Acute Onset Dysphagia Research Articles

Abstract 094: Sudden Onset Dysphagia: A Symptom To Be Aware of During Code Strokes

Introduction Lateral medullary infarction (LMI) can present with dysphagia, dysphonia, dysarthria, vertigo, nausea, skew deviation, and ipsipulsion. Patients may also exhibit sensory loss and ipsilateral Horner’s syndrome. LMS often develops because of an acute infarct from the vertebral arteries or posterior inferior cerebellar arteries (PICA). The most common mechanism of stroke usually is atherothrombosis, followed by cardioembolic, dissection and embolic source of undetermined source (ESUS). While dysphagia often accompanies the constellation of LMS symptoms, it is rarely the first symptom and has only been reported in a few cases in the literature. In this report we describe the case of a man in his 40s with acute onset dysphagia as the presenting finding ahead of an LMS diagnosis. Methods The patient was identified in routine clinical practice. Results A man in his 40s with medical history of HTN, type 2 DM and polycystic kidney disease, presented with sudden‐onset dysphagia which started while he was drinking alcohol. Later he noticed that he was unable to keep his balance. His National Health Institute Stroke Scale was 4. Neurologic exam was pertinent for left‐sided miosis, ptosis, and dysmetria. Pinprick and temperature sensation were decreased on the right arm and leg. Facial sensation to light touch was diminished on the left. Brain MRI showed an acute infarct in the left lateral medulla (Figure A). CTA showed calcified atherosclerosis of the V4 segment of left vertebral artery (Figure B). Mechanism of ischemic stroke was artery to artery thromboembolism from the left V4 segment of vertebral artery. For secondary prevention, dual antiplatelet therapy, high intensity statin, and optimization of his risk factors were initiated. Conclusion This case report demonstrates that dysphagia can be the initial symptom of an acute ischemic stroke. Diagnosis and recognition of an atypical presentation of lateral medullary syndrome can pose a particular challenge especially in this era of “time is brain” but is of the utmost importance to facilitate good outcomes. Patients presenting with dysphagia who have risk factors for stroke and no other obvious etiology for their symptoms should be worked up for possible cerebrovascular etiology.

Dysphagia Secondary to Vocal Cord Paralysis: A Case Report

A 51-year-old man with a 10-day history of acute-onset dysphagia presented with inability to swallow anything orally. The patient was unable to swallow any radiopaque contrast medium; therefore, a videofluoroscopic swallow study could not be performed. Brain imaging, neurological findings, and initial endoscopy findings were normal. Neck computed tomography suggested left vocal cord paralysis. The patient was diagnosed with diabetes one year prior to presentation but did not receive any treatment. Insulin therapy during hospitalization controlled the patient’s blood glucose levels, and his symptoms improved without any sequelae. We present a rare case of vocal cord paralysis secondary to controlled diabetes. The initial endoscopic examination did not include thorough evaluation of the vocal cords; therefore, accurate diagnosis was challenging in this case.

Asystole, A Rare Cardiac Complication of Lateral Medullary Infarction: Case report and Literature Review. (P2-5.010)

<h3>Objective:</h3> We report a case of lateral medullary infarction leading to asystole, and we discuss the diagnosis, management, and prognosis of patients with this rare complication. <h3>Background:</h3> Clinical presentations of lateral medullary stroke vary. Wallenberg syndrome is the most common presentation, which includes vertigo with nystagmus, ataxia, ipsilateral sensory deficits in the face, bulbar muscle weakness, and ipsilateral Horner’s syndrome. The nucleus tractus solitarius, the dorsal vagal nucleus, and the nucleus ambiguous in the lateral medulla oblongata play a critical role in autonomic regulation and have centers for respiratory, cardiac, and vasomotor reflexes. Despite this, cardiac arrhythmias such as asystole are a rare clinical manifestation of lateral medullary stroke. <h3>Design/Methods:</h3> Case report and literature review. <h3>Results:</h3> A 64-year-old man with hypertension, previously involved in a motor vehicle accident, presented with acute onset dysphagia, left facial droop, and left eye ptosis. CT of the head did not show any acute stroke or hemorrhage. CT angiography of the head and neck showed left vertebral artery (V3/V4 segment) occlusion. He received IV thrombolysis. Post thrombolysis, he had bradycardia evolving to asystole and brief cardiac arrest. MRI of the brain revealed acute left posterior lateral medullary stroke and MR angiography showed left vertebral artery dissection. Cardiac work-up was unrevealing, and he eventually required placement of a dual-chamber pacemaker. Given the absence of respiratory factors and structural heart disease, the bradycardia and asystole were attributed to the lateral medullary stroke. <h3>Conclusions:</h3> Despite the recognized role of the lateral medulla in autonomic regulation, cardiac arrhythmias are rarely associated with lateral medullary infarction. Precise mechanisms are yet to be elucidated, but it remains important to recognize them as a potential complication of this stroke. <b>Disclosure:</b> Dr. Gutierrez Quiceno has nothing to disclose. Dr. Gowda has nothing to disclose. Dr. Kakadia has nothing to disclose.

