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Biomedical subjects

B M Coull

Publications and source records attributed to B M Coull.

At least 55 records · Page 3Linked to original sources
PubMed1989

Ultrastructural and functional evidence for the survival of corticogeniculate neurons in kainic acid-lesioned lateral geniculate nucleus.

After a kainic acid lesion in the dorsal lateral geniculate nucleus of rat, retrograde axonal transport of fluorescent dyes is blocked in corticogeniculate but not in retinogeniculate neurons. This inhibition, however, can be reversed by electrical stimulation in the subcortical white matter (Woodward and Coull, Brain Research 454 (1988) 106-115). These observations suggest that retrograde axonal transport in corticogeniculate neurons is impulse-dependent and that neuronal activity in this pathway is reduced as a consequence of the lesions. To test this we examined retrograde transport of horseradish peroxidase (HRP) and cytochrome oxidase activity in the cortex of lesioned animals. Unilateral kainic acid lesions in the geniculate inhibit the retrograde transport of HRP, but this inhibition is reversed by electrical stimulation of white matter. Moreover, histochemical staining for cytochrome oxidase activity is less intense over visual cortex on the lesioned side, implying that cortical activity in intrinsic and efferent pathways is reduced as a consequence of removal of geniculate afferents. Inasmuch as the retrograde transport of HRP is dependent upon impulse activity in neurons and is thought to be mediated by synaptic vesicle recycling, these results suggest that terminals of corticogeniculate fibers survive the kainic acid lesions in the geniculate and are capable of releasing synaptic vesicles. Ultrastructural examination of lesioned geniculates strongly supports this conclusion and reveals the presence of axon terminal profiles which are filled with small round synaptic vesicles and have membrane specializations reminiscent of synaptic contacts. These terminal profiles are presumed to be of retinal and cortical origin.

Animals↗
PubMed1989

Neurological disease associated with antiphospholipid antibodies.

The Hemostasis and Thrombosis Laboratory at the Oregon Health Sciences University identified 80 patients with significantly elevated anticardiolipin antibody (ACLA) levels. We reviewed all of their available medical records and found that 25 of these patients had associated neurological symptoms or disorders. These symptoms and disorders could be grouped into four distinct clinical patterns comprising encephalopathy, multiple cerebral infarctions, migraine-like headaches, and visual abnormalities including amaurosis fugax and ischemic optic neuropathy. Cerebral ischemia best explained these neurological dysfunctions. There was no correlation between the presence or absence of neurological disease and ACLA levels, but ACLA levels were higher in patients with encephalopathy than in others with neurological involvement (p less than 0.05). How neurological dysfunction and the presence of these antiphospholipid antibodies are related remains to be clarified. Nevertheless, in patients with unexplained cerebral ischemia, establishing the presence of ACLA may have prognostic and therapeutic importance. In particular, acute immunosuppressive therapy and plasmapheresis may be useful in patients with acute ischemic encephalopathy.

Adult↗
PubMed1989

Anterior operculum syndrome.

The anterior operculum syndrome (AOS) is a well-defined clinical entity that has received little attention in the English literature. We report the clinical and CT findings in 3 cases of AOS; 2 were caused by bilateral cerebral infarctions secondary to bilateral internal carotid occlusion and 1 by the residual effects of viral encephalitis. Although there was variability in the range of deficits found in our cases, each of these patients presented with characteristic facio-pharyngo-glosso-masticatory diplegia with a dramatic automatic-voluntary movement dissociation. This syndrome deserves attention for its characteristic anatomic and prognostic implications.

Adult↗
PubMed1988

Effects of kainic acid lesions in lateral geniculate nucleus: activity dependence of retrograde axonal transport of fluorescent dyes.

Kainic acid lesions in the dorsal lateral geniculate nucleus of rats block the retrograde axonal transport of fluorescent dyes in corticogeniculate neurons without affecting the retrograde transport of D-aspartate or the orthograde transport of radiolabelled proteins in these neurons. This blocking of dye transport does not appear to be a consequence of kainic acid-induced damage to axon terminals in the geniculate since retinal ganglion cells are still able to transport dyes retrograde. A more likely explanation for these results is that fluorescent dye transport requires electrical activity in neurons, and elimination of the geniculate afferents to visual cortex reduces impulse traffic in cortical output fibers to a level below that required to support detectable dye transport. This interpretation is supported by the observation that kainic acid lesions also reduce retrograde transport of dyes in cortical neurons which project to the superior colliculus. Electrical stimulation in the subcortical white matter restores the transport of dye compounds in corticogeniculate neurons: evidence consistent with an activity-dependent mechanism of retrograde transport for these substances. These results provide evidence that axon terminals of retinal ganglion cells and corticogeniculate neurons survive in kainate-lesioned geniculates and are capable of normal neuronal function.

Amidines↗
PubMed1986

Organic solvent-induced encephalopathy in industrial painters.

