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Biomedical subjects

W S Smith

Publications and source records attributed to W S Smith.

At least 37 records · Page 2Linked to original sources

Endovascular stenting of an acutely thrombosed basilar artery: technical case report and review of the literature.

OBJECTIVE AND IMPORTANCE: The goal of this report was to describe the successful percutaneous endovascular use of a Gianturco-Roubin-2 coronary stent in the treatment of an acute atherothrombotic occlusion of the basilar artery. To our knowledge, the percutaneous endovascular deployment of an intra-arterial stent for the treatment of an acute atherothrombotic occlusion of the basilar artery and the percutaneous endovascular placement of a Gianturco-Roubin-2 stent in the basilar artery have not been previously reported. CLINICAL PRESENTATION: An 83-year-old man presented with a recurrent, transient, locked-in syndrome resulting from a lower basilar artery occlusion caused by vertebrobasilar thrombosis superimposed on severe proximal basilar artery atheromatous stenosis. INTERVENTION: After successful superselective intra-arterial thrombolysis of the vertebrobasilar clot, balloon angioplasty of the underlying basilar artery stenosis was performed, without significant angiographic improvement. Percutaneous endovascular deployment of a Gianturco-Roubin-2 coronary stent of 4-mm diameter was subsequently performed, with excellent angiographic results. CONCLUSION: The patient made a very good neurological recovery but unfortunately died as a result of cardiogenic shock and sepsis. Detailed neuropathological follow-up results are presented; stent patency was revealed in the postmortem examination. The anatomic and pathophysiological considerations of basilar artery stent placement for the treatment of acute basilar artery occlusion related to atherosclerotic stenosis are discussed.

Acute Disease↗

Endovascular recanalization with balloon angioplasty and stenting of an occluded occipital sinus for treatment of intracranial venous hypertension: technical case report.

OBJECTIVE AND IMPORTANCE: Dural sinus thrombosis can lead to intracranial venous hypertension and can be complicated by intracranial hemorrhage. We present a case report of a patient who underwent endovascular recanalization and stenting of a thrombosed occipital sinus. CLINICAL PRESENTATION: A 13-year-old patient with a history of chronic sinus thrombosis refractory to anticoagulant therapy presented with acute onset of aphasia and hemiparesis. Computed tomography and magnetic resonance imaging revealed hydrocephalus and cerebral edema. Angiography delineated multiple dural arteriovenous fistulae and persistent occlusion of the posterior sagittal, occipital, and bilateral transverse dural sinuses with retrograde cortical venous drainage. INTERVENTION: After embolization of the dural arteriovenous fistulae, a transvenous approach was used to recanalize and perform balloon angioplasty of the right internal jugular vein and the occipital and left transverse sinuses, resulting in subsequent clinical improvement. The patient's condition deteriorated 3 days later with reocclusion of both balloon-dilated sinuses. Repeat angioplasty and then deployment of an endovascular stent in the occipital sinus were performed, and reestablishment of venous outflow was achieved, resulting in a decrease of intracranial venous pressure from 41 to 14 mm Hg and neurological improvement. At the 3-month follow-up examination, the stented occipital sinus remained patent and served as the only conduit for extracranial venous outflow; the patient remained neurologically intact at the 12-month follow-up examination. CONCLUSION: This is the first report of mechanical recanalization, balloon angioplasty, and stent deployment in the occipital sinus to provide sustained venous outflow for the treatment of venous hypertension with retrograde cortical venous drainage in a patient with dural pansinus thrombosis refractory to anticoagulant therapy.

Adolescent↗

Practice variability in management of transient ischemic attacks.

To define practice patterns in the management of transient ischemic attacks (TIAs), we surveyed practicing neurologists attending an educational conference in San Francisco, evaluating management decisions in 2 TIA case vignettes. In a vignette describing a hemispheric TIA 1 day prior with ipsilateral bruit, 53% chose admission, 47% elected an outpatient work-up, 28% treated with intravenous heparin and 70% chose aspirin, reflecting the disagreement about medical management of carotid stenosis in the literature. There was more agreement in the second case, a posterior circulation TIA 1 day prior with atrial fibrillation, in which 84% chose hospital admission, 74% chose intravenous heparin and 90% treated with some form of anticoagulation. There are areas of important practice variability in the management of TIAs. Further research is justified to guide patient care decisions in TIA patients.

Aged↗

Neurologic manifestations of spinal epidural arteriovenous malformations.