Dysphagia in the Presence of Varicella-Zoster Virus and SARS-CoV-2: A Case Report on the Role of Speech-Language Pathology

Purpose: Dysphagia due to cranial nerve neuritis is a rare complication of varicella-zoster virus reactivation. In this case report, we describe a single patient diagnosed with varicella-zoster virus meningitis with acute onset dysphagia, the instrumental assessments and interventions employed by speech-language pathologists (SLPs), and discuss the role of these clinicians in the management of these patients. Conclusion: The results of this case study demonstrate the importance of a multidisciplinary team approach and the vital role of SLPs in the evaluation and treatment of dysphagia of unknown etiology.

Intraoperative Traction May Induce Acute Onset Dysphagia With Diffuse Idiopathic Skeletal Hyperostosis After Anterior Cervical Discectomy

Diffuse idiopathic skeletal hyperostosis (DISH) is a systemic bone-forming disease, and its pathogenesis remains unknown. Moreover, the incidence of DISH increases with age. DISH may be an age-related disorder that occurs more frequently in degenerative spines than in healthy spines. Most patients with DISH of the cervical spine are asymptomatic; however, mechanical compression of the esophagus by the cervical spine can induce dysphagia, hoarseness, and dyspnea. In most cases, dysphagia progresses slowly. Most cases of postoperative dysphagia after anterior cervical spine surgery occurred within 1 month, and most patients recovered spontaneously. Severe dysphagia is relatively uncommon. Here, we report a case of acute-onset dysphagia with DISH that occurred immediately after anterior cervical discectomy. We should consider the possibility of dysphagia occurring immediately after anterior cervical discectomy in patients with DISH, even in those without dysphagia before surgery. Furthermore, surgical treatment for severe postoperative dysphagia associated with DISH may be a good option.

Autoimmune Neurogenic Dysphagia.

Autoimmune neurogenic dysphagia refers to manifestation of dysphagia due to autoimmune diseases affecting muscle, neuromuscular junction, nerves, roots, brainstem, or cortex. Dysphagia is either part of the evolving clinical symptomatology of an underlying neurological autoimmunity or occurs as a sole manifestation, acutely or insidiously. This opinion article reviews the autoimmune neurological causes of dysphagia, highlights clinical clues and laboratory testing that facilitate early diagnosis, especially when dysphagia is the presenting symptom, and outlines the most effective immunotherapeutic approaches. Dysphagia is common in inflammatory myopathies, most prominently in inclusion body myositis, and is frequent in myasthenia gravis, occurring early in bulbar-onset disease or during the course of progressive, generalized disease. Acute-onset dysphagia is often seen in Guillain–Barre syndrome variants and slowly progressive dysphagia in paraneoplastic neuropathies highlighted by the presence of specific autoantibodies. The most common causes of CNS autoimmune dysphagia are demyelinating and inflammatory lesions in the brainstem, occurring in patients with multiple sclerosis and neuromyelitis optica spectrum disorders. Less common, but often overlooked, is dysphagia in stiff-person syndrome especially in conjunction with cerebellar ataxia and high anti-GAD autoantibodies, and in gastrointestinal dysmotility syndromes associated with autoantibodies against the ganglionic acetyl-choline receptor. In the setting of many neurological autoimmunities, acute-onset or progressive dysphagia is a potentially treatable condition, requiring increased awareness for prompt diagnosis and early immunotherapy initiation.

