The Role of the Insular Cortex in Dysphagia

The Role of the Insular Cortex in Dysphagia

Stephanie K. Daniels, MS, CCC1 and Anne L. Foundas, MD21Audiology/Speech Pathology Service,2Neurology Service, Veteran’s Affairs Medical Center, New Orleans, Louisiana, USA and1,2Department ofPsychiatry and Neurology, Tulane University School of Medicine, New Orleans, Louisiana, USA

Abstract. Recent data indicate that dysphagia may oc-cur following unilateral cortical stroke; however, the elu-cidation of specific cytoarchitectonic sites that producedeglutition disorders remains unclear. In a previous studyof unilateral cortical stroke patients with dysphagia,Daniels et al. [8] proposed that the insula may be impor-tant in swallowing as it was the most common lesion sitein the patients studied. Therefore, 4 unilateral stroke pa-tients with discrete lesions of the insular cortex werestudied to further facilitate understanding of the role ofthe insula in swallowing. Dysphagia, as confirmed byvideofluoroscopy, was evident in 3 of the 4 patients; allhad lesions that involved the anterior insula, whereas theonly patient without dysphagia had a lesion restricted tothe posterior insula. These data suggest that the anteriorinsula may be an important cortical substrate in swal-lowing. The anterior insula has connections to the pri-mary and supplementary motor cortices, the ventropos-terior medial nucleus of the thalamus, and to the nucleustractus solitarius, all of which are important regions inthe mediation of oropharyngeal swallowing. Therefore,discrete lesions of the anterior insula may disrupt theseconnections and, thereby, produce dysphagia.

Key words: Stroke — Insula — Videofluoroscopy —Deglutition — Deglutition disorders.

Traditionally, dysphagia has been associated with brain-stem or bilateral cortical lesions [1], and deglutitiondisorders resulting from these lesions have been welldocumented [2–7]. Although recent studies have demon-strated that dysphagia may also occur following unilat-

eral cortical stroke [1,8–16], the specific cortical lesionsthat may produce dysphagia remain unknown [8–10,16–19]. To date, most studies of unilateral stroke and dys-phagia have focused upon differences in patterns of dys-phagia in left vs. right hemispheric stroke [9,10,16–19].To our knowledge, only one study attempted to docu-ment the precise neuroanatomical location of strokes thatproduce dysphagia [8]. In that study, Daniels et al. [8]studied dysphagia following unilateral stroke in 8 pa-tients with left hemispheric damage (LHD) and 8 withright hemispheric damage (RHD). The insular cortex wasthe most common site of involvement, as it was lesionedin 11 of the 16 unilateral stroke patients with dysphagia.This finding was unexpected as lesions to the insula hadnot previously been associated with dysphagia. There-fore, Daniels et al. postulated that the insula may beimportant in swallowing because of its connectivity tocrucial cortical, subcortical, and brainstem sites knownto be important in swallowing.

As the insula has been associated with relatedswallowing and nutritional properties such as coordi-nated interaction of oral musculature, gustation, and au-tonomic functions, through connectivity or inherentproperties of its own [20–27], it was hypothesized thatthe insula, particularly the anterior insula, may contributeto oral and pharyngeal motility. To further elucidate thepossible role of the insula in deglutition, 4 cases of uni-lateral stroke patients with discrete lesions of the insulawere investigated. Neuroimaging studies, neurologicalexamination, videofluoroscopy, bedside swallowingevaluation, and clinical oropharyngeal examination wereperformed on all patients. The clinical findings and theextent of the insular lesions in these 4 patients demon-strate the probable importance of the anterior insula inthe mediation of swallowing.

Subjects and Methods

Subjects were selected from a sample of patients (n4 39) enrolled ina prospective dysphagia study consisting of consecutive unilateral

Correspondence to:Stephanie K. Daniels, M.S., CCC, Speech Pathol-ogy Service (126), VA Medical Center, 1601 Perdido Street, NewOrleans, LA 70146, USA

Dysphagia 12:146–156 (1997)

© Springer-Verlag New York Inc. 1997

stroke patients with new neurological deficits admitted to the VeteransAffairs Medical Center in New Orleans. The participants had no priorhistory of dysphagia, dementia, or neurodegenerative disorders. Theyconsisted of 4 males, ages 50–63 years (mean age 55.5 years) who hadsustained a unilateral cortical stroke with the lesion isolated to theinsular cortex, as documented on computed tomography (CT) scan ofthe head. Four additional patients in the larger stroke sample had le-sions that included portions of the insula and adjacent cortical regions.Three of these 4 had dysphagia. However, given that the lesions inthese additional 4 patients extended beyond the insular cortex, theywere not included in further analysis.

