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Year : 2010  |  Volume : 58  |  Issue : 4  |  Page : 596-598

Unilateral diaphragmatic paralysis following dengue infection

Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Acceptance17-Jul-2010
Date of Web Publication24-Aug-2010

Correspondence Address:
Sanjeev Jha
Department of Neurology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.68662

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How to cite this article:
Ansari M K, Jha S, Nath A. Unilateral diaphragmatic paralysis following dengue infection. Neurol India 2010;58:596-8

How to cite this URL:
Ansari M K, Jha S, Nath A. Unilateral diaphragmatic paralysis following dengue infection. Neurol India [serial online] 2010 [cited 2023 Feb 9];58:596-8. Available from: https://www.neurologyindia.com/text.asp?2010/58/4/596/68662


Dengue is the most common arboviral infection in tropical and sub-tropical climates. Clinical presentation varies from a severe flu-like illness to a potentially lethal dengue hemorrhagic fever. Various neurological manifestations of dengue include myositis, polyradiculopathy and Guillain-Barre syndrome. [1],[2],[3] Isolated phrenic neuropathy and diaphragmatic paralysis following dengue is extremely rare and only a single such association has been described. [4] We report the second such patient.

A 38-year-old school teacher presented with fever, rashes and generalized body pains of 4 days duration. On examination, he was febrile (102°F), with a pulse of 128/min and a blood pressure of 120/78 mmHg. The rash was macular and blanching and generalized. Petechiae were present over the thighs and abdomen. Neurological examination at this stage was essentially normal. Total platelet counts were 7,000/mm 3 and total leucocyte count was 10,200/mm 3 with lymphocyte predominance. Serology for dengue IgG and IgM was positive. Results of the liver function tests are: total bilirubin 1.07 mg/dl; SGOT 262 U/L, SGPT 85 U/L; alkaline phosphatase 318 U/L. Coagulation profile and renal functions were normal.

He was given supportive care and transfusion of platelet concentrates. Within 6 days of onset of symptoms, he had a significant relief of his ailments. His hospital stay was uneventful, except for body ache, particularly along the right shoulder and interscapular region, which responded to oral analgesics. After 1 week of a symptom-free interval, he developed shortness of breath and chest discomfort on physical exertion and talking, especially while delivering lectures to his students. These symptoms were nonprogressive, but persisted for 1 month when he was re-hospitalized for evaluation. General physical examination was unremarkable and there were no focal neurological deficits. The X-ray of chest showed elevated right hemidiaphragm [Figure 1]. Fluoroscopy for diaphragmatic movements demonstrated minimal excursion of right diaphragm with no paradoxical motion on sniff test [Figure 2]a and b. Electrodiagnostic studies revealed nonrecordable compound muscle action potential (CMAP) from right phrenic nerve [Figure 3] and [Figure 4]. There was no electrophysiological evidence of involvement of other components of the right brachial plexus. The pulmonary function test (PFT) in the sitting position was suggestive of restrictive pattern. The contrast-enhanced computed tomography of thorax was normal.
Figure 1 : X-ray chest (PA view) showing elevated right hemidiaphragm

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Figure 2 : (a) Fluoroscopy for diaphragmatic movements demonstrating negligible descent of right hemidiaphraghm with inspiration. (b) Expiratory film showing negligible ascent of right hemidiaphragm and no paradoxical movement

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Figure 3 : Upper panel - nonrecordable right phrenic nerve compound muscle action potential (CMAP) before treatment. Lower panel - low amplitude but recordable right phrenic nerve CMAP after 4 weeks of intravenous immunoglobulins

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Figure 4 : Upper panel - left side phrenic nerve compound muscle action potential (CMAP) before treatment. Lower panel - left side phrenic nerve CMAP after 4 weeks of intravenous immunoglobulins

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Post dengue, right phrenic neuropathy was considered and he was managed with oral steroids and supervised chest physiotherapy. He also received intravenous immunoglobulins for 5 days. At 4 weeks of follow-up he had significant relief in symptoms. Repeat PFTs showed significant increase in expiratory forced vital capacity and forced expiratory volume during the first second. Repeat phrenic nerve conduction study showed low amplitude but recordable right phrenic nerve CMAP [Figure 3] and [Figure 4].

