DOCSLIB.ORG

Pseudo Bulbar Palsy: a Rare Cause of Extubation Failure

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Pseudo Bulbar Palsy: a Rare Cause of Extubation Failure Letters to the Editor 2. Deepak N A, Patel ND. Differential diagnosis of acute liver failure in Access this article online India. Ann Hepatol 2006;5:150‑6. Quick Response Code: 3. Singh V, Bhalla A, Sharma N, Mahi SK, Lal A, Singh P, et al. Website: Pathophysiology of jaundice in amoebic liver abscess. Am J Trop Med www.ijccm.org Hyg 2008;78:556‑9. 4. Kamarasu K, Malathi M, Rajagopal V, Subramani K, Jagadeeshramasamy D, Mathai E, et al. Serological evidence for wide DOI: distribution of spotted fevers & typhus fever in Tamil Nadu. Indian J 10.4103/ijccm.IJCCM_244_18 Med Res 2007;126:128‑30. 5. Poomalar GK, Rekha R. Scrub typhus in pregnancy. J Clin Diagn Res 2014;8:1‑3. How to cite this article: Mahto SK, Sheoran A, Goel A, Agarwal N. This is an open access journal, and articles are distributed under the terms of the Creative Uncommon cause of acute liver failure with encephalopathy. Indian J Crit Commons Attribution‑NonCommercial‑ShareAlike 4.0 License, which allows others to Care Med 2018;22:619‑20. remix, tweak, and build upon the work non‑commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms. © 2018 Indian Journal of Critical Care Medicine | Published by Wolters Kluwer ‑ Medknow Pseudo Bulbar Palsy: A Rare Cause of Extubation Failure Sir, Extubation Failure (EF) following weaning trials is a well known entity in Intensive Care Units (ICUs). The varied prevalence (2%–25%) of EF depends on the population studied and the time frame (24–72 h) included for analysis.[1] Airway edema and nonresolution of the primary disease are a common cause. Swallowing dysfunction as a cause of EF may at times account for more than 50% of patients.[1] We report an unusual presentation of lacunar stroke with pseudobulbar palsy presenting with EF. An 80‑year‑old woman a known case of hypertension and Type 2 diabetes mellitus with good premorbid functional status, presented with 10 days history of intermittent fever associated with chills and rigor, nausea, and episodes of loose stools. History also included increased urinary urgency and Figure 1: Indirect laryngoscopy showing vocal cord palsy frequency and urinary incontinence. Four days after the illness, she developed shortness of breath. She was referred to our ICU on the 8th day of her illness. In our initial assessment, she was conscious, oriented, and cooperative. Her limb power as assessed both at distal and at proximal joints were 5/5, with flexor plantars and normal deep tendon reflexes. She had dysphonia at presentation. She had distressed breathing, bilateral basal crepts on auscultation, shock with cold peripheries, and ongoing noradrenaline dose of 0.2 mics/kg/min. She was managed as per the ICU protocols. She was weaned off the ventilator, and after a successful spontaneous breathing trial, she was extubated. Within 2 h of extubation, she had stridor, drooling of saliva, and dysphagia. Airway edema was suspected. Measures taken to reduce edema included adrenaline nebulizations and systemic steroid, to which she did not show any improvement. She was re‑intubated and subsequently tracheostomized. Upper airway Figure 2: Hyperintensities noted in centrum semi ovale, thalmi, cortical bronchoscopy was done which was suggestive of hypotonic areas in T2 flair pharyngeal muscle with no vocal cord movements. Indirect laryngoscopy (IDL) performed by ears, nose, and throat neurological examination revealed a brisk jaw jerk reflex with surgeon validated the above findings [Figure 1]. Further bulbar weakness clinically evident as swallowing dysfunction. 