Dysphagia after pediatric functional hemispherectomy

Clinical article

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Object

Functional hemispherectomy is a well-recognized surgical option for the treatment of unihemispheric medically intractable epilepsy. While the resultant motor deficits are a well-known and expected consequence of the procedure, the impact on other cortical functions has been less well defined. As the cortical control of swallowing would appear to be threatened after hemispherectomy, the authors retrospectively studied a pediatric population that underwent functional hemispherectomy for medically intractable epilepsy to characterize the incidence and severity of dysphagia after surgery.

Methods

A retrospective cohort (n = 39) of pediatric patients who underwent hemispherectomy at a single institution was identified, and available clinical records were reviewed. Additionally, the authors examined available MR images for integrity of the thalamus and basal ganglia before and after hemispherectomy. Clinical and video fluoroscopic assessments of speech pathology were reviewed, and the presence, type, and duration of pre- and postoperative dysphagia were recorded.

Results

New-onset, transient dysphagia occurred in 26% of patients after hemispherectomy along with worsening of preexisting dysphagia noted in an additional 15%. Clinical symptoms lasted a median of 19 days. Increased duration of symptoms was seen with late (> 14 days postoperative) pharyngeal swallow dysfunction when compared with oral dysphagia alone. Neonatal stroke as a cause for seizures decreased the likelihood of postoperative dysphagia. There was no association with seizure freedom or postoperative hydrocephalus.

Conclusions

New-onset dysphagia is a frequent and clinically significant consequence of hemispherectomy for intractable epilepsy in pediatric patients. This dysphagia was always self-limited except in those patients in whom preexisting dysphagia was noted.

Abbreviations used in this paper:CSE = clinical swallow evaluation; VFSS = videofluoroscopic swallow study.

Abstract

Object

Functional hemispherectomy is a well-recognized surgical option for the treatment of unihemispheric medically intractable epilepsy. While the resultant motor deficits are a well-known and expected consequence of the procedure, the impact on other cortical functions has been less well defined. As the cortical control of swallowing would appear to be threatened after hemispherectomy, the authors retrospectively studied a pediatric population that underwent functional hemispherectomy for medically intractable epilepsy to characterize the incidence and severity of dysphagia after surgery.

Methods

A retrospective cohort (n = 39) of pediatric patients who underwent hemispherectomy at a single institution was identified, and available clinical records were reviewed. Additionally, the authors examined available MR images for integrity of the thalamus and basal ganglia before and after hemispherectomy. Clinical and video fluoroscopic assessments of speech pathology were reviewed, and the presence, type, and duration of pre- and postoperative dysphagia were recorded.

Results

New-onset, transient dysphagia occurred in 26% of patients after hemispherectomy along with worsening of preexisting dysphagia noted in an additional 15%. Clinical symptoms lasted a median of 19 days. Increased duration of symptoms was seen with late (> 14 days postoperative) pharyngeal swallow dysfunction when compared with oral dysphagia alone. Neonatal stroke as a cause for seizures decreased the likelihood of postoperative dysphagia. There was no association with seizure freedom or postoperative hydrocephalus.

Conclusions

New-onset dysphagia is a frequent and clinically significant consequence of hemispherectomy for intractable epilepsy in pediatric patients. This dysphagia was always self-limited except in those patients in whom preexisting dysphagia was noted.

Functional or disconnective hemispherectomy is a surgical procedure used in intractable, lateralized epilepsy. First conceived as an anatomical resection of the involved hemisphere, it demonstrated acceptable seizure control but was limited by postoperative complications, especially superficial cerebral hemosiderosis and hydrocephalus.12,16 In response, Rasmussen developed the functional hemispherectomy, which aimed to provide a complete functional disconnection while minimizing resection of the cerebrum.30 This trend of functional disconnection without resection has continued in recent years with the development of a number of hemispherotomy techniques.4,23,25 Current literature reports a seizure freedom rate ranging from 61% to 85% after hemispherectomy for medically intractable epilepsy of all causes.10,19,26,29 Data on other complications of the procedure are more limited and are primarily concerned with the incidence of posthemispherectomy hydrocephalus, which has been reported in 5.3%–23% of patients.13,26 Liégeois et al. reported persistent mild dysarthria in pediatric patients undergoing assessment from 1 to 13 years posthemispherectomy; none of these patients was noted to have a swallowing issue.14 No prior literature exists specifically detailing the incidence and severity of dysphagia after hemispherectomy.

