Clinical review: Prognostic value of magnetic resonance imaging in acute brain injury and coma
© BioMed Central Ltd 2007
Published: 18 October 2007
Progress in management of critically ill neurological patients has led to improved survival rates. However, severe residual neurological impairment, such as persistent coma, occurs in some survivors. This raises concerns about whether it is ethically appropriate to apply aggressive care routinely, which is also associated with burdensome long-term management costs. Adapting the management approach based on long-term neurological prognosis represents a major challenge to intensive care. Magnetic resonance imaging (MRI) can show brain lesions that are not visible by computed tomography, including early cytotoxic oedema after ischaemic stroke, diffuse axonal injury after traumatic brain injury and cortical laminar necrosis after cardiac arrest. Thus, MRI increases the accuracy of neurological diagnosis in critically ill patients. In addition, there is some evidence that MRI may have potential in terms of predicting outcome. Following a brief description of the sequences used, this review focuses on the prognostic value of MRI in patients with traumatic brain injury, anoxic/hypoxic encephalopathy and stroke. Finally, the roles played by the main anatomical structures involved in arousal and awareness are discussed and avenues for future research suggested.
Severe brain impairment, most notably persistent coma, may follow traumatic brain injury (TBI), anoxic/hypoxic encephalopathy, or stroke. Although progress in the management of critically ill neurological patients has led to improved survival rates , some survivors remain in a persistent vegetative or minimally conscious state. Up to 14% of patients with TBI remain in a persistent vegetative state after 1 year [2–4], and their medical cost has been estimated at US$1 to 7 billion per year in the USA . The possibility that aggressive medical management may lead to survival with severe brain impairment raises ethical issues. Adapting the level of medical care to long-term neurological prognosis is a major challenge for neurological intensive care. The first step in meeting this challenge is validation of tools that accurately predict long-term neurological outcome after severe cerebral insult.
Magnetic resonance imaging (MRI) is more sensitive than computed tomography at detecting stroke in the early phase, subtle abnormalities related to anoxic/hypoxic encephalopathy, and diffuse axonal injury (DAI) in patients with TBI. MRI provides valuable diagnostic information, although it is cumbersome to perform in the acute phase in comatose patients who are undergoing mechanical ventilation. Several MRI sequences and techniques have been used to explore the structures, metabolism and functions of the brain. The data supplied by these methods could be used to predict long-term neurological outcome.
In this review we briefly describe the MRI sequences and techniques used in critically ill neurological patients, and then we discuss their prognostic value in comatose patients with TBI, anoxic/hypoxic encephalopathy, or stroke. Finally, we discuss the prognostic influences of the main anatomical structures that are involved in arousal and awareness, and we suggest avenues for future research.
Magnetic resonance imaging sequences and techniques
Conventional magnetic resonance imaging
Conventional MRI provides an initial evaluation of brain lesions. However, when it is used alone it fails to predict outcome accurately.
Magnetic resonance spectroscopy
Diffusion tensor magnetic resonance imaging
Diffusion tensor imaging (DTI), derived from DWI, measures the degree and direction of water diffusion (anisotropy). Water diffusion anisotropy reflects the integrity of white matter tracts. Pathophysiological mechanisms that can alter water diffusion anisotropy include DAI, effects of intracranial hypertension and disconnection of white matter tracts.
Magnetization transfer imaging
This sequence is based on the principle that structure-bound protons undergo T1 relaxation coupling with protons in the aqueous phase. Saturated protons in macromolecules exchange longitudinal magnetization with protons in the aqueous phase, leading to a reduction in signal intensity. Magnetization transfer imaging has been found to be sensitive for detecting white matter lesions in several neurological conditions [11, 12].
Functional magnetic resonance imaging
Functional MRI may reveal foci of cerebral dysfunction in regions that look structurally intact on conventional MRI. Imaging is based on changes in the oxidative state of haemoglobin, which reflects regional brain activation. Functional MRI remains difficult to perform in critically ill unstable patients and, consequently, few teams have acquired the equipment and experience necessary to apply this technique . The few available studies conducted in comatose patients with TBI showed a correlation between prefrontal/cingulated cortical activation disturbation and cognitive impairments [14, 15]. However, functional MRI was performed in these studies at a distance from the injury.