Procedures

A neurological examination was completed upon hospital admission.Speech-language testing, oromotor examination, and bedside swallow-ing assessment were conducted within the first week of hospitalization,except for Case 2, who was referred for evaluation 4 months after thestroke. Each patient underwent a CT scan and videofluoroscopic swal-low study (VSS) within 1 week of stroke onset, except for Case 2 whounderwent the VSS 4 months after the stroke.

Neurological ExaminationThe neurological evaluation included mental status examination and anelemental neurological assessment (Appendix 1). The mental statusexamination included tests of memory, intention, attention, languageand related functions, neglect, and visuospatial abilities. The elementalneurological assessment included cranial nerve examination, sensory(pain, temperature, proprioception, and vibration), motor (bulk, tone,strength, movement disorders), cerebellar, gait and station, deep tendonreflexes, and pathological reflexes (Babinski response and frontal re-lease signs).

Speech-Language AssessmentSpeech assessment included evaluation of articulatory precision andagility, fluency, resonance, and intelligibility. Language assessmentconsisted of evaluation of auditory comprehension, verbal fluency,naming, repetition, reading comprehension, and writing. Standardizedtesting in all areas was completed, as warranted, and consisted of theWestern Aphasia Battery [28] and the Boston Naming Test [29].

Oromotor ExaminationAssessment of oral musculature symmetry, strength, agility and sensa-tion was completed (Appendix 2). Features of the oromotor examina-tion included measurements of isolated movement as well as continualspeech and nonspeech movements of the mandible, lips, tongue, velum,and larynx. Light touch of the face was examined as well as the pres-ence of gag and volitional cough. Identification of dysphonic voicequality was made and classified as wet-hoarseness, strained, breathy, ornonspecific hoarseness.

Bedside Swallowing ExaminationThe clinical swallowing assessment consisted of administration of liq-uid, semisolid, and solid consistencies at varying calibrated volumeswith assessment of oral transition, oral retention, initiation of laryngealelevation, laryngeal excursion, voice quality after swallow, and spon-taneous cough. Assessments were initiated with a 3-ml liquid bolus andprogressed with increasing volumes as tolerated by the patient. Semi-solid and solid volumes were initiated at half teaspoon volumes andprogressed to continuous ingestion. Administration of a consistencywas terminated if a patient demonstrated, on two swallows, either acough or voice changes after the swallow.

Fluoroscopic ExaminationThe VSS was performed by speech pathology in conjunction withradiology. VSS samples were recorded using a Super-VHS videocas-sette recorder which was coupled to a counter timer that encoded digitaltime in hundredths of a second on each video frame. A video recordingof the oral cavity (anterior to the lips) and the pharynx (inferior to theupper esophageal sphincter) was obtained in the lateral plane, as thepatient swallowed liquid barium at volumes of 3, 5, 10, and 20 ml, and1⁄2 teaspoon barium paste, twice each.

