What could be the cause of new onset left-sided weakness in a patient with a history of right Middle Cerebral Artery (MCA) infarct, now presenting with hyponatremia and no evidence of new infarct or bleed on MRI/Magnetic Resonance Angiography (MRA)?

Recrudescence of Prior Stroke Deficits Due to Hyponatremia

The most likely explanation for this patient's new left-sided weakness is recrudescence (reappearance) of her prior right MCA stroke deficits triggered by the acute metabolic stress of hyponatremia and systemic infection, rather than a new structural brain lesion.

Primary Mechanism: Metabolic Unmasking of Prior Infarct

The combination of hyponatremia (128 mmol/L) and acute infection has unmasked neurological deficits from her previous right MCA territory damage through several mechanisms:

• Hyponatremia causes cerebral edema and increased intracranial pressure, which disproportionately affects previously damaged brain tissue that has impaired autoregulation and reduced functional reserve 1, 2
• Acute hyponatremia creates an osmotic gradient that promotes water movement into brain cells, causing cerebral edema that is particularly pronounced in areas with prior ischemic injury 3
• The old infarct zone has compromised blood-brain barrier integrity and abnormal osmoregulation, making it more vulnerable to metabolic disturbances than healthy brain tissue 4

Supporting Evidence for Recrudescence

Clinical Pattern Recognition

• Hyponatremia at 128 mmol/L is sufficient to cause neurological symptoms, particularly in patients with pre-existing brain lesions 1
• Focal neurological deficits can occur with acute hyponatremia, mimicking acute ischemic stroke even without new structural lesions 5
• The absence of new infarct or hemorrhage on MRI/MRA confirms this is not a new vascular event but rather functional impairment of previously damaged tissue 6, 7

Pathophysiological Mechanisms

• Hyponatremia in neurologic patients causes more aggressive cerebral edema due to impaired osmoregulation in pathologic brain lesions, increasing intracranial pressure 4
• Previously infarcted brain tissue has lost organic osmolytes during the initial injury and has impaired capacity to regulate cell volume during subsequent metabolic stress 3
• Systemic infection compounds the problem by causing inflammatory mediators, fever, and metabolic derangements that further stress the compromised brain tissue 2

Differential Considerations

Seizure Activity (Less Likely)

• Post-stroke seizures typically present with positive phenomena (twitching, jerking) rather than pure weakness 1, 7
• Todd's paralysis could cause transient weakness, but this patient's symptoms have persisted for 3 days without witnessed seizure activity 7
• EEG would be indicated if there were episodic symptoms or altered consciousness, but pure persistent weakness is more consistent with metabolic recrudescence 7

Hemorrhagic Transformation (Excluded)

• MRI/MRA has ruled out new hemorrhage, which would be visible on gradient-echo sequences 7

New Ischemic Stroke (Excluded)

• Diffusion-weighted MRI is highly sensitive for acute infarction and was negative 6, 7

Management Approach

Immediate Priorities

• Correct the hyponatremia gradually to avoid osmotic demyelination syndrome, targeting 4-6 mEq/L increase per 24 hours, not exceeding 8 mEq/L per 24 hours 1
• Treat the underlying infection aggressively, as sepsis and systemic inflammation worsen cerebral edema 2
• Avoid overly rapid correction in this elderly patient with chronic brain injury, as she is at higher risk for osmotic demyelination 1, 8

Hyponatremia Correction Strategy

• For moderate hyponatremia (120-125 mEq/L), water restriction to 1,000 mL/day is recommended, though this patient at 128 mEq/L may need less aggressive restriction 1
• Monitor serum sodium every 4-6 hours initially during correction to prevent overcorrection 1
• Consider isotonic saline rather than hypertonic saline given the moderate severity and need for controlled correction 8

Expected Clinical Course

• Neurological deficits should improve as hyponatremia corrects and infection resolves, typically within 48-72 hours 5
• If weakness persists despite sodium normalization, reconsider alternative diagnoses including delayed seizure activity or undetected small vessel disease 7

Critical Pitfalls to Avoid

• Do not assume new stroke without imaging confirmation - metabolic disturbances commonly unmask old deficits 5
• Do not correct hyponatremia too rapidly - this elderly patient with chronic brain injury is at high risk for osmotic demyelination syndrome, which can cause permanent neurological damage 1, 8, 3
• Do not overlook the infection - systemic illness is a major contributor to neurological decompensation in patients with prior stroke 2, 4
• Do not start empiric anticoagulation without confirming new ischemic stroke, as this patient's symptoms are metabolic rather than thrombotic 6

Monitoring Parameters

• Serial neurological examinations every 4-6 hours to track improvement with metabolic correction 7
• Serum sodium measurements every 4-6 hours during active correction phase 1
• Reassess with repeat imaging only if clinical deterioration occurs or if improvement does not follow sodium correction 6, 7