Recovery of swallowing after dysphagic stroke relates to functional reorganization in the intact motor cortex

Hamdy, Shaheen; Aziz, Qasim; Rothwell, John C.; Power, Maxine; Singh, Krish Devi; Nicholson, D A; Tallis, Raymond; Thompson, David G.

doi:10.1016/s0016-5085(98)70081-2

Cited by 322 publications

(262 citation statements)

References 15 publications

Supporting

Mentioning

241

Contrasting

Unclassified

Order By: Relevance

“…No relation between specific lesion location and the presence or absence of swallowing difficulties was observed in CVAi or CVAh. Some studies have demonstrated that the location and severity of the lesion in patients with CVA determines the effect on swallowing (2) , whereas others did not confirm the correlation between swallowing disorders and location of the lesion (12,36) . Magnetic transcranial stimulation reveals that dysphagic patients with a unilateral stroke have lower pharyngeal representations in the unaffected hemisphere than patients with unaltered swallowing regardless of the depth of the lesion (cortical or subcortical).…”

Section: Discussionmentioning

confidence: 97%

“…These findings indicate interhemispheric asymmetry of swallowing motor function, suggesting that lesions in the hemisphere with a dominant swallowing center result more frequently in oropharyngeal dysphagia (11) . Recovery of swallowing in dysphagic patients after a CVA is associated with increased pharyngeal representation in the unaffected hemisphere, suggesting the possibility of reorganization of this hemisphere (12) . This may explain why some patients develop dysphagia and others do not despite the same location of the lesion (13) .…”

Section: Discussionmentioning

confidence: 98%

See 1 more Smart Citation

Risk factors for swallowing dysfunction in stroke patients

Baroni

Fábio

Dantas

2012

Arq. Gastroenterol.

View full text Add to dashboard Cite

-Context -Stroke is a frequent cause of dysphagia. Objective -To evaluate in a tertiary care hospital the prevalence of swallowing dysfunction in stroke patients, to analyze factors associated with the dysfunction and to relate swallowing dysfunction to mortality 3 months after the stroke. Methods -Clinical evaluation of deglutition was performed in 212 consecutive patients with a medical and radiologic diagnosis of stroke. The occurrence of death was determined 3 months after the stroke. Results -It was observed that 63% of the patients had swallowing dysfunction. The variables gender and specific location of the lesion were not associated with the presence or absence of swallowing dysfunction. The patients with swallowing dysfunction had more frequently a previous stroke, had a stroke in the left hemisphere, motor and/or sensitivity alterations, difficulty in oral comprehension, alteration of oral expression, alteration of the level of consciousness, complications such as fever and pneumonia, high indexes on the Rankin scale, and low indexes on the Barthel scale. These patients had a higher mortality rate. Conclusions -Swallowing evaluation should be done in all patients with stroke, since swallowing dysfunction is associated with complications and an increased risk of death. HEADINGS -Stroke. Deglutition disorders.

show abstract

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 98%

Risk factors for swallowing dysfunction in stroke patients

Baroni

Fábio

Dantas

2012

Arq. Gastroenterol.

View full text Add to dashboard Cite

show abstract

“…25,26 Therefore, a benign and transient dysphagia would be expected in a unilateral hemispheric stroke due to bilateral cortical representation. 27 However, in WS, the main abnormality was observed in the pharyngeal phase of the swallowing reflex, and this cannot be solely explained by the dysfunction of some of the corticobulbar fibers, because in such an anatomic involvement, the swallowing reflex would remain normal. 12,15,16 Therefore, in WS due to LMI, the main reason for an abnormal swallowing function should be sought within the neural structures located in the medulla oblongata.…”

Section: Discussionmentioning

confidence: 99%

Dysphagia in Lateral Medullary Infarction (Wallenberg’s Syndrome)

