severe cases, cerebral herniation. [2,4]. External ventricular drainage is commonly used as an emergency, life-saving method of CSF diversion in acute hydrocephalus and intracranial hypertension. It allows temporary drainage of CSF and, when appropriately equipped, monitoring of intracranial pressure. However, EVD is associated with potential complications including infection, hemorrhage, catheter malposition and obstruction. [5,6]. We present a case of acute severe obstructive hydrocephalus caused by a lesion at the foramen of Monro in a young adult, complicated by extensive ischemic infarctions involving the brainstem, bilateral thalami, gangliocapsular regions, cerebellum and posterior cerebral artery territories. The patient required emergency EVD followed by permanent CSF diversion with bilateral VP shunts, prolonged critical care, tracheostomy and neuro-rehabilitation.

Anatomy of the Third Ventricle and Foramen of Monro

The ventricular system is a network of interconnected cavities containing CSF. The lateral ventricles are paired structures located within the cerebral hemispheres. Each lateral ventricle communicates with the third ventricle through the foramen of Monro, also known as the interventricular foramen. [3,7]. The third ventricle is a narrow, vertically oriented cavity situated between the right and left thalami and hypothalamic structures. Anteriorly, it is related to the columns of the fornix and anterior commissure, while posteriorly it communicates with the cerebral aqueduct. [7]. The foramen of Monro represents a critical anatomical pathway because it provides the connection between the lateral ventricles and the third ventricle. A lesion in this region can therefore interrupt the normal movement of CSF. The strategic location of colloid cysts is particularly important. These lesions usually occur in the anterior third ventricle near the foramen of Monro. Their clinical effect is determined largely by their relationship to CSF pathways rather than by their absolute size. [1,2]

Physiology of Cerebrospinal Fluid

CSF is continuously produced within the ventricular system, predominantly by the choroid plexus. It circulates through the ventricles before entering the subarachnoid space. [3,7]

The conventional pathway of CSF circulation is:

Lateral ventricles → Foramen of Monro → Third ventricle → Cerebral aqueduct → Fourth ventricle → Foramina of Luschka and Magendie → Subarachnoid space → CSF absorption pathways.

The foramen of Monro is therefore an important point in the normal CSF circulation pathway. [3,7]. Normally, CSF production and absorption remain in dynamic equilibrium. When CSF flow is interrupted, fluid accumulates proximal to the site of obstruction. In obstructive hydrocephalus caused by a lesion at the foramen of Monro, the lateral ventricles may enlarge because CSF cannot pass normally into the third ventricle. [1,3]

Hydrocephalus in Adults

Definition

Hydrocephalus is characterized by abnormal CSF accumulation associated with ventricular enlargement and altered intracranial dynamics. Adult hydrocephalus may occur because of impaired CSF circulation, impaired absorption or, less commonly, abnormalities of CSF production. [3]

The major clinical categories include:

  • Obstructive/non-communicating hydrocephalus
  • Communicating hydrocephalus
  • Normal-pressure hydrocephalus

The present case represents acute obstructive hydrocephalus, because a structural lesion was identified at the foramen of Monro.

Mechanism of Obstructive Hydrocephalus

When an obstruction develops within the ventricular system, CSF production continues despite the blockage. Consequently, CSF accumulates upstream from the obstruction. This produces ventricular enlargement and may increase intracranial pressure. [3,4]. In adults, the skull is a relatively rigid compartment. Although compensatory mechanisms initially allow some displacement of CSF and venous blood, these mechanisms are limited. Once intracranial compliance is exhausted, a relatively small additional increase in intracranial volume may cause a marked increase in intracranial pressure. [4]. The resulting increase in intracranial pressure can reduce cerebral perfusion and produce secondary neurological injury.

Obstruction at the Foramen of Monro

The foramen of Monro is particularly important because it is a narrow CSF pathway. A lesion in this region can produce significant obstruction despite its relatively limited anatomical size. A colloid cyst may obstruct the foramen of Monro and interfere with CSF drainage from the lateral ventricles. This may result in ventricular enlargement, trans ependymal CSF movement and raised intracranial pressure. [1,2]

Patients may present with:

  • Headache
  • Nausea and vomiting
  • Altered consciousness
  • Visual symptoms
  • Memory disturbance
  • Gait disturbance
  • Papilledema
  • Seizures
  • Sudden neurological deterioration in severe cases

The clinical presentation depends on the degree and rapidity of obstruction. [1,2]

Acute Hydrocephalus in the Present Case

In this patient, the clinical course was consistent with acute severe obstructive hydrocephalus. He initially developed headache and vomiting and subsequently became suddenly unconscious. Emergency CT demonstrated severe obstructive hydrocephalus associated with a lesion at the foramen of Monro. The sudden deterioration suggests that the obstruction had significant effects on intracranial CSF dynamics. The emergency need for bilateral EVD placement further reflected the severity of the hydrocephalus. Follow-up CT after EVD placement showed reduction in ventriculomegaly, reopening of the basal cisterns and reduction in mass effect over the brainstem, supporting the clinical importance of the obstructive component.