620 Indian Journal of Critical Care Medicine ¦ Volume 22 ¦ Issue 8 ¦ August 2018 Page no. 62 Letters to the Editor clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest. Ritu Singh, Monalisa Nayak, Sunil Kumar Jena, Afzal Azim Department of Critical Care Medicine, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India Address for correspondence: Dr. Afzal Azim, Department of Critical Care Medicine, Sanjay Gandhi Postgraduate Institute of Figure 3: Hyperintensities noted in bilateral cortical and subcortical Medical Sciences, Lucknow, Uttar Pradesh, India. areas in T2 flair E‑mail: [email protected] Her laboratory parameters including sodium were within REFERENCES normal limits throughout her stay in ICU. Magnetic resonance 1. Rothaar RC, Epstein SK. Extubation failure: Magnitude of the problem, imaging (MRI) brain was done which was suggestive of impact on outcomes, and prevention. Curr Opin Crit Care 2003;9:59‑66. multiple foci of confluent long hyperintensities in bilateral 2. Puvanendran K, Wong PK, Ransome GA. Syndrome of Dejerine’s cortical and subcortical areas [Figures 2 and 3]. After 2 weeks fourth reich. Acta Neurol Scand 1978;57:349‑53. 3. Huang CY, Broe G. Isolated facial palsy: A new lacunar syndrome. of ICU stay, she was discharged with a tracheostomy tube J Neurol Neurosurg Psychiatry 1984;47:84‑6. in situ, and routine tracheostomy care was taught to the 4. Besson G, Bogousslavsky J, Regli F, Maeder P. Acute pseudobulbar or relatives. She has been advised for a 2 weekly follow‑up. suprabulbar palsy. Arch Neurol 1991;48:501‑7. Informed consent was taken from the relatives of the patient. This is an open access journal, and articles are distributed under the terms of the Creative The isolated pseudo bulbar weakness with no limb weakness Commons Attribution‑NonCommercial‑ShareAlike 4.0 License, which allows others to is a rare entity with only a few reported cases.[2,3] Unilateral remix, tweak, and build upon the work non‑commercially, as long as appropriate credit lacunar stroke limited to corticonuclear pathways may be is given and the new creations are licensed under the identical terms. asymptomatic. When symptomatic, unilateral pathway damage Access this article online usually produces only lower facial weakness, and mostly Quick Response Code: [4] without significant limb weakness. Other symptoms of Website: dysarthria, drooling, speech abnormities, nasal regurgitation, www.ijccm.org and emotional liability are common.[3] Our case report highlights an atypical presentation of stroke as a cause of DOI: EF. A high clinical suspicion, vocal cord palsy on IDL and 10.4103/ijccm.IJCCM_78_18 microangiopathic changes in MRI, confirmed our diagnosis. Declaration of patient consent How to cite this article: Singh R, Nayak M, Jena SK, Azim A. Pseudo The authors certify that they have obtained all appropriate bulbar palsy: A rare cause of extubation failure. Indian J Crit Care Med patient consent forms. In the form the patient(s) has/have 2018;22:620‑1. given his/her/their consent for his/her/their images and other © 2018 Indian Journal of Critical Care Medicine | Published by Wolters Kluwer ‑ Medknow Unusual Cause of Hypotension in a Polytrauma Victim: A Case of Fahr’s Syndrome Sir, On arrival at the emergency department, the patient was Shock in polytrauma patient is believed to be due to conscious, responding but tachypneic (respiratory rate 30 hemorrhage until proven otherwise.[1] A 28‑year‑old male breaths/min) with bilateral equal air entry and in the state patient presented to the trauma center with a history of of shock (blood pressure was 80/40 mmHg, and heart rate blunt trauma to the chest and abdomen following fall from was 130/min). Pupils were bilaterally equal and reactive. height. He had a medical history of seizure disorder for He was resuscitated in the emergency department (ED) with the past 5 years for which he was on antiepileptic drugs. 2 L of crystalloids and two units of packed red blood cells. Indian Journal of Critical Care Medicine ¦ Volume 22 ¦ Issue 8 ¦ August 2018 621 Page no. 63.