Magnetic resonance imaging findings in specific critical neurological conditions
Traumatic brain injury
Conventional magnetic resonance imaging
Conventional magnetic resonance in traumatic brain injury
Kampfl, 1998 
Firsching, 1998 
Pierallini, 2000 
Yanagawa, 2000 
Paterakis, 2000 
Firsching, 2001 
Firsching, 2002 
Wedekind, 2002 
Carpentier, 2006 
T1, T2, FLAIR
T1, T2, T2*
MRS, T2, T2*
VS between 6 and 8 weeks
Admission in coma (duration >24 hours)
GCS score <8, coma >1 week, post-traumatic amnesia >4 weeks
Alive after 1 week
Discrepancy between CT scan and neurological status
Admission in coma (duration >24 hours)
GCS score <8
GCS score <8
Number of patients
Delay to MRI
6 to 8 weeks
60 to 90 days
1 to 39 days
17.5 ± 6.4
Outcome Variable of Interest
GOS score (2 versus 3–5) at 2, 3, 6, 9 and 12 months
Clinical assessment at 3, 6 and 12 months
GOS score at 3 months
GOS score (2–3 versus 4–5) at 6 months
Mortality and outcome at 3 months to 3 yearsb
Mortality at 6 months
GOS score, DRS >6 months (mean delay: 11.3 months)
GOS score (1–2 versus 4–5) and DRS at 18 months
Independent factor of poor outcome on multivariate analysis. Corpus callosum: OR 213.8 (95% CI 14.2 to 3213.3). Brainstem lesions OR 6.9 (95% CI 1.1 to 42.9)
Brainstem lesions: mortality rate of 44%. Bilateral brainstem lesions: mortality rate of 100%
Volume of FLAIR corpus callosum lesions correlated with first clinical evaluation. Volume of FLAIR frontal lobe lesion correlated with clinical outcome at 1 year
Number of T2 lesions correlated with GOS score. Number of T2* lesions correlated with GOS score
DAI stages correlated with outcome. No patient with good outcome had haemorrhagic DAI
Bilateral pons lesions: mortality rate of 100%. Outcome correlated with presence/absence and unilateral/bilateral brainstem lesions
Bilateral upper pontine lesion predicts mortality
More lesions of corpus callosum, basal ganglia and (para-)hippo-campal lesions in patients with brainstem lesions
Total burden of FLAIR and T2* lesions correlated with DRS and GOS score
DAI is the most common primary lesion in TBI patients [22, 23] and may be the most common cause of poor outcome [22–24]. DAI may be ischaemic or haemorrhagic [7, 8]. Ischaemic DAI is seen as a hypersignal on DWI or FLAIR, with no abnormality on the T2* sequence . The hypersignal with DWI disappears within about 2 weeks. Conversely, haemorrhagic DAI appears as a hyposignal on the T2* sequence, with normal DWI findings. It has been proposed  that DAI location could be classified into the following stages: stage 1, frontal and temporal white matter; stage 2, lobar white matter and posterior part of corpus callosum; and stage 3, dorsolateral midbrain and pons. With outcomes defined as Glasgow Outcome Scale  scores of 2 to 3 versus 4 to 5, none of the 33 patients with good outcome in another study  had haemorrhagic DAI (Table 1). DAI appears to be a major determinant of poor outcomes, although its use as an outcome predictor in the individual patient remains difficult. Whether the correlation between DAI and outcome is due to the total lesion burden or to DAI location remains debated.
In several prospective studies, lesion burden was associated with outcome irrespective of DAI location (Table 1) [17, 19, 28]. Among 40 prospectively enrolled patients with severe TBI, lesions by FLAIR and T2*-weighted sequences increased progressively with GOS score groups 1 to 2, 3, and 4 to 5 . Similar results were obtained in a study comparing 42 patients with persistent vegetative state with 38 patients who recovered consciousness .