S1995 Dysphagia Secondary to Acute Stroke Masquerading as Food Impaction

INTRODUCTION: Dysphagia is a commonly encountered symptom in gastroenterology, and esophageal food impaction is a common cause of acute onset dysphagia presenting in the emergency room. As such, gastroenterologists are often among the first to evaluate patients with a chief complaint of dysphagia. Here, we present a case of acute onset dysphagia concerning for food impaction, where the patient was then noted to have multiple neurologic deficits suggestive of acute stroke. CASE DESCRIPTION/METHODS: The patient is a 54 year-old male with history of hypertension who presented with acute onset dysphagia for two hours. His symptoms began with lightheadedness, and subsequently developed inability to swallow liquids. His symptoms did not develop acutely after ingestion of any solid foods. He then noted discomfort in his neck, prompting presentation to the emergency department. On arrival, he was hemodynamically stable. Initial labs were unremarkable. Physical exam at time of arrival notable for normal cardiovascular and neurologic exams. Oropharyngeal exam was abbreviated as he was wearing a mask due to the COVID-19 pandemic. GI was consulted for concern for food impaction. While plans were being made for urgent endoscopy, he developed a left facial droop, nystagmus and gait ataxia concerning for acute posterior circulation stroke. He underwent CTA which was notable for occlusion of right vertebral and proximal basilar arteries. He promptly received tPA and was admitted to the stroke service. His neurologic exam improved over the course of his hospitalization and tolerated pureed diet by time of discharge, though with some residual dysphagia. DISCUSSION: The differential diagnosis for dysphagia is commonly differentiated into oropharyngeal and esophageal pathologies. Within each of these categories, there are both neuromuscular and structural processes which can manifest with symptoms of dysphagia. As gastroenterologists, we are frequently exposed to common esophageal pathologies. However, maintaining a broad differential and avoiding anchoring bias is key for timely recognition of a multitude of diagnoses. Urgent diagnoses which can present with acute onset dysphagia include oropharyngeal infections, acute stroke, and food and/or foreign body impaction. This case highlights the importance of the gastroenterologist, who may be the first person to evaluate a patient with acute onset dysphagia, in maintaining a broad and appropriate differential diagnosis to ensure appropriately and timely treatment of the patient.

S2022 Rare Cause of Acute Onset Dysphagia and Treatment With Z-Peroral Endoscopic Myotomy (Z-POEM)

INTRODUCTION: Zenker's Diverticulum (ZD) is a rare disease with a prevalence of 0.01 to 0.11% in the general population.It is commonly associated with symptoms of progressive and chronic symptoms of dysphagia and weight loss. We describe a rare case of acute onset of dysphagia related to ZD and its management with a novel endoscopic technique. CASE DESCRIPTION/METHODS: An 82-year-old female with multiple co-morbidities presented to the hospital with acute onset dysphagia to solids and liquids since last 2 weeks. She lost 10 lbs and started coughing incessantly with any solids or liquid intake. Vital signs and routine laboratory values were within normal limits. On examination by speech and language pathologist, she was noted to have severe oropharyngeal dysphagia and frank aspiration with all consistencies. A modified barium swallow showed a large ZD and aspiration. Neurology consultation was sought given acuity of dysphagia, however there were no local neurological deficits on imaging and physical exam. Subsequently an Esophagogastroduodenoscopy (EGD) was performed which showed a 4-5 cm ZD and the septum separating the diverticulum from the pinpoint esophageal lumen. The case was discussed at a multidisciplinary conference involving gastroenterology, ENT and radiology and decision was made to proceed with endoscopic septotomy. A Z-peroral endoscopic myotomy (POEM) was performed with septotomy. It was technically challenging to expose the anterior aspect of the septum secondary to significant fibrosis and difficulty with dissection. Therefore a partial septotomy was performed extending to about 2 cm distally at the posterior aspect of the septum. The scope was withdrawn and reintroduced into the true esophageal lumen more easily despite the anterior aspect of the septum not being completely dissected. Patient was started on clear liquid diet after 48 hours with gradual advancement and tolerated it well. On a 4-week follow up visit, patient continued to tolerate diet well with weight gain and no signs of aspiration. DISCUSSION: Treatment of ZD can be accomplished with open surgery, a rigid endoscope, flexible endoscope or more recently, the novel Z-POEM procedure. Z-POEM utilizes the concept of submucosal tunneling endoscopic septum division (STESD) technique and has permitted complete muscular septum dissection while maintaining the mucosal integrity. It is associated with fewer rates of complications and symptom recurrence as compared to septotomy with standard flexible endoscopy.Figure 1.: Z-Per oral endoscopic myotomy.

