LETTER TO EDITOR
Year : 1999 | Volume
: 9 | Issue : 4 | Page : 202--203
Cerebral toxoplasmosis in a patient with AIDS
PV Ramachandran, Jacob P Alappat, KS Madhusudan, VP Vijayan, P Sanal Kumar
CT Scan Centre, Medical College Hospital, Calicut, India
P V Ramachandran
CT Scan Centre, Medical College Hospital, Calicut
|How to cite this article:|
Ramachandran P V, Alappat JP, Madhusudan K S, Vijayan V P, Kumar P S. Cerebral toxoplasmosis in a patient with AIDS.Indian J Radiol Imaging 1999;9:202-203
|How to cite this URL:|
Ramachandran P V, Alappat JP, Madhusudan K S, Vijayan V P, Kumar P S. Cerebral toxoplasmosis in a patient with AIDS. Indian J Radiol Imaging [serial online] 1999 [cited 2018 Jan 22 ];9:202-203
Available from: http://www.ijri.org/text.asp?1999/9/4/202/28357
Toxoplasmosis is the most well known frequent cause of intracranial mass lesions in patients with AIDS, accounting for 50-70% of all mass lesions in this population . It is also the most common opportunistic infection involving the brain in patients with AIDS. The probability of ever developing toxoplasma encephalitis after the onset of AIDS has been estimated at 28%. It is said to be the most eminently treatable among all the CNS infections in this population . However, a high index of suspicion is necessary so as not to miss the diagnosis in a new patient. This communication becomes important because of the sequence of events that lead to the diagnosis, though the disease itself is very common in HIV positive patients.
A thirty-six-year-old gentleman was admitted to our hospital with a history of right-sided weakness and difficulty in talking for one week. Neurological examination revealed right pyramidal signs. There was global aphasia and the fundi showed bilateral papilledema. Since there was chronic suppurative otitis media of the left ear, a brain abscess was suspected and a CT was performed. Plain scans showed a hypodense lesion with an isodense peripheral margin involving the left basal ganglia, thalamus and left frontoparietal lobe associated with surrounding edema and mass effect [Figure 1]. The contrast enhanced scans showed mild ring enhancement of the isodense margin [Figure 2]. The diagnostic possibility of a brain abscess or a granulomatous lesion such as a tuberculoma was considered. The patient was started on an anti-TB regime with steroids, on an empirical basis.
Since the site was unusual for an otogenic abscess, the neurosurgeon tried a twist drill aspiration. This did not yield any pus. Since there was a history of drug addiction, the patient's blood was sent for HIV and HbsAg screening. The test results were negative. The patient was posted for a burr hole aspiration under general anesthesia. Since the attempt for aspiration with a brain cannula gave a solid feel, the burr hole was enlarged into a craniectomy. The lesion was avascular and firm. A biopsy was obtained and intraluminal decompression was done. Postoperatively, anti convulsants and an anti-TB regime were continued and the blood was sent again for repeat HIV and HbsAg tets. The ELISA test for HIV was positive. Histopathology of the brain lesion in the mean time showed massive infiltration of the brain parenchyma with Toxoplasma gondii. The anti-TB drugs and steroids were discontinued and the patient was started on pyrimethamine. The patient was taken home against medial advice and later succumbed to the disease.
CNS complications are quite common in AIDS patients and are often the cause of severe morbidity and mortality. Broadly they can be classified into HIV associated diseases, opportunistic infections and neoplasia. Of the opportunistic infections, the most common cause of focal brain involvement is Toxoplasma gondii. The infection has a predilection for the grey-white junction, basal ganglia and thalamus. Though the lesions are typically supratentorial, they have been also noted in the cerebellum and brain stem and rarely in intraventricular locations. The lesions can be small or large, multiple and bilateral or solitary. On NCCT the lesions appear as relatively isodense, rounded masses associated with edema and mass effect. Lesions can appear hyperdense due to hemorrhagic necrosis. CECT reveals homogeneous nodular or ring-like enhancement. Enhancement may be mild or absent in individuals with severely diminished cellular immunity. Demonstration of response to empirical anti toxoplasmosis therapy is taken as a presumptive evidence of the lesion and lack of response to it as negative.
We feel our study points to certain facts:
(a) Since HIV infection is becoming more and more prevalent, cerebral toxoplasmosis should also be considered for differential diagnosis in mass lesions detected byimaging for any given patient from a general population.
(b) A cerebral abscess, when atypical, also should raise concern.
(c) An acute stroke like presentation is also possible with toxoplasma abscess, though this occurs only in a minority of patients.
(d) The general trend is to rely on therapeutic trials for a diagnosis, reserving brain biopsy for treatment failures or atypical patients who are seronegative. Though definitive diagnosis requires the demonstration of the parasite in the brain tissue, many clinicians feel that brain biopsy is contraindicated because of increased morbidity and mortality. The option then is a therapeutic trial .
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