|LETTER TO EDITOR
|Year : 2014 | Volume
| Issue : 4 | Page : 295-296
Bilateral facial palsy in acute seroconversion illness: An uncommon scenario
Department of General Medicine, Institute of Post-Graduate Medical Education and Research, Kolkata, West Bengal, India
|Date of Web Publication||16-Oct-2014|
Department of General Medicine, Institute of Post-Graduate Medical Education and Research, Kolkata, West Bengal
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Chakrabarti S. Bilateral facial palsy in acute seroconversion illness: An uncommon scenario. CHRISMED J Health Res 2014;1:295-6
|How to cite this URL:|
Chakrabarti S. Bilateral facial palsy in acute seroconversion illness: An uncommon scenario. CHRISMED J Health Res [serial online] 2014 [cited 2020 Nov 27];1:295-6. Available from: https://www.cjhr.org/text.asp?2014/1/4/295/143011
Bilateral facial nerve paralysis is a distinctly rare although recognized complication in HIV and few cases have been reported in literature thus far. The author reports such a case where a patient developed bilateral facial nerve paralysis along with aseptic meningitis during acute HIV seroconversion illness.
A 30-year-old unmarried heterosexual male truck driver presented with complaints of difficulty in closing his eyes, left worse than right, and inability to close his mouth completely causing food to dribble out of his mouth for last 2 days. For last 10 days, he was experiencing an episode of low-grade fever, sore throat, and malaise. He had multiple unprotected sexual exposures in last 9 years but denied any intravenous drug use. Multiple small and insignificant palpable cervical lymph nodes were noted in general survey. Neurological examination revealed bilateral lower motor neuron type facial diplegia with left-sided involvement more than right [Figure 1]. Meningeal signs were absent; sensory and motor systems were normal. Reflexes were intact in all 4 limbs; plantar responses were flexor bilaterally. Rest of the general and systemic examination was within normal limits. Blood biochemistry (including liver enzymes), blood counts, and cell indices were also within normal limits. Serological studies for herpes simplex virus 1 and 2, enterovirus, campylobacter, cytomegalovirus, hepatitis viruses, Epstein-Barr virus, and Toxoplasma gondii were all negative. Angiotensin-converting enzyme level and vasculitis profile including ANA, Rheumatoid Factor, C3, and C4 were within normal limits. Nerve conduction velocity (NCV) revealed a demyelinating type of facial palsy bilaterally (left-sided abnormality more than right) with absent blink reflexes and severely diminished conduction velocity, prolonged distal motor latency and F wave latency. NCV results of limbs were within normal limits. Brain magnetic resonance imaging (MRI) showed normal findings. Cerebrospinal fluid analysis revealed raised opening pressure; glucose content of 69 mg/dl (serum glucose at that time was 134 mg/dl), protein content of 81 mg/dl, and 21 cells/mm 3 (all lymphocytes). A Gram-stained smear and culture of CSF for bacteria and mycobacteria revealed no organism, and viral PCR was negative. Considering his high-risk behavior, HIV serology was sent and HIV-1 infection was diagnosed by using enzyme-linked immunosorbent assay (ELISA). Positivity was confirmed by Western blot. CD4+ T lymphocyte count was 932/μL and viral load was 470,000 copies/mL. He was ultimately diagnosed as a case of aseptic meningitis with bilateral peripheral facial nerve palsy secondary to acute HIV seroconversion. As there was no indication for starting HAART, it was not instituted. However, symptomatic treatment for aseptic meningitis was started and patient asked for regular follow up. Follow up over 3 months revealed almost complete recovery in his facial palsies; the patient was asymptomatic. At that time, CD4 count was 726/uL and viral load 410,000/mL.
Neurological manifestations in patients infected with HIV include meningitis, encephalitis, cranial or peripheral nerve palsy, etc.  Both unilateral and bilateral facial nerve paralysis occurs nearly 100 times more commonly in the HIV-1-infected population (4.1%) than in the non-HIV-infected population (0.04%).  Facial nerve involvement occurring during acute HIV infection-related seroconversion illness is more common than during advanced stage by opportunistic infections (such as toxoplasmosis) and malignancies (such as Non-Hodgkin lymphoma). Host immune responses, which are comparatively intact in early stages, probably lead to autoimmune demyelination of neurons similar to a regional Guillain-Barre syndrome. 
Symptomatic acute retroviral infection (also called HIV seroconversion illness or acute retroviral syndrome) occurs in 10-90% of patients with primary HIV infection coinciding with high levels of viremia and the host's initial immunological response. Symptoms typically occur 2-6 weeks after exposure and usually last for 14 days. 
The entity frequently remains misdiagnosed or under-diagnosed primarily due to the non-specific features of the illness. An acute infectious mononucleosis-like illness occurs in majority of patients. Nausea, vomiting, diarrhea, cough, headache, aseptic meningitis, encephalitis, and cranial or peripheral nerve palsy can also be seen. Leucopenia and lymphopenia, thrombocytopenia, and raised transaminases have been reported. Presence of low-grade fever, sore throat, and malaise for last 10 days prior to onset of facial palsy, along with presence of cervical lymphadenopathy and aseptic meningitis are clinical hints in this case. Opportunistic infections and malignancies as well as other unrelated causes of bilateral facial nerve paralysis, such as neurosarcoidosis and brain stem encephalitis, were ruled out by clinical examination and relevant investigations. 
Diagnosing seroconversion illness is important since a person in the stage of primary HIV infection is highly infectious with extremely high levels of viremia and continuous shedding of the virus. In addition, symptomatic seroconversion predisposes to more rapid immunological deterioration (CD4 depletion and/or progression to AIDS)  and an earlier neurocognitive decline (mainly dementia).  Normal CD4 decline in HIV+ individuals is roughly 50/uL.  CD4 count dropped from 932/uL to 726/uL within 3 months in the index case; however, a rapid and precipitous drop in CD4 in the weeks immediately after seroconversion may have contributed to this significant decline.
Since facial palsy can be an initial clinical presentation of HIV infection and can aid in early diagnosis, evaluation for HIV should not be missed in such scenario, especially in high-risk groups, and wrongly stratifying these cases as idiopathic Bell's palsy should be avoided.
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