Sonja Suntrup

Functional oropharyngeal sensory disruption interferes with the cortical control of swallowing

BackgroundSensory input is crucial to the initiation and modulation of swallowing. From a clinical point of view, oropharyngeal sensory deficits have been shown to be an important cause of dysphagia and aspiration in stroke patients. In the present study we therefore investigated effects of functional oropharyngeal disruption on the cortical control of swallowing. We employed whole-head MEG to study cortical activity during self-paced volitional swallowing with and without topical oropharyngeal anesthesia in ten healthy subjects. A simple swallowing screening-test confirmed that anesthesia caused swallowing difficulties with decreased swallowing speed and reduced volume per swallow in all subjects investigated. Data were analyzed by means of synthetic aperture magnetometry (SAM) and the group analysis of the individual SAM data was performed using a permutation test.ResultsThe analysis of normal swallowing revealed bilateral activation of the mid-lateral primary sensorimotor cortex. Oropharyngeal anesthesia led to a pronounced decrease of both sensory and motor activation.ConclusionOur results suggest that a short-term decrease in oropharyngeal sensory input impedes the cortical control of swallowing. Apart from diminished sensory activity, a reduced activation of the primary motor cortex was found. These findings facilitate our understanding of the pathophysiology of dysphagia.

Tactile thermal oral stimulation increases the cortical representation of swallowing

BackgroundDysphagia is a leading complication in stroke patients causing aspiration pneumonia, malnutrition and increased mortality. Current strategies of swallowing therapy involve on the one hand modification of eating behaviour or swallowing technique and on the other hand facilitation of swallowing with the use of pharyngeal sensory stimulation. Thermal tactile oral stimulation (TTOS) is an established method to treat patients with neurogenic dysphagia especially if caused by sensory deficits. Little is known about the possible mechanisms by which this interventional therapy may work. We employed whole-head MEG to study changes in cortical activation during self-paced volitional swallowing in fifteen healthy subjects with and without TTOS. Data were analyzed by means of synthetic aperture magnetometry (SAM) and the group analysis of individual SAM data was performed using a permutation test.ResultsCompared to the normal swallowing task a significantly increased bilateral cortical activation was seen after oropharyngeal stimulation. Analysis of the chronological changes during swallowing suggests facilitation of both the oral and the pharyngeal phase of deglutition.ConclusionIn the present study functional cortical changes elicited by oral sensory stimulation could be demonstrated. We suggest that these results reflect short-term cortical plasticity of sensory swallowing areas. These findings facilitate our understanding of the role of cortical reorganization in dysphagia treatment and recovery.

Intravenous lacosamide—An effective add-on treatment of refractory status epilepticus

Status epilepticus (SE) is a frequent neurological emergency requiring immediate treatment. Therapy usually requires intravenous anticonvulsive medication. Lacosamide is a novel anticonvulsant drug that is available as infusion solution. We describe seven patients with focal SE who were treated with intravenous Lacosamide. All patients in our case series were unsuccessfully treated with other antiepileptic drugs before Lacosamide i.v. was added. In all cases, SE was terminated within 24 h after Lacosamide. There were no serious side effects or adverse events attributable to Lacosamide i.v. Our data suggest that Lacosamide might be an effective add-on treatment, if standard drugs fail or are unsuitable.

Cortical swallowing processing in early subacute stroke

BackgroundDysphagia is a major complication in hemispheric as well as brainstem stroke patients causing aspiration pneumonia and increased mortality. Little is known about the recovery from dysphagia after stroke. The aim of the present study was to determine the different patterns of cortical swallowing processing in patients with hemispheric and brainstem stroke with and without dysphagia in the early subacute phase.MethodsWe measured brain activity by mean of whole-head MEG in 37 patients with different stroke localisation 8.2 +/- 4.8 days after stroke to study changes in cortical activation during self-paced swallowing. An age matched group of healthy subjects served as controls. Data were analyzed by means of synthetic aperture magnetometry and group analyses were performed using a permutation test.ResultsOur results demonstrate strong bilateral reduction of cortical swallowing activation in dysphagic patients with hemispheric stroke. In hemispheric stroke without dysphagia, bilateral activation was found. In the small group of patients with brainstem stroke we observed a reduction of cortical activation and a right hemispheric lateralization.ConclusionBulbar central pattern generators coordinate the pharyngeal swallowing phase. The observed right hemispheric lateralization in brainstem stroke can therefore be interpreted as acute cortical compensation of subcortically caused dysphagia. The reduction of activation in brainstem stroke patients and dysphagic patients with cortical stroke could be explained in terms of diaschisis.