Pathophysiology

The pathophysiological sequence in this case can be understood as follows:

Foramen of Monro lesion
↓
Obstruction of CSF circulation
↓
Acute ventricular enlargement and obstructive hydrocephalus
↓
Rise in intracranial pressure
↓
Reduced intracranial compliance and possible reduction in cerebral perfusion
↓
Neurological deterioration
↓
Emergency CSF diversion with EVD
↓
Persistent need for CSF diversion
↓
Bilateral VP shunt placement

The patient’s subsequent extensive ischemic lesions represented an additional major neurological complication. CT demonstrated new hypodensities involving the midbrain, bilateral thalami, gangliocapsular regions, splenium of the corpus callosum, left medial temporal and occipital regions and the anterior cerebellum. The radiological impression was of extensive acute infarction involving multiple territories. MRI subsequently demonstrated extensive ischemic infarctions involving the midbrain, right cerebellum in the superior cerebellar artery territory, bilateral thalami, bilateral medial temporal and occipital regions in the posterior cerebral artery territories, hypothalamic regions, gangliocapsular areas, corpus callosum and cerebral cortices. Microhaemorrhages were noted in the pons along with diffuse cerebral edema. The precise mechanism responsible for the extensive multi-territorial infarction could not be established from the available clinical records. Severe intracranial pressure disturbances and associated cerebrovascular compromise may have contributed, but a direct causal relationship should not be assumed without further vascular and hemodynamic evidence.

Case Presentation

A man in his mid-thirties presented to the emergency department on 6 June 2026 with a history of headache and vomiting. During the acute episode, he suddenly became unconscious and was brought to the emergency department for further evaluation. On arrival, he had a markedly depressed level of consciousness. The documented emergency assessment included a Glasgow Coma Scale of approximately E1 M2 V1, bilateral pupils measuring approximately 5 mm and non-reactive to light, blood pressure of 190/90 mmHg and pulse rate of 40/min. He was immediately intubated and placed on mechanical ventilation. Bilateral EVDs were placed and he was transferred to intensive care for further management. The clinical examination after stabilization documented the patient on mechanical ventilation with depressed consciousness and bilaterally non-reactive pupils. The available record did not identify a significant documented previous neurological disorder. A possible history of previous eye surgery was mentioned, although records were unavailable. There were no known drug allergies.

Diagnostic Assessment

Initial CT Brain

An emergency plain CT brain performed on 6 June 2026 demonstrated acute severe obstructive hydrocephalus secondary to a lesion at the foramen of Monro. The lesion was initially considered possibly a colloid cyst or neoplasm. The anatomical location of the lesion was highly significant because obstruction at the foramen of Monro can rapidly interfere with CSF circulation. [1,2]

Post-EVD CT

A follow-up CT after EVD placement showed interval placement of the ventricular drainage catheters with reduction in ventriculomegaly. There was opening of the basal cisterns and reduction in mass effect over the brainstem. Post-procedural imaging also demonstrated intraventricular pneumocephalus, small areas of extra-axial and intraparenchymal air, minimal intraventricular hemorrhage and the presence of the EVD catheters.

Development of Cerebral Infarctions

A CT performed on 8 June 2026 showed new patchy hypodensities in the midbrain, bilateral thalami, gangliocapsular regions and splenium of the corpus callosum. A large wedge-shaped hypodensity was seen involving the left medial temporal and occipital lobes, with another smaller wedge-shaped hypodensity in the anterior cerebellum. The overall findings were consistent with extensive acute infarctions involving the brainstem, bilateral thalami, gangliocapsular regions, right cerebellum and left medial temporal/occipital regions corresponding to the posterior cerebral artery territory. Diffusion-weighted MRI was suggested for further evaluation.

MRI Brain

MRI of the brain with contrast performed on 9 June 2026 demonstrated a well-defined, smooth, oval-shaped intraventricular lesion at the foramen of Monro with internal haemorrhagic components.

The radiological differential diagnosis included:

  • Atypical colloid cyst
  • Astrocytoma with internal hemorrhage

Biopsy was advised for definitive confirmation.