Eight patients with spinal epidural arteriovenous malformations presented with progressive myelopathy (3), hemorrhage (3), and tinnitus/bruits (2). MRI suggested a vascular malformation in four (of seven) patients. Spinal angiography was necessary for diagnosis. Treatment by endovascular embolic occlusion (with balloons, particles, or coils) (7 patients) or surgical resection (4 patients), or both, temporarily arrested progression of neurologic symptoms, but recurrence of symptoms in two patients was associated with development of collateral arterial supply to the malformation.

Aged↗

Rapid development of giant fusiform cerebral aneurysms in angiographically normal vessels.

Several reports have mentioned formation of new saccular aneurysms in previously normal-appearing vessels, but de novo fusiform aneurysms have not been reported. We describe three children who initially presented with giant fusiform aneurysms involving the cervical and petrous portions of the internal carotid artery and were treated with balloon occlusion. Between 2 and 6 years later, they were found to have new giant fusiform aneurysms in the vertebrobasilar system.

Basilar Artery↗

Induction of antigen-specific tolerance for the treatment of ongoing, relapsing autoimmune encephalomyelitis: a comparison between oral and peripheral tolerance.

Experimental autoimmune encephalomyelitis (EAE) is a T cell-mediated autoimmune demyelinating disease of the central nervous system that serves as an animal model for multiple sclerosis. Various forms of Ag-specific tolerance have been used prophylactically to prevent development of acute EAE. Here we compare the induction of Ag-specific tolerance using two regimens, proteolipid protein 139-151 (PLP139-151) peptide-coupled splenocytes and oral administration of PLP139-151, for efficacy in the reduction of established, chronic clinical EAE. PLP139-151-coupled splenocytes and not oral administration of PLP139-151 was able to down-regulate established EAE, including subsequent relapses. PLP139-151 peptide-coupled splenocytes were effective at reducing Ag-specific T cell proliferation and IL-2 and IFN-gamma production, while concomitantly increasing IL-4 production. Oral administration of PLP139-151 did not reduce IL-2 or IFN-gamma production and appeared to increase Ag-specific T cell proliferation. Neither multiple high nor low doses of PLP139-151 were effective at decreasing ongoing clinical EAE or PLP139-151-specific IL-2 and IFN-gamma production. These results suggest that PLP139-151 peptide-induced tolerance is an efficacious treatment for ongoing, R-EAE when the peptide is coupled to chemically fixed splenocytes and not when given orally.

Administration, Oral↗

Differential CC chemokine-induced enhancement of T helper cell cytokine production.

Chemokines are a family of small m.w. cytokines that induce chemotaxis and chemokinesis of leukocytes. These molecules are ligands for seven-transmembrane, Gi protein-linked receptors that induce a signaling cascade in human T cells and provide costimulation for T cell activation, in addition to participating in transendothelial migration of leukocytes. To address the role of chemokines in the regulation of Th cell cytokine production, we utilized an OVA-specific TCR transgenic (Tg+) model. Cells stimulated through the TCR and incubated in the presence of macrophage inflammatory protein-1alpha (MIP-1alpha) showed enhanced IFN-gamma production, whereas cells incubated in the presence of monocyte chemotactic protein-1 (MCP-1) showed enhanced IL-4 production. Similar results were obtained whether TCR Tg+ T cells were stimulated with anti-CD3 mAb or OVA peptide. Primary stimulation of T cells in the presence of chemokines, followed by secondary stimulation and tertiary stimulation with anti-TCR clonotype mAb alone (no exogenous chemokines), revealed an enhanced IFN-gamma production for MIP-1alpha stimulation and IL-4 production for MCP-1 stimulation. Naive Tg+ T cells, obtained from Tg+ mice crossed to RAG-1-deficient mice, showed enhanced IFN-gamma production when incubated with MIP-1alpha and enhanced IL-4 production when incubated with MCP-1. These results suggest CC chemokines play a role in regulating naive Th cell cytokine production, in addition to regulating leukocyte trafficking.

Animals↗

Evidence for a hydrostatic mechanism in human neurogenic pulmonary edema.

