Persistent Neurological Impairment Following Falcine Meningioma Resection
This 77-year-old woman's reduced attention and severely reduced initiation 20 days post-operatively, combined with unilateral increased intraocular pressure, most likely represents a combination of post-operative cerebral edema affecting frontal-subcortical circuits and a secondary ocular complication requiring urgent ophthalmologic intervention to prevent permanent vision loss.
Differential Diagnoses
Primary Neurological Causes
Cerebral edema with frontal lobe dysfunction is the most likely primary cause of the attention and initiation deficits, as falcine meningiomas commonly cause post-operative edema that can persist for weeks and specifically impair executive functions when involving parasagittal regions 1, 2.
Post-operative hemorrhage or infarction must be excluded urgently, as spontaneous intratumoral infarction can occur in meningiomas and present with new neurological deficits, though this typically occurs earlier in the post-operative course 3.
Residual tumor or incomplete resection affecting frontal regions can cause persistent cognitive deficits, particularly in elderly patients where gross total resection may be limited by hemostatic challenges 4, 2.
Hydrocephalus from altered CSF dynamics should be considered, as increased intracranial pressure can manifest with cognitive slowing and attention deficits 5.
Venous infarction from sacrifice of cortical veins during surgery, though modern microsurgical techniques aim to preserve major cortical veins 2.
Ocular Complications
The unilateral increased intraocular pressure on day 20 requires immediate ophthalmologic evaluation as this represents a vision-threatening emergency that can cause irreversible optic nerve damage 6.
Corticosteroid-induced IOP elevation is the most common cause, as prolonged high-dose dexamethasone (typically used for post-operative edema management) causes significant IOP elevation in a substantial proportion of patients 7, 8.
Pupillary block or angle closure from positioning, medications, or direct orbital involvement during surgery should be assessed with urgent gonioscopy 7.
Elevated intracranial pressure with papilledema can cause secondary IOP elevation and should be evaluated with fundoscopy looking for optic disc swelling 7, 5.
Sixth nerve palsy with venous congestion from cavernous sinus involvement or back-pressure can cause chemosis with increased IOP 7.
Immediate Management Algorithm
Step 1: Urgent Neuroimaging (Within 24 Hours)
Obtain MRI brain with and without contrast immediately to exclude hemorrhage, infarction, residual tumor, or hydrocephalus 5, 4.
Look specifically for: posterior globe flattening (56% sensitivity for elevated ICP), empty sella (56% sensitivity), optic nerve sheath enlargement, and signs of venous congestion 5.
If MRI unavailable, perform urgent CT brain followed by MRI when available 5.
Step 2: Ophthalmologic Emergency Management
Immediately initiate aggressive aqueous suppression with topical beta-blockers (timolol 0.5% twice daily), carbonic anhydrase inhibitors (dorzolamide or brinzolamide), and alpha-2 agonists to prevent irreversible optic nerve damage 6.
Check IOP within 30 minutes to 2 hours after initiating treatment, then every 2-4 hours until below 30 mmHg, with target IOP <21 mmHg 6.
Perform slit-lamp examination and gonioscopy (once corneal clarity permits) to identify mechanism: pupillary block, angle closure, or steroid-induced elevation 6.
If IOP >40 mmHg despite maximum medical therapy for 2-4 hours, consider urgent surgical intervention 6.
Taper or discontinue corticosteroids if steroid-induced IOP elevation is confirmed, balancing cerebral edema management against vision preservation 7, 8.
Step 3: Neurological Management
Continue high-dose dexamethasone (4mg every 6 hours) with gradual taper over 1-2 weeks if cerebral edema is confirmed on imaging, while closely monitoring IOP 8.
Elevate head of bed to 30-45 degrees to promote venous drainage 8.
Implement fluid restriction and osmotic diuretics (mannitol) if significant cerebral edema is present, maintaining euvolemia for adequate cerebral perfusion 8.
Perform serial neurological examinations every 4-6 hours looking for deterioration or signs of increased intracranial pressure 8.
Step 4: Cognitive Assessment and Rehabilitation
Initiate formal neuropsychological testing once acute issues are stabilized, as 69% of meningioma patients demonstrate cognitive dysfunction pre-operatively in multiple domains (memory, attention, executive function, processing speed) 1.
Attention and executive function deficits are the most sensitive domains affected by falcine meningiomas and typically improve post-operatively in the majority of patients 7, 1.
Refer to neuro-rehabilitation for cognitive therapy targeting attention and initiation deficits, as these can significantly improve with structured intervention 1.
Prognosis
Visual Prognosis
Vision preservation depends entirely on rapid IOP control within hours to days, as prolonged elevation causes irreversible optic nerve damage 6.
If steroid-induced, IOP typically normalizes within days to weeks after steroid taper with appropriate topical therapy 7.
If related to elevated intracranial pressure, prognosis depends on addressing the underlying cause (edema, hydrocephalus) 5.
Cognitive Prognosis
Cognitive improvement is expected in the majority of patients, as 44% of meningioma patients show normal cognitive function by 3 months post-operatively compared to 69% with dysfunction pre-operatively 1.
Test performance improves in all cognitive domains post-operatively except psychomotor speed and reaction time, which may remain impaired 1.
Age 77 is a negative prognostic factor, as elderly patients have more limited cognitive reserve and slower recovery, though improvement still occurs in most cases 7, 1.
Attention, executive functions, and memory remain in the low-average range even after improvement, suggesting persistent mild deficits are common 7.
Peak cognitive recovery occurs between 3-12 months post-operatively, with continued gradual improvement possible up to 44 months 7, 1.
Functional Prognosis
Favorable neurological outcome is expected if acute complications (hemorrhage, infarction, uncontrolled IOP) are excluded and managed appropriately 2, 9.
Modern microsurgical techniques for falcine meningiomas achieve gross total resection in 87.5% of cases with no mortality and new/worsened deficits in only 3% of patients 2.
Quality of life assessment at long-term follow-up shows 17% of patients report diminished functioning, primarily related to residual cognitive deficits rather than motor deficits 7.
Critical Monitoring Protocol
Follow-up schedule: Daily until IOP controlled and neurological status stable, then at 1 week, 2 weeks, 1 month, 3 months, 6 months, and 12 months 6, 1.
Each visit should include: IOP measurement, fundoscopy for papilledema, neurological examination, and assessment of cognitive function 6, 5.
Repeat MRI at 3 months to assess residual tumor and resolution of edema 4, 2.
Formal neuropsychological testing at 3 months and 12 months to document cognitive trajectory and guide rehabilitation 1.
Common Pitfalls to Avoid
Do not attribute all symptoms to "expected post-operative course" without excluding acute complications like hemorrhage, infarction, or hydrocephalus 3.
Do not continue high-dose corticosteroids without monitoring IOP, as steroid-induced glaucoma can develop insidiously and cause permanent vision loss 7, 6.
Do not delay ophthalmologic consultation when IOP is elevated, as hours matter in preventing irreversible optic nerve damage 6.
Do not assume cognitive deficits are permanent at 20 days post-operatively, as the majority of patients show significant improvement over 3-12 months 1.
Do not perform lumbar puncture before neuroimaging in a patient with potential mass effect or elevated ICP 5.