Dysphagia is defined as a clinically evident impairment in swallowing. The swallow process is classically divided into the oral, pharyngeal, and esophageal phases.20,24 The oral phase consists of chewing and bolus formation via the tongue and hard palate. It is under voluntary control, and oral-phase dysphagia most frequently manifests as oral residue and difficulty with formation and control of the food bolus. The pharyngeal phase is an involuntary process involving coordinated movements in the pharyngeal musculature, vocal cords, and epiglottis that move the food bolus through the pharynx into the esophagus and prevent entry into the trachea. Pharyngealphase dysphagia is the most critical and typically results in aspiration and its associated symptoms. The esophageal phase consists of involuntary peristaltic movement of the bolus into the stomach.

Neurological disease resulting in dysphagia most commonly affects the oral and less commonly the pharyngeal phases of swallowing,21,22 with approximately one-third of patients demonstrating oropharyngeal dysphagia early after unilateral stroke.2,6 The swallow reflex is mediated by both cortical and brainstem input,24 with lesions of the primary sensorimotor cortex, insula, frontal operculum, anterior cingulate cortex, internal capsule, and supplementary motor area all being associated with dysphagia.9,11,17,22 Hemispheric dominance of swallowing appears to be present but highly variable between individuals7,15,24 with a suggestion that it shifts between hemispheres at different stages during the swallow.27

As prior studies have not specifically addressed these findings, and the cortical control of swallowing would seem to be at risk with the hemispherectomy procedure, we performed a retrospective analysis of our functional hemispherectomy procedure to assess for postoperative dysphagia.

Methods

Patient Selection

We retrospectively identified 39 pediatric patients who underwent functional hemispherectomy at Seattle Children's Hospital between 1997 and 2012 and who had adequate documentation to assess pre- and postoperative swallowing function. This review was performed in a manner approved by the Seattle Children's Hospital Institutional Review Board. The majority of procedures were performed by the senior author (J.G.O.). All patients had a diagnosis of intractable epilepsy and were evaluated by an epileptologist and a multidisciplinary epilepsy board prior to hemispherectomy. The majority of procedures were performed using the approach of Schramm et al.,25 namely, resection of the anterior and mesial temporal lobe, corpus callosotomy, frontobasilar and occipital disconnection, and insular resection.

Assessment of Dysphagia

The presence of dysphagia symptoms was determined preoperatively and postoperatively by examining patient records. Dysphagia was defined by documentation of clinical symptoms, initiation of dysphagia diet precautions, and the need for enteral nutrition and/or supplementation. When available, the results of clinical swallow evaluations (CSEs) and videofluoroscopic swallow studies (VFSSs) were used to assess for the presence of dysphagia and to characterize the type and severity of dysphagia present. Clinical documentation was reviewed by a speech pathologist (T.M.). Patients were then stratified using the following classification to characterize the presence of dysphagia after hemispherectomy: new dysphagia, preexisting dysphagia with worsening, preexisting dysphagia without worsening, and no dysphagia. Those patients with new or worsened dysphagia were additionally subdivided into those with evidence of dysphagia on CSE or VFSS and those with clinical evidence only. The duration and severity of symptoms were assessed during the postoperative follow-up period.

Imaging Assessment

Postoperative MR images were examined separately by a neurosurgical resident (R.T.B.) and senior attending neurosurgeon (J.G.O.). Magnetic resonance imaging was used to assess for resection of specific anatomical structures including full cortical disconnection, insular resection, and integrity of the basal ganglia and thalamus before and after hemispherectomy.

Statistical Analysis

Statistical significance was determined using the Fisher's exact test and the exact Mann-Whitney test using the PASW Statistics 18 (SPSS, Inc.) toolset with a p value < 0.05 deemed significant. Multivariate analysis was additionally performed with a p value of 0.05 deemed significant.

Results

Thirty-nine patients met inclusion criteria. The median age was 5.7 years (range 28 days to 18.9 years). Of the 39 patients the most common indications for surgery were disorders of cortical development (hemimegalencephaly, polymicrogyria, and cortical dysplasia; n = 12, 30.8%), stroke (n = 11, 28.2%), and Rasmussen encephalitis (n = 4, 10.33%), followed by unknown neonatal (n = 3, 7.7%), nonaccidental trauma and Sturge-Weber syndrome (n = 2, 5.1% each) and West syndrome, anaplastic oligodendroglioma, choroid plexus papilloma, encephalitis, and Wolf-Hirschhorn syndrome (n = 1, 2.6% each) (Table 1).

