Can a patient have persistent left-sided hemiplegia after a remote Transient Ischemic Attack (TIA) with no evidence of chronic infarct on brain Magnetic Resonance Imaging (MRI)?

Persistent Left-Sided Hemiplegia After TIA Without MRI Evidence of Chronic Infarct

No, a patient cannot have persistent left-sided hemiplegia after a remote TIA with no evidence of chronic infarct on brain MRI, as this contradicts the fundamental definition of a TIA, which by definition resolves completely without permanent neurological deficits or evidence of infarction.

Understanding TIA vs. Stroke

A Transient Ischemic Attack (TIA) is defined as:

• A brief episode of neurological dysfunction caused by focal brain or retinal ischemia with clinical symptoms typically lasting less than one hour and without evidence of acute brain infarction 1
• Neurological signs or symptoms lasting <24 hours presumed to be due to focal brain, spinal cord, or retinal ischemia, but without evidence of acute infarction by neuroimaging or pathology 2

In contrast, an ischemic stroke is characterized by:

• Acute onset of focal neurological signs or symptoms conforming to a vascular territory with signs or symptoms lasting ≥24 hours or until death, with pathology or neuroimaging evidence of CNS infarction 2
• Symptoms lasting <24 hours but with pathology or neuroimaging confirmation of CNS infarction in the corresponding vascular territory 2

Why Persistent Hemiplegia Cannot Be from a TIA

1. Diagnostic contradiction: By definition, TIA symptoms resolve completely, typically within 24 hours. Persistent hemiplegia (lasting beyond 24 hours) would classify the event as a stroke, not a TIA 1.

2. Imaging expectations:

   • If a patient has persistent neurological deficits, brain imaging (particularly MRI with diffusion-weighted imaging) would be expected to show evidence of infarction 1.
   • Even in cases where symptoms resolve within 24 hours (meeting the time-based definition of TIA), diffusion-weighted MRI can detect infarction in 30-50% of these patients, reclassifying them as strokes 3.

3. Pathophysiological basis:

   • TIA represents a temporary ischemic penumbra that resolves without permanent tissue damage 4.
   • Persistent deficits indicate progression from penumbra to infarction, which would be visible on MRI 4.

Alternative Explanations for This Clinical Scenario

If a patient presents with persistent left-sided hemiplegia and no evidence of infarct on MRI, consider:

1. Timing of MRI: Was the MRI performed too early after symptom onset? Diffusion changes may take time to develop.

2. MRI quality and technique: Standard MRI sequences might miss small infarcts. Diffusion-weighted imaging (DWI) is more sensitive for detecting acute ischemic changes 5.

3. Alternative diagnoses:

   • Functional neurological disorder
   • Todd's paralysis following seizure
   • Hemiplegic migraine
   • Multiple sclerosis or other demyelinating conditions
   • Conversion disorder
   • Small vessel disease with cumulative effects not visible as a single lesion

4. Rare exceptions: There are rare case reports of reversible DWI lesions in TIA patients without arterial recanalization 6, but these patients' symptoms resolved completely (unlike persistent hemiplegia).

Clinical Approach to This Scenario

When faced with persistent hemiplegia without MRI evidence of infarction:

1. Repeat imaging: Consider repeat MRI with DWI and perfusion studies if initial imaging was negative 1.

2. Comprehensive vascular assessment: Complete CTA or MRA from aortic arch to vertex to identify potential vascular abnormalities 2, 1.

3. Cardiac evaluation: Perform ECG, echocardiography to identify potential cardioembolic sources 1.

4. Consider alternative diagnoses: Evaluate for other neurological conditions that could mimic stroke symptoms.

Conclusion

The presence of persistent left-sided hemiplegia without evidence of infarction on MRI is inconsistent with the diagnosis of a remote TIA. This clinical presentation requires further investigation to determine the true etiology of the persistent neurological deficit, as it cannot be attributed to a TIA by definition.