Tips and tricks for detecting diffuse axonal injury on CT and MR neuroimaging

Transcription

1 Tips and tricks for detecting diffuse axonal injury on CT and MR neuroimaging Poster No.: C-3080 Congress: ECR 2018 Type: Educational Exhibit Authors: M. Marinkic, D. Zadravec ; Zagreb/HR, Zageb/HR Keywords: Neuroradiology brain, Emergency, CNS, MR, CT, CT-High Resolution, Diagnostic procedure, Imaging sequences, Education, Acute, Trauma, Hemorrhage DOI: /ecr2018/C Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. Page 1 of 19

2 Learning objectives The purpose of this educational exhibit is to identify the radiological and pathological features of diffuse axonal injury (DAI). Page 2 of 19

3 Background DAI is a severe form of traumatic brain injury which mostly occurs in high-speed motor vehicle accidents. It is considered to be one of the most common types of primary neuronal injury in patients with severe head trauma representing approximately one half of all intra-axial traumatic lesions. Overall incidence is 200 per person. It mostly occurs in younger population and it is the most common cause of persistent vegetative state. Therefore, it is a serious medical condition representing a great tragedy for the patients and their family. DAI rarely occurs in isolation. It is usually accompanied by other traumatic brain injuries such as hemorrhagic contusion or extra-axial hematoma. ETIOLOGY DAI results from high energy trauma. Mostly from motor vehicle crashes and, in some cases, from falls and assaults. Beside the direct impact force, the inertial forces which are the result of rapid head rotational motions also play a significant role in pathogenesis. Those forces deform the white matter and lead to DAI, commonly referred to as "shearing" brain injury. BIOMECHANICS OF DAI AND AXONAL PATHOLOGY As the name implies, DAI is characterized by widespread disruption of axons as a consequence of enduring intense acceleration or deceleration forces. Those forces, caused by unrestricted head movement instantly after injury, are forcing the cerebrum to move back and forth, pivoting around the upper brainstem. The brainstem, together with the cerebellum, is held firmly fixed by the tentorium, and the falx prevents side-toside motion. Axons are stretched but do not snap from this injury. These stretching of the axons is known as "tensile elongation" of axons, and it is thought to result in damage of the axonal cytoskeleton. Subsequently, the axons start to swell. Calcium entry into damaged axons initiates further damage by the activation of proteases. Swollen axons may become disconnected and contribute to additional neuropathologic changes in brain tissue. Page 3 of 19

4 Axonal injuries can occur anywhere but are particularly common in the parasagittal parts of the brain, the corpus callosum, fornix, internal capsule, and the brain stem. Microscopic examination of the brain tissue, which can be done post-mortem, reveals the pathologic signature of DAI: a multitude of swollen and disconnected axons. Axonal swellings can be detected with hematoxylin and eosin (H&E) and silver stains 15 hours after the injury. In highly severe causes, axons are not only swollen, further mechanisms also lead to tissue tears and consequent intraparenchymal hemorrhage. Axonal swellings can take a chronic form and persist for years. Distal to the swellings, axons and myelin degenerate and gliosis develops over time. Severe DAI may cause the decrease of white matter volume, atrophy of the corpus callosum, and dilatation of the lateral ventricles. CLINICAL PRESENTATION Loss of consciousness at the moment of impact is typical and it occurs in almost all cases. In severe DAI loss of consciousness is prolonged and it leads to coma. There is a likelihood of a vegetative state or even death. As in any trauma patient it is obligatory to determinate GCS (Glasgow Coma Scale) (Table.1). Based on GCS, traumatic brain injury can be classified as mild, moderate or severe. Patients with GCS score from 13 to 15 are considered to have mild traumatic brain injury Patients with GCS score from 9 to 12 are considered to have moderate traumatic brain injury Patients with GCS score 8 or below are considered to have severe traumatic brain injury Most head trauma patients have higher GCS score and consequently, mild traumatic brain injury. Sometimes DAI can occur with milder symptoms such as symptoms of cerebral concussion. Possible symptoms, which are nonspecific symptoms of any traumatic brain injury are: disorientation or confusion headache Page 4 of 19

5 nausea or vomiting drowsiness or fatigue trouble sleeping sleeping longer than normal loss of balance or dizziness The Adams classification is commonly used to classify the severity of of DAI (Table.2). The loss of consciousness in concussion probably happens due to a functional disturbance of the reticular activating substance in the brainstem. Since DAI is rarely an isolated finding in traumatic brain injury, clinically it is hard to distinguish the symptoms from other accompanied injuries (Fig.1). It is important to understand that is difficult to diagnose DAI in the acute phase. Clinical signs and neuroimaging findings may suggest the diagnosis, but confirmation is only possible post-mortem. TREATMENT Treatments of patients with diffuse axonal injury is primary supportive care. There is no specific treatment. The main goals are prevention of secondary injuries and facilitating rehabilitation. In the acute phase secondary injuries (cerebral edema, impaired metabolism, free radicals formation, excitotoxicity) lead to increased mortality. Therefore, it is important to focus the treatment of DAI on preventing hypotension, hypoxia, cerebral edema, and elevated intracranial pressure (ICP) since those factors can facilitate further brain damage by causing low oxygen delivery. ICP (intracranial pressure) monitoring is indicated in patients with severe head injury (GCS score 8 or below). Short-term anticonvulsant treatment can be used to prevent early post-traumatic seizures. Steroids are sometimes used as part of therapy for reduction of cerebral edema. PROGNOSIS Page 5 of 19

