Mrs A, an 81-year-old woman, was admitted to the Department of Infectious Diseases of The First Affiliated Hospital, Zhejiang University School of Medicine because of disturbance in her level of consciousness. Before this admission, the patient was diagnosed with CM in a neighboring hospital, where the diagnosis of CM was made after finding Cryptococcus in the CSF, and she underwent ventriculopuncture and implantation of Ommaya reservoir because of severe hydrocephalus. However, the patient had been previously diagnosed with cerebral infarction before diagnosing CM.
Nearly half a year prior to this admission, the patient ventured out and cut firewood alone after quarreling with her family members. Three days later, she began to feel headache, muscle soreness, and fatigue. Her condition worsened in the following days and she felt extremely weak and even could not walk or eat by herself. The patient was then sent to a local hospital. Cranial MRI revealed multiple ischemic foci located in the junction of cortex and medulla of bilateral frontoparietal region, the periventricular area, and the centrum semiovale. Cranial magnetic resonance angiography (MRA) revealed regional stenosis in the A1 segment of the left anterior cerebral artery and the P2 segment of the right posterior cerebral artery. Carotid artery ultrasound reported multiple plaques in the right common carotid artery with appropriately 79% stenosis. Systemic and supportive treatment did not help to improve her condition. The patient still complained of extreme weakness and poor appetite. Four weeks later, another cranial MRI indicated new-onset lacunar infarction in the bilateral frontal lobe. Cranial CT indicated high-density image near the anterior horn of the right lateral ventricle. Four months before this admission, the patient developed disturbance in her level of consciousness and psychotic symptoms, including persecutory delusion and visual hallucination. Her weight had decreased by 3.5 kg since she fell ill. She was then admitted to the Department of Psychiatry of our hospital. At that time, the patient failed to cooperate with physical examination and psychiatric interview. No pathological reflection of Babinski sign was induced. Occasionally, she would have incontinence of feces and urine. She reported congenital absence of left kidney and uterus duplex. No history of hypertension, diabetes mellitus, heart disease, or tuberculosis was reported. She did not drink or smoke or have long-term medications. Laboratory examinations, including arterial blood gas analysis; routine tests of blood, stool, and urine; liver and kidney functions; thyroid hormones; tumor biomarkers; myocardial enzymes; infectious profiles of HIV; syphilis; and hepatitis B and C, were all within normal limits. The serum D-dimer level was extremely high, and the potassium level was a bit low. The third cranial MRI indicated acute cerebral infarction in the bilateral frontoparietal region and ischemic changes in the periventricular area and the centrum semiovale (Figures 1 and 2). Thoracic CT revealed scattered infectious loci in the bilateral lungs. Neurological consultation was obtained, and the diagnosis was considered to be cerebral infarction. However, the patient was physically weak and uncooperative, and lumbar puncture was not performed due to the potential risk. Nutritional support and symptomatic treatment were prescribed, but the outcome was unsatisfactory. Her psychotic symptoms were well controlled by low-dose of quetiapine (50 mg per night). The patient was then transferred to a local hospital for further rehabilitation.
However, her condition did not improve. She raved occasionally and complained of headache and weakness. Cranial CT reported patch-shaped low-density areas around the bilateral periventricular region, which indicated hydrocephalus. Her illness further worsened in the following days and she developed lethargy, conscious disturbance, and retching. Consequently, she was transferred to a neighboring hospital to ours. An enhanced cranial MRI scanning indicated supratentorial obstructive hydrocephalus and interstitial encephaledema in bilateral periventricular region. Lumbar puncture was performed, and examination of CSF indicated cryptococcal antigen (+), India ink stain (+), chlorine 109.1 mmol/L ( ), glucose 0.1 mmol/L ( ), protein 336.5 mg/dL ( ), karyocyte count 24x106/L, and lymphocyte (98%). She was diagnosed with CM, received ventriculopuncture and implantation of Ommaya reservoir, and initiated antifungal interventions. Five days later, she was sent to the Department of Infectious Diseases of our hospital for further treatment. Given the potential renal toxicity of amphotericin B and absence of left kidney in our patient, 800 mg fluconazole per day was used for induction therapy against C. neoformans. Mannitol was used to reduce intracranial pressure. The patient began to show clinical improvement under intensive nursing and management. Three weeks after admission, lumbar puncture was performed again, and no Cryptococcus was found in the CSF. The patient was then discharged from our hospital, and her condition further improved in the follow-ups.
This case study was approved by the institute ethical committee of the First Affiliated Hospital, Zhejiang University School of Medicine. Written informed consent was obtained from the guardians of this patient to publish the case details.