Recovery from electroencephalographic slowing and reduced evoked potentials after somatosensory cortical damage in cats

Glassman, Robert B.; Malamut, Barbara L.

doi:10.1016/s0091-6773(76)90688-x

Cited by 28 publications

(3 citation statements)

References 20 publications

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“…These altered CA levels following cortical injury may result from damage to CA axons, producing a shift from transmitter production to protein synthesis for repair (Ross, Joh, & Reis, 1975). Evidence for RFD after injury to the brain is also provided by several histochemical studies (Cooper, Thurlow, & Rooney, 1984;Dail, Feeney, Murray, Linn, & Boyeson, 1981;Frey & Agranoff, 1983;Pappius & Wolfe, 1983;Reinstein, Isaacson, & Dunn, 1979;Schwartz, Sharp, Gunn, & Evarts, 1976) and by studies employing electrophysiological techniques (Glassman, 1970;Glassman & Malamut, 1976;Kempinsky, 1954Kempinsky, , 1956Kempinsky, , 1958Pittman, Feeney, & Spiker, 1976).…”

Section: Discussionmentioning

confidence: 98%

The locus coeruleus and cerebral metabolism: Recovery of function after cortical injury

et al. 1985

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Cerebral metabolic effects of locus coeruleus (LC) lesion or drugs affecting LC were investigated after unilateral injury of sensorimotor cortex in rats. Sensoriomotor cortex ablation produced a widespread depression of cerebral 14C-2-deoxyglucose utilization which was reversed by amphetamine (AMP, 2 mg/kg) and worsened by haloperidol (HAL, 0.4 mg/kg). Lesion of LC alone did not affect cerebral oxidative metabolism, measured by a stain for the enzyme alphaglycerophosphate dehydrogenase (a-GPDH). Lesion of LC prior to undercut laceration of motor cortex shortened time to onset of a-GPDH cortical paling. Treatment with AMP (2 mg/kg) blocked cortical paling ofthe enzyme stain at 4 days postinjury, an effect prevented by concomitant HAL (0.3 or 0.6 mg/kg). Apomorphine (1 mg/kg) did not block cortical paling. These data parallel effects of these drugs on recovery of function. The results suggest that a metabolic "remote functional depression" (RFD) is alleviated by catecholamine activation after cortical injury, whereas onset of RFD is accelerated by LC lesions and exacerbated by catecholamine blockade.The locus coeruleus (LC) may have an important role in neuronal development and plasticity (Felton, Hallman,

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Section: Discussionmentioning

confidence: 98%

The locus coeruleus and cerebral metabolism: Recovery of function after cortical injury

et al. 1985

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“…The factors underlying recovery of brain activity after injury are incompletely understood. In part it is related to reversal of functional depression of injured cells, and restoration of signalling between interconnected structures (Glassman & Malamut, ). Neuronal activity itself is critical for cell viability and closely interacts with trophic growth factor release.…”

Section: The Mechanisms Of Hypothermic Neuroprotectionmentioning

confidence: 99%

A working model for hypothermic neuroprotection

Wassink

Davidson

Lear

et al. 2018

The Journal of Physiology

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Therapeutic hypothermia significantly improves survival without disability in near-term and full-term newborns with moderate to severe hypoxic-ischaemic encephalopathy. However, hypothermic neuroprotection is incomplete. The challenge now is to find ways to further improve outcomes. One major limitation to progress is that the specific mechanisms of hypothermia are only partly understood. Evidence supports the concept that therapeutic cooling suppresses multiple extracellular death signals, including intracellular pathways of apoptotic and necrotic cell death and inappropriate microglial activation. Thus, the optimal depth of induced hypothermia is that which effectively suppresses the cell death pathways after hypoxia-ischaemia, but without inhibiting recovery of the cellular environment. Thus mild hypothermia needs to be continued until the cell environment has recovered until it can actively support cell survival. This review highlights that key survival cues likely include the inter-related restoration of neuronal activity and growth factor release. This working model suggests that interventions that target overlapping mechanisms, such as anticonvulsants, are unlikely to materially augment hypothermic neuroprotection. We suggest that further improvements are most likely to be achieved with late interventions that maximise restoration of the normal cell environment after therapeutic hypothermia, such as recombinant human erythropoietin or stem cell therapy.

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“…In the last few decades, a wealth of new studies involving neurotransmitter assays, metabolic measures, and pharmacological agents have been designed to test the theory of diaschisis. 32,[47][48][49][50][51][52][53][54] The results of these studies have been mixed, causing debates in the literature. [55][56][57][58] Today, no one who works with clinical patients or brain-damaged laboratory animals doubts that acute brain injuries can have secondary effects.…”

Section: Current Statusmentioning

confidence: 99%

The Monakow Concept of Diaschisis

Finger¹,

Koehler²,

Jagella³

2004

Arch Neurol

147

109

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The idea that damage to one part of the nervous system can have effects at a distance was popular during the 19th century. Constantin von Monakow, MD, accepted this idea and blended it with the newly formulated neuron doctrine early in the 20th century to account for ipsilateral paralyses and recovery of function. He called his theory of neural depression caused by loss of inputs to structures tied to the damaged area diaschisis. In this article, we examine the origins of diaschisis and the goals of Monakow. Credit is given to Monakow for drawing needed attention to the dynamics of the nervous system, remote lesion effects, and recovery of function, even though the fine details or specifics of his theory have had a mixed reception.

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Recovery from electroencephalographic slowing and reduced evoked potentials after somatosensory cortical damage in cats

Cited by 28 publications

References 20 publications

The locus coeruleus and cerebral metabolism: Recovery of function after cortical injury

The locus coeruleus and cerebral metabolism: Recovery of function after cortical injury

A working model for hypothermic neuroprotection

The Monakow Concept of Diaschisis

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