STUDY OBJECTIVES: To identify the relative contribution of hydrostatic and permeability mechanisms to the development of human neurogenic pulmonary edema. DESIGN: Retrospective review of patients with neurogenic pulmonary edema who had pulmonary edema fluid analysis. SETTING: University hospital ICU. PATIENTS: Twelve patients with neurogenic pulmonary edema in whom the associated neurologic condition was subarachnoid hemorrhage (n = 8, 67%), postcraniotomy (n = 2), and stroke (n = 2). MEASUREMENTS: Protein concentration was measured from pulmonary edema fluid and plasma samples obtained shortly after the onset of clinical pulmonary edema. RESULTS: The mechanism of pulmonary edema was classified according to the initial alveolar edema fluid to plasma protein concentration ratio. A hydrostatic mechanism (ratio < or = 0.65) was observed in seven patients, none of whom had cardiac failure or intravascular volume overload. Five patients had evidence for increased permeability (ratio > 0.70). Patients with a hydrostatic mechanism had better initial oxygenation (mean +/- SD PaO2/FIO2 [fraction of inspired oxygen] = 233 +/- 132) compared with patients with increased permeability (PaO2/FIo2 = 80 +/- 42), and oxygenation improved more rapidly in the hydrostatic patients. Overall mortality (58%) was high, but it was related to unresolved neurologic deficits, not to respiratory failure. CONCLUSION: Many of our patients had a hydrostatic mechanism for neurogenic pulmonary edema. This is a novel observation in humans since prior clinical case reports have emphasized increased permeability as the usual mechanism for neurogenic pulmonary edema. These findings are consistent with pulmonary venoconstriction or transient elevation in left-sided cardiovascular pressures as contributing causes to the development of human neurogenic pulmonary edema.

Adult↗

Inhibition of relapsing experimental autoimmune encephalomyelitis in SJL mice by feeding the immunodominant PLP139-151 peptide.

Peripheral antigen-specific tolerance can be induced by feeding protein antigens. The mechanism has been described as either clonal anergy/deletion or induction of antigen-specific regulatory cells that produce transforming growth factor-beta (TGF-beta). These two mechanisms have been linked to the magnitude and frequency of the dose of antigen fed; a single high dose induces anergy/deletion, whereas multiple low doses of antigen induce TGF-beta-secreting regulatory cells. In the present study, we investigated the mechanisms of feeding soluble peptides of proteolipid protein (PLP) for prevention of experimental autoimmune encephalomyelitis (EAE) induced by either intact PLP or the immunodominant PLP139-151 peptide. Feeding PLP139-151 prevented acute and relapsing EAE induced by either PLP139-151 or intact PLP. PLP139-151 feeding induced anergy in the T helper 1 (Th1) population as measured by an inhibition of both proliferation and interferon-gamma (IFN-gamma) production. Interleukin-4 (IL-4) production was increased, but increased TGF-beta production was not observed. Importantly, PLP139-151 feeding induced anergy in peripheral and central nervous system (CNS)-in-filtrating T cells. Feeding of the subdominant PLP epitope (PLP178-191) failed to inhibit EAE induced by PLP139-151; therefore, oral tolerance was not due to induction of bystander suppression. These results demonstrate that both acute and relapsing paralysis in EAE can be prevented by feeding the immunodominant peptide of PLP.

Administration, Oral↗

From the archives of the AFIP. Primary tumors of the spine: radiologic pathologic correlation.

Primary tumors of the spine are relatively infrequent lesions compared with metastatic disease, multiple myeloma, and lymphoma. However, when a solitary lesion of the spine occurs, these neoplasms represent an important group of entities for diagnostic consideration. A wide variety of benign neoplasms can involve the spine, including osteoid osteoma, osteoblastoma, aneurysmal bone cyst, giant cell tumor, enostosis, and osteochondroma. Common primary nonlymphoproliferative malignant neoplasms of the spine include chordoma, chondrosarcoma, Ewing sarcoma or primitive neuroectodermal tumor, and osteosarcoma. The imaging features of these lesions of the spine are often characteristic. These changes include a small sclerotic focus with irregular thorny margins in the vertebral body (enostosis), a small radiolucent nidus with central calcification in the posterior elements of the vertebral body (osteoid osteoma), a large expansile lesion with multiple fluid-fluid levels (aneurysmal bone cyst), and an aggressive mineralized mass (chondroid or osteoid) with osseous and soft-tissue involvement (chondrosarcoma or osteosarcoma). Radiologists should be aware of the appearance of these unusual neoplasms in order to provide a complete differential diagnosis and to guide clinical colleagues in patient treatment.

Adolescent↗

Granulocyte colony-stimulating factor versus placebo in addition to penicillin G in a randomized blinded study of gram-negative pneumonia sepsis: analysis of survival and multisystem organ failure.

