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 forty year old previously healthy Sri Lankan male presented with acute onset bilateral leg weakness which was progressive over two days following a brief febrile illness of three days. He did not give any history of trauma nor there was any history of tuberculosis. Initially he did not have urinary retention nor there was any sensory symptoms. He did not complain of shortness of breathing.\nOn examination he was found to have asymmetric flaccid paralysis of bilateral lower limbs with power grade one to two. Reflexes were diminished bilaterally and Babinski sign was equivocal. Examination of optic fundi and cranial nerves were normal. There was no demonstrable sensory level and joint position sense was initially preserved. Upper limbs were neurologically normal. Respiratory movements and sphincter function were preserved. Depending on initial findings a clinical diagnosis of Guillain-Barré syndrome was suspected and he was closely observed for the development of respiratory paralysis with monitoring of forced vital capacity and oxygen saturation.\nOn the fifth day of onset of symptoms his weakness worsened with additional flaccid paralysis of upper limbs and neck muscles. He was catheterized for acute retention of urine. Patient was urgently transferred to a high dependency unit but he did not develop respiratory paralysis necessitating ventilator support. Later he developed bilateral spastic paraparesis and positive Babinski sign with mild paraesthesia of lower limbs. But he did not develop a definite sensory level at anytime during the course of his illness.\nA nerve conduction study failed to show demyelination or axonal loss. Magnetic resonance imaging study of the spine showed hyperintensity of central portion of mid cervical cord from C 2 to C 5 level in T2 weighted and FLAIR images (Figure \n) There was mild swelling of cervical cord without significant change of signal intensity on T1 weighted image (Figure \n).\nBasic investigations were as follows; Na+ 139 mmol/l, K+-4.2 mmol/l, Serum creatinine-62 μmol/l, blood urea 8.7 mmol/l, White cell count 5000/mm3(N-76,L-18), platelet count 17500/mm3. Haemoglobin 9.3 g/dl, AST-51u/l, ALT-74u/l, Bilirubin 12 μmol/l, ESR-12 mm/hr, CRP-0.4 mg/dl, VDRL-negative, Fasting blood sugar 5.4 mmol/l.\nCerebrospinal fluid analysis done on the tenth day after onset of weakness was suggestive of a viral CNS infection with a protein content of 300 mg/l, glcose 4.3 mmol/l(RBS 10.9 mmol/l) and a leukocyte count of 350/mm3(92% lymphocytes). CSF infectious screen was positive for cytomegalovirus PCR(sensitivity more than 100copies/ml). This test was repeated and result was confirmed. Cytomegalovirus IgG and IgM were not detected in CSF. Polymerase chain reaction of CSF for herpes simplex virus(HSV) and Japanese encephalitis virus(JEV) were negative. Oligoclonal bands were not detected in CSF.\nConsidering the overall clinical picture, a working diagnosis of CMV associated transverse myelitis was made. Immunoglobulin levels and lymphocyte subset analysis failed to identify any immunodeficiency while HIV serology was negative.\nPatient received treatment with intravenous ganciclovir for a duration of 21 days starting on the 10th day of illness. He was also given maximal supportive care with physiotherapy and psychological support. A second CSF analysis done 22 days after the onset of symptoms revealed no cells and protein content of 390 mg/l. (CSF glucose 3.6 mmol/l RBS-6.5 mmol/l) Repeated CMV serology in blood, CSF and CSF PCR for CMV were negative on the 22nd day of illness.\nOne month after the onset of symptoms the upper limb power was improved (grade 5) but the lower limb power remained grade 3. He was transferred to a long term rehabilitation facility.