Eight features of oropharyngeal dysmotility were evaluated.In the oral stage these features were anterior bolus loss, delayed ini-tiation of movement, and uncoordinated initiation of oral transfer. An-terior bolus loss was identified as spillage from the lips. Delayed ini-tiation of movement was identified as inability to begin oral transferupon command to swallow. Uncoordinated initiation of oral transferwas defined as groping and effortful labial, lingual, and mandibularmovements. The pharyngeal stage dysmotility patterns evaluated weredelayed pharyngeal swallow, reduced laryngeal excursion, penetrationinto the laryngeal vestibule, aspiration, and stasis. Delayed pharyngealswallow was measured from the time the bolus head reached the pointwhere the ramus of the mandible bisects the base of the tongue until theonset of laryngeal excursion [30]. The delay was rated as mild (0.45–2sec delay), moderate (3–5 sec delay), and severe (6 sec or greaterdelay). Patients with delay times <0.45 sec were considered withinnormal limits, a designation consistent with Tracy et al. [31] whoidentified average delay time for normal controls under age 60 as 0.24sec, and 0.36 sec for those over age 60. Vallecular and hypopharyngeallocations of the bolus prior to elicitation of the pharyngeal swallowwere identified as pooling. Decreased laryngeal elevation was identi-fied as reduced anterior, superior hylolaryngeal excursion. Stasis wasidentified as pharyngeal residue after the swallow. The specific locationof stasis (valleculae, pyriform sinus, or both areas) was noted and ratedon a scale of 1 (coating) to 3 (complete filling of space). Supraglotticpenetration was identified as entry of barium into the laryngeal vesti-bule superior to the true vocal folds, and aspiration was defined as entryof barium inferior to the level of the true vocal folds. The speechpathologist reviewing these cases had no prior knowledge of lesionlocalization.

Neuroimaging LocalizationCT scans were performed on a Picker 1200SX Expert or a PickerPQ2000. A series of 7-mm slices was obtained from the foramen mag-num to the vertex. Neuroimaging studies were reviewed and localizedusing Damasio and Damasio’s [32] technique, which utilizes standard-ized templates of axial CT sections at various angles to the canthome-atal line. Parameters of the lesion were mapped out within and acrosseach CT slice on the template. Once the lesion was mapped, the loca-tion of the lesion and cytoarchitectonic regions involved were deter-mined using standardized templates [32,33]. CT scans were obtainedwithin 1 week of the acute stroke. Although lesion localization on a CTscan within 1 week of the stroke may not be as circumscribed as CTscan localization at 1–2 months poststroke, the behaviors tested in thisstudy were assessed at the same time as the CT scan was obtained inorder to directly evaluate brain-behavior relationships.

The insular cortex lies buried in the depths of the lateralsulcus, and is overgrown by the frontal, temporal, and parietal opercula.Therefore, the insula is not visible when viewing the lateral surface ofthe cerebral hemisphere, but can be visualized when the frontal, tem-poral, and parietal lobes are separated. The insula forms a triangularcortical area with the apex directed forward and downward. Thus, theanterior and posterior extent of the insula are radially oriented, and theprecise extent of these regions is not well demarcated. However, thecentral sulcus of the insula can be used to divide the insula into anteriorand posterior portions [34,35]. Therefore, the anterior and posterior

S.K. Daniels and A.L. Foundas: Insular Cortex in Dysphagia 147

portions of the insula were determined based on the location of thecentral sulcus derived from lateral reconstructions of the lesions onstandardized templates. When the central sulcus is extended ventrallyonto the insular cortex, it is continuous with the central sulcus of theinsula. The full extent of the insula is best visualized in the axial plane,and therefore, standard axial CT scan images were used for lesionmapping.

Case Reports

Case 1

The first case is a 55-year-old male who presented witha 1-day history of dysarthria and left upper extremityweakness. Previous medical history was significant forhypertension. Neurological examination was unremark-able except for a mild left facial asymmetry consistentwith a left upper motor neuron (CN VII) lesion. Speechand language testing revealed dysarthria and dysphoniacharacterized by articulatory imprecision, strained vocalquality, and restricted volume and pitch ranges. Neitherbuccofacial nor speech apraxia was evident on examina-tion. A bedside swallowing assessment revealed inter-mittent coughing after ingestion of liquids, but there wasno wet hoarseness.

Fluoroscopic ExaminationOral stage functioning was intact. A mild delay in thepharyngeal swallow was evident with all volumes andconsistencies. Pooling in the valleculae and pyriform si-nuses was evident secondary to the delayed pharyngealswallow. Penetration and aspiration were not apparent.Pharyngeal stasis was not present.

Neuroimaging LocalizationLesion mapping demonstrated a 2 cm × 2 cmarea ofdecreased attenuation limited to the anterior extent of theinsula cortex in the right cerebral hemisphere. The insu-lar lesion extended across two consecutive axial imageswith a small extension superiorly into subcortical whitematter (Fig. 1).

