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Biomedical subjects

L S Adelman

Publications and source records attributed to L S Adelman.

At least 37 records · Page 2Linked to original sources
PubMed1992

Cavernous angiomas of the central nervous system in children.

A surgical series of 19 patients under the age of 18 years with pathologically verified cavernous angioma is presented. Most lesions were located in the cerebral hemispheres, but four were in the pons or midbrain, two in the diencephalon, and one in the spinal cord. Fourteen patients presented with an acute or progressing neurological deficit, three with seizures, one infant with irritability, and one with headache alone. Five patients had family histories of vascular malformations of the central nervous system, and five had multiple lesions. Surgery for small or deep lesions was aided considerably by intraoperative ultrasonographic or stereotactic localization techniques. Pathological examination of the resected malformations revealed a complex histology containing not only typical closely approximated cavernous vessels, but also areas of marked proliferation of granulation tissue and partially re-endothelialized hemorrhage, suggesting a mechanism for the apparent growth of certain cavernous angiomas. The postoperative results were good, with only one patient suffering a permanent worsening of neurological status after surgery. Incomplete resection was initially carried out in five patients, two of whom rebled within 1 year after operation. Long-term follow-up findings in these patients have emphasized the unusual history of certain of these malformations.

Adolescent↗
PubMed1991

Eosinophilia-myalgia syndrome associated with ingestion of L-tryptophan: muscle biopsy findings in 4 patients.

Muscle biopsies of 4 patients with the eosinophilia-myalgia syndrome associated with ingestion of L-tryptophan showed lymphocytic infiltrates with occasional eosinophils largely restricted to interstitial fibrous tissue and perivascular areas. There was inflammation and fibrosis of muscle spindle capsules in 3 patients. In the 2 sickest patients, there was profound muscle atrophy, affecting both muscle fiber types.

Adult↗
PubMed1991

Fatal brainstem stroke following internal jugular vein catheterization.

Neurologic complications of central venous catheterization are uncommon, and there are no reports of cerebrovascular events. We report a case of massive postoperative vertebrobasilar territory stroke following internal jugular vein cannulation due to inadvertent vertebral artery injury. Autopsy revealed thrombosis at the site of puncture wound in the right vertebral artery, with emboli present in the distal basilar artery.

Adult↗
PubMed1990

Progressive myopathy in hyperkalemic periodic paralysis.

A progressive degenerative myopathy has been well described in hypokalemic periodic paralysis but is not as widely recognized in hyperkalemic periodic paralysis. We studied four families with the latter disease in which some members developed a progressive myopathy. Episodes of paralysis were prolonged, lasting for months in some cases, and in one case paralysis was sufficiently severe to require ventilatory support. The progressive myopathy tended to develop at a time when attacks of paralysis were decreasing in frequency. Muscle biopsy specimens showed variability in fiber size, internal nuclei, and fibers with vacuoles. Electron microscopy showed myofibrillary degeneration and tubular aggregates. An abnormal biopsy specimen was more common in older patients. Our experience suggests that a progressive myopathy is as common in hyperkalemic periodic paralysis as it is in the hypokalemic disorder.

Adolescent↗
PubMed1989

Experimental trials with Gd(DO3A)--a nonionic magnetic resonance contrast agent.

Gd(DO3A), a member of a new family of nonionic MRI contrast agents, was evaluated in vivo in a rat model. In 10 animals, enhancement of an intracerebral glioma was studied following Gd(DO3A) injection. Correlation with tissue pathology was obtained in all cases. Comparative studies of renal enhancement were performed in 15 animals, utilizing disodium Gd(DTPA)2-, sodium-Gd(DOTA)-, and Gd(DO3A). With the glioma model, Gd(DO3A) administration provided enhancement of tissue with an altered blood brain barrier, thus permitting identification of the bulk of the neoplastic lesion. Comparative studies revealed that enhancement of normal renal medulla was equal or superior with Gd(DO3A).

Animals↗
PubMed1989

Glial hyaluronate-binding protein in polar spongioblastoma.

