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Biomedical subjects

D M Moody

Publications and source records attributed to D M Moody.

At least 73 records · Page 4Linked to original sources
PubMed1979

Radionuclide sinography: diagnosis of lateral sinus thrombosis by dynamic and static brain imaging.

Four patients with lateral sinus thrombosis were studied by radionuclide (RN) dynamic studies and RN static brain scans. Findings included: (a) abrupt termination of RN activity in the midportion of a lateral sinus ("stump sign"); (b) nonvisualization on dynamic, increased visualization on static images ipsilateral to a prominent sinus groove on a plain skull radiograph; and (c) increased activity on static images with nonfilling on angiography. RN demonstration of the "stump sign" is pathognomonic of lateral sinus occlusion; the latter two patterns require radiographic demonstration of an ipsilateral sinus groove or angiography for significance.

Adult↗
PubMed1978

Clinical and computerized tomographic study of hypertensive intracerebral hemorrhage.

Historical, neurological, and computerized tomographic findings were correlated in 32 patients with hypertensive intracerebral hemorrhage. The mortality figures given in standard texts appear to be too high; the more acceptable figure would seem to be approximately 40%. Special attention was given to intraventricular rupture, which complicated 62% of the cases. Sudden onset of coma appears to correlate with the presence of intraventricular rupture. The "ring sign," if looked for, will be seen in most cases of resolving intracerebral hematoma.

Brain↗
PubMed1978

Computed tomography in late-infantile metachromatic leukodystrophy.

Computed tomography of 2 patients with late-infantile metachromatic leukodystrophy (MLD) demonstrated generalized white matter lucency and moderate ventricular enlargement. CAT scan findings in other white matter diseases likely to be confused clinically with MLD are sufficiently dissimilar to allow differentiation.

Brain↗
PubMed1978

Computerized cranial tomography of free intracranial fat in congenital tumors.

Three additional cases of free intracranial fat associated with congenital tumors are reported. The migration of fat with positional change is detailed. Free intraventricular fat may present without transcerebral rupture of the tumor. Our experience with these three patients, plus the two previously reported, suggest that two conditions must be present for oily material to enter the ventricular system through the outlets of the fourth ventricle: first, there must be a reversal of bulk flow of cerebrospinal fluid; second, the oily material must have a specific gravity less than that of cerebrospinal fluid. Also noted from our series is the absence of serious clinical sequelae associated with rupture or leakage of fatty tumors.

Adipose Tissue↗
PubMed1978

Computed cranial tomographic findings in cerebral sinovenous occlusion.

Eleven patients with angiographically and/or pathologically verified cerebral sinovenous occlusions not directly caused by trauma were studied by computed cranial tomography (CCT). Static radionuclide brain scans and dynamic radionuclide flow studies were also obtained in four patients; in two, findings diagnostic of lateral sinus thrombosis were noted. These comprised a "negative on dynamic, hot on static" image, as well as a "hot on static with nonfilling on angiography." Computed cranial tomography findings included visualization of the thrombosed vein ("cord sign") or sinus ("empty triangle" or "delta sign"), multiple focal bilateral parasagittal hemorrhages, intense tentorial enhancement, gyral enhancement indistinguishable from infarct, solitary intracerebral hematoma, small ventricles, and normal scan. Excluding the patients with underlying meningioma, all three of whom survived, seven of the remaining eight patients expired during the acute phase of their illness, an 88% mortality. This group includes one patient who had normal CCT findings, albeit without contrast enhancement, who was diagnosed as pseudotumor cerebri. The need for full neuroradiological evaluation, including angiography, is thus stressed if this highly fatal yet treatable condition is not to remain undiagnosed.

Adult↗
PubMed1978

Resolving intracerebral hematoma: alteration of the "ring sign" with steroids.

A ring of contrast enhancement is seen on CT scans of resolving intracerebral hematomas. This ring can be modified with steroid administration in the early stages; however, enhancement seen in the later stages is not affected. Evidence suggests that the early ring is due to blood-brain barrier breakdown, and the later enhancement is due to vascular granulation tissue. The following six stages of hematoma resorption were identified depending on the hematoma density, the presence or absence of a ring of enhancement, and the response of the ring to steroid administration: I = dense hematoma without enhancement; II = decreasing density, enhancement, modification of enhancement with steroid; III = isodense hematoma, enhancement, modification with steroid; IV = lucent hematoma, enhancement, modification with steroid; V = lucent hematoma, enhancement, no modification with steroid; and VI = healed, no enhancement.

Blood-Brain Barrier↗
PubMedDate not supplied

Immunohistochemical assessment of constitutive and inducible heat-shock protein 70 and ubiquitin in human cerebellum and caudate nucleus.