Load more

Recommended publications
  • Melioidosis: a Potentially Life Threatening Infection
    CONTINUING MEDICAL EDUCATION Melioidosis: A Potentially Life Threatening Infection SH How, MMed*, CK Liam, FRCP*· *Department of Internal Medicine, Kulliyyah of Medicine, International Islamic University Malaysia, FO.Box 141, 27510, Kuantan, Pahang, Malaysia, **Department of Medicine, Faculty of Medicine, University of Malaya, 50603, Kuala Lumpur, MalaysIa Introduction example in Thailand, it is most commonly seen in the north-eastern region with an incidence of 4.4 per Melioidosis is caused by the gram-negative bacillus, 100,000 population per year'. In Northern Australia, Burkholderia pseudomallei, a common soil and fresh the incidence is higher (16.5 per 100,000 populations water saprophyte in tropical and subtropical regions. It 4 per yearY than that in Thailand • The incidence in is endemic in tropical Australial and in Southeast Asian Pahang and Singapore is 6.1 per 100, 000 population 23 4 countries, particularly Malaysia , Thailand and per year3 and 1.7 per 100,000 population per yearS, Singapores. However, only few doctors in these respectively. However, the true incidence may be endemic areas are fully aware of this infection. Hence, higher than that reported as most of these studies the management of this infection is often not included culture-confirmed cases only. Furthermore, appropriate and suboptimal. A recent study in Pahang some patients with mild infection from the rural areas has shown the incidence of this infection in Pahang3 is may not present to the hospital. More and more 4 comparable with that in northern Thailand • The melioidosis cases are being reported from previously overall mortality from this infection remains extremely unreported parts of the world especially southern high despite recent advancement in its treatment.
    [Show full text]
  • Cranial Nerve Disorders 11/05/2012
    Version 2.0 Cranial Nerve Disorders 11/05/2012 General Lesion possible locations: muscle, NMJ, nerve outside or inside brainstem Conditions that can affect any CN: DM, MS, Tumours, Sarcoid, Vasculitis (e.g. PAN), SLE, Syphilis, chronic meningitis (tends to pick off lower CN one by one). Olfactory (I) Nerve • Anatomy: Olfactory cells are a series of bipolar neurones which pass through the cribriform plate to the olfactory bulb. • Signs: Reduced taste and smell, but not to ammonia which stimulates the pain fibres carried in the trigeminal nerve. • Causes: Trauma; frontal lobe tumour; meningitis. Optic (II) Nerve • Anatomy: The optic nerve fibres are the axons of the retinal ganglion cells. Fibres from the nasal parts of retina decussate at optic chiasm, join with the non-decussating fibres and pass back in optic tracts to visual cortex. • Signs and causes: o Visual field defects: Field defects start as small areas of visual loss (scotomas). Monocular blindness: Lesions of one eye or optic nerve eg MS, giant cell arteritis. Bilateral blindness: Methyl alcohol, tobacco amblyopia; neurosyphilis. Bitemporal hemianopia: Optic chiasm compression eg internal carotid artery aneurysm, pituitary adenoma or craniopharyngioma Homonymous hemianopia: Affects half the visual field contralateral to the lesion in each eye. Lesions lie beyond the optic chiasm in the tracts, radiation or occipital cortex e.g. stroke, abscess, tumour. o Pupillary Abnormalities see pupillary abnormalities article. o Optic neuritis (pain on moving eye, loss of central vision, afferent pupillary defect, papilloedema). Causes: demyelination; rarely sinusitis, syphilis, collagen vascular disorders. o Optic atrophy (pale optic discs and reduced acuity): MS; frontal tumours; Friedreich's ataxia; retinitis pigmentosa; syphilis; glaucoma; Leber's optic atrophy; optic nerve compression.
    [Show full text]
  • The Management of Motor Neurone Disease
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.74.suppl_4.iv32 on 1 December 2003. Downloaded from THE MANAGEMENT OF MOTOR NEURONE DISEASE P N Leigh, S Abrahams, A Al-Chalabi, M-A Ampong, iv32 L H Goldstein, J Johnson, R Lyall, J Moxham, N Mustfa, A Rio, C Shaw, E Willey, and the King’s MND Care and Research Team J Neurol Neurosurg Psychiatry 2003;74(Suppl IV):iv32–iv47 he management of motor neurone disease (MND) has evolved rapidly over the last two decades. Although still incurable, MND is not untreatable. From an attitude of nihilism, Ttreatments and interventions that prolong survival have been developed. These treatments do not, however, arrest progression or reverse weakness. They raise difficult practical and ethical questions about quality of life, choice, and end of life decisions. Coordinated multidisciplinary care is the cornerstone of management and evidence supporting this approach, and for symptomatic treatment, is growing.1–3 Hospital based, community rehabilitation teams and palliative care teams can work effectively together, shifting emphasis and changing roles as the needs of the individuals affected by MND evolve. In the UK, MND care centres and regional networks of multidisciplinary teams are being established. Similar networks of MND centres exist in many other European countries and in North America. Here, we review current practice in relation to diagnosis, genetic counselling, the relief of common symptoms, multidisciplinary care, the place of gastrostomy and assisted ventilation, the use of riluzole, and end of life issues. c TERMINOLOGY c Motor neurone disease (MND) is a synonym for amyotrophic lateral sclerosis (ALS).