The MRI also demonstrated extensive ischemic infarctions involving the midbrain, right cerebellum, bilateral thalami, bilateral medial temporal and occipital regions, hypothalamic regions, gangliocapsular areas, corpus callosum and cerebral cortices. Microhaemorrhages were noted in the pons along with diffuse cerebral edema. MRI appearances of colloid cysts can be variable, and atypical intraventricular lesions may overlap radiologically with other third-ventricular tumours. Therefore, imaging alone may not always establish the definitive histological diagnosis. [1,7,8]. Importantly, no histopathological diagnosis was documented in the available records. Therefore, the lesion cannot be described as a confirmed colloid cyst.

Therapeutic Intervention

Emergency External Ventricular Drainage

Because of severe obstructive hydrocephalus and neurological deterioration, emergency EVD placement was performed under general anaesthesia on 6 June 2026. Bilateral ventricular drains were placed at the Kocher’s point region for CSF diversion. EVD is a commonly used emergency intervention for acute hydrocephalus because it can rapidly divert CSF and reduce the consequences of raised intracranial pressure. [5,6]. Following placement, imaging demonstrated improvement in ventricular enlargement and reduction of brainstem mass effect.

Subsequent Neurological Complications

Despite initial ventricular decompression, the patient’s neurological status remained poor. Serial imaging demonstrated extensive cerebral and posterior circulation infarctions with diffuse cerebral edema. The infarctions remained radiologically stable over subsequent CT examinations, although subtle hyper density within some subacute infarcts raised concern for early haemorrhagic transformation. There was no major increase in mass effect documented. Patients with large cerebral or cerebellar infarctions complicated by swelling require intensive neurological monitoring because progressive edema may result in further deterioration. [9]

Tracheostomy

Because of the prolonged critical illness and continued requirement for airway support, a percutaneous tracheostomy was performed on 11 June 2026 using a Ciaglia single-stage technique under ultrasound guidance. An 8-mm cuffed tracheostomy tube was inserted. The procedure facilitated continued airway management and subsequent ventilator weaning.

Transition from EVD to Permanent CSF Diversion

During the hospital course, the EVD was removed after the initial period of drainage. However, the patient continued to have a low level of consciousness and subsequently demonstrated an increase in the size of the lateral ventricles when the EVD was blocked. This indicated persistent dependence on CSF diversion.

In view of the persistent hydrocephalus, a decision was made to proceed with permanent CSF diversion. Bilateral VP shunts were placed on 13 June 2026 under general anaesthesia. Postoperative CT demonstrated cranial shunt catheters in position without significant hydrocephalus. The third-ventricular lesion remained unchanged. The progression from temporary EVD to permanent CSF diversion is consistent with the established role of EVD as an acute treatment while persistent hydrocephalus may require longer-term CSF diversion. [5,6]

Clinical Course

The patient’s clinical course was prolonged and required multidisciplinary neurocritical care.

Following emergency EVD placement, he required mechanical ventilation and intensive care monitoring. Serial neuroimaging was performed to assess ventricular size, infarction, cerebral edema, intraventricular haemorrhage and the status of the EVD. The neurological imaging demonstrated extensive infarction involving multiple vascular territories. Despite these complications, there was no significant progressive mass effect or major hemorrhagic transformation documented on subsequent CT examinations. The patient underwent tracheostomy during the hospital stay and was subsequently gradually weaned from ventilatory support. After VP shunt placement, postoperative imaging demonstrated no significant hydrocephalus. He was then shifted from intensive care to ward-level care when clinically stable. Neuro-rehabilitation was initiated, with continued physiotherapy directed toward limb and chest care. At discharge, the patient remained neurologically severely impaired, with a documented GCS of E2 M3 Vt and bilateral pupils measuring 3 mm that were non-reactive to light. The VP shunt incision had healed well. He remained on enteral feeding, had a tracheostomy and Foley catheter, and was transferred to a neuro-rehabilitation facility.

Timeline of the Case

DateClinical event
06 June 2026Presented with headache and vomiting followed by sudden loss of consciousness.
06 June 2026Severe obstructive hydrocephalus identified on CT; lesion at foramen of Monro.
06 June 2026Intubation, mechanical ventilation and bilateral EVD placement.
06 June 2026Post-EVD CT showed reduction in ventriculomegaly and brainstem mass effect.
08 June 2026CT demonstrated extensive acute infarctions involving brainstem, thalami, gangliocapsular regions, cerebellum and PCA territories.
09 June 2026MRI demonstrated foramen of Monro lesion with internal hemorrhage; atypical colloid cyst vs astrocytoma considered.
11 June 2026Percutaneous tracheostomy performed.
11–13 June 2026Serial CT monitoring showed persistent infarcts, edema and evolving hemorrhagic changes without major mass effect.
13 June 2026Bilateral VP shunt placement for persistent CSF diversion requirement
After VP shuntVentricular size improved; ventilator weaning and neurorehabilitation initiated.
01 July 2026Discharged/transferred to neurorehabilitation with persistent severe neurological impairment.