Sepsis is a common cause of morbidity and mortality. Neutrophils are the major defense against bacterial invasion, and granulocyte colony-stimulating factor (G-CSF) augments both neutrophil number and function. In our study, 160 rabbits were inoculated transtracheally with 0.5 mL of a solution containing 10(4) colony forming units per milliliter of Pasteurella multocida. Twenty-four hours later, chest x-rays and quantitative blood cultures demonstrated pneumonia and bacteremia. Therapy was then begun with penicillin G and either recombinant human G-CSF (rG-CSF; 5 to 8 micrograms/kg subcutaneously) or placebo every day for 5 days. Arterial blood gases and 23 other parameters of organ function were performed before inoculation and serially thereafter. All rabbits underwent histologic examination of organs at the time of septic death or when sacrificed on day 6. A total of 149 rabbits survived long enough to initiate therapy. A significant increase in leukocytes by day 4 was found in the rG-CSF-treated group. There was a trend towards improved survival in the rG-CSF group (77% v 67%; P = .13, n = 149). Analysis of pretreatment variables revealed sepsis-induced leukopenia (< or = 2,800/microL) as the only predictor of significantly improved survival with rG-CSF treatment (57% v 39%; P = .04, n = 73). The majority of the survival benefit occurred within the first 24 hours of treatment. This was before the time that a significant difference in mean white blood cell (WBC) count was observed between the study groups, making intravascular leukocytosis an unlikely explanation for the survival advantage in the rG-CSF group. No significant difference in laboratory variables reflecting organ function was demonstrated between the groups. Histologic grading of inflammation (0, normal, to 6, necrosis) in seven organs revealed that the surviving rabbits had mild but statistically significant increased inflammation in the liver, spleen, and noninoculated lung in the rG-CSF versus placebo groups (liver: 2.6 v 1.5, P < or = .0001; spleen: 3.2 v 2.3, P < or = .0001; and noninoculated lung: 2.9 v 2.5, P = .04). Administration of rG-CSF, in addition to penicillin G, in immune competent rabbits with gram-negative sepsis complicated by leukopenia significantly improved survival over antibiotics alone. The administration of rG-CSF in early sepsis for a short therapeutic duration was not associated with any clinically evident toxicity. Clinical trials using rG-CSF in septic patients with leukopenia are indicated.

Animals↗

From the archives of the AFIP. Musculoskeletal angiomatous lesions: radiologic-pathologic correlation.

Vascular lesions of bone and soft tissue are relatively common musculoskeletal neoplasms. Hemangioma is the most frequently encountered angiomatous lesion. Osseous hemangioma commonly involves the spine and calvaria and often has a characteristic radiographic appearance, with either coarsened trabeculae lying adjacent to the vascular channels or multifocal lytic areas creating a honeycomb pattern. Soft-tissue hemangioma is the most frequent soft-tissue neoplasm of infancy and childhood. Radiography and computed tomography (CT) may show phleboliths in cavernous soft-tissue hemangioma. The magnetic resonance (MR) imaging appearance, however, is often more distinctive, because fat overgrowth and serpentine vascular channels can be seen. Lymphangioma usually occurs in the neck and axillae of young children as a soft-tissue mass composed of large cavernous spaces and is well evaluated with CT, ultrasound, or MR imaging. Vascular lesions can also diffusely involve both bone and soft tissue in angiomatosis. A group of more aggressive vascular neoplasms, including hemangioendothelioma, hemangiopericytoma, and angiosarcoma, may have a nonspecific imaging appearance; however, the vascular pattern can be recognized in some cases, allowing radiologic diagnosis. Imaging is important throughout the evaluation of angiomatous lesions for detection, diagnosis, preoperative assessment, and treatment.

Adolescent↗

Streptococcus pneumoniae-induced hemolytic uremic syndrome: a case for early diagnosis.

Hemolytic uremic syndrome associated with infection by neuraminidase-producing Streptococcus pneumoniae usually presents with fulminant pneumonia and has a high mortality rate. Post-pneumococcal hemolytic uremic syndrome may occur earlier in life than classical hemolytic uremic syndrome. We describe an 18-month-old male with hemolytic uremic syndrome, S. pneumoniae pneumonia, and T-antigen activation characteristic of neuraminidase activity. We have summarized the features of this case and 11 previously reported children. As the use of blood products containing IgM may aggravate this disorder, early recognition of hemolytic uremic syndrome associated with S. pneumoniae neuraminidase production may lead to improved patient outcome through the judicious use of blood products.

Agglutination Tests↗

Cerebral aneurysm presenting as cough headache.

The diagnosis of benign cough headache syndrome currently requires non-invasive brain imaging to exclude structural and mass lesions. We describe a patient with a cerebral aneurysm who presented with recurrent cough headache as her initial symptom. Conventional cerebral angiography was required for the diagnosis. Cerebral aneurysm should be considered in the differential diagnosis of cough headache syndrome.

Adult↗