S1998 Acute Dysphagia Due to Malignant Aerodigestive Fistula

INTRODUCTION: Patients with cancer may develop dysphagia during the course of anti-neoplastic treatment. While esophagitis is common in this population, aerodigestive fistulae should be considered in the differential diagnosis. We present a case of a tracheoesophageal fistula caused by a lung metastasis. CASE DESCRIPTION/METHODS: A 51 year old female with breast cancer metastatic to brain, lungs, and bones, previously treated with breast radiation and currently on treatment with oral alpelisib, presented with acute-onset dysphagia. Vital signs, chest X-ray, and leukocyte count were unremarkable. A bedside swallow test with clear liquid demonstrated immediate coughing and regurgitation of the fluid. The physical examination was otherwise unremarkable. Suspecting oropharyngeal dysphagia, speech and language pathology were consulted. A modified barium swallow was performed and revealed a tracheoesophageal fistula (Figure 1). A tracheoesophageal fistula was identified (Figure 2) on upper endoscopy and a fully covered metal stent was deployed. Pulmonology then conducted a bronchoscopy which revealed a patent airway. After 48 hours, an esophagram demonstrated the stent in appropriate position (Figure 3). She was discharged on post-procedure day 5, tolerating a modified diet. During the follow-up period, her cancer progressed despite therapy and she elected for hospice care. DISCUSSION: Malignant aerodigestive fistulae may complicate the management of cancers involving the esophagus, trachea or, less commonly, the lungs. The incidence increases with tumor size and sensitivity to chemotherapy or radiotherapy: treatment-related tumor necrosis may lead to fistulization in large, sensitive cancers. Once reserved for palliation of aerodigestive fistulae, endoscopic management is increasingly employed as definitive therapy. Several treatment strategies have been investigated, with the largest body of evidence supporting the use of partially or fully covered self-expanding metallic stents (SEMS) in the esophagus. Respiratory stent placement may be an alternative or complementary therapy for some patients. Treatment with a combination of esophageal and tracheal stents should be considered for large fistulae or when there is risk of respiratory tract compression from placement of the esophageal stent. Other endoscopic therapies include fistula closure using over-the-scope clips, tissue adhesives, or endoluminal vacuum-assisted closure.Figure 1.: Modified barium swallow demonstrates contrast in the right mainstem bronchus and secondary bronchi.Figure 2.: Upper endoscopy shows a fistula (arrow) in the distal esophagus.Figure 3.: Esophagram reveals an esophageal stent without leakage of contrast.

S1986 Mucous Membrane Pemphigoid: A Rare Cause of Hematemesis

INTRODUCTION: Mucous membrane pemphigoid (MMP) rarely presents with esophageal involvement [1-3]. We present a case of a 57 year old man who was evaluated for acute onset dysphagia and severe hematemesis. He denied any caustic ingestion. EGD revealed severe esophageal mucosal injury with bleeding, mucosal sloughing with exposure of the submucosal layers, and mid-esophageal narrowing. Biopsies were non-diagnostic. Physical exam revealed erythematous plaques and few bullae on his extremities. Shave biopsies were positive for linear basement membrane (BM) immunofluorescent staining, consistent with MMP. Serum ELISA was positive for Anti-BP180 Ab, which along with the clinical presentation, confirmed the diagnosis of MMP. The patient was started on corticosteroids and mycophenolate mofetil with resolution of his symptoms and evidence of mucosal healing on repeat EGD. CASE DESCRIPTION/METHODS: MMP with esophageal involvement typically presents with longstanding dysphagia due to esophageal strictures that often require dilation. In this atypical case, the patient developed acute dysphagia and hematemesis. EGD revealed an esophageal stricture which was not traversed initially given sloughing mucosa and concern for causing perforation. Fortunately, there was no apparent stricture on repeat EGD done after immunosuppressive therapy was started. Establishing a diagnosis of MMP is essential as treatment requires systemic immunosuppression [1,4]. Esophageal biopsies with direct immunofluorescence (DIF) is the gold standard for diagnosis, but biopsies are frequently inconclusive [2,5]. Therefore, both lesional and perilesional biopsies are recommended for histologic and DIF staining, respectively [2,6]. Indirect immunofluorescence (IIF) and serum ELISA testing can help distinguish MMP from other entities [6]. Anti-BP180 Ab was elevated in our patient and down-trended with immunosuppression. Other more specific IIF tests can help distinguish MMP from bullous pemphigoid. DISCUSSION: MMP involving the esophagus should be considered for patients with unexplained hematemesis or dysphagia, particularly when presenting with mucosal sloughing or strictures. The diagnosis is made with the combination of clinical assessment, histopathology and specialized testing. A high index of suspicion is required to make the diagnosis given that biopsies are often inconclusive. This case stresses the significance of a thorough physical exam and the importance of obtaining lesional and perilesional biopsies to establish a diagnosis of MMP.Figure 1.: Endoscopic Evaluation.

