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The neuroimaging challenges in hemispherectomy patients
Published in Mark J. Ashley, David A. Hovda, Traumatic Brain Injury, 2017
Zachary Jacokes, Avnish Bhattrai, Carinna Torgerson, Andrew Zywiec, Sumiko Abe, Andrei Irimia, Meng Law, Saman Hazany, John Darrell Van Horn
Hemispherectomy has become an established surgical treatment for carefully selected pediatric patients who suffer from intractable and pharmacologically resistant epilepsy. Recent published perioperative data report low mortality and seizure reduction rates of 50%–89% with no major trends reported with regard to postoperative complications.9 Postsurgical improvement of cognitive and behavioral functions has been observed in children following hemispherectomy and suggests plastic reorganization of the brain.24–28 For instance, changes in DTI metrics, such as fractional anisotropy and mean diffusivity, may reflect Wallerian and/or transneuronal degeneration of the WM tracts within the remaining hemisphere. In patients with acquired pathologies, postsurgical fractional anisotropy values have been noted to correlate positively with the time elapsed since the operation, indicating a greater ability for recovery in contrast to patients with congenital pathologies necessitating hemispherectomy.29 Indeed, the use of neuroimaging has provided unique insights into the initial need for and the recovery outcomes of hemispherectomy.27,30–36
Acute Brain and Somatic Injury
Published in Rolland S. Parker, Concussive Brain Trauma, 2016
Transneuronal degeneration: Neurons in a circuit interact in more ways than exchange of impulses; their metabolic equilibrium may derive from their interactions. Two types of degeneration are recognized. A severed axon may result in atrophy of skeletal muscle, though not usually postsynaptic neural effects. With cellular damage, transneuronal effects occur in the CNS and the PNS in a retrograde and orthograde direction. Neurons up to the tertiary level may become involved (Angevine, 2002).
Developing the theory of the extended amygdala with the use of the cupric-silver technique
Published in Journal of the History of the Neurosciences, 2023
Soledad de Olmos, Alfredo Lorenzo
Transneuronal degeneration occurs when a neuron that critically depends on a particular afference suddenly ceases to receive it, causing the neuron to degenerate. After successive modifications of the original Cu-Ag technique (de Olmos, 1969b), a newer version allowed these axons to be stained (Carlsen and de Olmos 1981). Therefore, when Heimer edited the book, Neuroanatomical Tract-Tracing Methods (Heimer and Robards 1981), de Olmos participated and published the 1981 version of the Cu-Ag technique (de Olmos, Ebbesson, and Heimer 1981). The effectiveness of the new 1981 Cu-Ag technique led him to detect exitotoxic-like neurodegeneration as soon as 10 minutes after inducing ischemia in an animal model.
Optical coherence tomography in the investigation of systemic neurologic disease
Published in Clinical and Experimental Optometry, 2019
Sangeetha Srinivasan, Nathan Efron
Thinning of the retinal nerve fibre layer may be a squealae to transneuronal degeneration because of the lesions in the optic radiations and/or beyond.2015 Although the exact mechanism for this neuroaxonal degeneration is not known, it has been hypothesised that there could be: (i) retrograde degeneration in the presence of mild subclinical optic neuritis; (ii) primary degeneration of ganglion cell complex and retinal nerve fibre layers due to multiple sclerosis; and (iii) degeneration due to lesions in the optic radiation via trans‐synaptic degeneration.2018