    [Show full text]
  • The Etiology and Pathogenesis of Poliomyelitis
    University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1937 The Etiology and pathogenesis of poliomyelitis Robert B. Johnson University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Johnson, Robert B., "The Etiology and pathogenesis of poliomyelitis" (1937). MD Theses. 517. https://digitalcommons.unmc.edu/mdtheses/517 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. THE ETIOLOGY AND PATHOGENESIS OF POLI0~1YELITIS by Bobert B. johnson Senior Thesis Presented to the College of Medioine University of Nebraska, Omaha 1937 """"------------------------------.-----------------r----,.-./ INDEX Page Introduction ..••.••.•••...••••••.•.•••••••••• Hi stOIj7 ...................... 4' ••••••••• ., • • • • .. • 1 Etiology •••••• • • • • .. •• • • • • • • • • • • • • • • • * ........ 6 Pathogenesis ••••..••••••••••••••••••••••••••• 22 Sw:rmary-• • " • • • • • • • • .. .. • • • • • • • • • • • • .. ,. • • • • .. • • • • • • 38 Bibliography ••••••••••••••••••••••••••••••••• 40 480877 INTRODUCTION This subject was chosen for my senior thesis primarily
    [Show full text]
  • Cranial) - Ophthalmoplegia, Field Defects, Facial Nerve Palsy
    Common neuro conditions (cranial) - Ophthalmoplegia, field defects, facial nerve palsy Examination sequence STANDARD examination sequence (WIPER, observe, inspect, palpate, percuss, auscultate, thank) Particulars: 1 (smell), 2 (visual acuity, fields, pupils), 3/4/6 (eye movements, pupils, accommodation, nystagmus), 5 (facial sensation), 7 (facial movements, taste), 8 (hearing), 9 (uvula), 10 (cough), 11 (SCM, shoulder), 12 (tongue) Commonly missed: smell, covering OWN eye for visual fields and not being 1m away, sternum for sensation, hearing Completion: formal tests (1 – scents, 2 – Snellen and Ischiara charts, 3/4/6 – fundoscopy, corneal reflex, 7 – jaw jerk, 9 – gag reflex), full neurological examinations (upper/lower, cerebellum) Presentation - WHAT; KEY positive; IMPORTANT negative: meningism; completion • I was asked to examine the cranial nerves of this elderly lady • On examination I found – failure of lateral gaze in the right eye. • There was no evidence of meningism; all other eye movements were intact, visual acuity was normal and there were no visual field defects, nor abnormalities in any of the other cranial nerves. • DDx – 6th nerve palsy • I would like to perform tests for completion as above. Common findings and viva questions - Investigations: o Bedside: urine dip (glucose, blood) o Bloods: FBC, U&E, LFTs, ceruloplasmin, INR, auto-antibodies, glucose, B12/folate o Culture: Blood, CSF o Imaging: CXR (paraneoplastic), CT, MRI (posterior lesions, cord), DAT scan o Special: LP (cells, oligoclonal bands, xanthochromia); nerve
    [Show full text]
  • Mrcp Paces Manual
    MRCP PACES MANUAL Louise Pealing MA Hons (Cantab) MBBS MSc MRCP MRCGP General Practitioner and Clinical Research Fellow, Nuffield Department of Primary Care Health Sciences, University of Oxford Benjamin Mullish MB BChir MA (Cantab) MRCPAFHEA Specialty Registrar/Academic Clinical Fellow, Gastroenterology and Hepatology, St Mary’s Hospital, London Philip J Smith BMedSci (Hons) BMBS (Hons) MRCP MSc (Nutrition) Gastroenterology Specialist Registrar and MRC Clinical Research Training Fellow Gastroenterology Department, University College London Hospital, London Edited by Douglas C Macdonald BM (Hons) BSc (Hons) MRCP PhD Consultant Hepatologist, Royal Free London NHS Foundation Trust Royal Free Hospital, London Contents Preface vi Introduction vii STATION 1 ^ Respiratory and Abdominal Examinations 1 The abdominal examination 3 Abdominal scenarios 7 The respiratory examination 47 Respiratory scenarios 52 STATION 2 ^ History-Taking Examination 71 History-taking scenarios 77 STATION 3 ^ Cardiovascular and Neurological Examinations 169 The cardiovascular examination 170 Cardiovascular scenarios 175 The neurological examination 220 Neurological scenarios 241 STATION 4 ^ Communication skills and Ethics’ Examination 353 Approach to the communication skills and ethics station 355 Communication skills and ethics scenarios 359 STATION 5 ^ Integrated Clinical Assessment 393 Approach to Station 5 398 Integrated clinical assessment scenarios 407 Abbreviations 599 Index 605 v Station 3 Neurological scenarios 1. Multiple sclerosis 17. Median nerve palsy 2. Parkinson’s disease 18. Ulnar nerve palsy 3. Motor neuron disease 19. Radial nerve palsy 4. Hemiparesis 20. Common peroneal nerve 5. Spastic paraparesis palsy and L4–5 root lesions 6. Cervical myelopathy 21. Nystagmus 7. Syringomyelia/Syringobulbia 22. Ophthalmoplegia 8. Myotonic dystrophy 23. Visual field defect 9. Myasthenia gravis 24.
