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Biomedical subjects

R R Smith

Publications and source records attributed to R R Smith.

At least 217 records · Page 12Linked to original sources

Anaplastic transformation of verrucous carcinoma following radiotherapy.

A 58-year-old man with a verrucous carcinoma of the larynx initially underwent partial laryngectomy followed by radiotherapy when the carcinoma recurred locally. Subsequently, he developed an anaplastic spindle cell carcinoma of the larynx ten months after radiotherapy, which eventuated in his death. The role of radiotherapy in the treatment of verrucous carcinoma remains controversial, and the risk of transforming the low-grade verrucous carcinoma to an anaplastic, metastasizing carcinoma is a real, although uncommon, complication.

Biopsy↗

Adenoid cystic carcinoma of the supraglottic larynx: report of a case and review of the literature.

Although adenoid cystic carcinoma is the most common malignant tumor of the minor salivary glands, it seldom occurs in the larynx. Less than 0.25 per cent of all laryngeal carcinomas are adenoid cystic, and only 15 such cases of supraglottic origin are recorded in the literature. In only four cases the details of treatment and outcome are described. We report another case and review the literature in order to define the entity of adenoid cystic carcinoma of the supraglottic larynx. This case reveals the aggressive nature of the disease, which is often associated with the solid variant histology and also demonstrates the most rapid course of any cases described in the literature. Other histologic variants of adenoid cystic carcinoma of the supraglottic larynx follow a more prolonged course that can extend many years even with persistent local disease. However, development of distant metastases may eventually occur. Therefore, 5-year statistics are not adequate, and 10 or 20 years' follow-up is required to evaluate the curability of this disorder. Evaluation, treatment, and clinical course of adenoid cystic carcinoma of the supraglottic larynx are discussed.

Carcinoma, Adenoid Cystic↗

Neuroradiologic review of intracranial infection.

The detection of intracranial infection continues to be a common reason for neuroradiologic examination. This review covers the neuroradiologic findings of the variety of common infections. It includes meningitis and its complications, as well as bacterial, viral, tuberculous, fungal, and parasitic diseases. Finally, a review of the common infections associated with AIDS is presented. With an increased ability to recognize such infections, radiologists should be able to supply their clinical colleagues with more specific diagnoses.

AIDS-Related Opportunistic Infections↗

Gadolinium-DTPA enhanced MR imaging of septic dural sinus thrombosis.

We present a case of septic transverse/sigmoid sinus thrombosis imaged with gadopentetate dimeglumine enhanced magnetic resonance (MR). The appearance of the septic thrombus was atypical and did not conform to the usual blood degradation products probably because of the septic nature of the process. Enhanced T1-weighted images demonstrate both the "delta" sign and the tentorial enhancement as previously seen with contrast enhanced CT. Surgical correlation was obtained and helps to account for the appearance of the clot on MR.

Adult↗

Toxoplasmic myelitis in AIDS: gadolinium-enhanced MR.

An acquired immunodeficiency syndrome (AIDS) patient developed acute symptoms suggestive of a lower spinal cord lesion. Magnetic resonance imaging was performed and demonstrated an enhancing lesion of the conus medullaris. Surgical biopsy revealed Toxoplasma gondii. Disease processes involving the spinal cord in AIDS patients are reviewed and differential diagnosis for the lesion in this patient is discussed.

Acquired Immunodeficiency Syndrome↗

Gadolinium enhancement in acute disseminated encephalomyelitis.

Acute disseminated encephalomyelitis (ADEM) is a widespread CNS inflammation that usually follows an infection or vaccination. We present a case of ADEM, which in addition to the typical MR findings, demonstrates gadolinium enhancement of several of the lesions. Since ADEM is usually a monophasic illness, it has been postulated that all lesions might enhance with paramagnetic contrast medium since they would all be expected to be active. Our case demonstrates enhancement of some of the lesions, without enhancement of others.

Acute Disease↗

Gadolinium enhancement in the center of a spinal epidural hematoma in a hemophiliac.

Spinal epidural hematoma (SEH) is an uncommon complication of hemophilia. It is a neurologic and neurosurgical emergency and prompt diagnosis is imperative. The utility of MRI in the diagnosis of hemorrhage is well established. We present a case of an SEH in a hemophiliac patient that demonstrated gadolinium enhancement.

Adult↗

MR of intracranial Langerhans cell histiocytosis.

Langerhans cell histiocytosis (LCH) is a disease of children characterized by idiopathic proliferation of histiocytes in the reticuloendothelial system. Intracranial LCH involving the brain is uncommon. We present a case of LCH involving the dural venous sinuses and choroid plexus. Contrast MRI provided an excellent means of identifying the extent of tumor involvement and showed that the patient was at risk for venous sinus thrombosis.

Adolescent↗

Foreign body giant cell reaction associated with epidermoid tumor: CT and MR findings.

A patient with a known epidermoid tumor presented with a new large ring-enhancing mass adjacent to the cyst. Histopathology showed foreign body giant cell reaction adjacent to the epidermoid cyst. The CT and MR imaging appearances are described. The neuroimaging findings are identical to malignant degeneration to squamous cell carcinoma.

Aged↗

The jugular foramen: a review of anatomy, masses, and imaging characteristics.

