Intracranial transthecal subarachnoid fat emboli and subarachnoid haemorrhage arising from a sacral fracture and dural tear.

We present the case of a 28-year-old man with an unusual aetiology of lipid-dense material in the subarachnoid space. CT of the head at presentation was normal. MRI of the spine revealed a defect in the dura at L5/S1, with avulsed left L5 and S1 nerve roots. Haematoma and marrow fat were observed in close relation to the dural tear adjacent to the sacral fracture. Head CT and MRI subsequently demonstrated new lipid-dense material and haemorrhage in the subarachnoid space after sacral instrumentation, presumably owing to transthecal displacement of fatty marrow.

Resolution of existing intimal plaque in a patient with carotidynia.

We present a case of carotidynia that was imaged with 3 techniques: sonography, CT angiography, and gadolinium-enhanced MR imaging. We describe a previously unreported finding, the resolution of an intimal plaque noted on imaging at the time of initial presentation, presumably due to changes induced by the healing phase of the carotid inflammatory process.

Lightning strike: a rare cause of bilateral ossicular disruption.

Otologic injury associated with fatal and nonfatal lightning strikes has been sporadically reported in the literature. The most common acoustic insult is a conductive hearing loss secondary to rupture of the tympanic membrane. Although conjecture has been made of the theoretic possibility of ossicular injury from lightning strike, to our knowledge, none has been demonstrated intraoperatively or postmortem. We report the first documented case of ossicular disruption in a lightning-strike victim.

Calcified cerebral emboli.

Intracranial calcifications may represent calcified cerebral emboli. Calcified emboli may be overlooked even though cerebral CT is widely used as a stroke assessment. We report 4 cases of calcified cerebral emboli and demonstrate the value of CT in the diagnosis and temporal evaluation of such emboli.

Diffusion-weighted imaging findings in Balo concentric sclerosis.

Balo concentric sclerosis is a rare demyelinating disease. Pathognomonic features have been previously described. Diffusion-wighted imaging findings have not been previously described in Balo concentric sclerosis. We describe the diffusion-weighted imaging findings in a 45-year-old lady with Balo concentric sclerosis. Diffusion-weighted imaging offers insight into the possible pathophysiology of this rare disease.

Baló's concentric sclerosis: surviving normal myelin in a patient with a relapsing-remitting dinical course.

Baló's concentric sclerosis is a demyelinating disorder in which bands of demyelination alternate with concentric bands of myelin preservation. The pathogenesis of the lesion is unknown. Previous reports using modern histopathologic techniques have shown the bands of myelin preservation to be comprised of remyelinated or partially demyelinated myelin. Here we report a case of Baló's concentric sclerosis in a 24-year-old East Indian patient with a previous history of relapsing-remitting multiple sclerosis (MS). Pathologically, the bands of myelin preservation showed myelin sheaths of normal thickness, with focal areas of demyelination. The findings, taken together with those of previously reported cases, suggest that Baló's concentric sclerosis is a variant of MS, and the concentric lesion may be an intermediary form in evolution of a chronic active MS plaque. The pathogenesis of this concentric lesion may be explained by periodic suppression of demyelination in the rapidly expanding border, allowing remyelination or only transient incomplete demyelination to occur.

Intravenous tissue plasminogen activator for acute ischemic stroke: A Canadian hospital's experience.

BACKGROUND AND PURPOSE: In the United States, tissue plasminogen activator (tPA) was approved for treatment of acute ischemic stroke in 1996. Its use has only recently been approved in Canada. We sought to evaluate the safety, feasibility, and efficacy of treatment in a Canadian hospital setting. METHODS: A combined retrospective and prospective review is presented of 46 consecutive patients treated with intravenous tPA at our hospital with a treatment protocol similar to that of the National Institute of Neurological Disorders and Stroke (NINDS) trial. RESULTS: Symptomatic intracranial hemorrhage at 36 hours occurred in 1 patient (2.2%). The median time to treat was 165 minutes, with a median "door-to-needle" time of 84 minutes. Compared with patients presenting initially at our hospital, patients transferred from another institution for tPA therapy were treated closer to the 3-hour time window (mean 173 versus 148 minutes, P:<0.001) but had a shorter door-to-needle time (43 versus 102 minutes, P:<0.001). For every 10 minutes closer to the 3-hour time window that any patient arrived at the hospital, 7 minutes was saved in the door-to-needle time (correlation coefficient 0.9, P:<0.001). Patient outcome did not differ from that in the NINDS trial (P:>0.75). CONCLUSIONS: Our safety and patient outcome data compare favorably with NINDS and Phase IV data. Although a 3-hour treatment window was feasible, the median door-to-needle time lengthened as more treatment time was available and the door-to-needle time was beyond recommended standards. This review has prompted changes in our community to improve treatment efficiency.

