Albert B. Butler

Epidural steroid effects on nerves and meninges.

There have been encouraging reports of symptomatic improvement in patients with low back pain following injection of a mixture of a local anesthetic and a corticosteroid into the lumbar epidural space. However, there is a lack of animal or human studies which examined possible long-term effects of this combination on the exposed neural tissues. This study evaluated by both light and electron microscopy the effect of triamcinolone diacetate in vehicle and of the vehicle itself (both in 2% lidocaine) in 48 cats after percutaneous epidural injections were done at the lumbosacral space. When the animals were killed at 30 or 120 days, specimens of the spinal root, the root exit zone, and the meninges at the level of injection and level above and below were obtained. Because all of the histologic findings were found to be mild, it is concluded that local anesthetic-steroid combinations do not cause significant damage to neural tissues.

Lidocaine or thiopental for rapid control of intracranial hypertension

The effectiveness of intravenously administered lidocaine for rapid control of acute intracranial hypertension was compared to the effectiveness of thiopental in 20 patients with brain tumors undergoing craniotomy. Despite normal radial arterial and intracranial pressures (ICP) after induction of N2O-O2-morphine anesthesia, mean ICP increased from 13.8 torr ± 1.5 SE to 31 torr ± 2.3 SE (p < 0.001) in response to application of a pin-holder or scalp incision. To treat the elevated ICP a bolus injection of lidocaine, 1.5 mg/kg IV, was given to 10 patients, whereas the other 10 received thiopental, 3 mg/kg IV. Lidocaine reduced ICP 15.7 torr ± 5.6 SE (p < 0.025) but did not significantly affect mean arterial pressure. In contrast, thiopental lowered ICP 18.4 torr ± 9.6 SE (p < 0.02) and also lowered mean arterial pressure by 26.1 torr ± 9.6 SE (p < 0.025). Mean time for injection of medication to ICP nadir was 66 seconds ± 10 SE after lidocaine versus 48 seconds ± 9 SE after thiopental (p > 0.20). It is concluded that lidocaine is as effective as thiopental for rapid reduction of intraoperative intracranial hypertension but that it causes less cardiovascular depression. Lidocaine may be of particular benefit to patients with both intracranial hypertension and marginal circulatory function.

Pigmented Ganglioneuroblastoma: Relation of Melanin and Lipofuscin to Schwannomas and Other Tumors of Neural Crest Origin

An unusual case of ganglioneuroblastoma containing melanin is presented. Electron microscopy revealed various stages of development of melanosomes in neoplastic cells of Schwann, the first direct demonstration in human material that these cells are melanogenic. The frequent occurrence of neuromelanin in autonomic ganglia and in ganglioneuromas is interpreted as the presence of altered lipofuscin. Review of ultrastructural and other observations indicates a relation between various pigmented tumors, the cell of Schwann, and other cells arising from the neural crest.

Haematoma following epidural anaesthesia

SummaryA case is presented of a 70-year-old man who developed progressive quadriplegia associated with epidural catheterization while on anticoagulation therapy. At operation a large liquid epidural haematoma was found extending from c-3 to l-2. Essentially no recovery of function was noted to time of death. If epidural anaesthesia is to be used in anticoagulated patients, there must be recognition of the signs of onset of neurological complications so that surgical therapy is instituted immediately rather than after a delay of several hours.RéSuméOn cite le cas ďun homme de 70 ans qui a présenté une quadriplégie progressive au cours ďun cathétérisme épidural alors que ce malade était soumis à un traite-ment anticoagulant. A ľopération on a trouvé un hématôme liquide considérable qui s’étendait de c-3 à l-2. On n’a noté aucun retour de fonction jusqu’à la mort du patient.Si on doit utiliser ľanesthésie épidurale chez les malades soumis aux anticoagulants, il faut noter précocement les signes de complications neurologiques afin que le traitement chirurgical soit pratiqué immédiatement plutôt qu’aprés un délai de plusieurs heures.

Neuronal compartmentation of ionic cobalt in rat cerebral cortex during initiation of epileptiform activity

Abstract An understanding of the mechanisms responsible for chronic epileptiform discharge induced by topical application of metallic cobalt to the cerebral cortex of the rat has been complicated by the progressive inflammation and necrosis of cortical tissue. In this study, ionic cobalt was transferred from a pipette on the pial surface into rat sensorimotor isocortex at a rate of 4 μg/min using an iontophoretic current of 3 μamp. Bilateral discharges of high voltage associated with brief bursts of ictal spike and polyspike activity were observed after transfer of 100 μg of cobalt. No histologic evidence of tissue damage was found by light microscopy. Quantitative and qualitative histochemical analysis revealed that cobalt was confined to the upper three cortical layers, occupying a circular area 1 mm in diameter on the pial surface. Although 75% of the heavy metal was found in layer I, neurons and their processes were intensely stained in layers II, and III. Hence, epileptiform discharge originated from neuronal aggregates which have a selective affinity for ionic cobalt and occupy a focal site in upper layers of sensorimotor cortex.

