PICTORIAL COMMENTARY
Cerebral Rabies
Contributed by: S.K.Shankar, MD and Anita Mahadevan, MD Department of Neuropathology, National Institute of Mental Health & Neurosciences, Bangalore -560029 and MS. Suja, PhD, Rajiv Gandhi Centre for Biotechnology, Trivandrum – 695014, Kerala, India
A sixteen year old male presented with acute onset of paresthesias in lower limbs of 10 days duration in the form of tingling sensation, followed by weakness of right lower limb and later of the left lower limb. Paresthesias ascended up to the groin in both lower limbs. Weakness started distally and progressed rapidly to involve the entire lower limbs. Upper limb paresthesias started 4 days later and ascended up to the neck, followed by similar weakness in upper limbs. He developed respiratory difficulty and dysphagia 3 days prior to admission and also retention of urine. Five days prior to admission he had intermittent moderate degree of fever associated with chills and rigors and diffuse back pain. There was no history of disturbance in consciousness or behavior or hydrophobia. There was no history of any antecedent illness or animal bite. He had hypotonia of all limbs, generalized areflexia, absent superficial reflexes, neck and truncal weakness. He had symmetrical limb weakness. He was bed bound at the time of presentation to the hospital.
Results of routine blood biochemistry and haematological investigations and cerebrospinal fluid (CSF) analysis were within the normal range. Results of other investigations were as follows:
Anti HSV antibody – 1:125; Anti JE antibody – negative; HSV 1 and 2 PCR – Negative; PCR for West Nile – Negative; Anti-rabies antibody – Positive; PCR for Rabies – Positive; HIV1 and 2: Non reactive.
Electrocardiogram was normal. Chest X-ray PA view and Brain CT Scan were normal. MRI Brain with contrast showed T2 and T2F FLAIR hyperintensities in bilateral medial temporal regions, insula, cingulated gyrus and basal ganglia and cerebellar hemispheres symmetrically. Meningeal enhancement was noted. Patchy enhancement were seen in the cerebellar lesions.
A diagnosis of HSV-1 encephalitis was made and the patient was prescribed methylpredinisoline, antibiotics and acyclovir. He was maintained on ventilator support and other general supportive measures.
Diagnostic possibility considered was acute disseminated encephalomyelitis secondary to Herpes Simplex infection based on MRI features. A possibility of rabies was also considered but history of animal bite was not forthcoming and the patient had no features of hydrophobia. Patient continued to deteriorate during the hospital stay, lapsed into coma and succumbed to his illness on 7th day of admission. CSF studies were positive for antirabies antibodies. Immunohistochemistry of brain section using polyclonal antibody to nucleoprotein of rabies virus revealed extensive distribution of the viral antigen, discordant with MRI feature of medial temporal and multiple cerebellar intensities.
Take home message: In addition to HSV, other viral conditions can also produce medial temporal intensities on MRI.
Rabies viral antigen can be a good neuroanatomical tracer, labelling the neurons and dendritic branches.
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