MRI brain lesion patterns in patients in anoxia-induced vegetative state

Ammermann, Heidi; Kassubek, Jan; Lotze, Martín; Gut, E.; Kaps, M.; Schmidt, Joachim; Rodden, Frank A.; Grodd, Wolfgang

doi:10.1016/j.jns.2007.03.026

Cited by 31 publications

(23 citation statements)

References 24 publications

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“…Some authors have tried to explain the phenomenology of NDE by diverse physiological explanations such as anoxic brain damage (Rodin, 1980; Blackmore, 1993; Greyson, 1998; Els et al, 2004; Woerlee, 2005; Ammermann et al, 2007), hypoxia (Lempert et al, 1994), hypercapnia (Klemenc-Ketis et al, 2010), abnormal temporal lobe dysfunctions (Blanke et al, 2002, 2004; Britton and Bootzin, 2004; Blanke and Mohr, 2005; Arzy et al, 2006; Hoepner et al, 2013), administration of sedatives (Cobcroft and Forsdick, 1993; Osterman et al, 2001; Lopez et al, 2006), or sleep abnormalities (Nelson et al, 2006, 2007). However, to the best of our knowledge, previous studies on NDE after coma have not aimed at identifying differences in NDE characteristics depending on the etiology (i.e., traumatic, non-traumatic anoxic or non-traumatic other acute brain insults) of the prolonged loss of consciousness.…”

Section: Discussionmentioning

confidence: 99%

Near-death experiences in non-life-threatening events and coma of different etiologies

Charland‐Verville

Jourdan²,

Thonnard

et al. 2014

Front. Hum. Neurosci.

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Background: Near death experiences (NDEs) are increasingly being reported as a clearly identifiable physiological and psychological reality of clinical significance. However, the definition and causes of the phenomenon as well as the identification of NDE experiencers is still a matter of debate. To date, the most widely used standardized tool to identify and characterize NDEs in research is the Greyson NDE scale. Using this scale, retrospective and prospective studies have been trying to estimate their incidence in various populations but few studies have attempted to associate the experiences' intensity and content to etiology.Methods: This retrospective investigation assessed the intensity and the most frequently recounted features of self-reported NDEs after a non-life-threatening event (i.e., “NDE-like” experience) or after a pathological coma (i.e., “real NDE”) and according to the etiology of the acute brain insult. We also compared our retrospectively acquired data in anoxic coma with historical data from the published literature on prospective post-anoxic studies using the Greyson NDE scale.Results: From our 190 reports who met the criteria for NDE (i.e., Greyson NDE scale total score >7/32), intensity (i.e., Greyson NDE scale total score) and content (i.e., Greyson NDE scale features) did not differ between “NDE-like” (n = 50) and “real NDE” (n = 140) groups, nor within the “real NDE” group depending on the cause of coma (anoxic/traumatic/other). The most frequently reported feature was peacefulness (89–93%). Only 2 patients (1%) recounted a negative experience. The overall NDE core features' frequencies were higher in our retrospective anoxic cohort when compared to historical published prospective data.Conclusions: It appears that “real NDEs” after coma of different etiologies are similar to “NDE-like” experiences occurring after non-life threatening events. Subjects reporting NDEs retrospectively tend to have experienced a different content compared to the prospective experiencers.

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Section: Discussionmentioning

confidence: 99%

Near-death experiences in non-life-threatening events and coma of different etiologies

Charland‐Verville

Jourdan²,

Thonnard

et al. 2014

Front. Hum. Neurosci.

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“…Structural and functional imaging studies, including FDG PET, have illustrated widespread damage to areas that are part of cortical networks implicated in consciousness and its constituent processes, including memory, attention and language 23. Marked structural loss has been found using both conventional MRI sequences24 and voxel-based morphometry 25. In a small sample size of five patients, with IHI VS, decreased volumes were found in the inferior parietal and superior/medial frontal cortices, insula, temporal lobes, cingulum, midbrain, dorsal pons, caudate, cerebellum and thalamus 25.…”

Section: Discussionmentioning

confidence: 99%

Aetiological differences in neuroanatomy of the vegetative state: insights from diffusion tensor imaging and functional implications