1773 Esophageal Obstruction From a “Cough Pill”: Case Report

INTRODUCTION: Foreign body obstruction in the elderly is usually due to an identifiable underlying cause such as psychiatric disease, substance-intoxification, secondary gain, or accidental food related event. Most esophageal obstructions are asymptomatic and usually result in the passage of the foreign body. However, some patients may present with acute onset dysphagia, choking, hypersalivation, blood-tinged saliva, regurgitation, and wheezing. Rarely, foreign body impaction occurs as a complication of pill ingestion. In the cases where a foreign body has been identified in the esophagus endoscopic intervention is indicated in only one out of five cases. This is a rare case of esophageal obstruction due to pill ingestion that resulted in endoscopic intervention. CASE DESCRIPTION/METHODS: Patient is an 80 year old male with a medical history of HTN, atrial fib/flutter, and history of throat cancer in 2003 s/p chemo and radiation who presented to the ED after he felt a "tablet stuck in his throat". He is unable to swallow saliva, with frequent spitting of blood. He had intermittent difficulty swallowing solid food prior to admission. Patient had an esophagram done previously in 2013 which showed slight narrowing of the esophagus at C7 (Figures 1.1 and 1.2). EGD was done which revealed a whitish foreign body in the upper esophagus which was subsequently removed (Figure 1.3), and patient was then able to swallow. DISCUSSION: Pill-induced esophageal obstruction is a rare but serious cause of obstruction. Patients presenting similarly to this case with dysphagia, hypersalivation, blood-tinged salvia, and regurgitation should have thorough history taken to elicit any previous pill ingestion. Prolonged time to diagnosis will lead to delayed intervention, and increased risk of pill-induced esophagitis. Women and elderly are at an increased risk due to higher medicine usage, and decreased saliva production and motility in the elderly. Additionally, radiation therapy to the head and neck greatly impacts swallowing, and is exacerbated by chemotherapy. In cases with elderly patients small pills and liquid formula should be considered to prevent pill impaction. The prolonged transit or stasis of a pill increases the interaction between the pill and the esophageal mucosa causing esophagitis. Pill induced esophagitis will produce ulcers, and presents with dysphagia, difficult swallowing, and odynophagia. sIncreased ability to recognize these patients will lead to more expedient intervention and reduce risks for complications.

1789 Pseudotumor Esophagus: Acute Dysphagia Secondary to Mallory-Weiss Tear Associated Blood Clots

INTRODUCTION: Acute onset dysphagia secondary to the mass effect from blood clots related to Mallory-Weiss tears (MWT) has not been reported in the literature. We present two such cases, both of which initially were thought to have a neoplastic etiology. CASE DESCRIPTION/METHODS: Case 1: A healthy 60-year-old woman developed acute dysphagia following impaction of a piece of steak. She forcefully regurgitated it with a coat of blood but continued to have substernal chest pressure and dysphagia with sticking at her suprasternal notch. A chest x-ray raised concern for pneumomediastinum, prompting an esophagram that showed a distal esophageal filling defect suggestive of obstructive neoplasm (Figure 1A). An upper endoscopy showed a long mucosal tear in the distal esophagus with a large adherent blood clot at the apex that could not be dislodged. The patient remained nil per os over the next couple of days with improvement in her discomfort. A repeat esophagram showed no filling defects (Figure 1B). Upon resumption of her diet, she experienced no further dysphagia. Case 2: An 80-year-old man with severe ischemic cardiomyopathy presented with volume overload. He was started on a heparin drip after an atrial thrombus was found on echocardiogram. One day later, he had sudden onset projectile vomiting and subsequent dysphagia with substernal sticking. An upper endoscopy showed a 3 cm fixed, partially obstructive mass-like lesion in the lower third of the esophagus with oozing at the base (Figure 2A). Biopsies showed non-specific findings including necrosis and foreign material. The following day, the patient tolerated solid food without dysphagia. A second upper endoscopy showed a 3 cm esophageal tear with a small adherent clot at the site of the previously noted mass-like lesion (Figure 2B). He continued to tolerate a regular diet without further symptoms. DISCUSSION: The presentation of MWT associated blood clots causing dysphagia and resembling distal esophageal neoplasms is novel. Both our cases experienced forceful regurgitation or emesis prior to the onset of dysphagia, suggesting a mucosal tear as the instigator with subsequent development of a large clot in the esophageal lumen. In each instance, resolution of symptoms correlated temporally with clearance of the clot. MWT are most likely to present with hematemesis but in rare cases may form a large blood clot mimicking a neoplastic process with resultant dysphagia. Awareness of such presentations may prevent unnecessary workups.

