A 25-year-old man with no history of alcohol or illegal drug use.
One month ago he had been diagnosed with AIDS (CD4 count of 113 cells/ul and viral load 220,000 copies/mL).
Two weeks prior to admission to the Hospital del Salvador, outpatient treatment with zidovudine, lamivudine, lopinavir and ritonavir that did not tolerate was initiated, presenting headache, vomiting and sensation of intellectual clumsiness on the seventh day of treatment.
The first scheme was substituted by Emtricita, Tenofovir, Lopinavir and Ritonavir, and the need to assess postural instability was hospitalized and v. persistence of the first scheme that originated was due to the persistence of subjectivity.
He was admitted tolerating the new treatment well with normal vital signs and a general examination that showed no alterations, except the presence of cervical lymphadenopathy.
The neurological examination showed an oriented patient with normal intelligence and conserved language.
In the examination of cranial nerves, the only compromise was a horizontal nystagmus that was not very relevant with a rapid phase on the right.
There was no gait disturbance, muscle power was preserved, with normal osteotendinous reflexes and plantar flexor reflexes, without sensory or cerebellar compromise.
Nystagmus disappeared the following day, although vertigo persisted with postural changes.
Laboratory tests showed pancytopenia (hepatitis pigmentosa) without albumin 26.5%, hemoglobin 9.3 g/dl, white blood cell count and platelet count 3.970 ul and 86.800 ul respectively), and hypoalbuminemia (
Brain MRI performed on the second day of admission and on the asymptomatic patient revealed central pontine hyperintensity in T2 and FLAIR sequences, with diffusion restriction, without contrast enhancement with MCP.
Cerebrospinal fluid (CSF) analysis showed 0.8 cells mm3 (100% mononuclear), protein 0.17 g/L and glucose 0.64 g/L, negative VDRL and adenosine deaminase 1.3 IU/L culture was normal.
The VIII nerve pair study showed no abnormalities.
Somatosensory evoked potentials and motors by transcranial magnetic stimulation were normal.
During hospitalization, the treatment instituted was maintained and the patient remained without counter-time.
One-month follow-up brain MRI revealed complete regression of the pontine image.
After 1 year of clinical follow-up, the patient was neurologically asymptomatic.