TABLE 1:

Clinical characteristics in the 39 children undergoing hemispherectomy*

Case No.Age at Op (yrs), SexHemisphereCause of EpilepsySeizure ControlFollow-Up (yrs)Postop HydrocephalusPreop DysphagiaNew/Worsened Dysphagia
10.8, FltWest syndromeno8.2nonono
21.7, Mrtunknownyes6.9noyesno
34.2, Frtstrokeyes3.5nonono
44.8, FrtPMGyes1.6nonoyes
55.7, Mltstrokeyes2.9nonono
69.0, Mrtstrokeyes5.7nonono
78.2, MltSturge-Weberyes5.7nonoyes
816.8, Mltstrokeyes2.9yesnoyes
96.0, Fltunknownyes0.8nonono
100.1, FrtHMEyes6.5noyesno
113.4, MltCPPyes4.8noyesyes
121.0, FltHMEyes0.8nonoyes
131.1, FltHMEyes3.9noyesyes
149.3, MrtHMEyes3.5noyesno
153.1, FltSturge-Weberyes0.3noyesyes
166.9, Frtstrokeyes6.3nonono
172.7, Frtanaplastic oligoastrocytomano2.6noyesyes
180.6, Mltdysplasiano6.3noyesno
1912.6, FrtREyes6.7nonono
2013.2, FrtREyes2.8nonono
215.6, FltHMEno10.6nonoyes
2217.2, Mltstrokeno0.6nonono
238.1, FrtREno6.3yesnoyes
2412.6, Mltstrokeyes1.7nonono
259.4, Frtdysplasiayes5.1nonoyes
267.9, Frtstrokeyes1.7nonono
274.5, FltNATno5.0yesnoyes
280.8, Frtdysplasiano9.3yesnono
2918.2, Mrtstrokeyes1.9nonono
3010.1, Fltstrokeyes1.7yesnono
314.5, MltNATno4.1noyesyes
3218.9, MltWolf-Hirschhornno2.3yesnono
339.7, MrtREyes0.4nonoyes
340.5, Mrtunknownyes5.5noyesyes
356.1, FrtHMEyes1.2nonono
368.0, Mltencephalitisno9.3noyesno
371.4, MrtHMEyes0.5nonoyes
382.1, Mltdysplasiayes1.5nonono
392.8, Mltstrokeyes6.6nonono

* CPP = choroid plexus papilloma; HME = hemimegalencephaly; NAT = nonaccidental trauma; PMG = polymicrogyria; RE = Rasmussen encephalitis.

Onset of new dysphagia symptoms was observed in 10 patients (25.6%) after hemispherectomy (Fig. 1A). Of these patients, 8 (80%) demonstrated a CSE or VFSS consistent with dysphagia while the remaining 2 (20%) had only clinical evidence of dysphagia. Preexisting dysphagia symptoms were identified by CSE or VFSS results in 11 patients (28.2%). Multiple assessments via CSE or VFSS were available in two-thirds of patients. Clinical worsening of dysphagia was observed in 6 patients (54.5%) after hemispherectomy with CSE or VFSS confirmation in all 6; there was no evidence of change in preexisting deficits in the 5 (45.5%) remaining patients. The remaining 18 patients (46.2%) did not have clinical evidence of dysphagia prior to or after hemispherectomy.

Of the patients who underwent CSE and/or VFSS for new and/or preexisting dysphagia in the early (< 14 days) postoperative period, dysfunction was identified in the oral phase in 3 (23.1%) and in the oral and pharyngeal (oropharyngeal) phase in 10 (76.9%) (Fig. 1B). For the patients with new dysphagia in the early postoperative period, 3 (42.9%) had impairment of the oral phase only and 4 (57.1%) had impairment of the oropharyngeal phase. All 6 patients whose preexisting symptoms worsened and who additionally had a CSE and/or VFSS performed in the first 2 weeks after hemispherectomy demonstrated impairment in the oropharyngeal phase of the swallow.

Fig. 1.
Fig. 1.

Incidence and characteristics of dysphagia following hemispherectomy. A: Presence or absence of dysphagia in children with and without preexisting deficits after surgery. Values on the y axis are the number of patients. B: Type of dysphagia. The gray bars indicate the early phase (< 14 days postoperative) and the black bars indicate the late phase (> 14 days postoperative). Values on the y axis are the number of patients. C: Median duration of late-phase dysphagia.

