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Rabies viral encephalitis – clinical determinants in diagnosis with special reference to paralytic form
  1. Girish Gadre1,
  2. Parthasarathy Satishchandra1,*,
  3. Anita Mahadevan2,
  4. MS Suja2,
  5. SN Madhusudana3,
  6. Challa Sundaram4,
  7. SK Shankar2
  1. 1 Department of Neurology, National Institute of Mental Health & Neurosciences, Bangalore, India;
  2. 2 Department of Neuropathology, National Institute of Mental Health & Neurosciences, Bangalore, India;
  3. 3 Department of Neurovirology, National Institute of Mental Health & Neurosciences, Bangalore, India;
  4. 4 Department of Pathology, Nizam's Institute of Medical Sciences, , Hyderabad, India
  1. Correspondence to: Satish P Chandra, Neurology, NIMHANS, Department of Neurology, NIMHANS, Bangaore, 560029, India; drpsatishchandra{at}yahoo.com

Abstract

Rabies is an important public health problem in developing countries like India where an alarmingly high incidence of the infection is reported every year despite availability of highly effective, potent and safe vaccines. In clinical practice, diagnosis of furious (encephalitic) form of rabies poses little difficulty. In contrast paralytic form poses a diagnostic dilemma, to distinguish it from Guillain Barre syndrome. The problem is further compounded in absence of history of dog bite, clinical features resembling a psychiatric syndrome. The present study analyzed the spectrum of neurological manifestations in 47 cases of rabies encephalitis [34 - paralytic, 6 – encephalitic, and 7 had psychiatric manifestations] from two hospitals in south India, confirmed at post mortem by demonstration of viral antigen in brain. History of dog bite was elicited in 33 patients and fox bite in one. Twenty-two patients received post exposure prophylaxis. Incubation period ranged from 7 days to 4 years. Clinical features were analyzed looking for any clinical pointers that provide clue to diagnosis of paralytic rabies. Fever, distal paresthesias, fasciculation, alteration in sensorium, rapid progression of symptoms, and pleocytosis in CSF should alert the neurologist to consider rabies encephalomyelitis. Detection of viral antigen in corneal smear, skin biopsy from nape of the neck had limited usefulness in antemortem diagnosis. Although a few clinical pointers may help suspect rabies encephalomyelitis antemortem, confirmation requires neuropathological / neurovirological assistance. The preponderance of atypical/paralytic cases in this series suggests that neurologists and psychiatrists need to have a high index of clinical suspicion particularly in absence of history of dog bite.

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