Acute Onset Dysphagia: An Atypical Presentation of Idiopathic Achalasia

We are presenting a unique case of achalasia of primary idiopathic etiology mimicking Pseudoachalasia. A 50 Year old Hispanic female presented to our GI clinic with severe complains of dysphgaia to both solids and liquids and regurgitation for past 4 weeks. It has gotten worse over the past few days now associated nausea, vomiting and 15 pounds of weight loss. In her last three ER vists in the last 4 weeks, she was diagnosed as GERD and treated with PPI, Sucralfate and antiemetics. She denied any significant pertinent past medical and surgical history. Her vital signs and physical examination were unremarkable. She was admitted for the evalaution of worsening Dysphagia. Endoscopic Gastroduodenoscopy was done, which revealed moderately diffuse dilation of the body of the esophagus with semi solid food coating of the mucosa. The endoscope met mild resistance while crossing the gastroesophageal junction into the stomach. The CT Chest reported negative for intrathorasic masses, but displayed dilated and asymmetric mural thickening of esophagus. With gastric fundus adenocarcinoma and esophageal cancer ruled out on EGD and CT Chest and keeping in mind the atypical presentation of this achalasia; we ordered Endoscopic Ultrasonography-EUS to rule out intrathoracic or intraabdominal neoplasms in and around the lower esophageal sphincter. EUS rulled out Intraluminal or Extraluminal GE junctional masses or Paraesophageal lymphadenopathy. However non-appreciable esophageal motility and a hypertonic lower esophageal sphincter was observed. Our suspicion for idiopathic achalasia was thus enhanced, which was confirmed on Esophageal Motility study. She was reffered to Surgery for Heller's myotomy. It is well known that achalasia is a chronic disease that starts gradually and worsens with increasing dysphagia over time. On the contrary, Pseudoachalasia is a term used to define a malignant neoplasm or stricture arising from the lower esophagus or upper stomach invading the esophageal lumen or nerve plexus. Our patient at first glance was thought to be a case of pseudoachalasia (malignancy causing achalasia). However as evident by all our extensive investigations we were quite surprisingly dealing with Primary idiopathic achalasia with atypical acute onset.

Endoscopic Variceal Band Ligation Leading to Acute Onset Dysphagia

Endoscopic Variceal Band Ligation Leading to Acute Onset Dysphagia

Lujan–Fryns Syndrome (LFS): A Unique Combination of Hypernasality, Marfanoid Body Habitus, and Neuropsychiatric Issues, Presenting as Acute-Onset Dysphagia

BACKGROUNDLujan–Fryns syndrome (LFS) is an extremely rare, X-linked disorder, for which the full clinical spectrum is still unknown. Usually, it presents with neuropsychiatric problems such as learning disabilities and behavioral issues in a typical combination with marfanoid features. Often, there is a positive family history for the disorder. However, sporadic cases have also been reported in males. More interestingly, there is no case of LFS presenting with acute-onset dysphagia in the English language medical literature.CASE PRESENTATIONA 17-year-old Pakistani mentally normal school boy was admitted for the workup of acute-onset dysphagia, hypernasal speech, and nasal regurgitation of liquids. He had no neuropsychiatric issues, and his family history was unremarkable. An obvious nasal twang, facial dysmorphism, and marfanoid body habitus were found on examination. The genetic tests revealed a pathogenic missense mutation in the MED12 gene on his X-chromosome.CONCLUSIONLFS can present as acute-onset dysphagia and in the absence of any neuropsychiatric issues or positive family history of the syndrome.

Lymphoma Presenting as Acute-Onset Dysphagia.

A 61-year-old man with recent Bell's palsy developed acute vocal cord paralysis causing severe dysphagia. CSF analysis showed elevated protein and a normal cell count; contrast-enhanced MRI of the brain was normal. He was treated with IVIG for a presumed bulbar-variant AIDP and gradually improved. Six months later, the patient developed rapidly progressive hearing loss and vestibular dysfunction. Repeat MRI revealed bilateral enhancement of the eighth cranial nerves and a hypercellular mass in the left temporal lobe. Biopsy of the mass confirmed the diagnosis of diffuse large B-cell lymphoma. Lymphomatous invasion of the cranial nerves should be considered in cases of relapsing cranial neuropathies.