Combined venous lymphatic malformations of the orbit (so-called lymphangiomas). Association with noncontiguous intracranial vascular anomalies.

OBJECTIVE: The authors present seven cases of orbital combined venous lymphatic vascular malformations (CVLVM) (lymphangioma) with evidence of noncontiguous intracranial vascular anomalies. DESIGN: The study design was a review. MAIN OUTCOME MEASURES: Radiologic studies of 25 patients with combined venous lymphatic vascular malformations were evaluated for noncontiguous intracranial vascular anomalies. Features of the intracranial anomalies and orbital lesions, their clinical presentation, and prognosis are described. RESULTS: Seven patients (28%) had associated noncontiguous intracranial vascular anomalies. Intracranial hemorrhage occurred in one of these patients. The intracranial anomalies had radiologic characteristics of developmental venous anomalies (DVAs). Diffuse orbital lesions with superficial and deep components (7/7), orbital bony expansion (7/7), and intraconal and extraconal components (4/7) were most common. They involved the inferior orbital fissure and extended into the pterygopalatine fossa in five patients. Involvement of the superior orbital fissure was noted in all seven patients with extension into the middle cranial fossa in three patients. At birth, these patients generally had a visible superficial component and then had episodes of sudden proptosis associated with deep orbital hemorrhages. Visual outcome was poor (20/200 or less) in four (57%) of seven cases. Anterior extension into soft tissues of the face and forehead and other associated vascular lesions, such as palatal involvement, were relatively common. In contrast, CVLVMs (lymphangiomas) without noncontiguous intracranial vascular anomalies were more anterior, less diffuse, less likely to extend into the soft tissues of the face, have associated vascular lesions, or have a poor visual outcome. CONCLUSIONS: Orbital CVLVMs (lymphangiomas) may be associated with noncontiguous intracranial vascular anomalies that may bleed. This association with intracranial DVAs has not been reported previously. The intracranial vasculature should be evaluated prospectively in these lesions, especially if they are diffuse.

Cardiac rupture complicating cerebral intraarterial thrombolytic therapy.

We report a case of fatal cardiac rupture occurring during intraarterial thrombolytic therapy for acute embolic stroke in a patient with recent myocardial infarction.

In vivo measurement of T2 distributions and water contents in normal human brain.

Using a 32-echo imaging pulse sequence, T2 relaxation decay curves were acquired from five white- and six gray-matter brain structures outlined in 12 normal volunteers. The water contents of white and gray matter were 0.71 (0.01) and 0.83 (0.03) g/ml, respectively. All white-matter structures had significantly higher myelin water percentages (signal percentage with T2 between 10 and 50 ms) than all gray-matter structures. The range in geometric mean T2 of the main peak for both white and gray matter was from 70 to 86 ms. T2 distributions from the posterior internal capsules and splenium of the corpus callosum were significantly wider (width is related to water environment inhomogeneity) than those from any other white- or gray-matter structures. Thus, quantitative measurement and analysis of T2 relaxation reveals differences in brain tissue water environments not discernible on conventional MR images. These differences may make short T2 components reliable markers for normal myelin.

In vivo visualization of myelin water in brain by magnetic resonance.

