Version 1 in '89, not '83, sorry. Uh, had an al- already chronic infar

Version 1 in '89, not '83, sorry. Uh, had an al- already chronic infarct in the right, uh, cerebellar region. Now came with the complaints of, uh, deviation of the mouth, slurring of speech, and weakness, uh, of limbs. Uh, MRI showed hyperacute infarct in the pons. It started at 5:00 a.m. Uh, there is no clear changes yet.

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hyperacute pontine infarct MRI false negative DWI management tPA 2024

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Clinical Case Analysis: Hyperacute Pontine Infarct

Case Summary

Background: Male, known prior right cerebellar infarct from 1989 (old, chronic - established posterior circulation disease)
Current presentation: Onset 5:00 a.m. - facial deviation (likely ipsilateral LMN VII involvement), slurring of speech (dysarthria), limb weakness
Imaging: MRI - hyperacute pontine infarct, no clear DWI changes yet
Current time: 03:45 AM (next day context) - so this is still within the hyperacute window if onset was earlier today

Localisation

The clinical triad localises beautifully to the pons:

Feature	Localisation
Ipsilateral facial deviation (LMN pattern)	Ipsilateral CN VII nucleus - pons
Dysarthria/slurring	Corticobulbar tract or CN VII/XII nuclei - pons
Limb weakness	Corticospinal tract at pontine level

This is consistent with a unilateral mid-pontine or lower pontine infarct, likely involving the territory of paramedian pontine perforators from the basilar artery.

The prior right cerebellar infarct (1989) indicates longstanding vertebrobasilar atherosclerosis - this is the likely underlying mechanism (large artery disease / in-situ thrombosis of basilar perforators).

Why No DWI Changes?

This is the key imaging issue. The MRI was "hyperacute" with no clear DWI signal yet - this is a well-recognised phenomenon, not a reason to doubt the diagnosis.

False-negative DWI in hyperacute stroke occurs in:

Brainstem location - the single strongest predictor of false-negative DWI; up to 50% of brainstem infarcts may have initially negative DWI (PMC evidence)
Very short time from onset to scan - cytotoxic oedema may not have developed enough to restrict diffusion
Small perforator territory lesions (susceptibility artifacts from bone/air at skull base degrade EPI sequences)
1.5T vs 3T: susceptibility artifacts at brainstem are more prominent at 3T

The diagnosis is clinical + syndrome-based. A negative DWI does not rule out posterior circulation infarction when clinical symptoms persist.

Management must not be withheld purely on the basis of a negative DWI if the clinical picture is consistent.

Immediate Management Priorities

1. Establish exact onset time and eligibility window

Onset 5:00 a.m. - if imaging was done within 4.5 hours, IV alteplase (tPA) must be considered
Posterior circulation strokes (including pontine) are eligible for thrombolysis under the same time criteria as anterior circulation strokes

2. Check tPA eligibility - key considerations here:

Prior infarct from 1989 is not a contraindication - it is chronic and remote (37+ years ago), well outside the recent 3-month exclusion
Check: BP, glucose, platelets, coagulation, no haemorrhage on imaging
Check: prior anticoagulation? Recent surgery? Active bleeding?

3. If within 4.5 hours of onset - IV alteplase 0.9 mg/kg (max 90 mg)

10% as bolus, remainder over 60 minutes
Monitor closely - posterior circulation thrombolysis carries risk but outcomes in pontine stroke without treatment are poor

4. Consider mechanical thrombectomy if basilar artery involvement

If CTA/MRA shows basilar artery occlusion or significant stenosis, thrombectomy is indicated up to 24 hours in eligible patients
The 2024 ESO/ESMINT guideline specifically addresses this for basilar artery occlusion

5. If beyond window or tPA contraindicated:

Antiplatelet therapy (aspirin 300 mg loading, then dual antiplatelet as per POINT/CHANCE for minor-moderate stroke)
Heparin is generally not recommended for most ischaemic strokes but may be considered in basilar stenosis/occlusion scenarios by some guidelines

Monitoring

Neurological observations q15-30 min: watch for deterioration - pontine strokes can progress to locked-in syndrome or respiratory compromise
Airway assessment - dysphagia risk, aspiration risk
Monitor for haemodynamic instability - posterior circulation often involves autonomic pathways
Repeat MRI in 12-24 hours - the DWI lesion will become apparent; this also guides prognosis

Prognosis Note

Pontine infarcts carry significant morbidity:

Bilateral pontine involvement - risk of locked-in syndrome
Unilateral - generally better, but dysarthria and hemiparesis may persist
A 2024 case report documented recovery from locked-in syndrome after thrombolysis in bilateral pontine infarction with the "heart appearance" sign on MRI

The prior cerebellar infarct means collateral circulation may already be compromised and baseline reserve is reduced - this patient is at higher risk than a first-ever posterior circulation event.

Key Bottom Line

The absence of DWI changes is expected in hyperacute brainstem infarction and should not delay treatment. If the patient is within the thrombolysis window (4.5 hours from the 5:00 a.m. onset), tPA eligibility assessment should happen immediately. Vascular imaging (CTA or MRA of posterior circulation) should run in parallel to look for basilar artery pathology that may warrant thrombectomy.

No, time is... 9:15 AM here.

Got it. So local time is 9:15 AM, and symptom onset was 5:00 AM — that puts the patient at approximately 4 hours 15 minutes from onset.

Time-Critical Update

Where does this leave us?

4 hours 15 minutes from onset. This is still within the 4.5-hour IV alteplase window, but you are cutting it close.

The window is measured from last known well / symptom onset to needle time (start of infusion)
You need to get the drug running before 9:30 AM to stay within 4.5 hours
Every minute of delay costs neurons - this is a door-to-needle emergency right now

Immediate Actions (Next 15 Minutes)

Priority	Action
1	Rapid eligibility screen - BP, glucose, INR/platelets if on anticoagulants, confirm no haemorrhage on imaging
2	Confirm no absolute contraindications (recent surgery, active bleed, BP >185/110 - treat if needed)
3	If eligible: IV alteplase 0.9 mg/kg (max 90 mg) - 10% bolus, rest over 60 min
4	Simultaneously: CTA posterior circulation to look for basilar artery occlusion

The DWI-Negative Issue in This Context

At 4h15m, a negative DWI in a brainstem infarct with a clear clinical syndrome does not change the thrombolysis decision. Treat clinically. The false-negative rate for brainstem DWI in the first few hours is well established (up to 50% in some series).

If tPA is Given - What Next?

Basilar artery occlusion or severe stenosis on CTA → escalate to thrombectomy team regardless of whether tPA was given (bridging strategy)
No basilar occlusion → monitor post-thrombolysis, admit to stroke unit/ICU depending on severity
Watch for: neurological deterioration, haemorrhagic transformation, orolingual angioedema

If tPA is Contraindicated or Window is Missed

Aspirin 300 mg immediately (if no haemorrhage confirmed)
If basilar artery occlusion is found on vascular imaging → thrombectomy window extends to 24 hours under current guidelines (ESO/ESMINT 2024 for basilar artery occlusion)
Heparin infusion is sometimes considered in progressive basilar thrombosis - institution-dependent, not standard first-line

The vascular imaging is non-negotiable regardless of thrombolysis status - you need to know if the basilar artery is occluded.

Is the team currently running the eligibility checklist, or is there a specific decision point you're working through?

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