Case 2

The second case is that of a 63-year-old male who wasadmitted to the hospital following the abrupt onset ofleft-sided weakness and inability to walk. Past medicalhistory was unremarkable. Neurological examination re-vealed anosognosia, left hemispatial neglect, left uppermotor neuron VII, and left hemiparesis. Speech and lan-guage testing revealed dysarthria and dysphonia charac-terized by articulatory imprecision, low volume, and wethoarseness. Neither buccofacial apraxia nor apraxia ofspeech was evident. A bedside swallowing examination

revealed anterior bolus loss, wet phonation after theswallow, but no elicitation of a cough.

Fluoroscopic ExaminationOral stage functioning was characterized by anterior bo-lus loss. A mild delay in the pharyngeal swallow yieldingvallecular and hypopharyngeal pooling was noted. Thedelayed pharyngeal swallow was evident only with liq-uid consistencies and resulted in penetration into the la-ryngeal vestibule without evidence of aspiration. Mild tomoderate vallecular stasis was noted with both consis-tencies.

Neuroimaging LocalizationLesion mapping demonstrated an area of decreased at-tenuation involving the anterior and posterior portions ofthe insular cortex in the right cerebral hemisphere. Thelesion extended 4 cm in the rostral-caudal plane on axialimage, with a medial-lateral depth of 2 cm. The insularlesion extended across two consecutive images, and in-volved small (<1 cm) portions of the frontal and tempo-ral opercula laterally, and extended to the image superiorto the insular cortex (Fig. 2).

Case 3

The third case is that of a 50-year-old male who devel-oped the abrupt onset of inability to speak 1 day afterhospitalization for chest pain. Previous medical historywas significant for atrial flutter and cardiomyopathy. Hesuffered a transient ischemic attack 7 months prior toadmission with transient dysarthria; however, no abnor-malities of language, deglutition, or gross motor func-tions were noted, and no lesions were evident on CTscan. Neurological examination on admission revealedmild distal weakness of the right upper extremity with aright Babinski response present. Speech and languageexamination demonstrated mild cortical stuttering char-

Fig. 1. Lesion mapping revealing right anterior insula localization inCase 1. Lesion localization was performed using Damasio and Dama-sio’s [32] method in all 4 cases.

148 S.K. Daniels and A.L. Foundas: Insular Cortex in Dysphagia

acterized by effortless sound and word repetitions andprolongations. Vocal quality was characterized by wethoarseness. Buccofacial apraxia, apraxia of speech, andasphasia were not present. A bedside swallowing exami-nation revealed intermittent wet hoarseness after inges-tion of liquids.

Fluoroscopic ExaminationOral stage functioning was intact. A mild delay in thepharyngeal swallow was evident with vallecular and hy-popharyngeal pooling. Penetration into the laryngeal ves-tibule was noted with liquid and semisolid consistencies,but aspiration was not identified. Laryngeal elevationwas reduced in maximum anterior-superior excursion.Mild to moderate stasis with both consistencies wasnoted in the valleculae and pyriform sinuses.

Neuroimaging LocalizationLesion mapping demonstrated an area of decreased at-tenuation of the anterior insular cortex in the left cerebralhemisphere. The lesion extended 1.5 cm in the rostral-caudal plane, with a depth of 1.5 cm medial-lateral oneach image. The full extent of the lesion involved twoconsecutive axial images (Fig. 3).

Case 4

The fourth case is that of a 54-year-old male who devel-oped the abrupt onset of mild word-finding difficulty.Past medical history was unremarkable. Neurological ex-amination revealed mild word-finding difficulty; cranialnerves, sensory, motor, cerebellar, gait, station, and re-flexes were intact. Speech and language testing revealedan anomic aphasia with lexical dysgraphia-dyslexia.Dysarthria, buccofacial apraxia, and apraxia of speechwere not evident. A bedside swallowing examination re-vealed no overt swallowing difficulty.

Fluoroscopic ExaminationThe VSS was unremarkable for any oral or pharyngealstage dysfunction. All parameters evaluated during theswallowing study were intact.