Although organic solvents are essential components of an industrial economy, they are not used without risk. The relationship between excessive exposure to organic solvents and subsequent development of chronic encephalopathy has been recognized for nearly 100 years. Fifteen industrial painters who underwent evaluation in an occupational health clinic for symptoms that they related to their work were found to have a high prevalence of neurasthenic symptoms, most frequently, memory loss and personality change. Although neurologic and screening laboratory examinations showed no consistent abnormalities, psychological tests documented poor short-term memory and an array of neuropsychologic deficits. Personality profiles revealed depression, anxiety, and preoccupation with somatic concerns. These findings agree well with previous reports of "chronic painter's syndrome." Heightened awareness among industrial physicians and prospective studies to evaluate existing threshold limit values and personal protective equipment requirements are indicated.

Adult↗
PubMed1985

Late stenosis of a superficial temporal-middle cerebral artery bypass: angiographic and histological findings.

The course of a patient with an initially widely patent superficial temporal artery-middle cerebral artery (STA-MCA) bypass and an enlarged donor vessel is presented. Over 17 months, the STA became markedly stenotic. Serial angiography is correlated with autopsy histological findings showing severe atherosclerotic changes throughout the donor vessel. The potential causative factors, both medical and surgical, are discussed and the appropriate literature is reviewed. Parallels are drawn from the cardiac bypass experience. The bypass itself may have precipitated or accelerated intimal hyperplasia, which stenosed (and may have eventually occluded) the vessel. Is this phenomenon more frequent than we realize?

Cerebral Angiography↗
PubMed1984

Localization and organization of geniculocortical and corticofugal fiber tracts within the subcortical white matter.

Reciprocal connections are formed between the dorsal lateral geniculate nucleus and the striate cortex in the mammalian visual system. The question of whether fibers of these corticopetal and corticofugal pathways are segregated or intermingled within the white matter is still open. In order to examine the organization of these fiber tracts within the white matter, we have used orthograde axonal transport of radiolabelled proteins and neuronal degeneration following kainic acid lesions in the geniculocortical and corticofugal pathways of the rat. Within the white matter the two pathways reside in different layers and are segregated from one another over a significant portion of their course, geniculocortical fibers lying in the external sagittal stratum and corticofugal fibers lying in the internal sagittal stratum of the white matter. In addition, the corticofugal pathways projecting to subcortical structures appear fasciculated in both the transport and the degeneration studies suggesting that axons of cortical output neurons are organized into fiber bundles. The separation of fibers within the white matter may be of potential use for selectively stimulating afferent and efferent pathways in electrophysiological studies in situ and in cortical slice preparations. In addition, the corticofugal fiber bundles may play an important role in guiding axons therein to appropriate targets during axonogeneis and may carry the output of columnar units within visual cortex.

Animals↗
PubMed1984

Prostacyclin infusion in acute cerebral infarction.

We gave prostacyclin infusions to seven patients with acute cerebral infarction. Patients without CT evidence of infarction improved, but those who already had hypodensities on CT did not benefit. Increased platelet activity, measured by plasma beta-thromboglobulin, decreased significantly (p less than 0.01) during prostacyclin administration to normal levels, but rose again after the infusion. These results indicate that prostacyclin can be given safely in doses adequate to suppress platelet function. Our findings encouraged us to proceed with a controlled trial of its clinical efficacy.

Acute Disease↗
PubMed1982

Studies of effects of kainic acid lesions in the dorsal lateral geniculate nucleus of rat.

Kainic acid has been described as a highly specific neurotoxin that when injected locally into the nervous system destroys neuronal perikarya but spares axons of passage and terminals in the vicinity of the injection site. The effects of injection of this agent into the rat dorsal lateral geniculate nucleus on geniculocortical and corticofugal pathways have been examined. Neuronal perikarya were absent from injected geniculates, and products of neuronal degeneration were observed in the external stratum of the optic radiation and in layer IV of striate cortex. Furthermore, no visually driven units could be found in physiological recordings from ipsilateral visual cortex, and no orthograde axonal transport of radioactivity to cortex was detectable by autoradiography. These observations are consistent with the complete destruction of the geniculocortical pathway. On the other hand orthograde axonal transport appeared normal in corticogeniculate and corticotectal neurons on the injected side. In addition to silver grains appearing over the geniculate and superior colliculus label was observed over corticofugal axons in the internal stratum of the optic radiation. It is noteworthy that axons of the corticofugal pathways are clearly segregated from geniculocortical axons over a part of their course through white matter. Corticogeniculate neurons on the injected side were able to transport D-aspartate but not nuclear yellow retrogradely to cell bodies in layer VI. These results are consistent with the notion that cortical neurons terminating in and passing through the kainate lesion site survive but suggests, however, that corticogeniculate neurons may be functionally altered by these lesions.

Animals↗
PubMed1981

The release of endogenous amino acids into the vitreous of the intact eye of the albino rat: effect of light, potassium, and ouabain.

