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|Year : 2000 | Volume
| Issue : 2 | Page : 185-7
A case of cerebral toxoplasmosis.
Alappat JP, Mathew CF, Jayakumar K, Suresh IC, Kumar S
Department of Neurosurgery, Medical College, Calicut, 673008, India.
Department of Neurosurgery, Medical College, Calicut, 673008, India.
A histopathologically proven case of cerebral toxoplasmosis in a young HIV positive patient has been presented. The clinical problems in management are highlighted.
|How to cite this article:|
Alappat J P, Mathew C F, Jayakumar K, Suresh I C, Kumar S. A case of cerebral toxoplasmosis. Neurol India 2000;48:185
Neurologic complications occur in nearly 40%
patients with AIDS. Autopsy studies show that central nervous system (CNS) abnormalities occur in at least 75% of HIV infected patients.,,,,
A thirty six year old man was admitted to Medical College, Calicut in June 1998 with history of weakness of the right side and difficulty in talking of one week duration. He had associated chronic suppuratory otitis media. An emergency CT scan showed a hypodense lesion with thin isodense peripheral margin involving the left basal ganglia, thalamus and left frontoparietal lobe, associated with surrounding oedema and mass effect. Contrast CT showed mild ring enhancement of the isodense margin of the lesion [Figure - 1]. A diagnostic possibility of a brain abscess or a granulomatous lesion like tuberculoma was considered. The patient was started on anti tuberculous drugs with steroids on an emperical basis. He was transferred to neurosurgical ward on 3.6.98. History revealed that he had divorced his wife and was a drug addict. On examination, he was anaemic and emaciated. Neurological examination revealed that he had global aphasia. Fundus showed bilateral papilloedema, right upper motor neuron type facial palsy and right pyramidal signs. Proper evaluation of sensory system could not be made. Neck stiffness was not present. Rest of systemic examination was within normal limits. Investigations showed a total leucocyte count of 8200/mm3, polymorphonuclear cells-52% and lymphocytes 48%. ESR was 10mm 1st hour. Blood sugar, urea and creatinine were with in normal limits. HIV serology and HBsAg were negative. Burrhole aspiration tried under general anaesthesia with brain cannula was not sucessful.Burrhole was enlarged into a craniectomy and the lesion approached through a cortical incision. Lesion was avascular and firm. Biopsy was taken and intralesional decompression done. There was no clear plane of cleavage from the surrounding brain. Post-operatively anticonvulsants, decongestants and anti tuberculous drugs were continued. HIV and HBsAg tests were repeated. ELISA test came positive. Histopathology showed areas of coagulative necrosis with surrounding area of chronic inflammation. This area showed free and encysted organisms. The free organisms were crescentic and the cysts were filled with ovoid bradyzoites. His anti tuberculous drugs and steroids were discontinued. Patient was started on pyremethamine 100 mg twice daily. He left the hospital against medical advice and succumbed to the disease, a few days later.
Toxoplasmosis is the most frequent cause of intracranial mass lesions in patients with AIDS, accounting for 50-70% of all mass lesions in this population. Toxoplasma gondii infection in the AIDS patient leads to brain abscess, which are often multiple with a predilection for the basal ganglia. The clinical presentation of CNS toxoplasmosis ranges from headache and fever without neurological symptoms to coma. Typically, the patient presents subacutely with a combination of focal neurological deficits and a non-focal encephalitic component. In some patients progressive focal deficit manifests, which relates to hemispherical lesions. An acute stroke like presentation occurs only in a minority of patients and most probably relates to a vascular compromise or haemorrhage associated with the toxoplasma abscess.
Multiple small, uniformly ring enhancing lesions with moderate to marked surrounding oedema in the basal ganglia and subcortical regions suggests the diagnosis., Double dose contrast CT or preferably MRI may help in clearly defining the lesions. Cerebral lymphoma may have a similar CT appearance although the lesions of lymphoma exhibit vague contrast enhancement and are located in white matter.
Majority of the patients with toxoplasmosis respond clinically and radiographically to an empirical trial of pyrimethamine and sulfadiazine and thus are never referred to by a neurosurgeon. If the mass lesion enlarges or remains unchanged in size despite adequate anti-toxoplasmosis therapy, a biopsy should be performed to rule out some other disease. After treatment of the acute infection, life long suppressive therapy with pyrimethamine and sulfadiazine is required to prevent reinfection.
It should also be recognized that because of the high prevalence of the AIDS dementia complex, it very frequently co-exists in patients with toxoplasmosis and other focal diseases. This can confuse the diagnosis and more particularly can confuse therapy since the background dementia will not clear even if parasitic infection is treated.
This case is being presented because of the following facts.
1. As HIV infection is becoming more prevalent, CNS complications of HIV are being encountered more in our clinical practice. This case presented as a mass lesion and had AIDS been in our differential diagnosis, we would have thought of toxoplasmosis.
2. An acute stroke like presentation occurs in a minority of the patients with toxoplasmosis.
3. In patients with cerebral toxoplasmosis and indeed all AIDS patients, steroids should be avoided. This is important when treatment is instituted as a therapeutic trial to differentiate between toxoplasmosis and CNS lymphoma. Since we did not suspect toxoplasmosis, ATT with steroids were started, which might have worsened his condition.
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