Neuroimaging LocalizationLesion mapping demonstrated an area of decreased at-tenuation limited to the posterior insular cortex in the leftcerebral hemisphere. The lesion extended 1.5 cm in therostral-caudal plane, with a depth of 1 cm medial-lateralon each image with the full extent of the lesion involvingtwo consecutive axial images (Fig. 4).

Results

Deglutition was evaluated by videofluoroscopy in 4 pa-tients with discrete lesions of the insular cortex (Table 1).Lesion mapping [24–27] of neuroimaging studies re-vealed that 2 subjects (Cases 1 and 2) had right insularlesions, 1 restricted to the anterior insula (Case 1) and theother involving anterior and posterior insula (Case 2).Two subjects (Cases 3 and 4) had left insular lesions, 1restricted to the anterior insula (Case 3) and the otherlesion isolated to the posterior insula (Case 4). Dyspha-gia, as identified by VSS, was evident in 3 (Cases 1, 2,3) of the 4 patients. Whereas dysphagia was present inthe subjects with lesions involving or restricted to theanterior insula, it was not present in the only patient witha lesion restricted to the posterior insular cortex (Case 4).A delayed pharyngeal swallow was the common dysmo-tility pattern in the 3 patients with dysphagia and resultedin supraglottic penetration in 2 of the 3 patients.

Discussion

Dysphagia, as verified by videofluoroscopy, was evidentin 3 of the 4 patients studied who had lesions of theinsular cortex. CT scan mapping of the lesions onto stan-

Fig. 2. Lesion mapping revealing right anterior and posterior insulalocalization in Case 2.

Fig. 3. Lesion mapping revealing left anterior insula localization inCase 3.


dardized templates demonstrated that all of the patientswith dysphagia had lesions involving the anterior insula;the lesion of the only patient without dysphagia wasrestricted to the posterior insula. These cases support ourhypothesis that the insular cortex may be an importantcortical substrate of swallowing. Furthermore, the disso-ciation of dysphagia by anterior-posterior involvementsuggests that the anterior insula may be more importantthan the posterior insula in swallowing. These findingsare provocative in that the insula, particularly the anteriorinsula, has not been previously implicated with dyspha-gia.

The anatomy and connectivity of the insula iscomplex, and little is known of the contribution of theinsular cortex to swallowing. To our knowledge, no pre-vious human studies have focused on the role of theinsular cortex in deglutition. Due to its redundant vascu-lar supply, focal lesions of this region are rare, and ad-jacent cortical and subcortical regions are generally in-volved and are often assumed to determine the resultantneurological deficits [20]. The insula lies deep to thesylvian fissure, and is covered by frontal, parietal, andtemporal opercula. The insula of the human brain has acentral sulcus, which divides the insula into anterior andposterior regions. The anterior insula consists of threeshort gyri (gyri breves), whereas the posterior insula con-sists of two long gyri (gyri longi) [36,37]. Histologicalstudies have identified three cytoarchitectonic subdivi-sions of the insula: agranular, dysgranular, and granular.The anterior insula is composed of a ventral-rostralagranular field, and the posterior insula is composed of adorsal-caudal granular field. A transitional area com-posed of a dysgranular field adjoins the agranular andgranular subdivisions [38]. Brodmann’s areas 14–16have been assigned to the agranular section of the insulawhereas area 13 is located in the granular section [37].

The anterior and posterior insula differ with re-gard to cytoarchitectonics and connectivity; therefore,these regions probably differ functionally. The anterior

insula appears to be a rich area of parallel connectivityclosely associated with many cortical and subcortical ar-eas that mediate swallowing. These areas include (1)premotor cortex; (2) gustatory, olfactory, limbic, and au-tonomic structures; (3) thalamus; and (4) nucleus tractussolitarius (NTS). The anterior insula has efferent connec-tions to premotor cortex (Brodmann’s area 6), whichcontains the motor representations for the face andmouth [20,21] with a rostral-caudal tonotopic organiza-tion [39,40]. It is well known that inferior and posteriorportions of the precentral gyrus (primary motor cortex),and portions of the supplementary motor cortex are im-portant in swallowing [review 41]. In primates, damageto the lateral precentral gyrus can disrupt oral transportand mastication [42,43], and repetitive electrical stimu-lation of the lateral and caudal surface of the precentralcortex can elicit swallowing alone, as well as combinedmastication and swallowing [44]. Magnetic stimulationstudies in humans implicate the lower precentral andposterior inferior frontal gyri for control of the oralphase, and the anterior inferior and middle frontal gyrifor pharyngeal and esophageal control [45]. Thus, dam-age to the anterior insula may produce deglutition disor-ders by disrupting anterior efferent cortical pathways.

