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MRI appearances of the facial nerve in an HIV infected patient with acute facial nerve palsy
  1. K A MISZKIEL
  1. MRI Unit, Imaging Department at UCL Hospitals (NHS) Trust, London, UK
  2. Division of Pathology and Infectious Diseases
  3. UCL Medical School, Camden and Islington Community Health Services (NHS) Trust, The Middlesex Hospital, Mortimer Street, London, UK
  1. Dr Katherine Anne Miszkiel, Lysholm Department of Radiology, The National Hospital for Neurology and Neurosurgery, Queen Square, London WC1 3BG, UK. Telephone 0044 171 837 3611; email KAMiszkiel{at}aol.com
  1. R F MILLER
  1. MRI Unit, Imaging Department at UCL Hospitals (NHS) Trust, London, UK
  2. Division of Pathology and Infectious Diseases
  3. UCL Medical School, Camden and Islington Community Health Services (NHS) Trust, The Middlesex Hospital, Mortimer Street, London, UK
  1. Dr Katherine Anne Miszkiel, Lysholm Department of Radiology, The National Hospital for Neurology and Neurosurgery, Queen Square, London WC1 3BG, UK. Telephone 0044 171 837 3611; email KAMiszkiel{at}aol.com

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A 27 year old white HIV positive homosexual man presented with a 6 day history of right mandibular and posterior auricular pain progressing to right facial weakness on day 7. Examination showed a right lower motor neuron facial palsy. On MRI performed on day 7, coronal (fig A) and axial (fig B) T1 weighted unenhanced images showed swelling (arrow) and increased signal (curved arrow) of the intracanalicular segment of the right facial nerve. Corresponding images post-Gd-DTPA (figs C, D) showed enhancement of the right intracanalicular segment (arrow) and the geniculate ganglion (curved open arrow). In view of the well preserved CD4+ lymphocyte count of 460 ×106 /l (normal: 350–2200 × 106 /l), lumbar puncture was not performed as CSF leucocytosis would not have been an indication to start antiretroviral medication. The patient wastreated with 60 mg oral prednisolone daily for 10 days. Follow up MRI on day 76 (the facial palsy having completely resolved), showed reduction in swelling and enhancement of the affected facial nerve.

Facial nerve palsy is part of the clinical range of disease resulting from HIV infection and is more common in asymptomatic patients than in those with more advanced disease.1 The enhancement pattern of the affected facial nerve we describe is similar to that described in Bell’s palsy,2 a condition in which the neurotropic Herpes simplex virus type 1 is probably the major aetiological agent3; HIV is also neurotropic and virus localisation in the facial nerve or the geniculate ganglion may cause mast cell degranulation, with release of vasoactive substances altering the permeability of the blood-peripheral nerve barrier resulting in intraneural oedema and fibre swelling.2 The end result of these interactions may be seen on MRI as swelling and pathological enhancement of the affected facial nerve.

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