A number of studies have focused on the value of DAI location in predicting outcome [19, 29–31]. Brainstem lesions in the pons and mesencephalon appear to be the most potent markers of poor prognosis, most notably when they are bilateral and symmetrical [18, 19, 29, 31]. In a prospective study conducted in 61 patients (Table 1) who were studied within 7 days of TBI , all patients with bilateral pontine lesions died as compared with 9% of patients with no brainstem lesions. These results were confirmed by the same group in a prospective study of 102 comatose patients  using the following four-stage grading system: grade I, lesions of the hemispheres only; grade II, unilateral lesions of the brainstem at any level with or without supratentorial lesions; grade III, bilateral lesions of the mesencephalon with or without supratentorial lesions; and grade IV, bilateral lesions of the pons with or without any of the lesions of lesser grades. Mortality increased gradually from 14% with grade I lesions to 100% with grade IV lesions. These findings were corroborated by two independent studies [19, 31] (Table 1). We recently confirmed the prognostic value of brainstem lesions in the upper pons and lower midbrain in a study of 73 patients . Bilateral pontine lesions carry a high mortality rate and predict poor neurological outcomes.
Three studies showed that corpus callosum lesions were associated with poor outcomes [19, 30, 31] (Table 1). However, these lesions may merely represent markers for severe initial injury. In addition to lesion burden, both total lesion volume and frontal lobe lesion volume on FLAIR images correlated significantly with clinical outcomes . Nevertheless, evaluating DAI lesion volume is difficult (most notably when the lesions are small), time consuming, cumbersome and subject to inter-rater variability.
The presence of severe DAI and a heavy lesion burden are associated with permanent neurological impairment. However, these factors are difficult to use in the individual patient, especially to distinguish GOS score 2 from GOS score 3. In TBI patients, brainstem lesions are easily identified by MRI. In our experience, they are associated with poor outcomes, most notably when they are posterior and bilateral. Posterior brainstem lesions in the periaqueductal grey matter are probably more relevant than anterior brainstem lesions as predictors of poor outcomes in patients with brainstem stroke  or TBI . In clinical practice, treatment limitation may deserve consideration in patients who have large bilateral lesions in the posterior part of the pons after TBI.
Magnetic resonance spectroscopy
Outcome of traumatic brain injury by magnetic resonance spectroscopy
Choe, 1995 
Ricci, 1997 
Ross, 1998 
Friedman, 1999 
Garnett, 2000 
Sinson, 2001 
Uzan, 2003 
Carpentier, 2006 
Marino, 2006 
2 weeks to 11 months
1 to 90 months
1 to 74 days
45 ± 21 days/6 months
12 days (3–35)/6.2 months (2.9–50.6)
41 days (median)
6 to 8 months
17.5 ± 6.4 days
48 to 72 hours
Number of patients
10 TBI patients versus 10 control individuals
14 VS TBI patients
25 TBI patients (12 children)
14 TBI patients versus 14 control individuals
26 patients. Early study: 21. Late study: 15. Both: 10
30 TBI patients
14 VS TBI patients versus 5 control individuals
40 TBI patients
10 TBI patients versus 10 control individuals
Grey matter voxel location
White matter voxel location
Splenium of corpus callosum
Corpus callosum, mostly white matter
Outcome variable of interest
GOS score after MRI
GOS score (1–2 versus 3–5) at follow upa
ROS at discharge and follow upb
GOS score and neuropsychological performance
GOS score, DRS at 6 months
GOS score at 3 months (1–4 versus 5)
Aware versus not aware at >6 months
GOS score (1–2 versus 4–5), DRS at 18 months
GOS score at 3 months
NAA/Cr ratio lower in TBI patients. NAA/Cr ratio correlated with GOS score
NAA/Cr ratio and NAA/Cho ratio lower, Cho/Cr ratio elevated, and NAA/Cho lower in GOS score 1–2 versus GOS 3–5
NAA levels diminished. NAA/Cr ratio correlated with outcome
NAA levels in white matter lower in TBI patients. Early NAA levels in grey matter correlated with GOS