The vitreal space of the intact eye of albino rats was perfused in vivo. The concentration of several endogenous amino acids in the vitreal effluent was measured by the [3H]microdansylation procedure. GABA was never detected despite a sensitivity of the method of 0.5 pmol. In contrast to previous results obtained in pigmented rats, photic stimulation with flashing white light did not alter the release of glycine or any of the other amino acids. Potassium (60 mM) and ouabain (0.1 mM) evoked a specific release of glycine. The potassium-evoked release was blocked by magnesium suggesting a neuronal site of origin of glycine. Ouabain-evoked release was not blocked by magnesium. The results were contrasted with experiments on radiolabeled amino acid release from retinas preloaded and superfused in vitro, a condition in which glial localization of exogenous amino acids predominates.

Amino Acids↗
PubMed1978

Intermittent photic stimulation. Clinical usefulness of non-convulsive responses.

The clinical usefulness of non-convulsive responses induced by intermittent photic stimulation (IPS) was studied in 46 patients whose evaluation included both electroencephalography (EEG) and computerized cranial tomography (CT scan). Three patterns of photic responses were identified and related to background EEG activity and type of lesion seen on CT scan. An asymmetry in photic driving manifested only by a consistent amplitude difference greater than 50% was rarely associated with other EEG changes such as focal slowing or significant asymmetry in the alpha rhythm. In contrast, an asymmetry in development of the photic response correlated well with ipsilateral focal slowing and CT scan evidence of parenchymatous brain disease. Bilateral, symmetrical high amplitude single spikes evoked by individual light flashes were seen only in patients with diffuse encephalopathies. In no patient with structural brain disease as judged by CT scan was an abnormality in IPS the only EEG finding. There was also no apparent relationship between the anatomical site of a focal cerebral lesion and the type of response induced by IPS. Photic stimulation is of limited value in non-epileptic patients. Little clinical significance can be attached to nonconculsive responses in the absence of associated EEG changes which by themselves are generally more informative.

Adult↗
PubMedDate not supplied

Early recurrent embolism associated with nonvalvular atrial fibrillation: a retrospective study.

Nonvalvular atrial fibrillation (NVAF) can be a source of cardiogenic brain embolism. We retrospectively reviewed the clinical features of 56 patients with acute brain infarction and NVAF. Based on clinical criteria, 35 infarcts (63%) were classified as probably embolic, 13 infarcts (23%) as probably nonembolic and 8 infarcts (14%) as of indeterminate pathogenesis. Among the 35 patients with presumed embolic infarcts, 12 patients were immediately anticoagulated without hemorrhagic complications. Of 23 patients who did not receive immediate anticoagulation, three (13%) experienced recurrent embolism (one each to brain, kidney and leg) within 10 days of initial embolism. There were no early recurrent emboli in patients receiving immediate anticoagulation or patients in the nonembolic or indeterminate category. Five additional patients experienced probable brain or systemic emboli within the 11 days prior to the marker stroke event. Including these patients, 20% (8 of 40) of all NVAF patients who were not immediately anticoagulated experienced recurrent embolism within 11 days of the initial embolus. Early recurrent emboli are common in NVAF patients who experience embolic stroke.

Adult↗
PubMedDate not supplied

Cerebral infarction associated with lupus anticoagulants--preliminary report.

Hypercoagulability may contribute to stroke in young adults. Lupus anticoagulants (LA) were identified in six patients (4%) of 145 young adults with cerebral infarction. The clinical features of the 6 patients in this survey plus an additional patient from another institution with LA-associated stroke are presented. Four had systemic lupus erythematosus and 3 had idiopathic LA; all had mild thrombocytopenia. In 2 patients, no other conditions associated with stroke were discovered after thorough evaluation. Recurrent arterial thrombosis occurred in 4 of 7 patients during an average of two years of follow-up. Evidence suggests that inhibition of prostacyclin formation may occur with LA, promoting a prothrombotic state.

Adolescent↗
PubMedDate not supplied

Enhanced in vivo platelet activation in subtypes of ischemic stroke.

It remains uncertain whether platelet activation in ischemic stroke is contributory or secondary to brain ischemia. The efficacy of aspirin (ASA) in stroke prevention suggests that platelet activation contributes to the occurrence of stroke. On the other hand, platelet activation may be simply a generalized consequence of cerebral ischemic damage. To examine this issue, plasma levels of the platelet specific proteins beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4) were measured in fifty-eight patients with various defined types of acute ischemic strokes. beta-TG was a broader indicator of platelet activation than PF4. Compared with an age-matched control group, thromboembolic and cardioembolic stroke patients had significantly elevated beta-TG levels (p less than 0.001). Also, beta-TG levels in these stroke categories were significantly higher in samples drawn within the first week after the event than in those drawn later (p less than 0.001). In contrast, beta-TG levels in lacunar stroke patients and in most TIA patients were normal. beta-TG levels did not correlate with the volume of cerebral infarction as measured by planimetry from CT scans. Moreover, beta-TG levels in patients on chronic ASA therapy at the time of stroke did not differ from those in patients of the same diagnostic categories not taking aspirin. These data indicate that platelet activation may be important in some, but not all, subtypes of ischemic stroke and that platelet activation can occur in stroke even though the platelet cyclooxygenase pathway is suppressed.

Adult↗