Aydoğdu

Ertekin

Tarlacı

et al. 2001

Stroke

128

View full text Add to dashboard Cite

Background and Purpose-We have investigated the pathophysiological mechanisms of dysphagia in Wallenberg's syndrome (WS) that are due to lateral medullary infarction (LMI). Methods-Twenty patients with WS were evaluated by means of clinical and electrophysiological methods that measured the oropharyngeal phase of voluntarily initiated swallowing. For comparison, 22 patients with unilateral hemispheric infarction were investigated during the acute stage of stroke, and 4 patients with unilateral peripheral 9th and 10th cranial nerve palsies were studied. Age-matched 30 healthy control subjects were also included in the study. Results-It was found that dysphagia was clinically more severe in WS patients than in the patients in the other groups.The pharyngeal phase of swallowing was predominantly impaired, whereas in patients with hemispheric stroke, dysphagia was related only to the delay of triggering of the voluntarily induced swallowing. In WS patients, the swallowing reflex was extremely slow in spite of the unilateral involvement due to LMI, whereas the pharyngeal phase of reflex swallowing remained within normal limits in patients with unilateral hemispheric stroke and patients with unilateral peripheral 9th and 10th cranial nerve palsies. Conclusions-Although in WS the lesion due to LMI is unilateral, its effect on oropharyngeal swallowing is bilateral. In LMI, primarily the premotor neurons in the nucleus ambiguus and their connections seem to be affected. Consequently, a disruption and/or disconnection of their linkage to swallowing-related cranial motor neuron pools bilaterally and to the contralateral nucleus ambiguus could produce the swallowing disorders in WS. However, the remaining intact ipsilateral premotor neurons and the contralateral center in the medulla oblongata may eventually begin to operate and overcome the severity and long-term persistence of dysphagia.

show abstract

“…This asymmetry is independent of handedness and is greatest in the pharynx and esophagus. More recently, TMS has been used to measure pharyngeal responses in patients with brain injury on admission and at 1 and 3 mo after dysphagic hemispheric stroke (8). The study found that return of swallowing was associated with increased pharyngeal representation in the unaffected hemisphere, suggesting first that compensatory adaptation in the intact hemisphere drives much of this recovery and second that these responses have physiological relevance to swallowing recovery in stroke.…”

mentioning

confidence: 96%

Differential changes in human pharyngoesophageal motor excitability induced by swallowing, pharyngeal stimulation, and anesthesia

Fraser

Rothwell²,

Power³

et al. 2003

American Journal of Physiology-Gastrointestinal and Liver Physi

View full text Add to dashboard Cite

Hamdy. Differential changes in human pharyngoesophageal motor excitability induced by swallowing, pharyngeal stimulation, and anesthesia. Am J Physiol Gastrointest Liver Physiol 285: G137-G144, 2003. First published February 26, 2003 10.1152/ajpgi.00399.2002We investigated the effects of water swallowing, pharyngeal stimulation, and oropharyngeal anesthesia on corticobulbar and craniobulbar projections to human swallowing musculature. Changes in pathway excitability were measured via electromyography from swallowed intraluminal pharyngeal and esophageal electrodes to motor cerebral and trigeminal nerve magnetic stimulation. After both water swallowing and pharyngeal stimulation, pharyngoesophageal corticobulbar excitability increased (swallowing: pharynx ϭ 59 Ϯ 12%, P Ͻ 0.001; esophagus ϭ 45 Ϯ 20%, P Ͻ 0.05; pharyngeal stimulation: pharynx ϭ 76 Ϯ 19%, P Ͻ 0.001; esophagus ϭ 45 Ϯ 23%, P ϭ 0.05), being early with swallowing but late with stimulation. By comparison, craniobulbar excitability increased early after swallowing but remained unaffected by pharyngeal stimulation. After anesthesia, both corticobulbar (pharynx ϭ Ϫ24 Ϯ 10%, P Ͻ 0.05; esophagus ϭ Ϫ28 Ϯ 7%, P Ͻ 0.01) and craniobulbar excitability showed a late decrease. Thus swallowing induces transient early facilitation of corticobulbar and craniobulbar projections, whereas electrical stimulation promotes delayed facilitation mainly in cortex. With removal of input, both corticobulbar and craniobulbar projections show delayed inhibition, implying a reduction in motoneuron and/or cortical activity.

show abstract

Recovery of swallowing after dysphagic stroke relates to functional reorganization in the intact motor cortex

Cited by 322 publications

References 15 publications

Risk factors for swallowing dysfunction in stroke patients

Risk factors for swallowing dysfunction in stroke patients

Dysphagia in Lateral Medullary Infarction (Wallenberg’s Syndrome)

Differential changes in human pharyngoesophageal motor excitability induced by swallowing, pharyngeal stimulation, and anesthesia

Contact Info

Product

Resources

About