For patients with new-onset dysphagia, dysfunction in the late postoperative period (> 14 days) was noted in the oral phase in 2 (40%), pharyngeal phase in 2 (40%), and oropharyngeal phase in 1 (20%). For those children with new or worsened dysphagia that persisted longer than 2 weeks, the mean duration of symptoms with oral phase dysphagia only (n = 4) was 32 days compared with a mean duration of 393 days for those with pharyngeal phase dysphagia (n = 5) (Fig. 1C). There was a statistically significant association between pharyngeal swallow dysfunction in the late postoperative period and duration of symptoms (p = 0.016). For those patients with preexisting dysphagia, there was no clear association with the type of dysphagia identified and likelihood of clinical worsening after hemispherectomy.

Initiation of dysphagia diet modifications was required in 13 (81.3%) of the 16 children who developed new or worsened dysphagia; for the remaining 3 patients oral intake was initially deemed unsafe. A nasogastric tube was placed for complete or supplemental nutrition in 10 children (62.5%). The mean duration of nasogastric tube placement in all patients was 29 days (range 9–110 days). Additionally, long-term enteric supplementation via placement of a gastric feeding tube was required in 3 children (13.3%).

Dysphagia symptoms persisted for a median 19 days (range 8 days to 4.15 years) in all patients with new or worsened deficits after hemispherectomy as measured by the need for a dysphagia diet or enteral nutrition and/or supplementation. Of the patients with new dysphagia, the median duration of symptoms was 19.5 days (range 8 days to 1.42 years) and for worsened dysphagia the median duration was 19 days (range 12 days to 4.15 years). This postoperative dysphagia resolved in all patients with new or worsened dysphagia and in all except one patient with worsened dysphagia who continued to require enteral supplementation via gastric tube at last follow-up (4.1 years).

Stroke of all types was the most common etiology in patients without dysphagia (n = 11), with only one of those patients developing new dysphagia after hemispherectomy. There was a negative association between stroke and new or worsened dysphagia after surgery (p = 0.014). There was no other clear association with etiology and the incidence of posthemispherectomy dysphagia.

The median age for children with new dysphagia was 6.82 years, for preexisting dysphagia with worsening 2.87 years, for preexisting dysphagia without worsening 1.65 years, and for no dysphagia 6.50 years. The median age at the time of hemispherectomy in patients with new or worsened dysphagia was 4.49 years compared with a median age of 6.12 years for those without (Table 2). There was no significant association between age at the time of hemispherectomy and the occurrence of postoperative dysphagia (p = 0.275).

TABLE 2:

Association between clinical and radiological characteristics and presence or absence of posthemispherectomy dysphagia

CharacteristicNew or Worsened Dysphagia (n = 16)No or Stable Dysphagia (n = 23)p Value
median age at op (yrs)4.496.120.275
postop hydrocephalus3 (18.8%)3 (13.0%)0.674
absence of seizure freedom6 (37.5%)5 (21.7%)0.307
preop basal ganglia & thalamus damage4 (25%)9 (39.1%)0.726
postop preservation of thalamus5 (31.3%)1 (4.3%)0.073

Of the patients with new or worsened dysphagia 9 (56.3%) underwent a left hemispherectomy and 7 (43.8%) underwent a right hemispherectomy. There was no relationship with new or worsened dysphagia and whether the hemispherectomy was performed on the right or left side (p = 0.748).

Review of postoperative imaging demonstrated that all patients had resection of the insula. There was complete or partial preoperative infarction or absence of the thalamus and basal ganglia in 12 children (30.8%) and of the basal ganglia only in an additional 2 children (5.1%). Of those patients with absence of both (n = 9, 75%), the majority were secondary to neonatal stroke. Preoperative absence of the thalamus and basal ganglia did not influence development of dysphagia after hemispherectomy (p = 0.726). In those children with an intact ipsilateral thalamus prior to surgery, 19 (70.4%) had complete or partial injury as seen on postoperative CT and/or MRI. Of those who did not have injury of the thalamus, 5 (83.3%) developed new dysphagia posthemispherectomy. There was a trend toward association of a structurally preserved thalamus postoperatively and new dysphagia, but this did not achieve statistical significance (p = 0.073). Complete or partial resection or infarction of the basal ganglia was seen in all patients; this did not correlate with postoperative dysphagia.