6 In mild cases of DAI clinical abnormalities such as headache, memory and mild cognitive impairment, personality change (post-concussion syndrome) may persist for months or longer. In severe DAI a great number of patients remain unconscious and most likely, turn to persistent vegetative state. In patients who regain consciousness severe neurologic impairments are possible. For some patients, with most severe cases of DAI the outcome may be lethal. Page 6 of 19

7 Images for this section: Table 1 Table 2 Page 7 of 19

8 Fig. 1: Non-contrasted axial brain CT scan in a 23 year old patient with severe brain trauma (GCS 7) obtained on the day of accident. There are small hemorrhagic DAI lesions of deep white matter and one slightly bigger lesion at corticomedullary junction (red arrow). Other associated traumatic brain injuries are also present: subdural hematoma (yellow arrow), frontal bone fracture (green arrow), signs of brain edema (blue arrow). Page 8 of 19

9 Findings and procedure details On neuroimaging, axonal injury is seen as small focal white-matter lesions measuring from 1 to 15 mm in size (Fig.1, Fig.2, Fig.3). Traumatic microbleeds are considered to be important imaging marker for DAI. They are seen as punctate lesions at corticomedullary junction, corpus callosum, deep grey matter and brainstem. DAI is much more visible through MR (magnetic resonance) than CT (computed tomography). It is estimated that 50-80% of DAI patients have normal CT scan reading upon presentation. Therefore, brain magnetic resonance is the best imaging tool for DAI. CT Since the diagnosis of DAI in acute patient who suffered a significant head trauma is difficult to obtain clinically, using CT in the emergency settings is helpful in the identification of injuries and diagnosis. Initial CT scan can show no abnormalities or it can be positive for DAI and show small petechial hemorrhages located at the grey-white matter junction as well as in the corpus callosum and brainstem (Fig.1, Fig.2, Fig.3). Delayed brain CT usually demonstrates edema, which is a later finding associated with DAI (Fig.4). CT is particularly insensitive to non-hemorrhagic lesions which are rarely detected on CT scans (Fig.5, Fig.6). The larger and more hemorrhagic the lesion is, the easier it is to notice on the CT scan. Possible findings and lesion characteristics on non-contrasted brain CT in DAI are: Often normal (50-80%) Hemorrhagic lesions are hyperdense Non-hemorrhagic lesions are hypodense The lesions typically become more evident over the first few days as edema develops around them Although MR is more sensitive in the detection of subtle soft-tissue abnormalities, CT scanning is more available, and is therefore, usually performed as a primary, emergency neuroimaging tool in head trauma patients. Short examination time and its compatibility with life-supporting devices have made it a method of choice to evaluate head trauma patients. Page 9 of 19

10 MR Even though MR requires a longer image acquisition time and is not compatible with instruments having magnetic components, its ability to show small abnormalities in brain parenchyma has made it the best imaging tool for DAI. It is useful for assessing suspected diffuse axonal injury even in patients with entirely normal CT of the brain. Possible findings and lesion characteristics on brain MR are: Microbleeds Punctate lesions at corticomedullary junction, corpus callosum, deep gray matter, brainstem Size of lesions: up to 15 mm Morphology of lesions: punctate, round, ovoid foci; often hemorrhagic, nearly always multiple and bilateral Most common location of lesions is gray-white matter interface (67%), especially frontotemporal lobes, corpus callosum (20%) with common involvement of splenium and posterior body, brainstem, especially dorsolateral midbrain and upper pons. Involvement of corpus callosum, and particularly of the brain stem is related to poorer outcome. Less common locations of lesions are deep grey matter, internal/external capsule, tegmentum, fornix, corona radiata and cerebellar peduncles. Useful MR sequences for nonhemorrhagic lesions are FLAIR (fluid-attenuated inversion recovery) and DWI (diffusion-weighted images), and for hemorrhagic lesions SWI (susceptibility-weighted imaging) or T2* GRE (gradient echo). Nonhemorrhagic DAI lesions appear as small foci of increased signal on T2- weighted images (T2WI) and FLAIR within the white matter (Fig.6). On T1-weighted images (T1WI) they appear as subtle areas of decreased intensity. The lesions tend to be multiple and bilateral, especially in patients with severe head injury. Hemorrhagic lesions are best seen on SWI and T2* GRE imaging. On these sequences they appear as hypointense focal lesions as a result of susceptibility from blood products (Fig.7). Hemorrhagic lesions appear hyperintense on T1WI. The abnormal signal on gradient-echo images can persist for many years after the injury. That abnormal, low signal, represents hemosiderin-laden macrophages that occur adjacent to small vessels and are indicative of previous extravasation of blood. Page 10 of 19

