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Year : 2004  |  Volume : 52  |  Issue : 2  |  Page : 270-

Differentiating paralytic rabies from post antirabies vaccine polyradiculoneuropathy

S Kumar 
 Neurology Unit, Department of Neurological Sciences, Christian Medical College Hospital, Vellore, Tamilnadu - 632004, India

Correspondence Address:
S Kumar
Neurology Unit, Department of Neurological Sciences, Christian Medical College Hospital, Vellore, Tamilnadu - 632004

How to cite this article:
Kumar S. Differentiating paralytic rabies from post antirabies vaccine polyradiculoneuropathy.Neurol India 2004;52:270-270

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Kumar S. Differentiating paralytic rabies from post antirabies vaccine polyradiculoneuropathy. Neurol India [serial online] 2004 [cited 2021 Sep 24 ];52:270-270
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The recent report of flaccid paralysis following anti-rabies vaccine (ARV) was interesting, where Behari et al describe the diagnostic dilemma in a patient presenting with flaccid paralysis following administration of ARV.[1] They mention that measurement of rabies antibody titer in the serum and cerebrospinal fluid could help in differentiating paralytic rabies from post-ARV polyradiculoneuropathy (Guillain-Barre syndrome, GBS). However, I would like to make certain observations.

Firstly, there are several features that could be useful in differentiating paralytic rabies from polyradiculoneuropathy, which could be summarized as follows:

1. History of dog bite: In a person who has not been bitten by a dog (as in the case reported by Behari et al), there is virtually no possibility of rabies and the diagnosis of GBS is straightforward.

2. Incubation period: The mean incubation period in paralytic rabies is 49 days,[2] as compared to 14 days in case of post-ARV neurological syndromes.[3]

3. Clinical involvement: Sphincter disturbances and sensory symptoms (in addition to ascending flaccid paralysis) are common in paralytic rabies,[4] which is not the case with post-ARV polyradiculoneuropathy. This could be explained on the basis of direct involvement of brainstem and spinal cord by rabies virus, proven by autopsy studies.[2]

4. Disease progression: Paralytic rabies progresses rapidly with early respiratory paralysis and death ensues within 7-11 days of symptom onset in all cases.[2] On the other hand, post-ARV polyradiculoneuropathy has a better outcome with conservative management[5] or immunotherapy and the mortality is less than 10%.[3]

5. Magnetic resonance imaging (MRI): MRI of the brain in paralytic rabies shows exclusive involvement of the gray matter including the basal ganglia, thalami, pontine and midbrain nuclei. This is in contrast to the predominant white matter involvement in post-vaccinial acute disseminated encephalomyelitis.[6] Moreover, in polyradiculoneuropathy; MRI is usually normal (as in the case reported by Behari et al).

Secondly, Behari et al treated their patient with steroids. However, significantly better therapeutic results have earlier been shown with cyclophosphamide as compared to steroids.[3] Moreover, patients treated with steroids have a higher incidence of relapse of GBS.[7] Plasmapheresis or intravenous immunoglobulins are better options for treatment of these patients.


1Srivastava AK, Sardana V, Prasad K, Behari M. Diagnostic dilemma in flaccid paralysis following anti-rabies vaccine. Neurol India 2004;52:132-3.
2Chopra JS, Banerjee AK, Murthy JM, Pal SR. Paralytic rabies: A clinico-pathological study. Brain 1980;103:789-802.
3Swamy HS, Shankar SK, Chandra PS, Aroor SR, Krishna AS, Perumal VG. Neurological complications due to beta-propiolactone (BPL)-inactivated antirabies vaccination. Clinical, electrophysiological and therapeutic aspects. J Neurol Sci 1984;63:111-28.
4Warrell DA. The clinical picture of rabies in man. Trans R Soc Trop Med Hyg 1976;70:188-95.
5Arega D, Zenebe G. Peripheral neuropathy following administration of nerve tissue antirabies vaccine. Ethiop Med J 1999;37:269-73.
6Mani J, Reddy BC, Borgohain R, Sitajayalakshmi S, Sundaram C, Mohandas S. Magnetic resonance imaging in rabies. Postgrad Med J 2003;79:352-4.
7Dias-Tosta E, Brasil JP, Figueiredo MA. The use of corticosteroids in Guillain-Barre syndrome: study of 51 cases. Arq Neuropsiquiatr. 1986;44:117-24.