Adult‐onset GM2 gangliosidosis Seizures, dementia, and normal pressure hydrocephalus associated with glycolipid storage in the brain and arachnoid granulation

Ultrastructural and biochemical studies were performed on biopsy and postmortem tissue from a 22-year-old woman with generalized seizures and intellectual and behavioral deterioration. Her symptoms began at age 18 and, during the last year of life, normal-pressure hydrocephalus was demonstrated. Abnormal accumulation of granular periodic acid-Schiff (PAS)-positive material was found in the cytoplasm of cells of both brain and spleen. Numerous membrane-bound, multilamellar cytoplasmic inclusions were seen in cells of the brain, spleen, and arachnoid granulation. Tissue concentrations of lipid-bound sialic acid were 38 percent greater than age-matched control specimens. A marked increase of only the GM2 ganglioside was demonstrated by thin-layer chromatography. An eightfold increase in the quantity of GM2 ganglioside was found in the cerebral cortex. Total hexosaminidase activity was increased 85 percent, associated with an increase in the activity of both hexosaininidase A and B, resembling an adult onset form of the “AB variant” of GM2 gangliosidosis.

Focal alteration of dendrites and astrocytes in rat cerebral cortex during initiation of cobalt-induced epileptiform activity

Abstract The epileptic focus induced by pial surface iontophoresis of cobalt is exquisitely confined to the upper three laminae of sensorimotor cortex, occupying a tissue volume of 130 mm3 showing no light microscopic evidence of injury to neural cells. At the time of initiation of epileptiform discharge, ultrastructural cytopathology is relatively confined to dendrites and astrocytes, which are severely distended in association with dispersion of their organelles. Neuronal perikarya, axons, synaptic terminals, and blood vessels are relatively unaffected, and no alteration of fine structure is seen in lower cortical layers. Ionic cobalt induces a major disturbance of cation homeostasis in neural aggregates of cerebral cortex, manifested by cytopathologic effects during the initiation of epileptiform discharge, which are relatively confined to the intracellular compartment of dendrites and astrocytes.

Cytochemical affinity of pyramidal cell dendrites for divalent cobalt during initiation and calcium-induced blockade of epileptiform discharge

Abstract The epileptic focus induced by pial surface iontophoresis of 100 μg divalent cobalt is confined to 130 mm 3 of supragranular ioscortex and contains aggregates of pyramidal neurons which are selectively impregnated by the heavy metal. At the time of initiation of epileptiform discharge, neuropathologic change is evident only at the ultrastructural level of resolution, manifested by severe swelling of pyramidal cell dendrites in the zone of cobalt deposition. When calcium and cobalt are simultaneously iontophoresed, epileptiform discharge and Golgi-like staining of pyramidal neurons does not occur, despite flooding of the cortical site with free or loosely bound cobalt complexes that can be completely removed by glutaraldehyde perfusion. In contrast, when perfusion-fixation is carried out at the initiation of cobalt-induced epileptiform discharge, the heavy metal can readily be identified within pyramidal cell dendrites as insoluble complexes which are tightly bound to cytoplasmic organelles. Based on these observations we suggest that cobalt-induced epileptiform discharge may result from a disturbance in calcium homeostasis which is triggered by high-affinity binding of the heavy metal within the cytoplasmic compartment of pyramidal cell dendrites.

An improved design of the pneumatic counter-pressure trousers

Inflation of the circumferential pneumatic counter-pressure trousers was associated with the development of hemiparesis in a multiple trauma patient. We attribute this complication to the marked movement of the spinal cord that results from inflation of the circumferential abdominal compartment of the trousers. The design of the circumferential pneumatic counter-pressure trousers was recently modified so that the inflation portion of the abdominal compartment was restricted to the anterior portion of the abdomen. Inflation of the abdominal compartment of the modified trousers resulted in considerably less movement of the spine than with the trousers having the circumferential abdominal compartment.

Pre-hospital treatment of the spinal cord patient

Abstract The aims of emergency management of the spinal cord patient are to preserve maximal neurologic function and to assure that the emergency care will not expose the individual to additional neurologic injury. All health care personnel involved in the pre-hospital phase of the emergency medical system must be trained to recognize the mechanisms that produce spinal cord injuries and to initiate appropriate treatment. The guidelines for care of these patients are outlined in this paper.