    [Show full text]
  • Sarah Nichol (Glasgow) "Delayed Radiation-Induced Bulbar Palsy
    British Society for Clinical Neurophysiology Medical Student Essay Prize 2018 ‘How Clinical Neurophysiology helped in the diagnosis/management of a patient’ ​ Delayed radiation-induced bulbar palsy mimicking amyotrophic lateral sclerosis Sarah Nichol, University of Glasgow Summary This case report follows a 58 year old gentleman presenting with a one year progression of bulbar palsy signs and symptoms. His main complaint was difficulty in swallowing and slurring of his speech. He reported no upper or lower limb weakness. On neurological examination, there was visible atrophy of the tongue muscles as well as slight weakness of the tongue against resistance. Fasciculations of the tongue were present on visual examination. In any case of adult onset bulbar symptoms, amyotrophic lateral sclerosis (ALS) is a suggested diagnosis. This case shows how collation of clinical history, medical history and electrodiagnostic studies leads to the diagnosis of a known, but rare, mimic of bulbar-onset ALS. Background Amyotrophic lateral sclerosis (ALS) is a subtype of motor neurone disease (MND) characterised by progressive degeneration of motor neurons. It usually presents with both upper and lower motor neuron signs arising from one segment of the neuroaxis, typically beginning with either motor neuron degeneration in a cortical, bulbar or ventral cord location, to then spread to contiguous areas as the disease progresses [1]. Classic presenting signs and symptoms include weakness in lower limb or upper limb, muscle cramps and fasciculations. Other presenting symptoms are difficulty with speech and swallowing or even rarer, respiratory muscle problems and breathing difficulties. As the disease progresses muscles become weaker and more are affected, eventually leading to inability to chew or swallow, talk or walk [2].
    [Show full text]
  • Brainstem and Multiple Cranial Nerve Syndromes
    CHAPTER 21 Brainstem and Multiple Cranial Nerve Syndromes he brainstem is a compact structure, with cra- the lower motor neurons of the CN nuclei. With a nial nerve (CN) nuclei, nerve fascicles, and few exceptions, CNs innervate structures of the head T long ascending and descending tracts all and neck ipsilaterally. A process affecting the brain- closely juxtaposed. Structures and centers in the reticu- stem long tracts on one side causes clinical abnormal- lar formation control many vital functions. Brainstem ities on the opposite side of the body. For this reason, diseases are serious and often life threatening. focal brainstem lesions are characterized by “crossed” Involvement of the intricate network of neural struc- syndromes of ipsilateral CN dysfunction and contra- tures often causes a plethora of clinical findings. lateral long motor or sensory tract dysfunction. For Brainstem syndromes typically involve dysfunction of instance, in the right side of the pons, the nuclei for one or more CNs. Deficits due to dysfunction of indi- CNs VI and VII lie in proximity to the right corti- vidual nerves are covered in the preceding chapters. cospinal tract, which is destined to decussate in the This chapter discusses conditions that cause dysfunc- medulla to innervate the left side of the body. The tion beyond the distribution of a single CN, involving patient with a lesion in the right pons will have CN more than one CN, or conditions that involve brain- findings on the right, such as a sixth or seventh nerve stem structures in addition to the CN nucleus or fasci- palsy, and a hemiparesis on the left.