Evidence for adaptive cortical changes in swallowing in Parkinson’s disease

Dysphagia is a relevant symptom in Parkinsons disease, whose pathophysiology is poorly understood. It is mainly attributed to degeneration of brainstem nuclei. However, alterations in the cortical contribution to deglutition control in the course of Parkinsons disease have not been investigated. Here, we sought to determine the patterns of cortical swallowing processing in patients with Parkinsons disease with and without dysphagia. Swallowing function in patients was objectively assessed with fiberoptic endoscopic evaluation. Swallow-related cortical activation was measured using whole-head magnetoencephalography in 10 dysphagic and 10 non-dysphagic patients with Parkinsons disease and a healthy control group during self-paced swallowing. Data were analysed applying synthetic aperture magnetometry, and group analyses were done using a permutation test. Compared with healthy subjects, a strong decrease of cortical swallowing activation was found in all patients. It was most prominent in participants with manifest dysphagia. Non-dysphagic patients with Parkinsons disease showed a pronounced shift of peak activation towards lateral parts of the premotor, motor and inferolateral parietal cortex with reduced activation of the supplementary motor area. This pattern was not found in dysphagic patients with Parkinsons disease. We conclude that in Parkinsons disease, not only brainstem and basal ganglia circuits, but also cortical areas modulate swallowing function in a clinically relevant way. Our results point towards adaptive cerebral changes in swallowing to compensate for deficient motor pathways. Recruitment of better preserved parallel motor loops driven by sensory afferent input seems to maintain swallowing function until progressing neurodegeneration exceeds beyond the means of this adaptive strategy, resulting in manifestation of dysphagia.

Standardized endoscopic swallowing evaluation for tracheostomy decannulation in critically ill neurologic patients.

Objectives:Decisions regarding tracheostomy tube removal after mechanical ventilation often depend on the physician’s individual experience because evidence-based practice guidelines are still scarce, especially for critically ill neurologic patients. In these patients, the prevalence of aspiration is high and regarded as an important contributor to decannulation failure. The presence of severe neurological deficits may, however, give clinicians the subjective impression that a tracheostomy tube is still necessary although decannulation may actually be safe. It is therefore crucial to test swallowing function reliably prior to decannulation in this patient population. Design:Prospective observational study. Setting:University hospital, neurological ICU. Patients:One hundred tracheostomized patients with acute neurologic disease completely weaned from mechanical ventilation. Interventions:An endoscopic protocol evaluating readiness for decannulation and a conventional clinical swallowing examination were carried out by separate, experienced practitioners blinded to each other’s decisions. Patient management always followed the decision made with endoscopy. Measurements and Main Results:Practitioners’ decannulation decisions (yes/no) reached with both assessments were compared. Decannulated patients were monitored throughout their stay for complications related to tube removal. Endoscopy was performed successfully in all subjects without any complications. Following the protocol, the tracheostomy tube was successfully removed in 54 patients, whereas according to the clinical swallowing examination, only 29 patients would have been decannulated at that point. Only one patient needed recannulation due to respiratory problems, resulting in a failure rate of 1.9%. Conclusions:In neurologic patients, speech-language pathologists’ impressions about the patient’s state when clinically assessing indirect variables of swallowing function often lead to the unnecessary prolongation of cannulation time. Endoscopic evaluation has the advantage of objectively visualizing the patient’s ability to manage secretions directly and allows for faster but, nonetheless, safe decannulation. The endoscopic protocol proposed here is a safe, efficient, and objective bedside tool to guide decannulation decisions.

The impact of lesion location on dysphagia incidence, pattern and complications in acute stroke. Part 1: dysphagia incidence, severity and aspiration.

Although early identification of patients at risk for dysphagia is crucial in acute stroke care, predicting whether a particular patient is likely to have swallowing problems based on the brain scan is difficult because a comprehensive model of swallowing control is missing. In this study whether stroke location is associated with dysphagia incidence, severity and the occurrence of penetration or aspiration was systematically evaluated relying on a voxel‐based imaging analysis approach.