The timeline follows the documented sequence of emergency presentation, ventricular drainage, serial neuroimaging, tracheostomy, VP shunt placement and transfer to rehabilitation.

Discussion

This case demonstrates the complex interaction between an intraventricular lesion, acute obstructive hydrocephalus and extensive secondary neurological injury. Colloid cysts are uncommon benign lesions of the third ventricle, most frequently located near the foramen of Monro. They are often identified in adults, particularly during the third to fifth decades of life. Their clinical significance is primarily related to their potential to obstruct CSF flow. [1,2]. In symptomatic patients, headache associated with raised intracranial pressure and hydrocephalus is common. Because the foramen of Monro is a narrow CSF pathway, a lesion in this region can produce clinically significant obstruction. [1,2]

The present patient initially developed headache and vomiting and then experienced sudden deterioration in consciousness. The initial CT demonstrated severe obstructive hydrocephalus associated with a lesion at the foramen of Monro. This clinical-radiological relationship is important because it demonstrates how a strategically located lesion can produce a life-threatening neurological emergency. The first priority was therefore restoration of CSF flow. EVD provides a rapid means of ventricular decompression and is widely used as an emergency treatment for acute hydrocephalus. [5,6]. In this patient, post-EVD imaging showed reduction in ventriculomegaly and improvement in the basal cisterns and brainstem mass effect. This indicates that CSF diversion successfully addressed an important component of the acute intracranial pressure problem. However, the neurological course was complicated by extensive ischemic injury. The infarctions involved multiple structures, including the midbrain, bilateral thalami, gangliocapsular regions, right cerebellum and bilateral PCA territories. The extensive distribution makes the case particularly unusual and clinically significant.

The exact mechanism of these infarctions cannot be established solely from the available data. Severe intracranial pressure elevation and associated reduction in cerebral perfusion may have contributed, but other vascular or hemodynamic mechanisms cannot be excluded. Therefore, it would be inappropriate to state that the infarctions were definitively caused by hydrocephalus. The development of infarction in the cerebellum and brainstem was particularly concerning because posterior fossa swelling can result in brainstem compression and further neurological deterioration. AHA/ASA guidance emphasizes the importance of early neurocritical monitoring and appropriate neurosurgical intervention in patients with cerebellar infarction and swelling. [9]. Another important feature of this case was the persistence of the hydrocephalus after the initial EVD period. When the EVD was blocked, the lateral ventricles increased in size, indicating that the patient continued to require CSF diversion. Permanent diversion was therefore achieved with bilateral VP shunts. MRI characterization of the lesion was also important. The lesion was well-defined and oval-shaped at the foramen of Monro, with internal hemorrhagic components. The differential included an atypical colloid cyst and astrocytoma with internal hemorrhage. This illustrates an important diagnostic limitation: radiological appearance may suggest a colloid cyst, but definitive diagnosis requires histopathological correlation when tissue is obtained. [1,7,8]. The case therefore should not be interpreted simply as a case of a confirmed colloid cyst. Instead, it represents acute obstructive hydrocephalus caused by a third-ventricular lesion at the foramen of Monro, with atypical colloid cyst and neoplasm considered on imaging.

Importance of Early Recognition

The case emphasizes several important clinical lessons.

  • First, headache and vomiting in an adult should not always be considered benign, particularly when symptoms are sudden, severe or associated with altered consciousness. [1,2]
  • Second, lesions near the foramen of Monro deserve careful evaluation because even a relatively small intraventricular lesion can obstruct CSF circulation. [1,2]
  • Third, neurological deterioration in acute hydrocephalus can occur rapidly. Emergency imaging and early neurosurgical involvement are essential. [2,5]
  • Fourth, EVD can provide immediate CSF diversion in life-threatening obstructive hydrocephalus. However, the drain requires meticulous monitoring because infection, hemorrhage, malposition and obstruction are recognized complications. [5,6]
  • Finally, persistent dependence on CSF diversion may require transition from temporary EVD to a permanent VP shunt, as occurred in this patient. [5,6]

Role of Neuro-Rehabilitation

The patient’s neurological injury was extensive and involved multiple structures responsible for consciousness, motor control, coordination and autonomic function. Therefore, management did not end with surgical control of hydrocephalus.