The distributions of constitutive and inducible 70-kDa heatshock proteins (Hsc70 and Hsp70, respectively) and ubiquitin (Ub) were investigated in autopsy specimens from 24 adult human brains. The objectives were to verify that the milder fixation and celloidin embedding applied to those specimens preserved protein immunoreactivity in the tissue sections, even with extended intervals between death and fixation, and to determine the typical pattern of distribution of the proteins in aged human cerebellum and caudate nucleus. To achieve these objectives, the patterns of immunoreactivity in human specimens were compared with those in normal rat brain after three methods of immersion fixation: 1. 1% Formalin; 2. 10% Formalin; 3. Methacarn (a modification of Carnoy's solution). Additionally, some rats were left refrigerated, but unfixed for up to 24 h to mimic the postmortem interval that commonly occurs prior to fixation of human autopsy material. Tissues were embedded in celloidin, sectioned at 100 microns, and the celloidin dissolved to permit immunostaining. Immunoreactivity for all antigens was greatly diminished in the rat brain by fixation in 10% formalin compared to 1% formalin or methacarn. Rat and human brain tissues fixed in the latter two solutions showed similar patterns of low levels of Hsp70 immunostaining in gray matter and other areas where neuronal somata were concentrated, whereas Hsc70 immunostaining was much greater in those same areas. Little Hsc70 or Hsp70 immunoreactivity was detected in the white matter from either source, but immunoblots of human gray and white matter suggested that white matter contained more Hsc70 and Hsp70 than apparent by tissue section immunoreactivity. Ubiquitin immunostaining in rat and human brain showed the same high levels as Hsc70 in gray matter, but unlike Hsc70, was also visible in white matter. These patterns remained the same in rat brains even if fixation was delayed for 24 h. In three human brain specimens, elevated Hsc70 staining, but not Hsp70 or Ub, was found in a ring pattern similar to that described as the ischemic penumbra in experimentally induced brain ischemia. These results indicated that dilute formalin preserved Hsc/Hsp70 and Ub antigenicity well, and that the proteins had similar distributions in human and rat brains, despite the extended postmortem delay in fixation of the former. They also suggested that evidence of premortem, localized cellular metabolic stress may be preserved in the postmortem human brain by an alteration in the typical distribution of Hsc70.

Adult↗
PubMedDate not supplied

A morphologic study of the vasculature of malignant gliomas using thick celloidin sections and alkaline phosphatase stain.

The combination of 100 microm thick celloidin sections and alkaline phosphatase (AP) enzyme histochemistry of the vascular endothelium offers a greatly enhanced, 3D morphologic perspective and reveals intricate details of the vasculature of brain. A study of tumor specimens obtained at craniotomy from 6 patients with glioblastomas, 1 with anaplastic oligodendroglioma and 1 with juvenile pilocytic astrocytoma was undertaken using this technique. Five of the 6 glioblastomas, the anaplastic oligodendroglioma and the low-grade astrocytoma specimen showed uniform staining of afferent tumor blood vessels. In the glioblastomas, newly formed vessels formed dense, festooned networks at the advancing edges of the tumor. Feeding arteries entered the tumor at the junction between the edge of the tumor and adjacent brain or meninges and proceeded to form striking, coiled vessels and smaller branches. The density of both small arteries and veins was greatly increased within the tumor although there was much variability. Disordered arborization, arteriole to venous and arteriole to arteriole shunts were observed, leading to a situation where arteries connected directly to veins. In necrotic areas, there were often no AP-stained vessels. In many places, arterioles and capillaries were lacking. Numerous AP-negative veins of various sizes drained the tumors. Glomeruloid proliferations were presumptively identified as focal stain smudges or clusters of capillaries arising from nearby vascular channels. Increased alkaline phosphatase staining and/or focal new vessels were seen outside necrotic areas. The pilocytic astrocytoma and the oligodendroglioma showed less dense vascularity and no formation of the focal festoons of vessels shown by the glioblastomas. This technique may be useful for the study of tumor angiogenesis and to evaluate vascularity in experimental and human brain tumors after various therapies.

Adult↗
PubMedDate not supplied

A combined hematoxylin-eosin, alkaline phosphatase and high-resolution microradiographic study of lacunes.

Lacunar infarcts (lacunes) are small, cystic lesions of the brain in patients with hypertension and/or diabetes. In order to improve our understanding of the relationship between lacunes and their blood vessels, the alkaline phosphatase (AP) technique of microvascular staining and high-resolution microradiography were employed in a three-dimensional study of 31 lacunes from 15 hypertensive subjects. A second aim was to compare the usefulness of the techniques with that of routine hematoxylin-eosin (HE) stain employed by previous investigators. Arteries were traced throughout their course. The lesions identified included intimal hyperplasia, hyalinization and atherosclerosis with variable narrowing and occasional occlusions. The small arterioles in the lacune cavities supplied adjacent intact brain. The AP technique clearly distinguished true lacunar infarcts from dilated perivascular spaces. AP and microradiography were superior to HE in showing the three dimensional details with far fewer sections. Four different types of relationships were observed between nutrient arteries and their lacunes, indicating that patterns of vascular involvement can be elucidated in brains of subjects dying with lacunar syndromes by using special techniques such as AP. Such patterns can be correlated with clinical risk factors such as hypercholesterolemia, hypertension etc., singly and in combination. Our data suggest that the natural history of lacunar infarcts may be changing in two ways--the number of lacunes per patient may be diminishing and white matter involvement may be increasing. Possible explanations for these changes are suggested.

Aged↗