11 Sometimes DAI lesions can show restricted diffusion with high signal intensity on DWI sequences and hypointense signal intensity on ADC map. Cytotoxic edema may be a cause of those findings, but it is believed there are other possible mechanism and causes which are contributing to increased restricted diffusion in DAI The neuroimaging can also play a significant role in determining the outcome of patients after DAI. Some studies show that the greater the number of lesions observed early after trauma, the greater the impairment of functionality after 12 months. Besides the number of lesions, the location of lesions is also a very important factor which is related to severity of patient`s symptoms and severity of trauma. Patients with the mildest forms of injury have lesions in frontal and temporal white matter, near the gray-white junction. The lesions typically involve the parasagittal regions of the frontal lobes and periventricular regions of the temporal lobes. Patients with more severe trauma have DAI in deeper white matter as well as in the corpus callosum, especially the posterior body and splenium. Patients with brain stem injuries have poor outcome, sometimes leading to death. Page 11 of 19

12 Images for this section: Fig. 1: Non-contrasted axial brain CT scan in a 23 year old patient with severe brain trauma (GCS 7) obtained on the day of accident. There are small hemorrhagic DAI lesions of deep white matter and one slightly bigger lesion at corticomedullary junction (red arrow). Other associated traumatic brain injuries are also present: subdural hematoma (yellow arrow), frontal bone fracture (green arrow), signs of brain edema (blue arrow). Page 12 of 19

13 Fig. 2: Non-contrasted axial brain CT scan in a 22 year old male patient who suffered head trauma shows multiple bilateral hemorrhagic lesions of white matter in cerebral hemispheres and brain stem typical for DAI. Page 13 of 19

14 Fig. 3: Axial non-contrasted emergency CT scan in a 28 year old male trauma patient who was involved in a motor vehicle accident. A small focal hyperintensity is seen in dorsal part of corpus callosum which was later confirmed as DAI. Page 14 of 19

15 Fig. 4: Follow-up non-contrasted axial brain CT scan in a 16 year old male patient who suffered severe brain trauma obtained 10 days after trauma. Multiple hemorrhagic DAI lesions in white matter, corpus callosum, basal ganglia and mesencephalon are surrounded with edema which is a later stage in DAI and helps to easily visualise DAI lesions on CT scans. Page 15 of 19

16 Fig. 5: A) Non-contrasted axial brain CT scan obtained 2 days after head trauma in a 34 year old male. Hardly detectable, discrete hypodense foci is seen in left internal capsule. B) Follow-up non-contrasted axial brain CT scan in a same patient obtained 2 days later (4 days after trauma occured) shows the progression oof hypodense lesion in left internal capsule which implies non-hemorrhagic DAI lesion. Fig. 6: Axial T2 and FLAIR MR scans in the same patient as in Fig.5, obtained 16 days after head trauma show hyperintensity in left internal capsule confirming nonhemorrhagic DAI lesion. Page 16 of 19

17 Fig. 7: Axial T2* GRE scan in a 18 year old patient shows hypointense punctate lesion in splenium of corpus callosi - hemorrhagic DAI lesion. Page 17 of 19

18 Conclusion Being one of the most severe brain injuries in head trauma patients, it is essential to promptly recognise and understand DAI presentation on CT and/or MR scans. Page 18 of 19

19 References Su E and Bell M, Translational Research in Traumatic Brain Injury, Boca Raton, CRC Press/Taylor and Francis Group, Vieira R de CA et al., Diffuse Axonal Injury: Epidemiology, Outcome and Associated Risk Factors, Frontiers in Neurology, vol. 7, no. 1, 2016, pp.178. Davceva N, Sivevski A and Basheska N., Traumatic Axonal Injury, A Clinical-pathological Correlation, Journal of Forensic and Legal Medicine, vol. 48, no. 5, 2017, pp Meythaler JM et al., Current Concepts: Diffuse Axonal Injury-associated Traumatic Brain Injury, Archives of Physical Medicine and Rehabilitation, vol. 82, no. 10, 2001, pp Johnson VE, Stewart W and Smith DH, Axonal Pathology in Traumatic Brain Injury, Experimental Neurology, vol. 7, no. 1, 2016, pp.178. Yousem DM and Grossman RI, Neuroradiology: The Requisites, 3rd edn, Philadelphia, Mosby Elsevier, Jing S et al., Clinical Features of DIffuse Axonal Injury, Journal of Clinical Orthopaedics and Trauma, vol. 4, no. 11, 2001, pp Osborn A et al., Diagnostic Imaging: Brain, 3rd edn., Philadelphia, PA, Elsevier, Gaillard F et al., Diffuse Axonal Injury, Radiopaedia, [website], 2017, radiopaedia.org/articles/diffuse-axonal-injury, (accessed 10 November 2017). Page 19 of 19