A 28-year-old man presented with acute onset of vertigo, tinitus, and left limb and body numbness, together with unsteady gait. Physical examination revealed nystagmus, right VI and VII cranial nerve complete palsy (House-Brackmann grading 6/6), and left limb ataxia and deceased sensation. Imaging showed a pontine hematoma.
Surgical excision of the lesion was indicated because the patient was symptomatic with disabling neurological deficit due to hemorrhage of the cavernous malformation and the hematoma was shown to reach the surface of the floor of the fourth ventricle on T1-weighted MRI sequence. This suggested that it was feasible to reaching the lesion surgically with minimal damage to the brainstem. A posterior fossa craniotomy was performed for evacuation of the pontine hematoma through the floor of the fourth ventricle.
The patient was significantly improved 3 months postoperatively. He walked unaided. His facial palsy was mild (House-Brackmann grading 2/6). Pathological examination confirmed the diagnosis of cavernous malformation.
On MRI for investigation of a parotic cyst, this 14-year-old boy was found to have multiple brain lesions consistent with cavernous malformations.
The patient had acute onset of severe headache associated with double vision and right-sided numbness for one day in one year after his initial presentation. Physical examination revealed left VI cranial nerve palsy. CT of the brain showed multiple small lesions.
His MRI showed evidence of recent hematoma of the left pontine lesion (red arrows).
MRA showed no evidence of AVM. The diagnosis was cavernous malformation with bleeding of the pontine lesion. The patient was treated conservatively because the lesion did not reach the surface of the brainstem. His symptoms completely abated in 6 months. MRI 3 years later showed that the pontine lesion had decreased in size. However, 1 year later he developed sudden onset severe headache with double vision and right-sided weakness and numbness Physical examination revealed VI cranial nerve palsy, right hemparesis, and decreased sensory function. The symptoms progressed by the next day with decreased consciousness.
At this stage, surgical excision of the lesion was indicated in view of recurrent symptomatic hemorrhage with impaired consciousness, and the fact that the lesion reached the surface of the brainstem. Emergency surgery for evacuation of the hematoma and excision of the lesion was performed via a left retromastoid approach.
Pathological examination confirmed the diagnosis of cavernous malformation. On clinical follow-up 6 months postoperatively, the patient reported that he had returned to school and had only mild right-sided weakness and decreased in sensation.
A 12-year-old boy presented with insidious onset of a progressive left-sided weakness for 1 year. Physical examination revealed left-limb hemiparesis with upper motor neuron signs. On CT and MRI/MRA, there was a large lesion (red arrow) in the midbrain without evidence of AVM.
The lesion was totally excised. Intraoperative monitoring of the cranial nerves was used. Cranial nerve IV was identified and preserved. Because the lesion was highly vascular, circumferential excision was used. Postoperatively the patient had partial palsy of cranial nerves II and IV, which resolved in 6 months. Pathological examination of the lesion confirmed that it was a cavernous malformation.
Residual hemosiderin is seen on the T2-weighted image. This is not uncommon when resecting a cavernnoma in a critical area where radical resection, including the perilesional hemosiderin-laden tissue, is not possible. In noneloquent areas and for patients with epilepsy, resection of the hemosiderin-laden tissue should be the goal.
A 30-year-old man presented with sudden onset of diplopia.
A cavernous malformation was the leading differential diagnostic possibility. Although the patient was symptomatic with neurological deficit and the lesion reached the surface of the brainstem in the anterior medial aspect of the cerebral peduncle, surgical excision was not contemplated because entry through the interpeduncular region had a high chance of damaging cranial nerve III. The patient was treated conservatively, and MRI was repeated several months later.
The features were compatible with the diagnosis of cavernous malformation. Clinically, the patient’s diplopia had largely subsided with subtle residual left ptosis. However, he developed progressive left ptosis 1 year later Physical examination showed left ophthalmoplegia with fixed dilated pupils and ptosis. After he was admitted to the hospital, his condition deteriorated further to bilateral ophthalmoplegia, right-limb weakness, and impaired consciousness, which required ICU admission and tracheal intubation.
The patient underwent surgery for evacuation of the hematoma and excision of the cavernous malformation via a frontal interhemispheric transfornicial approach.
Pathological examination confirmed that the lesion was a cavernous malformation. The patient gradually recovered with residual left cranial nerve III palsy. . He returned to work as a bank clerk. There was no clinical or imaging evidence of further hemorrhage.