Postoperative hydrocephalus developed in 6 patients (15.4%), 3 (50%) of whom also had new dysphagia. There was no relationship between postoperative hydrocephalus and dysphagia after hemispherectomy (p = 0.674). Complete and durable absence of clinical seizure events after surgery occurred in 28 patients (71.8%), with a median length of follow-up of 3.54 years (range 0.3–10.6 years). Of the patients who had persistence or late recurrence of seizures, 6 (54.5%) had new or worsened dysphagia after hemispherectomy. There was no relationship between posthemispherectomy clinical seizure absence and the development of dysphagia (p = 0.307).

Discussion

This study represents the first examination of dysphagia after hemispherectomy in pediatric patients. In our series approximately one-quarter of children developed new-onset dysphagia after surgery, the majority of whom had observable pathology on clinical or fluoroscopic evaluation. This finding is in addition to the roughly one-quarter of children who had preexisting swallowing difficulties prior to hemispherectomy. Of these patients with preexisting deficits, a small majority clinically worsened after surgery.

Clinical symptoms in patients who had new-onset dysphagia were always temporary and typically resolved completely by the end of the 1st postoperative month. The duration of symptoms in patients with worsening of preexisting deficits typically improved to the child's baseline within the 1st month, but was more variable. The gradual recovery in swallowing function we observed supports the theory proposed by Hamdy et al. that there is a slow reorganization of the swallow control networks into the undamaged contralateral hemisphere after a unilateral hemispheric injury.8 This may also be influenced by the increased plasticity of the pediatric brain, which is critical for reorganization of cortical swallow networks necessary for recovery after dysphagia.3,5 Most children required diet modifications and enteral nutrition during the course of their posthemispherectomy dysphagia. Only one patient with new dysphagia required long-term nutritional supplementation via gastric tube; this was able to be removed by 18 months posthemispherectomy.

Oral-phase dysphagia was seen in all patients with new dysphagia after surgery. This pattern is commonly seen after stroke and with other cortical lesions affecting the primary somatosensory and cingulate cortex.11,21 The majority of children also had dysfunction in the pharyngeal phase in the early period after surgery. In those who had persistent pharyngeal-phase dysfunction, there was a significantly longer duration of symptoms. Follow-up clinical or videofluoroscopic swallow assessment in posthemispherectomy patients with persistent dysphagia is important for identifying this pharyngeal dysfunction and can help guide discussion and therapy.

There are data to suggest a role for the basal ganglia and insula in mediating the swallow reflex;9,11,15 however, there was no association with resection of the basal ganglia or insula and dysphagia in our series. There was a strong trend toward an association between posthemispherectomy dysphagia and new complete or partial damage to the ipsilateral thalamus on postoperative imaging. Interestingly, interruption of afferent pharyngeal sensory input to primary somatosensory cortex and other cortical mediators of the swallow reflex has been linked to the presence of dysphagia after neurological injury.1,28 This suggests that preservation of the ipsilateral thalamus in the context of the loss of associated inhibitory cortical modulation of brainstem swallow reflex centers18 after functional disconnection may predispose to dysphagia in these patients.

Occurrence of dysphasia after hemispherectomy was not dependent on the hemisphere resected, which correlates with the bilateral representation of swallowing and wide individual asymmetry in cortical dominance reported in the literature.15,18 In light of this variability, there may be a role for functional imaging assessment of the swallow prior to hemispherectomy as a mechanism to clarify postoperative dysphagia risk. This may be especially relevant in children with preoperative dysphagia for whom the risk of permanent deficit is present. There was no evidence that development of hydrocephalus or seizure freedom posthemispherectomy influenced the presence of dysphagia after surgery.

Based on the observed incidence and severity of dysphagia after hemispherectomy in children, we would not recommend routine preoperative formal swallow evaluation in the absence of clinical dysphagia. This is supported by the fact that in those children with known preexisting dysphagia, the identification of the specific area of the swallow reflex that was impaired did not help in predicting whether symptoms worsened after hemispherectomy. In those children with new or worsened dysphagia after surgery, CSE and/or VFSS are indicated to determine both the severity of symptoms and the specific treatment modality needed. For children with persistent dysphagia in the late postoperative period (> 14 days), repeat CSEs and/or VFSSs are recommended to assess for pharyngeal phase dysphagia; this is significantly associated with a prolongation in symptoms and need for treatment in our cohort.

This study is subject to the inherent limitations of a retrospective analysis. Additionally, preoperative swallow evaluation was unavailable except in patients with previously identified clinical dysphagia. Therefore, we cannot exclude subtle deficits that may not be clinically apparent that predispose children to developing dysphagia after hemispherectomy.