NAA/Cr ratio lower in TBI patients. Cho/Cr elevated in TBI patients. NAA/Cr ratio correlated with GOS score and DRS
NAA/Cr ratio lower. NAA/Cr correlated with GOS score
NAA/Cr ratio lower in VS. NAA/Cr ratio lower in patients remained in VS compared with patients who regained awareness
NAA/Cr ratio correlated to GOS score and DRS. No correlation between NAA/Cr ratio and lesions burden on FLAIR or T2*
NAA/Cr and NAA/all metabolites ratios lower. La/Cr and La/all metabolites ratios increased in TBI
Compared with control individuals, TBI patients exhibited decreased NAA levels, decreased NAA/creatine ratios and increased choline levels (Table 2) in all brain regions evaluated [35–39, 41, 42]. Increased lactate levels were seldom found in TBI patients, contrary to patients with other brain injuries . The NAA/creatine ratio appeared to be the best outcome predictor. Low NAA/creatine values correlated with poor outcomes when they were located in the frontal [37, 39], frontoparietal , or occipitoparietal lobes [36, 40]; the splenium of the corpus callosum ; the thalami ; the pons ; or a voxel including the corpus callosum, the white matter, and part of the hemispheric cortex .
These studies are heterogeneous (Table 2) in terms of patient selection, time from TBI to MRS, voxel location, method of outcome assessment and timing of outcome assessment. For instance, among studies of patients with TBI, one included only patients in a vegetative state , another included patients with severe TBI  and a third excluded patients with early initial coma . These differences in patient selection may be associated with differences in severity of brain oedema and in associated hypoxia and herniation, thereby introducing bias into the interpretation of the results. MRS findings vary greatly according to time since TBI. Four phases may be distinguished: an acute phase, which lasts 24 hours after TBI; an early subacute phase, which spans from the days 1 to 13; a late subacute phase, from days 14 to 20; and a chronic phase, which starts on day 21. Only two studies included patients at the acute phase [38, 40], and only one of these included all patients before 72 hours . Two studies were conducted from the early subacute phase to the first month [17, 37] and one began inclusion in the late subacute phase but included patients up to 11 months after TBI . Four studies focused on the chronic phase; in two of these studies, patients were included 3 weeks to 6 months after TBI [36, 39] and in the other two studies they were included 2 months to 8 months after TBI [39, 42].
Although NAA/creatine ratios were similar across studies, the results should be interpreted with caution because experimental in vitro and in vivo data suggest differences in the underlying pathophysiological mechanisms and in the time course of the lesions [44–46]. To interpret these results reliably, information on NAA values over time are needed. Experiments conducted in vitro  and in vivo [45, 46] show an early NAA decrease starting within a few minutes after TBI and reaching the trough value within 48 hours. This finding explains why spectroscopic disturbances may require 48 hours for visualization . NAA levels remain stable within the first month after TBI, supporting the validity of MRS assessment during the second or third week [48, 49]. Later on, between 6 weeks and 1 year after TBI, NAA levels may decrease [9, 37]. Partial recovery of NAA levels has been suggested and may indicate recovery of mitochondrial function .
Another important factor that varied across studies was MRS voxel location (Table 2). Voxels were located in the hemisphere (the occipitoparietal, frontoparietal, or frontal lobes), corpus callosum, thalamus, or brainstem (the pons). Because whole brain analysis is time consuming, voxels are typically restricted to the areas most affected by DAI, namely the lobar white matter, corpus callosum and upper brainstem . Estimation of NAA in the whole brain may improve the prognostic value of MRS . A good compromise may be a voxel encompassing the corpus callosum, white matter and part of the hemispheric cortex .
