We present a clinical case of a 31-year-old man diagnosed with HIV-1 infection, with CD4 T cell count of 35 cells/mm3 (4%) and HIV RNA 305349 copies/mL (log10 5.48) having initiated ART with abacavir/lamivudine and nevirapine. Around two weeks after starting ART, the patient is admitted due to a sudden cognitive impairment (anhedonia and memory loss) with progression to gait change and imbalance. The cranial computerized tomography (CT) scan showed no lesions but the cranial MRI revealed ventriculoencephalitis ().\nThe cerebrospinal fluid (CSF) had 38 nucleated cells/mm3, 175 mg/dL proteins and 37 mg/dL glucose (glycaemia 82 mg/dL). The CSF CMV and EBV viral load were 189000 (log10 5.28) and 799 (log10 2.90) copies/mL with negative CSF neurotropic microorganism serologies and molecular identification (HSV 1/2, VZV, Cryptococcus, Brucella, Treponema pallidum, Borrelia burgdorferi, JC virus, Mycobacterium tuberculosis, and Toxoplasma gondii). The final considered diagnostic was mainly CMV-related ventriculoencephalitis and ganciclovir was started.\nNevertheless, the patient started left conjugate horizontal gaze palsy with abducting horizontal saccadic (or jerk-type) nystagmus of the right eye as well as a slight anisocoria with left eye miosis. These changes were enclosed in the one-and-a-half syndrome and left-sided Horner's syndrome. The patient also presented a grade II-III paresis of the right lower limb. The cranial CT scan (performed fifteen days later) revealed a dubious right linear protuberancial hypodensity without signs of intracranial hypertension.\nCranial MRI was repeated one month later revealing improvement of the ventriculitis signs but a larger hippocampus and left mesial temporal region involvement with a discrete increase of the lateral ventricles dimensions.\nDue to these clinical and imagiological changes and because we could not exclude tuberculosis infection, classic first-line tuberculostatic therapy was empirically started (stopped after excluding this infection) and foscarnet was added to ganciclovir (until a negative CMV viral load was achieved). At this point, the hypotheses of limbic encephalitis, epileptic activity or paraneoplastic encephalitis could not be excluded. The lumbar puncture was repeated and CSF antineuronal antibodies, HHV-8, and other neurotropic microorganisms were negative.\nThe electroencephalogram (EEG) showed frontal and frontotemporal bilateral activity with occasional periodic discharges, independent of nonabrupt three-phase bifrontal lesions. Anticonvulsant therapy with levetiracetam and topiramate was started. One month later, the cranial MRI was repeated and a new frontal lesion was detected. The body CT scan was normal. The imagiological reevaluation showed a slight improvement of the frontal lesion with new cerebellum lesions. The suspicion of lymphoproliferative disease was meaningful. Cranial MRI with diffusion and perfusion study with spectroscopy was performed and revealed very suggestive images of CNS lymphoma (). For definitive diagnosis, a stereotactic brain biopsy was done. The histological study revealed a polymorphic cellular infiltrate with histiocytes, CD3+ T-lymphocytes, and CD 20+ B-lymphocytes (mixture of numerous small cells and large activated cells with positive hybridization results for EBV-encoded RNA (EBER)). The histology was suggestive of polymorphic lymphoproliferative EBV-positive disease. The molecular studies were not done because the sample was insufficient to perform the clonality analysis (CSF EBV viral load was 12405 copies/mL; CSF HIV and CMV viral load were both undetectable).\nAt this point, chemotherapy with rituximab was started and radiotherapy was scheduled. Nevertheless, the patient developed a sudden neurological worsening with a generalized tonic-clonic seizure, refractory to the instituted measures, culminating in death.
A 29 years-old man was admitted to our neurological department with five months of progressive disability in walking, paresthesia in the arms when bending the neck, numbness in the hands, and back pain. He had been treated for many years with aerosol salbutamol during exacerbations of asthma. Apart from periodic jaw spasms during the last five years, there were no apparent previous illnesses and no suspicion of infection within the last six months. During the last two years, he had been successfully treated for his injectable drug abuse with daily oral methadone. The patient had had negative hepatitis C virus RNA (HCV) serology two years before presentation. The neurological examination revealed positive Lhermitte`s sign, hypoesthesia in the hands, normal muscle strength in the upper limbs, reduced muscle strength in the legs (4 on a MRC scale), and reduced dorsiflexion of the feet (4 on a MRC scale). In addition, the patient had severe increased spasticity in the extensor muscles of the lower limbs, bilateral-positive Babinski, and a broad-based gait requiring support.\nSpinal cord MRI demonstrated extensive longitudinal spinal cord lesions from the cervical vertebral segment C1 to C5 and thoracic vertebral segment T2 to T11 (Figure ). The cervical lesion was located in the dorsal part and over a short distance in the lateral part on the right side on T2-weighted images. Discrete enhancement was found in the posterior part. Changes in the thoracic part were seen almost over the cord's entire cross section on the T2-weighted images, but enhancement was only demonstrated in the lateral part on both sides. The brain MRI was normal.\nA lumbar puncture was performed with cerebrospinal fluid showing slight pleocytosis with 11 mononuclear cells, a slightly increased protein to 0.64 g/l, normal IgG index and no oligoclonal bands, no antibodies against the varicella-zoster virus, herpes virus, entero-virus, or borrelia. The blood tests showed normal B12 vitamin, rheumatoid factor IgM and ANA, negative HIV serology, negative syphilis RPR, negative TB gamma interferon release assay, negative MOG- and AQP-4 antibodies, and increased ALAT to 200 U/l. Tests for HCV serology and HCV RNA were both positive.\nTreatment of HCV infection with Zepatier (elbasvir 50 mg and grazoprevir 100 mg) one tablet daily was initiated and continued for three months. Follow-up blood tests showed normalization of ALAT, negative HCV serology, and normalization of the spinal cord changes on MRI. The neurological findings were unchanged. There was no clinical suspicion of rheumatic, vascular or skin diseases and normal thyroid, white blood cells and renal function tests. With that condition, we found no indication for steroid treatment also taking into account previous episodes of psychosis in relation to his drug abuse.\nDespite a four-week course of inpatient rehabilitation, the physical condition was only slightly improved. Currently (two years later), walking distance is reduced, a stick is required when walking outside, and medication is still necessary for spasticity and neuropathic pain in the legs.