Franklin D. Westhout

Background: This report provides a rare documentation of spontaneous thrombosis of a ruptured aneurysm followed by delayed recanalization and subsequent rerupture. Case Description: A 47-year-old female presented with spontaneous subarachnoid hemorrhage (SAH). Four aneurysms were identified on CT angiogram including a basilar apex aneurysm, considered source of bleeding. Cerebral angiogram on postbleed day (PBD) #1 showed spontaneous thrombosis of basilar apex aneurysm. The patient was discharged to a nursing home on PBD #18 after two subsequent studies showed no recanalization of the basilar aneurysm. The patient returned on PBD #26 with a second episode of spontaneous SAH. The previously thrombosed basilar aneurysm had recanalized and reruptured, which was now treated with coil embolization. Conclusion: We are not aware of a previous report of saccular cerebral aneurysm documenting spontaneous thrombosis after SAH and recanalization with second hemorrhage. This occurrence presents a dilemma regarding the timing and frequency of subsequent cerebrovascular imaging and treatment.

Prolonged cerebrospinal fluid bathing of cranioplasty cement frequently results in breakdown of the cement implants. A 5-year-old boy with a history of severe head trauma at 2 weeks of age presented with marked protrusion of the entire superior temporal bone and inferior parietal bone. The defect was elevated by more than 1 cm and was associated with a 4.5 x 3-cm skull defect located above and behind the right ear. There also was pulsatile tissue at the depths of the defect. A computed tomographic scan taken of the head revealed an expanding skull fracture from a dural defect with underlying brain herniation. The cranial lesion was repaired with OsteoVation hydroxyapatite cement. Within 8 weeks, the fluid encased the cranioplasty site. This resolved following implantation of a shunting device. At 2 and 12 months after the repair, the implant was still palpably solid without breakdown and did not fragment despite the prolonged bathing in cerebrospinal fluid.

The authors report a case of short-term high-dose propofol-related metabolic acidosis in a 3-year-old girl. The patient initially presented at another institution with left fourth cranial nerve palsy, and examination revealed a large, wide-necked 19 x 22 x 17-mm aneurysm in the left internal carotid artery. She had undergone three previous unsuccessful attempts at endovascular coil embolization, which were complicated by repeated coil protrusions into the parent vessel. During angiography and a balloon occlusion test (BOT) 80 mg propofol was given for 3 hours followed by 200 microg/kg/min for another 4 hours. The 20-minute BOT was well tolerated, and the aneurysm was occluded with stent-assisted coil embolization. Following the procedure the patient developed severe acidosis, hypotension, tachycardia, and signs of cardiac failure. On postoperative Day 3 her metabolic acidosis resolved, and she was weaned off sedatives. She continued to improve and was discharged from the hospital on postoperative Day 7. The metabolic acidosis and hypotension were thought to be due to propofol-related infusion syndrome.

Background/Objective: Peripheral causes of foot drop are well recognized. However, causes stemming from the central nervous system represent rare, important, and underappreciated differential etiologies. Methods: Two cases of foot drop stemming from central causes are described. Patients: The first patient, a 46-year-old man with a remote history of lumbar spine fracture and L4-L5 instrumentation/fusion, presented with progressive weakness and numbness of the left foot, followed within 3 months by similar symptoms in the right foot. Lumbar spine imaging failed to reveal compressive nerve root pathology. Electromyography, nerve conduction studies, and muscle and nerve biopsy suggested a preganglionic lesion and ruled out a peripheral cause. Upper spine magnetic resonance imaging (MRI) revealed significant spinal stenosis at C4-C7 and T11 -T12. Patient 2 was a 66-year-old man with a known left parasagittal convex meningioma diagnosed 2 years prior presented with a progressive right foot drop over 2 months. Spine imaging was normal, and serial brain MRI confirmed a slowly enlarging parasagittal meningioma. Results: Following decompressive laminectomies at C4-C7 and T11-T12, patient 1's gait improved, with marked resolution of his right foot drop and significant improvement on the left. Patient 2 underwent craniotomy for microsurgical tumor resection. At the 2-weekfollow-up examination, he was taking daily walks. Conclusions: Central causes, although rare, need to be considered in the differential diagnosis of foot drop. Central causative lesions usually occur at locations where pyramidal tract connections are condensed and specific and the function is somatotopically organized. These cases confirm that good results can be achieved when correctable central causes of foot drop are recognized.

Lemierre syndrome is an extremely rare complication of mild-to-moderate pharyngeal infections. The authors pre sent an unusual case of Lemierre syndrome in a 16-year-old boy with cavernous sinus thrombosis and right internal carotid artery narrowing without neurological sequelae, right subdural empyema, and cerebritis in the right temporal and occipital lobes. Neuroimaging also demonstrated right jugular vein thrombosis. Cultures of samples from the blood proved positive for the presence of Fusobacterium necrophorum. The patient underwent unilateral tonsillectomy, drainage of the peritonsillar abscess, and a myringotomy on the right side. Postoperatively the patient was treated conservatively with antibiotic therapy resulting in an excellent outcome.