Why do patients with cortical embolism (CE) and stroke experience swallowing difficulties if the brainstem is not affected?

Why Cortical Strokes Cause Dysphagia Without Brainstem Involvement

Cortical strokes cause dysphagia because swallowing is controlled by bilateral cortical representations in addition to brainstem centers, and damage to the cortical swallowing network disrupts the voluntary and coordinating aspects of swallowing even when the brainstem remains intact. 1

The Cortical Control of Swallowing

While the brainstem contains the central pattern generator for swallowing reflexes, the cerebral cortex plays a critical role in the voluntary initiation, coordination, and modulation of swallowing. 1 This explains why purely cortical lesions can produce significant dysphagia:

• Swallowing requires intact cortical function for voluntary control of the oral preparatory and oral phases, as well as cortical modulation of the pharyngeal phase 1
• The cortex provides bilateral innervation to swallowing musculature, though this representation is asymmetric in most individuals 1
• Cortical damage disrupts the complex sensorimotor integration required for safe, efficient swallowing 1

Clinical Prevalence and Impact

The magnitude of this problem is substantial in cortical stroke:

• 51-64% of acute stroke patients develop dysphagia, even with cortical lesions 2
• Between 11% to 50% continue experiencing dysphagia at 6 months post-stroke despite initial recovery 3, 4
• The majority recover within 7 days, but persistent dysphagia significantly impacts mortality and quality of life 3, 4

Critical Clinical Pitfalls

Approximately 50% of aspirations from cortical stroke-related dysphagia are silent and go unrecognized until pulmonary complications develop. 4 This makes screening essential:

• All acute stroke patients must undergo dysphagia screening before any oral intake, regardless of lesion location 3
• Screening should occur within 24 hours of presentation using validated tools 3
• Dysphagia increases aspiration pneumonia risk 7-fold and is an independent predictor of mortality 4

Mechanism of Cortical Dysphagia

The specific mechanisms include:

• Disruption of voluntary swallowing initiation from damage to motor cortex and premotor areas 1
• Impaired sensory processing affecting the ability to recognize food bolus position and consistency 1
• Loss of cortical modulation of the brainstem swallowing centers, even though those centers remain structurally intact 1
• Aphasia and dysphasia are among the strongest predictors of prolonged dysphagia, indicating the importance of cortical language and motor planning areas 4

Recovery Through Cortical Plasticity

The fact that most patients recover suggests the remaining viable cortex can reorganize to compensate for damaged areas:

• Recovery occurs through plasticity and reorganization of the remaining cerebral cortex 1
• This explains why 73-86% of patients recover swallowing function within 7-14 days as cortical reorganization occurs 4
• The strongest predictors of prolonged dysphagia are stroke severity, aphasia, and specific lesion locations, not simply whether the brainstem is involved 4

Practical Management Implications

Given cortical control of swallowing:

• Never assume swallowing is safe based solely on brainstem integrity 3
• Maintain nil per os status until formal screening is completed 3
• Refer patients who fail screening to speech-language pathologists within 24 hours for comprehensive assessment 3
• Consider instrumental evaluation (videofluoroscopy or FEES) for suspected aspiration 3, 5
• Implement an interprofessional team approach including physicians, speech-language pathologists, dieticians, and nurses 3