Following stabilization, the patient was started on neuro-rehabilitation and physiotherapy for limb and chest care. At discharge, he continued to require enteral feeding, tracheostomy care and urinary catheterization and was transferred to neurorehabilitation.

For patients with severe neurological injury, rehabilitation should be individualized according to neurological status and may involve:

  • Physiotherapy
  • Positioning and pressure-injury prevention
  • Chest physiotherapy
  • Passive and active range-of-motion exercises where appropriate
  • Airway and tracheostomy care
  • Nutritional support
  • Swallowing assessment when clinically appropriate
  • Prevention of contractures
  • Occupational therapy
  • Speech and communication rehabilitation
  • Family education and caregiver training

In this case, rehabilitation represented an important continuation of care after the acute neurosurgical phase.

Discharge Management and Follow-Up

At discharge, the patient was transferred to neuro-rehabilitation with continued supportive management. The documented discharge medications included bromocriptine, midodrine, amantadine, Emrok-O, Duphalac as required, topical clotrimazole, lubricating eye drops, saline nebulization and ipratropium nebulization, with several medications prescribed for limited durations.

Follow-up with the neurosurgery team was advised after one month, with earlier review recommended for seizures, recurrent unconsciousness, limb weakness, vomiting, fever or other new abnormalities.

Strengths and Limitations

Strengths

This case provides a detailed clinical and radiological description of:

  1. Acute adult obstructive hydrocephalus.
  2. A lesion located at the foramen of Monro.
  3. Emergency EVD as initial CSF diversion.
  4. Extensive multi-territorial cerebral and posterior circulation infarctions.
  5. Persistent hydrocephalus requiring permanent VP shunting.
  6. The role of tracheostomy and neuro-rehabilitation in prolonged neurological illness.

Limitations

The major limitation is the absence of histopathological confirmation of the intraventricular lesion. Although imaging suggested an atypical colloid cyst versus astrocytoma with internal hemorrhage, the definitive pathological diagnosis remains unknown.

In addition, the available clinical records do not provide sufficient information to establish the exact mechanism of the extensive cerebral infarctions. Long-term neurological outcome after transfer to neurorehabilitation was also not available. These limitations should be clearly acknowledged in the final publication. The CARE guidelines emphasize transparent reporting of the diagnostic process, interventions, outcomes and limitations in case reports. [10]

Clinical Significance

This case is clinically significant because it demonstrates that adult obstructive hydrocephalus caused by a lesion at the foramen of Monro can present as a rapidly progressive neurological emergency.

The important sequence in this patient was:

Headache and vomiting
↓
Sudden loss of consciousness
↓
Severe obstructive hydrocephalus
↓
Emergency EVD
↓
Extensive cerebral and posterior circulation infarction
↓
Persistent CSF diversion requirement
↓
Bilateral VP shunt
↓
Tracheostomy and prolonged critical care
↓
Neurorehabilitation

The case emphasizes that successful ventricular decompression does not necessarily prevent secondary neurological injury once severe intracranial and vascular complications have developed.

Conclusion

Acute obstructive hydrocephalus in adults is a potentially fatal neurological emergency, particularly when obstruction occurs at a critical CSF pathway such as the foramen of Monro. In this case, a third-ventricular lesion produced severe obstructive hydrocephalus and rapid neurological deterioration requiring emergency EVD placement. Although initial ventricular decompression resulted in reduction of ventriculomegaly and brainstem mass effect, the patient subsequently developed extensive ischemic infarctions involving the brainstem, thalami, gangliocapsular regions, cerebellum and bilateral PCA territories. Persistent dependence on CSF diversion subsequently necessitated bilateral VP shunt placement. The radiological characteristics of the lesion suggested an atypical colloid cyst versus astrocytoma with internal hemorrhage; however, in the absence of histopathological confirmation, a definitive diagnosis cannot be made. The case highlights the importance of early recognition of acute hydrocephalus, prompt neuroimaging, emergency CSF diversion, serial neurological and radiological assessment, multidisciplinary critical care and early transition to neurorehabilitation.

References

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  9. Wijdicks EFM, Sheth KN, Carter BS, Greer DM, Kasner SE, Kimberly WT, et al. Recommendations for the management of cerebral and cerebellar infarction with swelling: a statement for healthcare professionals from the American Heart Association/American Stroke Association. 2014;45(4):1222-1238. doi:10.1161/01.str.0000441965.15164.d6.
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