A 36-year-old woman with a history of anorexia nervosa and was admitted to the Neurology Department after two episodes of simple partial seizures with secondary generalisation.
The crises began with paresthesia and numbness of the right upper limb and continued with generalized tonic-clonic movements and loss of consciousness.
Cranial computed tomography (CT) showed an intracerebral mass at the left parasagittal parietal level and electroencephalogram showed a left basal rhythm with presence of functional alterations in the left hemisphere.
Since admission the patient had normal general and neurological examinations.
Laboratory tests, including serological tests, microbiology and lumbar puncture were negative.
Corticosteroid treatment was established with a marked decrease in vasogenic edema that accompanied the lesion.
A magnetic resonance imaging (MRI) and a magnetic resonance spectroscopy study were then performed. The results showed a benign nature of the lesion, and a probable granulomatous atypical origin.
Subsequently, partial resection of the tumor was performed, with histological results of granulomas with doubtful necrosis.
Serum levels of angiotensin-converting enzyme were normal and complementary imaging tests (chest radiography and abdominal ultrasound) showed no pathological findings.
It was then decided to administer empirical tuberculous treatment while waiting for defnitive microbiological results.
In the follow-up one year later, a slow growth of the lesion was observed.
Moreover, the existence of mycobacteria was not demonstrated after microbiological analysis and seizures persisted quarterly despite having received several treatments (valproic acid, levetiracetam and clobazam).
A chest X-ray was then requested, showing the existence of mediastinal widening and bilateral hiliar growth.
A CT scan revealed multiple bilateral and mediastinal adenopathies.
No signs of interstitial thickening were observed in the lung parenchyma.
Because sarcoidosis was suspected, a new determination of plasma levels of angiotensin converting enzyme was performed.
The biopsy of mediastinal adenopathies with diagnosis of pulmonary sarcoidosis stage I.
It was concluded, therefore, that brain injury had been the first manifestation of sarcoidosis in this patient and treatment with corticosteroids was instituted.
The subsequent evolution was favorable.
Findings
Magnetic resonance imaging of the brain demonstrated the existence of a left parietal parasagittal lesion, cortico-subcortical, with minimal mass effect and moderate associated perilesional edema.
In the images obtained after intravenous contrast administration, a striking enhancement of the lesion with areas of annular uptake was observed.
Although no clear enhancement of the dura mater was identified, there was involvement and uptake of the leptomeninge adjacent to the lesions.
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The imaging study was completed with MR spectroscopy, which showed a slight increase in choline levels (Cho) and a minimal decrease in N-acetyl-aggressiveness (NAA), indicating a low aggressiveness lesion.
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The appearance of the lesions and the spectroscopy study showed an unfavourable granulomatous type origin, very suggestive of neurosarcoidosis.
Chest X-ray and chest CT performed two years later showed the appearance of hiliar and mediastinal lymph nodes.
