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 swallowing difficulties because the cerebral cortex plays a critical role in voluntary swallowing control, sensory processing, and coordination of the swallowing sequence—the brainstem pattern generators alone cannot execute safe swallowing without intact cortical input and modulation. 1, 2

The Cortical Control of Swallowing

Bilateral Cortical Network Required for Normal Swallowing

• The cerebral cortex provides essential voluntary control, sensory integration, and initiation signals that are necessary for safe swallowing, operating through a broad bilateral neural network spanning from cortex to subcortical structures to brainstem 2
• Cortical lesions disrupt this bilateral activation pattern, causing dysphagia even when brainstem swallowing centers remain anatomically intact 3
• Research using magnetoencephalography demonstrates that dysphagic patients with hemispheric stroke show strong bilateral reduction of cortical swallowing activation in the early subacute phase 3

Specific Cortical Functions Lost in Cortical Stroke

• The cortex controls the oral preparatory phase (voluntary food manipulation), initiates the pharyngeal swallow reflex, and provides sensory feedback for swallow coordination 4, 2
• Cortical damage causes delayed oral transit, impaired swallow initiation, and disrupted sensory processing—all leading to aspiration risk even with intact brainstem centers 4
• Videofluoroscopic studies identify delayed oral transit and penetration of the laryngeal vestibule as independent predictors of persistent dysphagia at 6 months, demonstrating that cortical control deficits have lasting functional consequences 4

Clinical Implications and Prevalence

High Frequency Regardless of Lesion Location

• Dysphagia occurs in 30% to 64% of acute stroke patients and 37% to 78% of the general stroke population, affecting both cortical and brainstem stroke patients 5
• Between 11% to 50% of patients continue experiencing dysphagia at 6 months post-stroke despite initial recovery 1
• All acute stroke patients must undergo dysphagia screening before any oral intake, regardless of whether the lesion involves the brainstem, because cortical strokes alone frequently cause dangerous swallowing impairment 1, 6

Critical Safety Concerns

• Approximately 50% of aspirations from dysphagia are silent and go unrecognized until pulmonary complications develop 1
• Dysphagia increases aspiration pneumonia risk 7-fold and serves as an independent predictor of mortality 1
• The delayed or absent swallowing reflex detected by videofluoroscopy is the single independent baseline predictor of chest infection during 6-month follow-up 4

Mechanism: Diaschisis and Loss of Cortical Modulation

Why Intact Brainstem Centers Cannot Compensate

• The reduction of cortical activation in dysphagic cortical stroke patients can be explained by diaschisis—the dysfunction of remote brain areas connected to the damaged cortex 3
• Even though bulbar central pattern generators in the brainstem coordinate the pharyngeal swallowing phase, they require intact cortical input for proper initiation, timing, and sensory feedback to function safely 3
• Cortical plasticity and reorganization of remaining viable cerebral cortex are necessary for recovery of swallowing function, explaining why some patients have persistent dysphagia despite anatomically intact brainstem structures 7

Practical Management Algorithm

Immediate Assessment (Within 24 Hours)

• Screen all awake and alert stroke patients for dysphagia before allowing any oral intake using validated screening tools 1, 6
• Keep patients who fail screening NPO until comprehensive assessment, preferably within 3 days of stroke onset 6
• Perform bedside swallowing evaluation followed by instrumental examination (videofluoroscopy or FEES) if clinical signs indicate aspiration risk 5, 6

Risk Stratification Based on Findings

• Patients with videofluoroscopic evidence of delayed oral transit, delayed/absent swallow reflex, or penetration into the laryngeal vestibule have the highest risk of persistent dysphagia and complications 4
• Age >70 years and male sex are additional independent predictors of swallowing impairment at 6 months 4
• Initial aspiration risk is the most critical factor for both short-term and long-term dysphagia outcomes 1

Treatment Approach

• Implement a multi-intervention dysphagia program including modified diet consistency, airway protection strategies (chin tuck, head rotation), and swallowing exercises 5, 6
• Provide swallowing therapy at least 3 times weekly for patients able to participate, continuing as long as functional gains are observed 6
• The chin-tuck posture provides aspiration protection in fewer than 50% of neurogenic dysphagia cases, so do not rely on compensatory strategies alone—they may protect against aspiration but do not lead to recovery of swallowing ability 5

Common Pitfalls to Avoid

• Never assume swallowing is safe based solely on brainstem integrity or absence of brainstem lesion on imaging 1
• Do not wait for "obvious" signs of aspiration—50% of aspirations are silent and require instrumental assessment to detect 1
• Avoid allowing oral intake before formal screening, even in alert patients with purely cortical strokes 1, 6
• Recognize that recovery can occur beyond 3 years in some patients, so continue reassessment and therapy as long as functional improvements are demonstrated 8, 6