Myasthenia gravis as a ‘stroke mimic’ – it’s all in the history

An 85-year-old man presented to hospital as an emergency having difficulties with swallowing and speech. In the emergency department, he was assessed as having acute onset dysphagia and dysarthria in keeping with an acute stroke. Subsequently, it became apparent that although the symptoms were indeed of relatively acute onset, there was a clear description by the patient of fatigability and diurnal variation, prompting a working clinical diagnosis of myasthenia gravis. The patient followed a turbulent clinical course, and interpretation of investigation results proved not to be straightforward in the acute setting. Myasthenia gravis is an uncommon disorder but it is more common in the elderly. This case provides key learning points, particularly highlighting the value of prompt, accurate clinical assessment and the importance of adhering to the clinical diagnostic formulation.

Acute Onset Dysphagia Secondary To Cervical Injury In A Young Male – A Case Report

Dysphagia may have oropharyngeal or esophageal causes. Extrinsic compression of oesophagus or intraluminal abnormalities in the esophagus can cause dysphagia. Anatomic causes of dysphagia are tumors, abscesses, and cervical bony outgrowths (osteophytes). Anterior cervical osteophytes can rarely cause dysphagia due to mechanical compression and inflammatory reactions in the tissues around the esophagus. For this reason Non steroidal anti-inflammatory drugs might have a role in improving patient symptomatology. We present a case of a young man with cervical osteophytes presenting with an acute onset of dysphagia following mechanical injury to the neck that improved rapidly with non steroidal anti-inflammatory medications. The report is discussed with a review of relevant literature.

Paliperidone-Induced Dystonic Dysphagia

Back to table of contents Previous article Next article LETTERFull AccessPaliperidone-Induced Dystonic DysphagiaDattatreya Namdeorao Mendhekar D.P.M.,Ashish Agarwal M.D.,Dattatreya Namdeorao Mendhekar D.P.M.Search for more papers by this author,Ashish Agarwal M.D.Search for more papers by this author,Published Online:1 Oct 2010https://doi.org/10.1176/jnp.2010.22.4.451.e37AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: Acute dystonic reactions are well recognized, but isolated dystonia of the pharyngeal muscle causing dysphagia is a rare occurrence with neuroleptic drugs. Extended-release paliperidone is a newly introduced atypical antipsychotic medication formulated using the principal active metabolite of risperidone, 9-hydroxyrisperidone. In contrast to risperidone, it provides consistent and smooth plasma drug concentrations over 24 hours. 1 We report a young man who developed acute-onset dysphagia after taking paliperidone. Case ReportMr. S, an 18-year-old male student, presented with a history of being suspicious, irritable, withdrawn, muttering to self, and having grandiose ideas and disturbed biological functions for a duration of 1 year. He was diagnosed with schizophrenia (DSM-IV-TR criteria). He was treated with divalproex sodium, 750 mg/day, olanzapine, 30 mg/day, and clozapine, 100 mg/day, with marked recovery in psychotic symptoms. He remained stabilized for 3 months while continuing the same treatment. Subsequently, he stopped taking medicine and had a relapse within 2 weeks. This time he was treated with divalproex sodium, 500 mg/day, and paliperidone, 3 mg/day. At day 3, the dosage of paliperidone was increased to 6 mg/day. After taking only two doses of paliperidone at 6 mg/day and within 12 hours of his last dose of paliperidone, he started complaining of a choking sensation in his throat if he tried to ingest any solid or semisolid food and made gurgling sounds. He had little difficulty taking liquids, but solid food would stick in his throat. He presented with severe anxiety and was calling for help. By the time he was brought to the treating psychiatrist, within 4 hours, he also had difficulty making sounds of any kind.Neurological examination did not show any evidence of organic illness, and no abnormal movements were noticed on other parts of the body. He was given intramuscular promethazine, 50 mg, and within 30 minutes he showed remarkable recovery in swallowing. Otolaryngological and gastroenterological evaluation did not find any organic causes and confirmed a case of drug-induced dysphagia. His organic workup for dystonia, including EEG and brain MRI, was negative. Paliperidone was replaced by clozapine, 200 mg/day, with no further recurrence of dysphagia.Discussion The association between paliperidone and dystonic dysphagia is irrefutable in this report; the complaints developed shortly after the introduction of paliperidone and resolved with an anticholinergic drug. Dysphagia may be a manifestation of extrapyramidal side effect when it is associated with neuroleptic therapy. 2 Literature shows that patients with dystonic dysphagia frequently have oromandibular dystonia or neck dystonia, 3 but in our case it was an isolated phenomenon. The mechanism of action of paliperidone is unclear. Paliperidone may cause dystonia due to its dopamine D 2 -serotonin 5HT2A antagonist property. 1 Further, it can block alpha 2 adrenoceptors which can increase noradrenergic activity by inhibiting the autoreceptors. 4 Animal study has suggested that enhanced activity of central noradrenergic nuclei is one of the pathophysiologies of dystonia. 5Complaints of dysphagia in patients with schizophrenia are often overlooked, and this report shows that early diagnosis of neuroleptic-induced dysphagia can avoid potential complications and prevent the patient from undergoing extensive diagnostic testing and various drug trials.Neuropsychiatry and Headache Clinic, New Delhi, IndiaDepartment of Psychiatry, GB Pant Hospital, New Delhi