A variety of lesions may occur in the jugular foramen, arising from the structures normally found within the jugular foramen or from contiguous structures. The most common jugular foramen lesions are nontumoral pseudolesions (eg, asymmetrically enlarged jugular foramen, high or protruding jugular bulb) and tumors (eg, paraganglioma, metastasis). In nontumoral pseudolesions, computed tomography (CT) demonstrates smooth, intact margins of the jugular foramen. Turbulent or slow flow in a high or protruding jugular bulb can result in loss of the flow void and contrast enhancement at magnetic resonance (MR) imaging, thereby mimicking real disease. Use of flow-sensitive techniques or MR angiography will help clarify confusing cases. In cerebral venous thrombosis, CT findings are often normal. At conventional MR imaging, flow-related enhancement and in-plane, turbulent, or slow flow can cause loss of the flow void and thus mimic thrombosis. Consequently, phase-contrast MR venography is the imaging modality of choice in the assessment of cerebral venous thrombosis. Most tumoral lesions of the jugular foramen manifest at CT as areas of infiltrative bone destruction, although schwannoma and meningioma cause smooth enlargement of the jugular foramen. In addition, most of these tumors have low to intermediate signal intensity on T1-weighted MR images and intermediate to high signal intensity on T2-weighted MR images and enhance strongly after the administration of contrast material. Careful analysis of these imaging features and correlation with clinical manifestations can allow a more specific diagnosis.

Brain Diseases↗

Imaging features and clinical significance of perineural spread or extension of head and neck tumors.

Perineural spread of head and neck tumors is a form of metastatic disease in which tumor disseminates to noncontiguous regions along the endoneurium or perineurium. Both computed tomography (CT) and magnetic resonance (MR) imaging can help detect perineural spread, although MR imaging is the modality of choice because of its multiplanar capability, its superior soft-tissue contrast, and the decreased amount of artifact from dental hardware. Perineural spread most commonly occurs in adenoid cystic carcinoma and squamous cell carcinoma. Nerve enlargement may lead to foraminal enlargement and, ultimately, to foraminal destruction, findings that are best seen at CT. Extension through the foramen ovale and involvement of the Meckel cave is best seen on coronal T1-weighted MR images, and nerve enhancement is best seen on fat-suppressed T1-weighted MR images. Other radiologic findings include obliteration of fat planes at foraminal openings, neuropathic atrophy, cavernous sinus enlargement, and replacement of the trigeminal subarachnoid cistern with soft tissue. The pathway of perineural tumor spread is predictable with knowledge of the pertinent cranial nerve anatomy; however, patients with radiologically or pathologically proved perineural spread may have normal nerve function at clinical examination. Therefore, it is imperative that the radiologist be familiar with both normal cranial nerve anatomy and the radiologic appearance and assessment of perineural tumor extension.

Cranial Nerve Neoplasms↗

Constrictive endarteropathy following experimental subarachnoid hemorrhage.

Rhesus monkeys were subjected to subarachnoid hemorrhage by either the introduction of blood into the subarachnoid space or by mechanically rupturing the middle cerebral artery. Local cerebral blood flow, vascular compliance studies, and histological studies (light and electron microscope) were made of the vessels of all animals. In animals hemorrhaged via vascular rupture, subintimal swelling and thickening was minimally present by 3 days, becoming progressively more severe by one month. Such changes consisted of severe subintimal proliferation, fibrosis of the medial smooth muscle layer and interruption of the internal elastic membrane. Cells in the subintimal proliferative areas examined by electronmicroscopy were seen to have ultrastructural characteristics of smooth muscle. In the subarachnoid-injected hemorrhaged animals, there was no evidence of intimal proliferation or other vascular changes, which was also true of all control vessels. There was a decrease in wall elasticity of vessels exposed to mechanical rupture when compared to those exposed only to injected subarachnoid blood or normal vessels. Local cerebral blood flow was affected very little following the 2 methods of subarachnoid hemorrhage.

Animals↗

The angiopathy of subarachnoid hemorrhage: angiographic and morphologic correlates.

In patients with subarachnoid hemorrhage, particularly hemorrhage due to aneurysmal rupture, there was a positive significant relation between angiographic vessel constriction and vessel pathology (angiopathy). Furthermore, there was a positive relationship between post-hemorrhage survival time and the severity of angiopathy. Factors such as age, sex, operations, steroid and CSF pressure seemed to have little affect on angiopathy following hemorrhage. Pathological changes were primarily limited to the involved major cerebral vessels themselves, with their branches rarely being affected. While intramural vascular hemorrhage was a common pathological feature in vessels showing severe pathology, the mere presence of blood surrounding an artery seemed to have little influence on vessel alterations.

Cerebral Angiography↗

The angiopathy of subarachnoid hemorrhage I. Role of vessel wall catecholamines.

Subarachnoid hemorrhage (SAH) due to rupture of the right middle cerebral artery (RMCA) produced specific anatomical and biophysiological responses in the involved feline vessels. The RMCA showed morphological alterations that became progressively more severe with time and were widespread within the cerebral vascular tree. SAH also resulted in an acute depletion of vessel catecholamine levels which remained depressed over a 30 day period. When the cerebral vessels of cats were severely depleted of catecholamines (using reserpine) prior to induced SAH, morphological alterations were significantly reduced both in severity and in degree of spread within the cerebral vascular network. The results of this study suggest that the concentration of norepinephrine within the vessel at the time of hemorrhage plays a significant role in the production of the angiopathy that follows SAH.

Angiography↗