Diaphragmatic paralysis is more common than clinically recognized and the etiology remains unidentified in more than two-third of the cases. [5] Post viral neuropathy and phrenic nerve involvement have been described following several viral infections like herpes zoster, poliovirus, West Nile virus and human immunodeficiency virus infections. [6],[7],[8],[9] Our patient had dengue infection complicated by right phrenic neuropathy, resulting in hemidiaphragmatic paralysis and respiratory insufficiency. Neurological and electrophysiological evaluation revealed only isolated right phrenic neuropathy and no evidence of brachial plexus involvement. The initial symptoms of pain along the right shoulder and interscapular region might have been due to brachial plexus involvement. However, the electrodiagnostic tests performed after 1 month of onset of these symptoms were not suggestive of brachial plexus involvement, except for right phrenic neuropathy. It is possible that this patient might have had brachial plexus involvement initially, where several of the features like weakness and wasting in the distribution of single or multiple motor nerves are absent or not readily recognized. [10],[11],[12] Phrenic nerve palsy has been described as an isolated involvement in brachial neuritis. [10]

Clinical course and management of postinfection phrenic neuropathy remains inconclusive. In the earlier reported case, the course was either benign or associated with poor outcome requiring prolonged mechanical ventilation. [8],[9] Considering the possible pathogenic mechanism being immune-mediated inflammatory reaction, these patients were given intravenous immunoglobulin. [6],[13]

 » References Top

1.Kalita J, Misra UK, Mahadevan A, Shankar SK. Acute pure motor quadriparesis: is it dengue myositis? Electromyogr Clin Neurophysiol 2005;45:357-61.  Back to cited text no. 1  [PUBMED]    
2.Santos NQ, Azoubel AC, Lopes AA, Costa G, Bacellar A. Guillain-Barre syndrome in the course of dengue: case report. Arq Neuropsiquiatr 2004;62:144-6.   Back to cited text no. 2  [PUBMED]  [FULLTEXT]  
3.Gulati S, Maheshwari A. Atypical manifestations of dengue. Trop Med Int Health 2007;12:1087-95.  Back to cited text no. 3  [PUBMED]  [FULLTEXT]  
4.Chien J, Ong A, Low SY. An unusual complication of dengue infection. Singapore Med J 2008;49:e340-2.  Back to cited text no. 4  [PUBMED]  [FULLTEXT]  
5.Baum GL, Crapo JD, Celli BR, Karlinsky JB. Pulmonary diseases. 6 th ed. Philadelphia, PA: Lippincott-Raven; 1998. p. 1185-8.  Back to cited text no. 5      
6.Piliero PJ, Estanislao L, Simpson D. Diaphragmatic paralysis due to isolated phrenic neuropathy in an HIV-infected man. Neurology 2004;62:154-5.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]  
7.Imai T, Matsumoto H. Insidious phrenic nerve involvement in postpolio syndrome. Intern Med 2006;45:563-4.  Back to cited text no. 7  [PUBMED]    
8.Stowasser M, Cameron J, Oliver WA. Diaphragmatic paralysis following cervical herpes zoster. Med J Aust 1990;153:555-6.  Back to cited text no. 8  [PUBMED]    
9.Betensley AD, Jaffery SH, Collins H, Sripathi N, Alabi F. Bilateral diaphragmatic paralysis and related respiratory complications in a patient with West Nile virus infection. Thorax 2004;59:268-9.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]  
10.Tsao BE, Ostrovskiy DA, Wilbourn AJ, Shields RW. Phrenic neuropathy due to neuralgic amyotrophy. Neurology 2006;66:1582-4.   Back to cited text no. 10      
11.Nardone R, Bernhart H, Pozzera A, Taddei M, Tezzon F. Respiratory weakness in neuralgic amyotrophy: report of two cases with phrenic nerve involvement. Neurol Sci 2000;21:177-81.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]  
12.Wilbourn AJ. Brachial plexus disorders. In: Dyck PJ, Thomas RK, Griffin JW, Low PA, Peduslo JF, editors. Peripheral neuropathy. 3rd ed. Philadelphia: Saunders; 1993. p. 933-4.  Back to cited text no. 12      
13.Nakajima M, Fujioka S, Ohno H, Iwamoto K. Partial but Rapid Recovery from Paralysis after Immunomodulation during Early Stage of Neuralgic Amyotrophy. Eur Neurol 2006;55:227-9.  Back to cited text no. 13  [PUBMED]  [FULLTEXT]  


  [Figure 1], [Figure 2], [Figure 3], [Figure 4]

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