Conclusions

This study provides evidence that dysphagia is a significant potential complication of hemispherectomy for intractable epilepsy in the pediatric population. This posthemispherectomy dysphagia is clinically significant but usually resolves on its own in the early postoperative period. In patients without identified preexisting deficits this posthemispherectomy dysphagia always resolved completely; permanent issues were only seen in those children with known dysphagia prior to surgery. It is important for neurosurgeons to be aware of the potential risk of dysphagia and resultant need for therapy and to communicate with families preparing for their child to undergo hemispherectomy.

Disclosure

The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper.

Author contributions to the study and manuscript preparation include the following. Conception and design: Buckley, Saneto, Ojemann. Acquisition of data: Buckley, Morgan. Analysis and interpretation of data: Buckley, Morgan, Barber, Ojemann. Drafting the article: Buckley, Saneto, Ellenbogen, Ojemann. Critically revising the article: all authors. Reviewed submitted version of manuscript: all authors. Approved the final version of the manuscript on behalf of all authors: Buckley. Statistical analysis: Buckley, Barber. Study supervision: Ojemann.

References

  • 1

    Aviv JEMartin JHSacco RLZagar DDiamond BKeen MS: Supraglottic and pharyngeal sensory abnormalities in stroke patients with dysphagia. Ann Otol Rhinol Laryngol 105:92971996

  • 2

    Barer DH: The natural history and functional consequences of dysphagia after hemispheric stroke. J Neurol Neurosurg Psychiatry 52:2362411989

  • 3

    Barritt AWSmithard DG: Role of cerebral cortex plasticity in the recovery of swallowing function following dysphagic stroke. Dysphagia 24:83902009

  • 4

    Delalande OBulteau CDellatolas GFohlen MJalin CBuret V: Vertical parasagittal hemispherotomy: surgical procedures and clinical long-term outcomes in a population of 83 children. Neurosurgery 60:2 Suppl 1ONS19ONS322007

  • 5

    Fraser CPower MHamdy SRothwell JHobday DHollander I: Driving plasticity in human adult motor cortex is associated with improved motor function after brain injury. Neuron 34:8318402002

  • 6

    Gordon CHewer RLWade DT: Dysphagia in acute stroke. Br Med J (Clin Res Ed) 295:4114141987

  • 7

    Hamdy SAziz QRothwell JCCrone RHughes DTallis RC: Explaining oropharyngeal dysphagia after unilateral hemispheric stroke. Lancet 350:6866921997

  • 8

    Hamdy SRothwell JCAziz QThompson DG: Organization and reorganization of human swallowing motor cortex: implications for recovery after stroke. Clin Sci (Lond) 99:1511572000

  • 9

    Hartnick CJRudolph CWillging JPHolland SK: Functional magnetic resonance imaging of the pediatric swallow: imaging the cortex and the brainstem. Laryngoscope 111:118311912001

  • 10

    Hauptman JSPedram KSison CASankar RSalamon NVinters HV: Pediatric epilepsy surgery: long-term 5-year seizure remission and medication use. Neurosurgery 71:9859932012

  • 11

    Humbert IARobbins J: Normal swallowing and functional magnetic resonance imaging: a systematic review. Dysphagia 22:2662752007

  • 12

    Krynauw ARRitchken HD: [Scope and results of hemispherectomy.]. Minerva Med 44:4905001953. (undetermined)

  • 13

    Lew SMMatthews AEHartman ALHaranhalli N: Posthemispherectomy hydrocephalus: results of a comprehensive, multiinstitutional review. Epilepsia 54:3833892013

  • 14

    Liégeois FMorgan ATStewart LHCross JHVogel APVargha-Khadem F: Speech and oral motor profile after childhood hemispherectomy. Brain Lang 114:1261342010

  • 15

    Lowell SYReynolds RCChen GHorwitz BLudlow CL: Functional connectivity and laterality of the motor and sensory components in the volitional swallowing network. Exp Brain Res 219:85962012

  • 16

    McKenzie K: The present status of a patient who had the right cerebral hemisphere removed. JAMA 111:1681938

  • 17

    Michou EHamdy S: Cortical input in control of swallowing. Curr Opin Otolaryngol Head Neck Surg 17:1661712009

  • 18

    Mistry SVerin ESingh SJefferson SRothwell JCThompson DG: Unilateral suppression of pharyngeal motor cortex to repetitive transcranial magnetic stimulation reveals functional asymmetry in the hemispheric projections to human swallowing. J Physiol 585:5255382007