We exploit the intrinsic difference in magnetic resonance spin-spin relaxation time, T2, between water associated with myelin sheaths and water in other central nervous system tissue in order to measure myelin water content within any region of an image or to generate indirectly a myelin map of the brain. In normal volunteers, myelin water maps give the expected myelin distribution. In multiple sclerosis patients, lesions exhibit different myelin water contents providing insight into the demyelination process unavailable from conventional magnetic resonance images. In vivo myelin measurement has important applications in the clinical management of multiple sclerosis and other white matter diseases.

Multidisciplinary approaches to complicated vascular lesions of the orbit.

BACKGROUND: Hemodynamically active vascular lesions of the orbit are often clinically challenging to treat, both because of the complexity of the vascular anatomy and the delicacy of the cardinal structures that are involved and vulnerable to damage. Attempts to achieve complete embolization of such vascular lesions may result in damage to vital visual structures. Conversely, incomplete closure of the feeders or vascular shunts will usually result in recanalization and, therefore, recurrence of such lesions. METHODS: Surgical excision after selective optimal embolizations may convert dynamic lesions into static ones with controlled surgical risks and could provide a solution to these problems. Cyanoacrylic polymerization was used to embolize the lesions, which were then excised with careful microsurgical and microvascular techniques. RESULTS: The authors present four cases of different hemodynamically active orbital vascular lesions (a post-traumatic arteriovenous fistula, a complex venous anomaly, a cavernous hemangioma of bone, and an arteriovenous malformation), which were treated successfully with the combination of presurgical embolization and surgery. CONCLUSION: The authors believe that, from their experience with these cases, a multidisciplinary approach to complicated orbital vascular lesions is ideal and practical.

Neurologic complications in allogeneic bone marrow transplant patients receiving cyclosporin.

Regimens using cyclosporin (CSP) and either methylprednisolone (MP) or methotrexate (MTX) have been useful in the prophylaxis of acute graft-versus-host disease (GVHD) after allogeneic bone marrow transplantation (BMT). However, CSP produces a number of side effects, including neurologic toxicity. A retrospective review of recipients of 239 BMTs given CSP-based prophylactic regimens revealed that 10 patients (4.2%, 95% confidence interval 0% to 10.4%) experienced a syndrome characterized by hypertension, severe visual disturbances, seizures and occipital lobe density changes on brain computed tomography (nine patients) or nuclear magnetic resonance imaging (one patient). Neurologic findings were reversible in all cases, usually after temporary discontinuation of CSP. Univariate analysis identified the following risk factors for neurotoxicity: use of unrelated or HLA-mismatched related donors, administration of etoposide (VP-16) or total body irradiation as part of conditioning, use of corticosteroids for prophylaxis or treatment of acute GVHD, or development of either acute GVHD or clinically significant microangiopathic hemolytic anemia (MAHA) post-BMT. In multivariate analysis, the most important predictors were the use of VP-16 (p = 0.008), the use of a continuous infusion CSP plus MP prophylactic regimen for GVHD (p = 0.003) and the development of MAHA after BMT (p less than 0.001). The strong association with MAHA suggests that endothelial damage is related to the development of this complication.

Carotid and vertebral artery trauma: clinical and angiographic features.

Injury to the carotid or vertebral artery is an important clinical entity that requires angiography for definitive diagnosis and evaluation. The common carotid artery may be injured by penetrating trauma while the internal carotid artery is usually damaged by either trivial or blunt trauma. With trivial trauma extracranial internal carotid artery dissection should be considered if there is unilateral headache, Horner's syndrome or delayed transient ischaemic attack, and intracranial dissection if a profound neurological defect occurs immediately following trauma. Injury to the internal carotid artery following blunt trauma includes dissection of the extracranial internal carotid artery, carotid-cavernous fistula and pseudoaneurysm formation. These should be considered in a patient with delayed neurological deficit, mandibular or skull fracture, a constellation of orbital signs or diffuse subarachnoid haemorrhage, respectively. Vertebral artery injury is less frequent. Dissection typically follows abrupt cervical rotation and occurs at C1-2, whereas penetrating trauma may involve either the proximal or distal vertebral artery and occlusion, arteriovenous fistula or pseudoaneurysm may be found. Endovascular techniques may be used in either the carotid or vertebral artery to close fistulae or occlude an extensively damaged vessel.