|Year : 1999 | Volume
| Issue : 3 | Page : 245--6
Basilar artery occlusion in cryptococcal meningitis.
D Goel, J Kalita, UK Misra
|How to cite this article:|
Goel D, Kalita J, Misra U K. Basilar artery occlusion in cryptococcal meningitis. Neurol India 1999;47:245-6
|How to cite this URL:|
Goel D, Kalita J, Misra U K. Basilar artery occlusion in cryptococcal meningitis. Neurol India [serial online] 1999 [cited 2023 Mar 25 ];47:245-6
Available from: https://www.neurologyindia.com/text.asp?1999/47/3/245/1603
Cryptococcal meningitis is being diagnosed with increasing frequency especially after appearance of AIDS, frequent use of immunosuppressive therapy in various autoimmune disorders and transplant patients. Cryptococcal meningitis is probably the second most common cause of chronic meningitis after tubercular (TB) meningitis in India. The clinical presentation of tubercular and cryptococcal meningitis are very similar although vasculitis is thought to be more common in TB meningitis. Infarction is rare in cryptococcal meningitis, although it has been reported in other fungal infections such as aspergillosis and zygomycosis., We report a rare patient with cryptococcal meningitis who developed basilar artery occlusion.
A 38 years old male was admitted in the emergency department with 2 days history of coma. He developed sudden visual impairment and soon became confused and delerious. He had a few vomitings and within 2 hours became deeply comatose. Review of his medical history revealed that 5 months back he had developed fever and abdominal distension, which was diagnosed as abdominal tuberculosis. He was prescribed antitubercular treatment. His abdominal complaints improved. However, 3 months later he developed jaundice. The antitubercular treatment was withdrawn temporarily and restarted while monitoring the liver function. After one month he developed fever, headache, vomiting and altered sensorium. His CSF revealed protein of 220 mg/dl, sugar 16 mg/dl and 180 cells/mm3, 75% of which were polymorphs. At this stage, the patient received a combination of antitubercular treatment, with ceftriaxone and penicillin. After 2 days, his sensorium improved although fever persisted. This treatment was continued for 2 weeks.
On examination the patient was comatosed and had repeated attacks of decerebration. His eyeballs were deviated down and medially. Fundus examination revealed bilateral papilloedema with superficial hemorrhages. Ultrasonography of abdomen revealed hepatomegaly with coarse echo pattern. Portal vein diameter was 12 mm, spleen was enlarged and there was free fluid in peritoneal cavity. Cranial CT Scan revealed obliteration of fourth ventricle and cisterns with cerebellar swelling. Urine revealed cryptococcal budding yeasts. Cryptococcal antigen was positive in both blood and urine. He was prescribed Inj. amphotericin B and fluconazol, which he received for 2 days. He expired two days after admission.
Sudden onset of visual impairment, delirium, deep coma and respiratory paralysis were suggestive of vertebrobasilar territory stroke. The characteristic down and in deviation of the eyes was suggestive of thalamic or upper midbrain involvement although CT scan done within 24 hours revealed only cerebellar oedema and distortion of fourth ventricle. The infarctions in the CT scan are usually visualised 36 to 72 hours after the ictus. The anatomical extent of infarction could have been better delineated, if repeat CT or MRI scan was carried out but was not possible due to critical condition of the patient. The clinical and radiological picture of our patient, however, was consistent with basilar artery occlusion. At the time of admission the patient had the signs of central herniation.
The presence of cryptococci in the urine and cryptococcal antigen in blood and urine were strongly suggestive of disseminated cryptococcosis and could be responsible for meningitis and basilar artery occlusion in our patient. The demonstration of cryptococci in the CSF was not possible because it was not advisable to repeat a lumbar puncture lest it could accelerate the herniation. In the earlier CSF specimens, unfortunately, the examination for fungal elements were not undertaken. The symptoms of meningitis in our patient had a fluctuating course which improved following course of antibiotic therapy. A fluctuating course of cryptococcal meningitis has been reported. Cryptococcal meningitis commonly occurs in immunocompromised patients. In about 50% patients, however, no cause for immunosuppression can be found. Our patient had the evidence of chronic liver disease as revealed by the history of jaundice, coarse echotexture of liver and enlarged portal vein on abdominal ultrasonography. Chronic liver disease may predispose for disseminated cryptococcal infection. However, liver disease itself may be a manifestation of systemic cryptococcosis.
Thus, cryptococcal meningitis may have a fluctuating course and may occasionally be complicated by stroke.
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