Paliperidone-Induced Dystonic Dysphagia

Back to table of contents Previous article Next article LETTERFull AccessPaliperidone-Induced Dystonic DysphagiaDattatreya Namdeorao Mendhekar D.P.M.,Ashish Agarwal M.D.,Dattatreya Namdeorao Mendhekar D.P.M.Search for more papers by this author,Ashish Agarwal M.D.Search for more papers by this author,Published Online:1 Oct 2010https://doi.org/10.1176/jnp.2010.22.4.451.e37AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor: Acute dystonic reactions are well recognized, but isolated dystonia of the pharyngeal muscle causing dysphagia is a rare occurrence with neuroleptic drugs. Extended-release paliperidone is a newly introduced atypical antipsychotic medication formulated using the principal active metabolite of risperidone, 9-hydroxyrisperidone. In contrast to risperidone, it provides consistent and smooth plasma drug concentrations over 24 hours. 1 We report a young man who developed acute-onset dysphagia after taking paliperidone. Case ReportMr. S, an 18-year-old male student, presented with a history of being suspicious, irritable, withdrawn, muttering to self, and having grandiose ideas and disturbed biological functions for a duration of 1 year. He was diagnosed with schizophrenia (DSM-IV-TR criteria). He was treated with divalproex sodium, 750 mg/day, olanzapine, 30 mg/day, and clozapine, 100 mg/day, with marked recovery in psychotic symptoms. He remained stabilized for 3 months while continuing the same treatment. Subsequently, he stopped taking medicine and had a relapse within 2 weeks. This time he was treated with divalproex sodium, 500 mg/day, and paliperidone, 3 mg/day. At day 3, the dosage of paliperidone was increased to 6 mg/day. After taking only two doses of paliperidone at 6 mg/day and within 12 hours of his last dose of paliperidone, he started complaining of a choking sensation in his throat if he tried to ingest any solid or semisolid food and made gurgling sounds. He had little difficulty taking liquids, but solid food would stick in his throat. He presented with severe anxiety and was calling for help. By the time he was brought to the treating psychiatrist, within 4 hours, he also had difficulty making sounds of any kind.Neurological examination did not show any evidence of organic illness, and no abnormal movements were noticed on other parts of the body. He was given intramuscular promethazine, 50 mg, and within 30 minutes he showed remarkable recovery in swallowing. Otolaryngological and gastroenterological evaluation did not find any organic causes and confirmed a case of drug-induced dysphagia. His organic workup for dystonia, including EEG and brain MRI, was negative. Paliperidone was replaced by clozapine, 200 mg/day, with no further recurrence of dysphagia.Discussion The association between paliperidone and dystonic dysphagia is irrefutable in this report; the complaints developed shortly after the introduction of paliperidone and resolved with an anticholinergic drug. Dysphagia may be a manifestation of extrapyramidal side effect when it is associated with neuroleptic therapy. 2 Literature shows that patients with dystonic dysphagia frequently have oromandibular dystonia or neck dystonia, 3 but in our case it was an isolated phenomenon. The mechanism of action of paliperidone is unclear. Paliperidone may cause dystonia due to its dopamine D 2 -serotonin 5HT2A antagonist property. 1 Further, it can block alpha 2 adrenoceptors which can increase noradrenergic activity by inhibiting the autoreceptors. 4 Animal study has suggested that enhanced activity of central noradrenergic nuclei is one of the pathophysiologies of dystonia. 5Complaints of dysphagia in patients with schizophrenia are often overlooked, and this report shows that early diagnosis of neuroleptic-induced dysphagia can avoid potential complications and prevent the patient from undergoing extensive diagnostic testing and various drug trials.Neuropsychiatry and Headache Clinic, New Delhi, IndiaDepartment of Psychiatry, GB Pant Hospital, New Delhi