Glial hyaluronate-binding (GHA) protein is a 60 kDa glycoprotein isolated from human white matter by affinity chromatography on immobilized hyaluronate. It is localized in white matter astrocytes by immunofluorescence with monoclonal antibodies. Amino acid sequences have not revealed similarities with other proteins except cartilage extracellular matrix proteins, the region of similarity being located within the hyaluronate-binding region. Cryostat sections of 13 intracranial neoplasms removed at surgery were tested for the presence of GHA protein by indirect immunofluorescence with monoclonal antibodies. These included seven astrocytomas, one oligodendroglioma, one medulloblastoma and one spinal cord ependymoma. All tumors were negative with the exception of one astrocytoma in which the GHA protein-positive areas had the typical appearance of polar spongioblastoma, i.e. small cells palisading around blood vessels and very delicate glial fibrillary acidic (GFA) protein-positive fibrils. Conversely, neoplastic as well as reactive GFA protein-positive astrocytes were GHA protein-negative. We suggest that polar spongioblastoma derives from a GHA protein-positive glial precursor and pertinent to this suggestion is the observation that the periventricular germinal layer was found GHA protein-positive in a 22-week human fetus.

Antibodies, Monoclonal↗
PubMed1989

Spontaneous intracranial carotid artery dissection.

A previously healthy 46-year-old woman had the abrupt onset of aphasia and right hemiplegia from a large left-hemisphere infarct. At postmortem examination the cause of the infarct was dissection and occlusion of the intracranial carotid artery. No preexisting abnormality was found to account for the dissection. This uncommon cause of stroke and its pathogenesis are discussed.

Aortic Dissection↗
PubMed1989

Stroke in patients with fusiform vertebrobasilar aneurysms.

We studied seven patients with brainstem infarction and large fusiform vertebrobasilar (VB) aneurysms to clarify the clinical, radiologic, and pathologic features. All presented with pontine infarcts; one also had a cerebellar infarct. VB TIAs preceded brainstem infarction in four patients. Angiography and CT documented VB fusiform aneurysmal dilatation. Four had intraluminal thrombi and one had severe basilar artery stenosis. Two distinct clinical pictures emerged: unilateral pontine infarcts with favorable outcome, presumably related to obstruction of a pontine penetrating artery at its origin from the posterior wall of the aneurysmal basilar artery, and major fatal bilateral pontine infarcts from basilar artery occlusion. Two patients came to autopsy. One had thrombus in the dilated basilar artery and a posterior cerebral artery branch embolus with hemorrhagic occipital infarction; the other had basilar artery thrombus with aneurysmal rupture and subarachnoid hemorrhage. Fusiform VB aneurysms caused brainstem stroke by intraluminal thrombus, local embolism, atherostenosis, and obstruction of paramedian penetrating arteries. Subarachnoid hemorrhage is an uncommon complication.

Adult↗
PubMed1989

Orbital myositis and giant cell myocarditis.

A 65-year-old woman developed progressive, bilateral ophthalmoplegia, with thickened extraocular muscles on CT. One month later, a cardiac arrhythmia led to her death. Pathologically, the extraocular and skeletal muscles showed diffuse mononuclear cell inflammation, while the heart contained granulomatous myositis. This patient's syndrome of idiopathic, orbital myositis and giant cell myocarditis may be a distinct nosologic entity.

Aged↗
PubMed1988

Lateral thalamic infarcts.

A patient with occlusion of the proximal posterior cerebral artery (PCA), a lateral thalamic infarct, and hemisensory loss later developed hemianopia and hemiparesis and had extensive PCA territory infarction in the midbrain, the lateral portion of the thalamus, and the occipital lobe noted at necropsy. Two other patients had lateral thalamic infarcts on computed tomography, normal angiographic findings, and presumed thalamogeniculate artery branch occlusion. There are three clinical syndromes associated with lateral thalamic infarction: (1) hemisensory loss, hemiataxia, and involuntary movements; (2) pure sensory stroke; and (3) sensory-motor stroke. Ataxia, adventitious movements, and sensory loss are due to infarction of the lateral, posterolateral, and posteromedial ventral nuclei caused by occlusion of the PCA proximal to the thalamogeniculate artery branches or by occlusion of large thalamogeniculate arteries. Pure sensory and sensory-motor strokes are due to smaller infarcts in the posterolateral-posteromedial ventral complex and adjacent internal capsule caused by occlusion of penetrating artery branches of the thalamogeniculate arteries.

Aged↗
PubMed1988

Polyneuropathies associated with IgM monoclonal gammopathies.

We studied ten patients with IgM monoclonal gammopathies. Five had M proteins that reacted with myelin-associated glycoprotein (MAG) and five had no recognizable antinerve activity. The neuropathy in the MAG-reactive patients was homogeneous by clinical and laboratory analysis, while the neuropathy in the MAG-nonreactive patients varied considerably. Both groups responded well to immunosuppressive therapy, which lowered the concentration of the serum M protein. The homogeneity of the MAG-reactive patients and their response to sustained lowering of the M protein levels support the concept that the IgM M protein directly damages nerve fibers and is the proximate cause of the polyneuropathy.