Studies also differed in their definitions of poor and good GOS outcome groups: comparisons involved GOS score 1 to 2 versus GOS score 3 to 5 , GOS score 1 to 4 versus GOS score 5 , or GOS score 1 to 2 versus GOS score 4 to 5 . Finally, the time from TBI to outcome assessment varied from 3 to 18 months (Table 2), further complicating comparisons because neurological status may improve for up to 1 year after TBI.
Although MRS has superseded conventional MRI, the combination of these two techniques may be useful . Variations in the NAA/creatine ratio over time have not been studied in a large TBI patient population. The above-mentioned variability in NAA levels constitutes the main limitation of this technique. To overcome this limitation, repeated studies at intervals of 1 to 2 weeks are probably needed. In our experience, variations in the NAA/creatine ratio are minimal in many patients. We agree with Sinson and coworkers  that whole brain NAA estimation might improve the prognostic value of MRS. Absence of dysfunction by MRS is a valuable finding; in a patient with normal results by both conventional MRI and MRS, a poor outcome is unlikely. However, we have seen a few patients with normal conventional MRI and MRS findings who had poor outcomes, probably related to white matter damage detected as DTI abnormalities.
Diffusion tensor magnetic resonance imaging
Initial reports of DTI in TBI patients suggest that this technique may demonstrate alterations in white matter connections that are missed by conventional MRI . DTI provides information on the physiological status of fibre bundles, thus complementing the metabolic and biochemical information supplied by MRS. At present, little is known about the prognostic value of DTI in patients with TBI. DTI findings correlated with clinical status in patients with multiple sclerosis or neurodegenerative disease [52, 53]. In a mouse model of TBI, DTI parameters were significantly reduced in the injured brain, whereas conventional MRI showed no significant changes . Furthermore, changes in relative anisotropy correlated significantly with the density of stained axons on histological sections.
In a study comparing 20 TBI patients and 15 healthy control individuals, fractional anisotropy was reduced in the internal capsule and splenium of the corpus callosum and correlated with Glasgow Coma Scale score and Rankin score at discharge in the TBI patients . Similar findings have been reported in children . Anecdotal case reports of DTI abnormalities in TBI patients have been reported [57, 58]. In two patients who recovered partially after 6 years and 19 years, respectively, in a minimally conscious state, DTI disclosed increased anisotropy within the midline cerebellar white matter over an 18-month period . This anisotropy increase correlated with an increase in resting metabolism, measured using positron emission tomography, which suggests that axonal regrowth might underlie increases in anisotropy. Larger studies of DTI variations over time are needed. In our institution, comatose patients have been included in a prospective DTI study for the past 3 years. Patients with major connectivity abnormalities in both hemispheres and the brainstem were at increased risk for poor outcomes. A large multicentre prospective study is ongoing in France to assess the usefulness of combining DTI with MRS.
Magnetization transfer imaging
Magnetization transfer imaging is sensitive for detecting white matter lesions in patients with multiple sclerosis, progressive multifocal leukoencephalopathy, or wallerian degeneration [11, 12]. Preliminary results in TBI are promising [60, 61]. The magnetization transfer ratio was decreased in TBI patients [60, 61]. Out of 28 TBI patients, eight had abnormal magnetization transfer ratios, and all eight had persistent neurological deficits . In another study, however, no correlation was found between GOS score and abnormal magnetization transfer ratio .