In addition to connections with premotor cortex,the anterior insula has reciprocal connections with gus-tatory, olfactory, limbic, and autonomic structures[20,25,46–48]. In primates and rodents, the primary gus-tatory cortex has been localized to the frontal operculumand adjacent anterior insula [22–24]. This area, particu-larly the anterior insula, has separate representations fordifferent tastes. Furthermore, insular neurons appear tobe more sensitive to taste qualities than neurons of theNTS [49]. Neuroanatomical tracings in the rhesus mon-key demonstrated reciprocal connections between the an-terior insula and amygdala [47,48] with additional con-nections to the prepiriform olfactory cortex [25]. There-fore, damage to the anterior insula may producedisturbances of taste and smell that may contribute todisturbances of swallowing and eating.

The anterior insula is also connected to specificthalamic nuclei. It has extensive preferential reciprocalconnections with the parvicellular component of the ven-troposterior medial nucleus (VPMpc) of the thalamus,which contains sensory representations for the face andoral cavity [25,26,50,51]. Furthermore, the VPMpc is theprimary target of projections from rostral NTS [52]. TheNTS is the medullary region important in the identifica-tion of a swallowing stimulus and is the initial relayreceptor for gustatory input [52]. The NTS has projec-tions to the nucleus ambiguus (NA), and together, theNTS and the NA form part of the medullary centralpattern generator, or swallowing center [53]. Studiessuggest that the anterior insula provides cortical repre-

Fig. 4. Lesion mapping revealing left posterior insula localization inCase 4.


sentation for the NTS [25,27] and that these regionsalong with VPMpc may form a neural network that is thefoundation for the processing of gustatory as well asvisceral and autonomic information [26]. Additional ani-mal studies in rats and rabbits have shown that the an-terior insula also projects to rostral levels of the NTS[27,54,55]. Thus, this reciprocal connectivity betweenthe anterior insula and the NTS may further influencedeglutition. With its direct and indirect connectivity tothe NTS, and its role as part of the cortical center ofgustation, the anterior insular cortex may further partici-pate in deglutition through this visceral sensorimotorroute.

In contrast to the anterior insula, the posteriorinsula has projections to the inferior parietal lobule, re-ciprocal projections with the primary auditory cortex,extensive connections with the ventroposterior inferiornucleus and the pulvinar nucleus of the thalamus, andreciprocal connections with caudal NTS [20,25,26,56].Therefore, based on its connectivity, the functions of theposterior insula include audition, somatosensory re-sponses, and cardiovascular autonomic responses such asblood pressure and respiratory regulation, and excludegustatory and oromotor functions.

The cases presented in this study had discretelesions of the insula. Three of the 4 cases had lesionsinvolving the anterior insula. Dysphagia was evident inthese 3 cases, thus supporting the notion that the insula,particularly the anterior insular cortex, may be importantin swallowing. These conclusions are supported by theconnectivity of the anterior insula. The anterior insulahas connections to the primary and supplementary motorcortices, which facilitate coordinated interaction of thetongue, face, and jaw in swallowing. The anterior insulahas connections with the VPMpc of the thalamus, whichhas sensory representations for face and oral cavity, andis the first relay nucleus of visceral and gustatory affer-ents of the NTS. Additionally, the anterior insula hasconnections with the NTS, which is part of the medullary

swallowing center. Furthermore, the anterior insula helpsform the primary gustatory cortex. Theoretically, basedon the connectivity to these remote regions or throughinherent properties of the insula, the anterior insula maybe a crucial component in the swallowing loop and mayproduce dysphagia when lesioned in isolation (Fig. 5).