Aged↗
PubMed1988

Acute fulminating fatal leukoencephalopathy as the only manifestation of human immunodeficiency virus infection.

A case of acute human immunodeficiency virus (HIV) infection manifested by a rapidly fulminating, necrotizing, demyelinating encephalopathy that led to brain death in 5 days is reported. Autopsy demonstrated predominant white matter lesions, acute neuronal damage, and scanty cellular response. Cultures of cerebrospinal fluid were positive for HIV, suggesting an acute infection.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Response to total body irradiation in dermatomyositis.

There were two patients with severe dermatomyositis refractory to immunosuppressive therapy treated with 150 rad of total body irradiation given over a period of 5 weeks. Both patients responded promptly with minimal side-effects and remain in partial remission 42 and 18 months after completion of the treatment. Total body irradiation is effective in some patients with dermatomyositis who are refractory to standard therapy.

Adult↗
PubMed1988

Lectin histochemistry of gangliosidosis. II. Neurovisceral tissues from patients with Sandhoff's disease.

Lectin histochemical studies were performed on selected formalin-fixed, paraffin-embedded tissues of patients affected with the O variant of GM2-gangliosidosis (i.e., Sandhoff's disease). The purpose was to identify specific sugar residues of undegraded "stored" substances in cytoplasm of affected cells. We studied neural tissues from 13 patients, visceral tissues from four patients, and placentae from three affected fetuses. Neurons in all 13 cases studied stained with Concanavalia ensiformis agglutinin (Con A) and with Ulex europaeus agglutinin-I (UEA-I). Succinylated wheat germ agglutinin (S-WGA) stained affected visceral cells and astrocytes and macrophages in the central nervous system. These results demonstrate that alpha-D-mannosyl and alpha-L-fucosyl residues, which bind Con A and UEA-I, respectively, are present in affected neurons. Furthermore, they revealed the affected non-neuronal cells and astrocytes contain complex carbohydrates with nonreducing terminal beta-N-acetylglucosamine, which binds S-WGA.

Brain↗
PubMed1988

MR imaging of rat brain glioma: Gd-DTPA versus Gd-DOTA.

The enhancement properties of gadolinium diethylenetriaminepentaacetic acid (DTPA) and gadolinium tetraazacyclododecanetetraacetic acid (DOTA) were compared using a rat glioma model. In vitro analysis included the calculation of T1 relaxivity and determination of characteristic curves. Enhancement of the intracerebral glioma was studied in 23 rats approximately 2 weeks after glioma implantation with Gd-DTPA in 12 rats and Gd-DOTA in 11 rats. Six rats were also studied 1 week after implantation. Gd-DTPA exhibited a slightly greater T1 relaxivity in vitro than Gd-DOTA. Enhancement of the glioma was also greater with Gd-DTPA than with Gd-DOTA (P less than .05).

Animals↗
PubMed1988

Dissection of the intracranial vertebral artery.

We describe four patients and review prior reports to clarify the clinical, radiographic, and pathologic findings of intracranial vertebral artery (VA) dissection. A 43-year-old man and a 33-year-old woman had chronic bilateral VA dissecting aneurysms. The man had multiple episodes of subarachnoid hemorrhage (SAH) and necropsy showed multiple dissections and defects in the internal elastica. The woman had many brainstem TIAs and strokes during 3 years. Two other patients had SAH and unilateral dissections. Intracranial VA dissection causes four overlapping syndromes: (1) brainstem infarcts are usually due to subintimal dissection extending into the basilar artery, affect younger patients, and often are single fatal events; (2) SAH is due to subadventitial or transmural dissection; (3) aneurysms cause mass effect on the brainstem and lower cranial nerves; and (4) chronic dissections due to connective tissue defects cause extensive bilateral aneurysms and repeated TIAs, small strokes, and SAH.

Adult↗
PubMed1988

Patterns of recurrence in glioma patients after interstitial irradiation and chemotherapy: report of three cases.

Three patients with malignant gliomas who developed dissemination of tumor at the time of recurrence are presented. All three patients received combination therapy including conventional radiotherapy and interstitial radiation therapy followed by systemic BCNU chemotherapy. A review of the literature on the development of glioma metastases and an analysis of the possible mechanisms of this uncommon growth pattern are presented.

Adult↗