    [Show full text]
  • Amyotrophic Lateral Sclerosis Considerations on Diagnostic Criteria
    Article Arq Neuropsiquiatr 2010;68(6):837-842 Amyotrophic lateral sclerosis Considerations on diagnostic criteria Marco A. Chieia, Acary S.B. Oliveira, Helga C.A. Silva, Alberto Alain Gabbai ABSTRACT Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder, compromising the motor neuron, characterized by progressive muscle weakness, with reserved prognosis. The diagnosis is based on inclusion and exclusion clinical criteria, since there is no specific confirmation test. The objective of this research is to critically examine the main diagnosis instrument - El Escorial revisited, from the World Federation of Neurology (1998). Of the 540 patients with initial ALS diagnosis, either probable or definite, seen at UNIFESP-EPM, 190 underwent thorough investigation, following regular clinical and therapeutic treatment for over two years. Thirty patients (15.78%) had their diagnosis completely changed. The false-positive diagnoses were related to: early age, clinical presentation of symmetry, weakness greater than atrophy, symptomatic exacerbation. In addition, three patients with myasthenia gravis developed framework for ALS, suggesting the post-synaptic disability as a sign of early disease. Key words: amyotrophic lateral sclerosis, correct diagnosis, El Escorial revisited. Esclerose lateral amiotrófica: considerações sobre critérios diagnósticos RESUMO Esclerose lateral amiotrófica (ELA) é uma doença neurodegenerativa, que compromete o neurônio motor, caracterizada por fraqueza muscular progressiva, com prognóstico reservado. O diagnóstico é baseado na inclusão e exclusão de critérios clínicos, uma vez que não existe um teste de confirmação específica. O objetivo desta pesquisa é analisar criticamente o instrumento de diagnóstico principal - El Escorial revisited, da Federação Mundial de Neurologia (1998). Dos 540 pacientes com diagnóstico inicial de ELA, seja provável ou definitiva, vistos pela UNIFESP-EPM, 190 foram submetidos a investigação aprofundada, após tratamento clínico e terapêutico regular há mais de dois anos.
    [Show full text]
  • Anti-Gt1a Igg in Guillain-Barré Syndrome M Koga, H Yoshino, M Morimatsu, N Yuki
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.72.6.767 on 1 June 2002. Downloaded from 767 PAPER Anti-GT1a IgG in Guillain-Barré syndrome M Koga, H Yoshino, M Morimatsu, N Yuki ............................................................................................................................. J Neurol Neurosurg Psychiatry 2002;72:767–771 Objective: To investigate the presence of serum anti-GT1a IgG in Guillain-Barré syndrome (GBS) and its relation to clinical manifestations. Background: Several patients with GBS and bulbar palsy have been reported to have serum anti-GT1a IgG. Most, however, also have anti-GQ1b IgG. A previous study failed to detect GT1a in human cranial nerves, but GQ1b was abundant in human ocular motor nerves. Whether anti-GT1a IgG itself determines the clinical manifestations is not yet clear. See end of article for Methods: The association of clinical manifestations with the presence of anti-GT1a IgG and with its authors’ affiliations cross reactivity was investigated. An immunochemical study was performed to determine whether ....................... GT1a is present in human cranial nerves. Correspondence to: Results: Anti-GT1a and anti-GQ1b IgG were positive in 10% and 9% respectively of 220 consecutive Dr M Koga, Department of patients with GBS. Patients with anti-GT1a IgG often had cranial nerve palsy (ophthalmoparesis, 57%; Neurology, Dokkyo University School of facial palsy, 57%; bulbar palsy, 70%), and 39% needed artificial ventilation. These features were also Medicine, Kitakobayashi seen in patients with anti-GQ1b IgG. There was no significant difference between the two groups with 880, Mibu, Shimotsuga, respect to the frequency of clinical findings. An enzyme-linked immunosorbent assay showed that anti- Tochigi, Japan; GT1a IgG cross reacted with GQ1b in 75% of the patients, GD1a in 30%, GM1 in 20%, and GD1b [email protected] in 20%.
