[The usefulness of 3D-CTA for the diagnosis of a ruptured aneurysm at the origin of the duplicated middle cerebral artery: case report].

Duplication of the middle cerebral artery is known as a rare anomalous vessel arising from the internal carotid artery and an aneurysm at the origin of the duplicated middle cerebral artery is very rare. We presented a case of ruptured aneurysm at the origin of the duplicated middle cerebral artery and discussed the usefulness of 3D-CTA (three-dimensional computed tomographic angiography) for its diagnosis. A 34-year-old female suffered from severe headache and was admitted to our hospital. CT scan revealed diffuse subarachnoid hemorrhage and angiography revealed duplication of the right middle cerebral artery and dilatation at its origin. We could not identify it as an aneurysm by angiography, so we performed 3D-CTA. 3D-CTA was able to demonstrate clearly the aneurysm at the origin of the duplicated middle cerebral artery and we performed neck clipping of the ruptured aneurysm. To our knowledge, previously there have been only 14 cases which reported such an aneurysm at the origin of a duplicated middle cerebral artery. We reviewed the 15 cases including ours and found that, in 4 cases, the aneurysm could not be detected by the initial angiography. We suspected that most of these aneurysms were small, so the detection of the aneurysms by angiography was difficult. We conclude that 3D-CTA is useful for diagnosing aneurysms at the origin of the duplicated middle cerebral artery even when thy can't be detected by angiography.

[A dissecting aneurysm of the posterior inferior cerebellar artery was reduced spontaneously during conservative therapy: case report].

We report here a case of a patient with a dissecting aneurysm of the anterior medullary segment of the posterior inferior cerebellar artery (PICA) which presented with Wallenberg's syndrome. A 32-year-male presented with an unusual case of Wallenberg's syndrome due to a dissecting aneurysm of the PICA manifesting as a sensation of heaviness in the occipital region and vertigo. The occipital symptoms persisted and vertigo and vomiting developed after 6 days. Numbness developed on the left side of the patient's face, and hyperalgesia on the right side of the body. The diagnosis of Wallenberg's syndrome was based on the above findings. MRI revealed infarction of the lateral aspect of the medulla oblongata and MR angiography revealed dilatation in the proximal portion of the left PICA. Digital subtraction angiography revealed that the left vertebral artery was essentially normal, but there was a spindle-shaped dilatation in the proximal portion of the left PICA. We carried out conservative therapy at the patient's request and 3D-CTA revealed that the dissecting aneurysm was markedly reduced in size seven months after the onset. Dissecting aneurysms of the intracranial posterior circulation have been shown to be less uncommon than previously thought. However, those involving the PICA without involvement of the vertebral artery at all are extremely rare. The natural history of the dissecting PICA aneurysm was unknown, and the indication for surgical treatment of such aneurysms remains controversial. Management options are conservative treatment, open surgical treatment including wrapping, trapping, and resection with reconstruction, but almost all of the patients underwent radical treatment to prevent rupture of the aneurysm. However we had no knowledge of the risk of rupture of a PICA dissecting aneurysm presenting with ischemic symptoms. We have reviewed the well-documented 15 cases of dissecting aneurysms of the PICA reported in the literature and we discuss the management of the dissecting PICA aneurysm presenting with ischemic symptoms.

[Calcified chronic subdural hematoma complicated with subcortical hemorrhage: case report].

The patient was a 46-year-old male, who suffered from mild head trauma in January 2002, and general convulsions with unconsciousness on February 28. Slight right hemiparesis and aphasia were presented after the epilepsy attack. CT scan revealed a large lesion of mixed density occupying the left temporal space. It showed linear high density in its medial margin and had compressed the left temporal lobe strongly, causing mid-line shift. The lesion was suspected to be a calcified chronic subdural hematoma and the patient was admitted to our hospital on February 28. The symptoms had improved the next day but they began to get worse again gradually after admission. T1-weighted MR image showed high intensity areas under the subdural hematoma, which were suspected to be subcortical hemorrhage. Six days after admission, consciousness disturbance became progressive. The calcified hematoma had not enlarged but brain edema had increased. On CT, an operation was performed and the calcified old hematoma and the new subdural hematoma surrounding it were removed. The diagnosis of organized chronic subdural hematoma was made at the time of the operation. The contents of this calcified subdural hematoma was mostly old dark-gray substance, but some fresh bleeding point was seen at the inner surface of the outer membrane. At the bottom there was a hard, calcified layer which adhered tightly to the brain. Adhesion between the inner membrane of the hematoma and brain surface which related to the subcortical hemorrhage was presented. It seemed impossible to remove the inner membrane without damaging the brain so no attempt was made to do so. The aphasia and right hemiparesis improved 3 weeks after the operation and the patient was discharged on April 4. He has no neurological deficits and is under periodic observation. A calcified chronic subdural hematoma has rarely been encountered and the etiology, imaging diagnosis, and management are unclear. We presented the interesting image findings on this case and discussed the etiology of this disease.

[Aseptic meningitis as a complication caused by an allergic reaction after microvascular decompression: two case reports].

We report here two cases of patients complicated with aseptic meningitis after microvascular decompression (MVD). The first case, a 56-year-old female complained of headache with high fever 18 days after the MVD for right trigeminal neuralgia. The amount of cells in cerebrospinal fluid (CSF) had so much increased that bacterial meningitis was suspected. However, there was no improvement after antibiotics therapy, so immune globulin was injected and the meningitis gradually improved. Eosinophilia remained in peripheral blood and the symptoms improved rapidly after the steroid therapy. Because of this, we suspected that meningitis was caused by an abnormal allergic reaction. The second case, a 30-year-old male complained of headache with mild fever 15 days after MVD for left hemifacial spasm. The amount of cells in CSF increased, so bacterial meningitis was suspected. Eosinophilia remained in peripheral blood and the steroid therapy proved very effective for the meningitis. Because of this, we suspected that meningitis was caused by an abnormal allergic reaction. We suspected that the two patients suffered from aseptic meningitis caused by allergic reaction, and the antigen for this abnormal allergic reaction was the foreign materials used for MVD. The materials were Dacron for prostesis, Goatex or Lyodula for dural plasty, fibrin glue for preventing CSF leakage. We ascertained that the abnormal allergic reaction was caused by human fibrinogen in the second case. It is important to be aware of such allergic reaction to fibrin glue in the post-operative stage after MVD.