  • 19

    Moosa ANGupta AJehi LMarashly ACosmo GLachhwani D: Longitudinal seizure outcome and prognostic predictors after hemispherectomy in 170 children. Neurology 80:2532602013

  • 20

    Morgan ATDodrill PWard EC: Interventions for oropharyngeal dysphagia in children with neurological impairment. Cochrane Database Syst Rev 10:CD0094562012

  • 21

    Otapowicz DSobaniec WOkurowska-Zawada BArtemowicz BSendrowski KKułak W: Dysphagia in children with infantile cerebral palsy. Adv Med Sci 55:2222272010

  • 22

    Pender MPFerguson SM: Dysarthria and dysphagia due to the opercular syndrome in multiple sclerosis. Mult Scler 13:8178192007

  • 23

    Rangel-Castilla LHwang SWAl-Shamy GJea ACurry DJ: The periinsular functional hemispherotomy. Neurosurg Focus 32:3E72012

  • 24

    Satow TIkeda AYamamoto JBegum TThuy DHMatsuhashi M: Role of primary sensorimotor cortex and supplementary motor area in volitional swallowing: a movement-related cortical potential study. Am J Physiol Gastrointest Liver Physiol 287:G459G4702004

  • 25

    Schramm JBehrens EEntzian W: Hemispherical deafferentation: an alternative to functional hemispherectomy. Neurosurgery 36:5095161995

  • 26

    Schramm JKuczaty SSassen RElger CEvon Lehe M: Pediatric functional hemispherectomy: outcome in 92 patients. Acta Neurochir (Wien) 154:201720282012

  • 27

    Teismann IKDziewas RSteinstraeter OPantev C: Time-dependent hemispheric shift of the cortical control of volitional swallowing. Hum Brain Mapp 30:921002009

  • 28

    Teismann IKSteinstraeter OStoeckigt KSuntrup SWollbrink APantev C: Functional oropharyngeal sensory disruption interferes with the cortical control of swallowing. BMC Neurosci 8:622007

  • 29

    Villarejo-Ortega FGarcía-Fernández MFournier-Del Castillo CFabregate-Fuente MÁlvarez-Linera JDe Prada-Vicente I: Seizure and developmental outcomes after hemispherectomy in children and adolescents with intractable epilepsy. Childs Nerv Syst 29:4754882013

  • 30

    Villemure JGRasmussen T: Functional hemispherectomy in children. Neuropediatrics 24:53551993

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Article Information

Address correspondence to: Robert T. Buckley, M.D., Department of Neurological Surgery, Seattle Children's Hospital, 4800 Sand Point Way NE, Seattle, WA 98105. email: robuck@uw.edu.

Please include this information when citing this paper: published online November 8, 2013; DOI: 10.3171/2013.10.PEDS13182.

© AANS, except where prohibited by US copyright law.

Headings

Figures

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    Incidence and characteristics of dysphagia following hemispherectomy. A: Presence or absence of dysphagia in children with and without preexisting deficits after surgery. Values on the y axis are the number of patients. B: Type of dysphagia. The gray bars indicate the early phase (< 14 days postoperative) and the black bars indicate the late phase (> 14 days postoperative). Values on the y axis are the number of patients. C: Median duration of late-phase dysphagia.

References

1

Aviv JEMartin JHSacco RLZagar DDiamond BKeen MS: Supraglottic and pharyngeal sensory abnormalities in stroke patients with dysphagia. Ann Otol Rhinol Laryngol 105:92971996

2

Barer DH: The natural history and functional consequences of dysphagia after hemispheric stroke. J Neurol Neurosurg Psychiatry 52:2362411989

3

Barritt AWSmithard DG: Role of cerebral cortex plasticity in the recovery of swallowing function following dysphagic stroke. Dysphagia 24:83902009

4

Delalande OBulteau CDellatolas GFohlen MJalin CBuret V: Vertical parasagittal hemispherotomy: surgical procedures and clinical long-term outcomes in a population of 83 children. Neurosurgery 60:2 Suppl 1ONS19ONS322007

5

Fraser CPower MHamdy SRothwell JHobday DHollander I: Driving plasticity in human adult motor cortex is associated with improved motor function after brain injury. Neuron 34:8318402002

6

Gordon CHewer RLWade DT: Dysphagia in acute stroke. Br Med J (Clin Res Ed) 295:4114141987