    [Show full text]
  • Comparison of Disordered Swallowing Patterns in Patients with Recurrent Cortical/Subcortical Stroke and First-Time Brainstem Stroke
    J Rehabil Med 2005; 37: 189–191 SHORT COMMUNICATION COMPARISON OF DISORDERED SWALLOWING PATTERNS IN PATIENTS WITH RECURRENT CORTICAL/SUBCORTICAL STROKE AND FIRST-TIME BRAINSTEM STROKE Der-Sheng Han,1 Yeun-Chung Chang,2 Chih-Huei Lu3 and Tyng-Guey Wang1 From the 1Department of Physical Medicine and Rehabilitation, 2Department of Image, National Taiwan University Hospital, Taipei, Taiwan and 3Foo-Yin Institute of Technology Hospital, Kaohsiung, Taiwan, ROC Objective: To describe the disordered swallowing patterns in mentioned that swallowing disorders may occur in patients with recurrent cortical/subcortical stroke and first-time brain- single hemispheric lesions, dysphagia is generally believed to be stem stroke. a common and serious problem in patients with bilateral cerebral Design: A retrospective study. hemispheric or brainstem lesions (3). Dysphagic patients with Subjects: Forty-seven consecutive patients, 28 with recurrent recurrent cortical/subcortical stroke (RS), affecting the upper cortical/subcortical stroke and 19 with first-time brainstem motor neurones of the swallowing pathway, display a clinical stroke, referred for dysphagic evaluation to the rehabili- symptom complex known as “pseudobulbar palsy”. Those with tation department of a medical centre. brainstem stroke (BS), affecting the lower motor neurones of the Methods: Thirty-five male and 12 female patients with a swallowing pathway, generate a symptom complex called mean age of 62.0 ± 11.5 years were included. The median “bulbar palsy” (4). To our knowledge, although a few studies post-stroke duration was 17.0 days. The records of clinical have described the clinical characteristics of bulbar and examination and a videofluoroscopic study of swallowing pseudobulbar types of dysphagia (4, 5), none has compared were collected through chart review.
    [Show full text]
  • Syringobulbia in Patients with Chiari Malformation Type I: a Systematic Review
    Hindawi BioMed Research International Volume 2019, Article ID 4829102, 8 pages https://doi.org/10.1155/2019/4829102 Review Article Syringobulbia in Patients with Chiari Malformation Type I: A Systematic Review Jian Shen,1 Jie Shen,1 Kaiyuan Huang,1 Yixin Wu,2 Jianwei Pan,1 and Renya Zhan 1 1 Department of Neurosurgery, First Afliated Hospital, School of Medicine, Zhejiang University, China 2Cancer Hospital of Zhejiang, China Correspondence should be addressed to Renya Zhan; [email protected] Received 7 September 2018; Accepted 26 February 2019; Published 19 March 2019 Guest Editor: Rong Xie Copyright © 2019 Jian Shen et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Tis study aimed to summarize the clinical features, diagnosis, and treatment of Chiari malformation type I- (CM-1-) associated syringobulbia. We performed a literature review of CM-1-associated syringobulbia in PubMed, Ovid MEDLINE, and Web of Science databases. Our concerns were the clinical features, radiologic presentations, treatment therapies, and prognoses of CM-1-associated syringobulbia. Tis review identifed 23 articles with 53 cases. Symptoms included headache, neck pain, cranial nerve palsy, limb weakness/dysesthesia, Horner syndrome, ataxia, and respiratory disorders. Te most frequently involved area was the medulla. Most of the patients also had syringomyelia. Surgical procedures performed included posterior fossa decompression, foramen magnum decompression, cervical laminectomy, duraplasty, and syringobulbic cavity shunt. Most patients experienced symptom alleviation or resolution postoperatively. A syringobulbic cavity shunt provided good results in refractory cases.
    [Show full text]