Secondary parkinsonism caused by chronic subdural hematomas owing to compressed cortex and a disturbed cortico-basal ganglia-thalamocortical circuit: illustrative case.

BACKGROUND: Chronic subdural hematoma (CSDH) is a commonly encountered condition in neurological and neurosurgical practice, but the presence of concomitant parkinsonism is extremely rare. Basal ganglia disturbance is a well-known underlying mechanism; however, few cases present with cerebral cortex compression as the cause of symptoms. OBSERVATIONS: A 52-year-old man was referred to the authors' hospital with a 5-week history of gait disturbance and suspected Parkinson's disease. Neurological examination revealed a mask-like face, stooped posture, left-predominant rigidity, and postural instability. The authors initiated dopamine agonist administration, and brain magnetic resonance imaging (MRI) was scheduled. One week later, MRI showed bilateral CSDHs. The hematomas markedly compressed the bilateral cerebral cortex, whereas the midbrain and basal ganglia structures were intact. The patient underwent burr hole drainage and was discharged after 9 days without sequelae. LESSONS: CSDH can cause parkinsonism by compressing the cerebral cortex, which is a part of the cortico-basal ganglia-thalamocortical circuit. Surgery leads to positive outcomes, as illustrated by this case, in which cerebral cortex compression caused parkinsonism.

Surgical treatment of a rare sublingual intramuscular arteriovenous malformation.

We describe an aggressive median mandibulotomy approach for a sublingual arteriovenous malformation. Sublingual region is very rare location for arteriovenous malformation and requires special attention. The median mandibulotomy approach provides us with a wide surgical field for the resection of sublingual lesions. The procedure is easy and safe and, after dysfunction, is minimal. Preoperative transarterial embolization is recommended to reduce intraoperative blood loss.

[A case report of arteriovenous malformation of the tongue: vascular anatomy and note for transarterial embolization].

Arteriovenous malformation (AVM) of the tongue is a rare lesion of the cranio-facial vascular anomaly. Decision making concerning the vascular anomaly is not established because there are complex classifications of diagnosis and many treatment options. We report a case of AVM of the tongue, and review vascular anatomy and knowledge for treating this lesion. A 50-year-old man presented with dysarthria, sleep apnea and snoring because of a mass lesion of his sublingual region that had become larger over a two-year period. Neuroradiological examination revealed lingual arteriovenous fistula (AVF) associated with AVM of the tongue base. We performed transfemoral transarterial embolization via both lingual arteries using Polyvinyl alcohol particles and Eudragit-E as non-adhesive glue material. Final angiograms after embolization revealed a small residual nidus fed by the right facial artery mental branch, but shunt flow was markedly reduced. This vascular malformation was removed after a day of TAE (transarterial embolization). The patients symptom was improved and relapse has not been confirmed though 18 months have passed since the surgery. Using classification proposed by Mulliken and Glowacki, vascular anomalies are divided into two groups: hemangiomas and vascular malformations (AVM/F, arterial, venous, capillary, lymphatic and combined). AVM/F is classified into high flow malformation. TAE is useful for high flow malformation and can be used as the sole treatment or as an adjunct. Treatment should be to eradicate nidus or fistula completely, which is the fundamental abnormality because even the smallest residual nidus will expand to cause recurrence. The treatment of Cranio-facial AVM's requires rigorous differential diagnosis and appropriate management. Inadequate treatment is thought to contribute to collateral flow and disease progression in advanced AVM, making further management difficult.

[A case report of severe cerebral sinus thrombosis treated by mechanical disruption using rheolytic catheter with balloon].

A 61-year-old man presented with consciousness disorders. Computed tomography revealed bilateral frontal SAH and hematoma in the right temporo-parietal region. His condition deteriorated despite conservative treatment and hematoma became enlarged. The angiographic diagnosis was extensive sinus thrombosis from the superior sagittal sinus to the bilateral transverse sinus. Therefore, mechanical clot disruption was performed under systemic anticoagulation using PTA balloons catheter and a rheolytic catheter via the right internal jugular vein. Excellent angiographic results were obtained, and the patient recovered gradually. Six months after treatment, the patient had only upper quadrant hemianopsia and no other neurologic deficit. Our experience suggests that mechanical clot disruption with systemic anticoagulation as a safe effective treatment for cerebral sinus thrombosis, especially in patient whom had large intraparenchymal hematoma.

[Case report of cholesterol crystal embolism 1 month after carotid stenting].

Cholesterol crystal embolism (CCE) is a systemic disease resulting from shedding of cholesterol crystals into the small vessels of multiple organs, including skin, kidney, gastrointestinal tract and others. Recently, neuroendovascular therapeutic procedures for athrosclerosis disease is increasing. We report a case of CCE after carotid stenting (CAS). A 73-year-old man with asymptomatic carotid stenosis was treated by percutanenous transluminal angioplasty with stenting. CAS was achieved in a short time without trouble. About 1 month after CAS, his renal function deteriorated and purpura appeared on both toe tips (blue toe syndrome) with muscle pain of the lower extremities. Under diagnosis of CCE, he was treated by Predonisolone 20 mg/day and Valsartan 160 mg/day, Pravastatin 10 mg/day. His symptom's dramatically improved, with partial recovery of renal function. CCE rarely occurs after angiographic or interventional procedures, but is difficult to diagnose clinically and there is no established therapy. For early diagnosis of CCE strict follow-up of a patients clinical presentation and laboratory data, especially in high risk patients, is needed.

Techniques for passing the PercuSurge Guardwire system through severe and tortuous stenotic lesions.

Distal embolism is one of the major causes of morbidity and mortality associated with treating stenotic lesions by endovascular procedures, such as percutaneous angioplasty and stenting. Many devices have been designed and used to prevent this complication. The PercuSurge Guardwire system is recognized as the best system available to prevent distal embolism during stenting. However, this system is sometimes hard to pass through severe stenotic, tortuous lesions because of the poor selectivity and support. The PercuSurge device was safely introduced into two cases of severe stenotic and tortuous lesions with a triple coaxial system and the buddy wire technique, and stenting was performed successfully. These techniques are very helpful for introducing and maintaining this system in the correct position across stenoses with unfavorable configurations.

[A case of subarachnoid hemorrhage associated with spontaneous intracranial hypotension].

Cerebrospinal fluid (CSF) leakage has recently been documented in most patients, as the main cause of spontaneous intracranial hypotension (SIH). No cases of SIH accompanying an episode of subarachnoid hemorrhage (SAH) has yet been reported and, to the best of our knowledge, this is the first report of a patient, who developed SAH during his clinical course of SIH. SAH was cured completely by surgical intervention. A 57-year-old man, with a history of a sustained postural headache, suffered the sudden onset of severe nuchal pain. SAH in the basal cistern, together with the finding of bilateral subdural fluid retention were verified by CT. Angiogram showed no vascular abnormalities of cerebral or cervical vessels. Gd-enhanced Magnetic Resonance Imaging (MRI) disclosed diffuse meningeal enhancement. RI cisternogram and CT-myelogram (CTM) suggested that the region of CSF leakage should be in the retrospinal area at the level of C1-2. Because orthostatic headache failed to resolve even with 3 weeks of bed rest, surgical intervention was successfully carried out to seal the site of CSF leakage with the use of a fascia and fibrin glue. We have speculated that the etiology of SAH might have been a secondary rupture of congestive intracranial veins, such as basilar plexus or bridging veins, induced by a decrease of intracranial CSF pressure.