Thalamic Nuclei After Human Blunt Head Injury

Department of Anatomy, Division of Neuroscience and Biomedical Systems, University of Glasgow, UK.
Journal of Neuropathology and Experimental Neurology (Impact Factor: 3.8). 06/2006; 65(5):478-88. DOI: 10.1097/01.jnen.0000229241.28619.75
Source: PubMed


Paraffin-embedded blocks from the thalamus of 9 control patients, 9 moderately disabled, 12 severely disabled, and 10 vegetative head-injured patients assessed using the Glasgow Outcome Scale and identified from the Department of Neuropathology archive. Neurons, astrocytes, macrophages, and activated microglia were differentiated by Luxol fast blue/cresyl violet, GFAP, CD68, and CR3/43 staining and stereological techniques used to estimate cell number in a 28-microm-thick coronal section. Counts were made in subnuclei of the mediodorsal, lateral posterior, and ventral posterior nuclei, the intralaminar nuclei, and the related internal lamina. Neuronal loss occurred from mediodorsal parvocellularis, rostral center medial, central lateral and paracentral nuclei in moderately disabled patients; and from mediodorsal magnocellularis, caudal center medial, rhomboid, and parafascicular nuclei in severely disabled patients; and all of the above and the centre median nucleus in vegetative patients. Neuronal loss occurred primarily from cognitive and executive function nuclei, a lesser loss from somatosensory nuclei and the least loss from limbic motor nuclei. There was an increase in the number of reactive astrocytes, activated microglia, and macrophages with increasing severity of injury. The study provides novel quantitative evidence for differential neuronal loss, with survival after human head injury, from thalamic nuclei associated with different aspects of cortical activation.

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Available from: William L Maxwell
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    • "The advent and continuing development of magnetic resonance imaging (MRI) techniques has allowed visualization of changes within the structure and size of the human brain in a variety of clinical conditions but, in particular, following a patient’s earlier exposure to traumatic brain injury (TBI) [1]. In overview, long term changes are loss of the total volume of the brain, loss of the volume of both cerebral white and grey matter, loss in volume of the corpus callosum, thalamus, hippocampus, amygdala, some association, callosal and projection pathways [1,2,3,4,5] and an increased relative volume of the brain ventricular system (Figure 1) have been widely reported [6,7] up to two years after TBI [8]. "
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    ABSTRACT: Abstract: There is increasing evidence in the experimental and clinical traumatic brain injury (TBI) literature that loss of central myelinated nerve fibers continues over the chronic post-traumatic phase after injury. However, the biomechanism(s) of continued loss of axons is obscure. Stretch-injury to optic nerve fibers in adult guinea-pigs was used to test the hypothesis that damage to the myelin sheath and oligodendrocytes of the optic nerve fibers may contribute to, or facilitate, the continuance of axonal loss. Myelin dislocations occur within internodal myelin of larger axons within 1–2 h of TBI. The myelin dislocations contain elevated levels of free calcium. The volume of myelin dislocations increase with greater survival and are associated with disruption of the axonal cytoskeleton leading to secondary axotomy. Waves of Ca2+ depolarization or spreading depression extend from the initial locus injury for perhaps hundreds of microns after TBI. As astrocytes and oligodendrocytes are connected via gap junctions, it is hypothesized that spreading depression results in depolarization of central glia, disrupt axonal ionic homeostasis, injure axonal mitochondria and allow the onset of axonal degeneration throughout an increasing volume of brain tissue; and contribute toward post-traumatic continued loss of white matter.
    Full-text · Article · Jun 2013
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    • "Although many patients show slow recovery from such injuries (Katz et al., 1987; van Domburg et al., 1996), persistent fluctuations in behavioral responsive are typical (Stuss et al., 1988; Van Der Werf et al., 1999) and similar to fluctuations seen in MCS patients with non-selective patterns of brain injury. Multi-focal brain injuries are known to have a disproportionate impact on the integrity of the central thalamus (Maxwell et al., 2006) along a continuum with chronic vegetative state associating with marked neuronal loss across central thalamic nuclei (Kinney et al., 1994; Maxwell et al., 2006). Based on the evident potential for recovery after enduring disorders of consciousness in some MCS patients and the impact of non-selective brain injuries on deafferenting these critical thalamic regions, Schiff (1997) proposed a strategy for patient selection based on fluctuations in conscious behaviors and selection of specific regions of the central thalamus for electrical stimulation. "
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    ABSTRACT: The past 15 years have provided an unprecedented collection of discoveries that bear upon our scientific understanding of recovery of consciousness in the human brain following severe brain damage. Highlighted among these discoveries are unique demonstrations that patients with little or no behavioral evidence of conscious awareness may retain critical cognitive capacities and the first scientific demonstrations that some patients, with severely injured brains and very longstanding conditions of limited behavioral responsiveness, may nonetheless harbor latent capacities for significant recovery. Included among such capacities are particularly human functions of language and higher-level cognition that either spontaneously or through direct interventions may reemerge even at long time intervals or remain unrecognized. Collectively, these observations have reframed scientific inquiry and further led to important new insights into mechanisms underlying consciousness in the human brain. These studies support a model of consciousness as the emergent property of the collective behavior of widespread frontoparietal network connectivity modulated by specific forebrain circuit mechanisms. We here review these advances in measurement and the scientific and broader implications of this rapidly progressing field of research.
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    • "The dorsolateral prefrontal circuit is most frequently associated with executive functions. The anterior thalami's connections to the frontal cortex are also implicated in the pathway underlying executive functions (Sandson et al., 1991; Carrera and Bogousslavsky, 2006; Maxwell et al., 2006; Van der Werf et al., 2003; Van der Werf et al., 2000). This circuit originates on the lateral surface of the anterior frontal lobes and projects to the dorsolateral head of the caudate nucleus, which then project to the mediodorsal globus pallidus interna and rostrolateral substantia nigra pars reticula. "
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    ABSTRACT: Thalamofrontal abnormalities have been identified in chronic primary generalized epilepsy, specifically in juvenile myoclonic epilepsy (JME). These regions also underlie executive functioning, although their relationship has yet to be examined in JME. This study examined the relationship between thalamic and frontal volumes and executive function in recent-onset JME compared to healthy control subjects and recent-onset benign childhood epilepsy with centrotemporal spikes (BCECTS), a syndrome not typically associated with thalamocortical or executive dysfunction. Twenty children with recent-onset JME were compared to 51 healthy controls and 12 children with BCECTS using quantitative magnetic resonance imaging (MRI) and measures of executive abilities. Quantitative thalamic and frontal volumes were obtained through semi-automated software. Subtests from the Delis-Kaplan Executive Function System (D-KEFS) and the Behavior Rating Inventory of Executive Function (BRIEF) were used to measure executive function. Executive functions were impaired in JME subjects compared to control and BCECTS subjects. Subjects with JME had significantly smaller thalamic volumes and more frontal cerebrospinal fluid (CSF) than control and BCECTS subjects. Thalamic and frontal volumes were significantly related to executive functioning in the JME group, but not in the other two groups. Children with JME have significant executive dysfunction associated with significantly smaller thalami and more frontal CSF. Children with recent-onset BCECTS do not display the same pattern. Frontal and thalamic volumes appear to mediate the relationship between executive functioning and brain structure in JME.
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