Chronological magnetic resonance imaging findings in anoxic/hypoxic encephalopathy
Acute phase (<24 hours)
Early subacute phase (24 hours to day 13)
Late subacute phase (days 14 to 20)
Chronic phase (>21 days)
Absence of brain swelling
Diffuse atrophy and dilatation of the ventricles
Hypersignals in the cortex, in the thalamus and in the basal ganglia
Hypersignals in the cortex, in the thalamus and in the basal ganglia
Progressive disappearance of hypersignals found previously
Hypersignals in the cortex, in the thalamus and in the basal ganglia
Hypersignals in the cortex, in the thalamus and in the basal ganglia. Possible subcortical hyposignals
Hypersignals of the cortex, the thalamus, the basal ganglia and the pons
Normal or possible hypersignals of the cortex, the thalamus, the basal ganglia and the pons
Possible spontaneous subcortical and basal ganglia hypersignals
Can be normal
T1 with gadolinium enhancement
Possible subcortical enhancement suggestive of cortical laminar necrosis
Possible subcortical enhancement suggestive of cortical laminar necrosis
DWI seems more sensitive to mild hypoxic/anoxic injury in the first hours, and the hypersignal in cerebral cortex seems more precocious than in the basal ganglia
Hypersignals on both DWI and T2 become more intense, particularly in the thalamus and the basal ganglia
In some cases, appearance of diffuse white matter, abnormalities of delayed anoxic leukoencephalopathy on both DWI and T2
In some cases, hypersignals of the cortex and hyposignals in the subcortical zone on both T2 and T1, suggestive of cortical laminar necrosis
The three main series published to date included ten , eight  and six  patients. Although the small numbers of patients is a limitation, the succession of four phases was confirmed in several case reports and supported by findings of histological and animal studies [9, 12, 16, 67], indicating far greater vulnerability of grey matter to hypoxia as compared with white matter. This difference in vulnerability may explain why some brain regions are more susceptible than others to diffuse insults such as hypoxia or anoxia [2, 11, 29, 66].
A few studies recorded both MRI findings and long-term outcomes in patients with hypoxic/anoxic encephalopathy [64, 67, 69]. Diffuse cortical abnormalities by DWI in the acute or early subacute phase appear to be of unfavourable prognostic significance. Of six patients with hypoxic encephalopathy investigated by sequential MRI, the only patient who recovered a GOS score greater than 3 had hypersignals in watershed zones in the parieto-occipito-temporal cortex without cortical hypersignal by DWI. In a study of 10 patients who had suffered a cardiac arrest, FLAIR and DWI showed that eight patients had diffuse abnormalities in the cerebellum, thalamus, frontal and parietal cortices, and hippocampus . None of the patients with cortical structure abnormalities recovered beyond a severely disabled state. In another prospective study, the prognostic value of DWI was evaluated in 12 patients within 36 hours after global cerebral hypoxia . DWI findings correlated with clinical outcomes after 6 months. The three patients with short resuscitation times had a good recovery and normal DWI findings. Of the remaining nine patients, all had DWI abnormalities and developed a vegetative state. Thus, diffuse cortical hypersignals by DWI appear to predict a poor outcome. Conversely, several reports describe delayed anoxic encephalopathy with a good final outcome and resolution of MRI abnormalities. Therefore, finding diffuse hypersignals in the white matter by either DWI or T2/FLAIR weighted sequences should not lead to treatment limitation decisions.
In general, whether MRI findings can be used to guide treatment limitation decisions remains unclear. In our unit, treatment limitation is considered in patients with diffuse cortical hypersignals by DWI or cortical laminar necrosis images after prolonged cardiac arrest, provided the MRI findings are consonant with the clinical examination or electrophysiological data. In contrast, a patient with normal MRI findings after anoxia should probably be re-evaluated 1 or 2 weeks later by clinical examination, electrophysiological testing and MRI.
Few data are available on MRS findings after anoxia [70, 71]. No studies were specifically designed to assess the prognostic value of DTI in patients with anoxic/hypoxic encephalopathy. The unique ability of DTI to distinguish between white matter and grey matter, allowing separate quantitative assessment of these two tissues, should be of particular interest in anoxic/hypoxic encephalopathy.
Severe hypoglycaemia has been likened to hypoxic encephalopathy. Imaging study data in patients with hypoglycaemic coma are scant [63, 72, 73]. Interestingly, DWI abnormalities can mimic stroke in patients with hypoglycaemic coma [74, 75]. Rapid improvements in DWI and MRI abnormalities after glucose infusion were recently reported .
Ischaemic stroke causes coma in two main settings, namely malignant stroke and basilar artery occlusion. We focus on these two situations, and we do not discuss the prognostic value of MRI after stroke without coma.