We postulate that lesions restricted to the anteriorinsula may produce dysphagia by disrupting the process-ing of gustatory input, which may in turn yield a delay intriggering a swallow response and impair pharyngealswallowing, as demonstrated in our case studies. A delayin elicitation of the pharyngeal swallow may result fromdisconnection of sensorimotor information between theNTS and the anterior insular cortex. Increasing sensorycharacteristics of a bolus (taste, volume, temperature)have been documented as reducing the delay in pharyn-geal swallow time in stroke patients [57–59]. Logemannet al. [58] identified a significant decline in the pharyn-geal delay time using a sour bolus. Intensifying gustatoryinput may result in stronger sensory signals from theoropharyngeal cavity to the brainstem and in turn to theanterior insula thus facilitating the timing of the swallow.Lesions to the anterior insula may reduce the magnitudeof sensory input, thus increasing the swallowing thresh-old and delaying elicitation of the pharyngeal swallow.

Though lesions to other cortical, subcortical, andbrainstem sites may produce changes in oral-pharyngealtransition, we suggest that isolated anterior insula le-sions produce a delayed pharyngeal swallow due to re-ductions in the processing of sensory input, which maybe primarily gustatory. In our study, the 3 patients withdysphagia had a delayed pharyngeal swallow as the com-mon dysphagia pattern. Delayed pharyngeal swallow isone of the most common features associated with dys-phagia after stroke [9,16,60]. Albeit these findings wereclinically mild in patients in this study, this delay in thepharyngeal swallow was significant enough to yield su-praglottic penetration in 2 of the 3 patients with dyspha-gia. Normal aging cannot account for this delay in the

Table 1. Age, lesion site, and clinical and fluoroscopic results for each patient

Caseno. Age Lesion Neurological deficits Speech/language VSS results

1 55 R anterior insula CN VII lesion Dysarthria, dysphonia Delayed swallow2 63 R anterior and posterior

insulaAnosognosiaL neglectL hemiparesis

DysarthriaDysphonia

Delayed swallowPenetrationStasis

3 50 L anterior insula R upper extremity weaknessR Babinski response

Cortical stutteringDysphonia

Delayed swallow↓Laryngeal elevationPenetrationStasis

4 54 L posterior insula No motor/sensory deficits Anomic aphasia, lexicaldysgraphia-dyslexia

Normal


pharyngeal swallow, which averaged between 1 and 2sec in each of our patients with dysphagia.

In a study of normal aging, Robbins et al. [61]found a positive average time for triggering a pharyngealswallow only in the oldest group (mean age 72 years),whereas the age groups below this had a negative aver-age time for elicitation of the swallow. The mean age ofour subjects was 55.5 years. It is also unclear whether thedysphagia observed in our patients was transient or per-sistent as repeat VSS was not performed. Although thera-peutic strategies and diet alterations were only tempo-rarily implemented in specific patients, the 1 patient(Case 2) who presented 4 months after the stroke didhave persistent dysphagia.

It is important to note that the majority of re-search concerning the insula has involved animal studies.Controversy exists partly because of the use of an animalmodel, but also because different anatomical boundarieswere used to delineate the anterior and posterior portionsof the insula. Although human studies of the insular cor-tex and swallowing are lacking, Penfield and Faulk [46]did identify alterations in gastrointestinal motility andsensations associated with digestion upon cortical stimu-lation of the anterior insula in humans.

Of note, in this larger series of 39 unilateralstroke patients from which the case studies were se-lected, only 4 had lesions restricted to the insular cortex.However, 4 additional patients had lesions that includedportions of the insula and adjacent cortical regions; 3 ofthese had documented dysphagia. These data provide ad-ditional support for the notion that the insula contributesto swallowing. Further investigation with a larger patientpopulation is warranted to support these preliminaryfindings. In addition, focusing on the effects of varyinggustatory stimuli upon timing of the pharyngeal swallowin patients with discrete lesions of the anterior insulamay facilitate understanding of the role of taste in swal-lowing elicitation. Animal studies with direct examina-tion of oropharyngeal motility after discrete anterior in-

sular lesioning may also clarify the neurophysiologicaland anatomical contributions of the insula to swallowing.

Acknowledgments.The authors gratefully acknowledge the ResearchService of VAMC, New Orleans, LA, and the critical review of themanuscript by Thomas W. Powell, Ph.D.

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The Role of the Insular Cortex in Dysphagia