Newcombe

Williams

Scoffings

et al. 2010

Journal of Neurology, Neurosurgery & Psychiatry

115

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Background An improved in vivo understanding of variations in neuropathology in the vegetative state (VS) may aid diagnosis, improve prognostication and help refine the selection of patients for particular treatment regimes. The authors have used diffusion tensor imaging (DTI) to characterise the extent and location of white matter loss in VS secondary to traumatic brain injury (TBI) and ischaemicehypoxic injury. Methods Twelve patients with VS (seven TBI, five ischaemic/hypoxic injuries) underwent MRI including DTI at a minimum of 3 months postinjury. Mean apparent diffusion coefficient, fractional anisotropy and eigenvalues were obtained for whole-brain grey and white matter, the pons, thalamus, ventral midbrain, dorsal midbrain and the corpus callosum. DTI measures of supratentorial damage were compared with a summed measure from the JFK modified Coma Recovery Scale (CRS-R) and with a three-point scale of functional magnetic resonance imaging (fMRI) response to an auditory paradigm to assess whether residual integrity of supratentorial white matter connectivity correlated with cortical processing. Results Conventional radiological approaches did not detect lesions in regions where quantitative DTI demonstrated abnormalities. There was evidence of marked, broadly similar, abnormalities in the supratentorial grey-and white-matter compartments from both aetiologies. In contrast, discordant findings were found in the infratentorial compartment, with DTI abnormalities in the brainstem confined to the TBI group. Supratentorial DTI abnormalities correlated with the CRS-R as well as responses to an fMRI paradigm that detected convert cognitive processing. Conclusions DTI may help to characterise differences in patients in VS. These findings may have implications for response to therapies, and should be taken into account in trials of interventions aimed at arousal in VS. INTRODUCTIONThe vegetative state (VS) encompasses a spectrum of patients who have emerged from coma to be awake, but show no indication of awareness. The aetiology of these clinical outcomes is varied and includes processes as disparate as traumatic brain injury (TBI), ischaemic/hypoxic injuries (IHI), intracerebral haemorrhage and infection. Modern imaging tools continue to provide more data on the neuroanatomical substrate of these conditions in vivo, and such information may be important to gain further insights into the disease process.The commonest aetiologies of VS are TBI and IHI. While it is widely accepted that both these conditions arise from either damage to the brainstem/midbrain structures and/or diffuse axonal/ cortical damage, most data come from histopathological studies. Such studies show that thalamic damage is common in the vegetative state secondary to both IHI (neuronal loss secondary to hypoxia) and TBI (retrograde thalamic degeneration and/or neuronal loss secondary to hypoxia). 2While brainstem lesions have been recognised in IHI, these appear to affect predominantly brainstem grey matter nuclei, whereas more extensiv...

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“…Despite these distinct, focal effects of gray matter damage resulting in hippocampal atrophy as a consequence of anoxia, there is evidence that cerebral hypoxia alters white matter (WM) integrity as well (see Ammermann et al, 2007;Arbelaez, Castillo, & Mukherji, 1999;Ginsberg, 1985;Prockop & Chichkova, 2007). Most research on memory impairment following hypoxic brain injury has specifically examined just the role of hippocampal damage, but the hippocampal formation has an elaborate WM afferent and efferent network of neural circuits involved in declarative memory.…”

Section: Introductionmentioning

confidence: 99%

White matter changes in patients with hypoxic amnesia

et al. 2011

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A deficit of declarative memory is a common sequela after a hypoxic episode. While the role of gray matter changes (i.e., atrophy of hippocampal formation) as mainly responsible for memory loss has been emphasized, the role of the white matter damage has so far been neglected. The present study was aimed at evaluating whether white matter damage, within the neural circuitry responsible for declarative memory functioning, is present in anoxic patients. We assessed, by means of voxel-based morphometry, the integrity of white matter regions in five patients with hypoxic amnesia. When anoxic patients were compared to healthy controls, significantly less white matter density was detected in the fornix, anterior portion of the cingulum bundle and uncinate fasciculus bilaterally. We conclude that cerebral hypoxia may alter, together with the hippocampi, the integrity of white matter fibers throughout the memory-limbic system.

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MRI brain lesion patterns in patients in anoxia-induced vegetative state

Cited by 31 publications

References 24 publications

Near-death experiences in non-life-threatening events and coma of different etiologies

Near-death experiences in non-life-threatening events and coma of different etiologies

Aetiological differences in neuroanatomy of the vegetative state: insights from diffusion tensor imaging and functional implications

White matter changes in patients with hypoxic amnesia

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