Cortical Processing of Swallowing in ALS Patients with Progressive Dysphagia – A Magnetoencephalographic Study

Amyotrophic lateral sclerosis (ALS) is a rare disease causing degeneration of the upper and lower motor neuron. Involvement of the bulbar motor neurons often results in fast progressive dysphagia. While cortical compensation of dysphagia has been previously shown in stroke patients, this topic has not been addressed in patients suffering from ALS. In the present study, we investigated cortical activation during deglutition in two groups of ALS patients with either moderate or severe dysphagia. Whole-head MEG was employed on fourteen patients with sporadic ALS using a self-paced swallowing paradigm. Data were analyzed by means of time-frequency analysis and synthetic aperture magnetometry (SAM). Group analysis of individual SAM data was performed using a permutation test. We found a reduction of cortical swallowing related activation in ALS patients compared to healthy controls. Additionally a disease-related shift of hemispheric lateralization was observed. While healthy subjects showed bilateral cortical activation, the right sensorimotor cortex was predominantly involved in ALS patients. Both effects were even stronger in the group of patients with severe dysphagia. Our results suggest that bilateral degeneration of the upper motor neuron in the primary motor areas also impairs further adjusted motor areas, which leads to a strong reduction of ‘swallowing related’ cortical activation. While both hemispheres are affected by the degeneration a relatively stronger activation is seen in the right hemisphere. This right hemispheric lateralization of volitional swallowing observed in this study may be the only sign of cortical plasticity in dysphagic ALS patients. It may demonstrate compensational mechanisms in the right hemisphere which is known to predominantly coordinate the pharyngeal phase of deglutition. These results add new aspects to our understanding of the pathophysiology of dysphagia in ALS patients and beyond. The compensational mechanisms observed could be relevant for future research in swallowing therapies.

Cortical compensation associated with dysphagia caused by selective degeneration of bulbar motor neurons

According to recent neuroimaging studies, swallowing is processed within multiple regions of the human brain. In contrast to this, little is known about the cortical contribution and compensatory mechanisms produced by impaired swallowing. In the present study, we therefore investigated the cortical topography of volitional swallowing in patients with X‐linked bulbospinal neuronopathy (Kennedy disease, KD). Eight dysphagic patients with genetically proven KD and an age‐matched healthy control group were studied by means of whole‐head magnetoencephalography using a previously established swallowing paradigm. Analysis of data was carried out with synthetic aperture magnetometry (SAM). The group analysis of individual SAM results was performed using a permutation test. KD patients showed significantly larger swallow‐related activation of the bilateral primary sensorimotor cortex than healthy controls. In contrast to the control group, in KD patients the maximum activity was located in the right sensorimotor cortex. Furthermore, while in nondysphagic subjects a previously described time‐dependent shift from the left to the right hemisphere was found during the one second of most pronounced swallow‐related muscle activity, KD patients showed a strong right hemispheric activation in each time segment analyzed. Since the right hemisphere has an established role in the coordination of the pharyngeal phase of swallowing, the stronger right hemispheric activation observed in KD patients indicates cortical compensation of pharyngeal phase dysphagia. Hum Brain Mapp 2009.

Dysphagia in X-linked bulbospinal muscular atrophy (Kennedy disease)

Dysphagia in X-linked bulbospinal muscular atrophy (Kennedy disease) has never been characterized in detail by objective swallowing studies. We assessed the nature of swallowing impairment in Kennedy disease by undertaking fiberoptic endoscopic evaluation of swallowing examinations of 10 genetically confirmed patients with Kennedy disease who were scored according to an ordinal rating scale including 25 different items. The results were compared to an age-matched control group of 10 healthy volunteers. Swallowing dysfunction was found in 80% of patients with Kennedy disease. The main pattern of dysphagia was an incomplete food bolus clearance through the pharynx with residues left in the valleculae overflowing into the laryngeal vestibule after the swallow. Total duration of the pharyngeal swallow was significantly shorter in patients with Kennedy disease compared to the control group. These findings suggest that dysphagia in Kennedy disease is predominantly characterized by an impairment of the pharyngeal phase of swallowing resulting from reduced base-of-tongue movement and bilateral paresis of pharyngeal and laryngeal muscles.