A 45-year-old man was admitted to our hospital with a series of focal and generalized epileptic seizures. Initial clinical presentation showed a disoriented patient with left-sided tongue bite. Neurological examination disclosed paresis of the left hand. Laboratory results were normal apart from low potassium and low haemoglobin levels. ECG and thoracic X-ray were also unremarkable. Computed tomography of the brain showed a haemorrhagic partially calcified lesion in the right parietal lobe. Subsequent MRI studies revealed a haemorrhagic transformed and space-occupying lesion diagnosed as a cavernoma (fig. 1, fig. 2). According to the clinical symptoms and the anatomical correlation, the cavernoma was the underlying lesion responsible for the new onset of focal epileptic seizures.
The patient's previous medical history included intensive treatment with various chemotherapeutic agents including cytarabine/idarubicin (first cycle), cytarabine/amsacrine (second cycle) and cytarabine/etoposide (third cycle) for the treatment of acute myeloid leukaemia (AML), subtype M2, in 1999. After early bone marrow recurrence in March 2000, he received reinduction chemotherapy (S-HAM) and an allogenic HSCT in July 2000. As part of the therapy, he was treated with TBI with 12 Gy in 6 fractions. After diverse infections (sinusitis, invasive pulmonary aspergillosis and mucositis) he finally achieved complete remission. Later on, he suffered from treatment-related secondary arterial hypertension most probably due to cyclosporine-associated renal impairment. He frequently complained about headaches which led to a first cerebral MRI in 2006 to exclude secondary causes. The MRI scan was entirely normal, without evidence of vascular lesions (fig. 3). Until 2011, neither a neurological evaluation nor a further radiological evaluation was performed.
According to the well-documented history including former cerebral MRI studies, we speculate that the newly diagnosed cavernoma in 2011 was triggered by TBI.