7

Hamdy SAziz QRothwell JCCrone RHughes DTallis RC: Explaining oropharyngeal dysphagia after unilateral hemispheric stroke. Lancet 350:6866921997

8

Hamdy SRothwell JCAziz QThompson DG: Organization and reorganization of human swallowing motor cortex: implications for recovery after stroke. Clin Sci (Lond) 99:1511572000

9

Hartnick CJRudolph CWillging JPHolland SK: Functional magnetic resonance imaging of the pediatric swallow: imaging the cortex and the brainstem. Laryngoscope 111:118311912001

10

Hauptman JSPedram KSison CASankar RSalamon NVinters HV: Pediatric epilepsy surgery: long-term 5-year seizure remission and medication use. Neurosurgery 71:9859932012

11

Humbert IARobbins J: Normal swallowing and functional magnetic resonance imaging: a systematic review. Dysphagia 22:2662752007

12

Krynauw ARRitchken HD: [Scope and results of hemispherectomy.]. Minerva Med 44:4905001953. (undetermined)

13

Lew SMMatthews AEHartman ALHaranhalli N: Posthemispherectomy hydrocephalus: results of a comprehensive, multiinstitutional review. Epilepsia 54:3833892013

14

Liégeois FMorgan ATStewart LHCross JHVogel APVargha-Khadem F: Speech and oral motor profile after childhood hemispherectomy. Brain Lang 114:1261342010

15

Lowell SYReynolds RCChen GHorwitz BLudlow CL: Functional connectivity and laterality of the motor and sensory components in the volitional swallowing network. Exp Brain Res 219:85962012

16

McKenzie K: The present status of a patient who had the right cerebral hemisphere removed. JAMA 111:1681938

17

Michou EHamdy S: Cortical input in control of swallowing. Curr Opin Otolaryngol Head Neck Surg 17:1661712009

18

Mistry SVerin ESingh SJefferson SRothwell JCThompson DG: Unilateral suppression of pharyngeal motor cortex to repetitive transcranial magnetic stimulation reveals functional asymmetry in the hemispheric projections to human swallowing. J Physiol 585:5255382007

19

Moosa ANGupta AJehi LMarashly ACosmo GLachhwani D: Longitudinal seizure outcome and prognostic predictors after hemispherectomy in 170 children. Neurology 80:2532602013

20

Morgan ATDodrill PWard EC: Interventions for oropharyngeal dysphagia in children with neurological impairment. Cochrane Database Syst Rev 10:CD0094562012

21

Otapowicz DSobaniec WOkurowska-Zawada BArtemowicz BSendrowski KKułak W: Dysphagia in children with infantile cerebral palsy. Adv Med Sci 55:2222272010

22

Pender MPFerguson SM: Dysarthria and dysphagia due to the opercular syndrome in multiple sclerosis. Mult Scler 13:8178192007

23

Rangel-Castilla LHwang SWAl-Shamy GJea ACurry DJ: The periinsular functional hemispherotomy. Neurosurg Focus 32:3E72012

24

Satow TIkeda AYamamoto JBegum TThuy DHMatsuhashi M: Role of primary sensorimotor cortex and supplementary motor area in volitional swallowing: a movement-related cortical potential study. Am J Physiol Gastrointest Liver Physiol 287:G459G4702004

25

Schramm JBehrens EEntzian W: Hemispherical deafferentation: an alternative to functional hemispherectomy. Neurosurgery 36:5095161995

26

Schramm JKuczaty SSassen RElger CEvon Lehe M: Pediatric functional hemispherectomy: outcome in 92 patients. Acta Neurochir (Wien) 154:201720282012

27

Teismann IKDziewas RSteinstraeter OPantev C: Time-dependent hemispheric shift of the cortical control of volitional swallowing. Hum Brain Mapp 30:921002009

28

Teismann IKSteinstraeter OStoeckigt KSuntrup SWollbrink APantev C: Functional oropharyngeal sensory disruption interferes with the cortical control of swallowing. BMC Neurosci 8:622007

29

Villarejo-Ortega FGarcía-Fernández MFournier-Del Castillo CFabregate-Fuente MÁlvarez-Linera JDe Prada-Vicente I: Seizure and developmental outcomes after hemispherectomy in children and adolescents with intractable epilepsy. Childs Nerv Syst 29:4754882013

30

Villemure JGRasmussen T: Functional hemispherectomy in children. Neuropediatrics 24:53551993

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