Diffusion-weighted MRI during early global cerebral hypoxia: a predictor for clinical outcome?

Els, T; Kassubek, Jan; Kubalek, Ralf; Klisch, Joachim

doi:10.1111/j.1600-0404.2004.00342.x

Cited by 131 publications

(72 citation statements)

References 39 publications

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“…Diffusion Weighted Images (DWI) and corresponding low signal on apparent diffusion coefficient (ADC) map due to cytotoxic edema. 2 Restricted diffusion was seen in this case in bilateral globus pallidus (Fig. 2a & b).…”

Section: Discussionsupporting

confidence: 49%

Hypoxic–Ischemic brain injury in an adult: Magnetic Resonance Imaging findings

Maurya

Ravikumar

Bhatia

et al. 2016

Medical Journal Armed Forces India

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Section: Discussionsupporting

confidence: 49%

Hypoxic–Ischemic brain injury in an adult: Magnetic Resonance Imaging findings

Maurya

Ravikumar

Bhatia

et al. 2016

Medical Journal Armed Forces India

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“…Although the amount of brain tissue with reduced ADC values is inversely related to clinical outcome in comatose patients after cardiac arrest, 124 -127 lack of any relevant lesions on DWI or T2-weighted MRI in the acute, subacute, and chronic period have been found repeatedly. 124,125,128,129 This absence of DWI abnormalities did not exclude severe functional deficits. In a recent prospective cohort study in patients with global cerebral ischemia after cardiac arrest, 3 out of 15 patients with poor neurological outcome had no DWI abnormalities at all after 2, 7, and 14 hours, respectively.…”

mentioning

confidence: 99%

Ischemic Cerebral Damage

Hofmeijer¹,

Putten²

2012

Stroke

223

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Abstract-In the human brain, Ϸ30% of the energy is spent on synaptic transmission. Disappearance of synaptic activity is the earliest consequence of cerebral ischemia. The changes of synaptic function are generally assumed to be reversible and persistent damage is associated with membrane failure and neuronal death. However, there is overwhelming experimental evidence of isolated, but persistent, synaptic failure resulting from mild or moderate cerebral ischemia. Early failure results from presynaptic damage with impaired transmitter release. Proposed mechanisms include dysfunction of adenosine triphosphate-dependent calcium channels and a disturbed docking of glutamate-containing vesicles resulting from impaired phosphorylation. We review energy distribution among neuronal functions, focusing on energy usage of synaptic transmission. We summarize the effect of ischemia on neurotransmission and the evidence of long-lasting synaptic failure as a cause of persistent symptoms in patients with cerebral ischemia. Finally, we discuss the implications of synaptic failure in the diagnosis of cerebral ischemia, including the limited sensitivity of diffusion-weighted MRI in those cases in which damage is presumably limited to the synapses. (Stroke. 2012;43:607-615.)Key Words: brain metabolism Ⅲ cerebral ischemia Ⅲ synaptic failure T he human brain is metabolically expensive. Although it represents only 2% of the body weight, it accounts for 20% of oxygen consumption and 25% of glucose utilization. 1,2 Cerebral ischemia is a pathological condition in which blood flow to the brain is insufficient to meet these metabolic demands, causing a loss of neuronal function and viability. Ischemia may be focal if a brain artery is occluded or global, for example, after cardiac arrest.In the 1950s, the concept of perfusion thresholds was introduced. 3 It was shown that functional activity became impaired with moderately reduced perfusion (14 -35 mL/100 g/min), along with electroencephalographic and evoked potential disturbances, whereas loss of ion gradients across the plasma membrane and subsequent cell swelling occur at lower perfusion levels Ϸ4.8 to 8.4 mL/100 g/min (Figure 1). [3][4][5] In focal brain ischemia, the brain tissue that is perfused in the flow range between these 2 levels is now called the penumbra. 6 The penumbra is considered structurally intact and viable, but functionally silent. The dysfunction is, in principle, reversible by restoration of blood flow. However, if oxygen and glucose are not resupplied in time, irreversible damage occurs.Knowledge on the distribution of energy usage among different neuronal activities may contribute to understanding the successive loss of cell function and cell damage in cerebral ischemia. In the human brain, Ϸ30% of the energy is spent on synaptic transmission. 7 Disappearance of synaptic activity is the earliest consequence of cerebral ischemia 8 and failure of synaptic transmission has been proposed to account for electric silence in the penumbra. 3,6,8 -10 The changes of syna...

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“…It is well known that DWI during the early phase after cerebral hypoxia is superior to conventional MRI for detecting ischaemia and can be used as a predictor of clinical outcome [16]. However, even severe cases of HIE may have normal or subtle findings on DWI initially (Figures 7 and 14).…”

Section: Resultsmentioning

confidence: 99%

“…However, measurement of ADC values and MR examinations over time when there is difficulty making the diagnosis initially can be crucial when evaluating HIE. Early detection will save time and provide more timely guidance to the clinical team concerning overall prognosis and give the patient and family better information about recovery [16].…”

Section: Resultsmentioning

confidence: 99%

Anatomical patterns and correlated MRI findings of non-perinatal hypoxic–ischaemic encephalopathy

White¹,

Zhang²,

Helvey³

et al. 2013

BJR

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ABSTRACT. Non-perinatal hypoxic-ischaemic encephalopathy (HIE) has varying anatomical patterns dependent on the type of insult, the degree and duration of cerebral hypoxia, or presence and degree of hypoperfusion. Profound insults can affect the entire cerebral cortex or just the perirolandic cortex, the cerebellum and the deep grey matter structures. Less severe insults may affect only the watershed regions. The objective of this article is to review the anatomical patterns of non-perinatal HIEs by MRI. Non-perinatal hypoxic-ischaemic encephalopathy (HIE) can be a devastating neurological injury and prompt recognition of it can result in significant changes in patient management. HIE insults develop in varying regions of the brain depending on the severity and duration of hypoperfusion or hypo-oxygenation [1]. Brain parenchyma changes have corresponding MR signal characteristics that are often obvious but can be subtle [2]. It is important for radiologists to be aware of the variations in the appearance of HIE in order to be alert to the diagnosis in subtle cases, recognise unusual patterns and be aware of the clinical ramifications.This review shows cases of HIE beyond the perinatal period. Aetiological factors and timing of imaging findings are delineated. The cases involve the usual HIE-specific neuroanatomical locations: the cerebral cortex, cerebellum, hippocampus, basal ganglia and thalamus. In addition, cases of HIE showing damage to the cerebral white matter and limbic system are demonstrated. Also, cases that mimic the appearance of HIE are presented. It is critical for a radiologist to be aware of potentially confounding cases.

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Diffusion-weighted MRI during early global cerebral hypoxia: a predictor for clinical outcome?

Abstract: Pathological DWI during the early phase after cerebral hypoxia might be superior to cMRI as a predictor of a worse clinical outcome.

Cited by 131 publications

References 39 publications

Hypoxic–Ischemic brain injury in an adult: Magnetic Resonance Imaging findings

Hypoxic–Ischemic brain injury in an adult: Magnetic Resonance Imaging findings

Ischemic Cerebral Damage

Anatomical patterns and correlated MRI findings of non-perinatal hypoxic–ischaemic encephalopathy

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