In a study of 37 patients with acute middle cerebral artery infarction, early quantitative DWI findings predicted progression to malignant stroke, which occurred in 11 patients . Factors that predicted malignant stroke were as follows: size of the region with apparent diffusion coefficient (ADC) < 80% greater than 82 ml; ADC in the core of the stroke < 300 mm2/s; and relative ADC within the ADC < 80% of the lesion under 0.62. Another study evaluated 28 patients, of whom 11 experienced malignant stroke . The best predictor of malignant stroke within 14 hours of stroke onset was infarct volume by DWI greater than 145 cm3, which was 100% sensitive and 94% specific. Regarding brainstem stroke, a retrospective study of 47 patients showed that coma, which was a feature in nine patients, was associated with lesions in the posterior pons and lower midbrain . The patients who died had all bilateral brainstem lesions in this area. None of the patients with bilateral lesions survived. Although the number of patients was small in the study, the results are consonant with clinical experience that brainstem stroke with coma and large brainstem lesions has a poor outcome and that some patients who are initially comatose with limited anterior brainstem infarction eventually experience good outcomes.
DTI has been used to assess outcomes after stroke , although we are not aware of studies of MRS or DTI to predict outcomes after malignant or brainstem stroke. In a study of 12 patients with subcortical infarcts involving the posterior limb of the internal capsule, a decrease in fractional anisotropy was detected by DTI, indicating secondary degeneration of the fibre tract proximal and distal to the primary ischaemic lesion . Fibre tract degeneration occurred gradually, which might have hampered functional recovery. In patients with brainstem stroke or malignant stroke, DTI may be of considerable value for assessing fibre tract degeneration, thus predicting chances of recovery.
Ascending reticular activating system and prognosis of brain injuries
Avenues for research
Data from patients with TBI, stroke, or anoxic encephalopathy suggest that specific MRI findings may hold promise for outcome prediction. Large studies are not yet available, even in patients with TBI. Given the major ethical, human and economic issues involved, there is an urgent need for large prospective multicentre studies. Only small numbers of patients eligible for such studies are admitted to medical or surgical intensive care units, and few neurosurgical or neurological intensive care units exist; therefore, a multicentre design is essential to ensure recruitment of a sufficiently large population. In our institution, which is a neurosurgical intensive care unit in a tertiary hospital, multimodal prospective imaging by conventional MRI, MRS and DTI is performed routinely in all patients who are still comatose after 2 weeks. A multicentre study funded by the French Ministry of Health is under way.
Patients with severe brain injury, most notably those who remain comatose, generate huge health care costs. Adapting the level of medical care to the neurological outcome is a major challenge currently faced by neurological intensive care. Meeting this challenge will require the development of tools that reliably predict long-term neurological outcomes.
Most MRI studies to date were conducted in patients with TBI. By conventional imaging, presence of bilateral lesions in the dorsolateral upper brainstem appears to be the factor of greatest adverse prognostic significance. With MRS, low NAA/creatine ratio in the hemispheres and in the pons predicts a poor outcome. In anoxic/hypoxic encephalopathy, the factor of greatest adverse significance appears to be the presence of diffuse cortical abnormalities by DWI. However, data are scarcer than in the field of TBI. Finally, regarding brainstem stroke, posterior lesions appear to be associated with poor outcome.
The prognostic value of imaging studies could be improved by combining several techniques and sequences, for instance by combining several MRI sequences or by combining MRI with electrophysiological studies or clinical data. Complete destruction of arousal structures is consistently associated with poor outcome. Multimodal MRI is a promising technique that can be expected to provide accurate prediction of neurological outcome in the near future.
apparent diffusion coefficient
ascending reticular activating system
diffuse axonal injury
diffusion tensor imaging
diffusion weighted imaging
fluid-attenuated inversion recovery
Glasgow Outcome Scale
magnetic resonance imaging
magnetic resonance spectroscopy
traumatic brain injury.
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