EMERGENCY NEURORADIOLOGY - PART 5 ppt

gendie. The ability of CT to detect SAH is di- rectly related to the quantity of extravasated blood as well as to the time from the traumatic incident; the SAH can be negative if the CT scan is performed some days after the event. SAH’s can sometimes be falsely simulated in certain particularly severe cases of diffuse cere- bral oedema, in which the brain appears rela- tively hypodense in comparison to the underly- ing dura mater and neural tissue (20). Subdural hygroma A subdural hygroma is an extraaxial collec- tion of CSF caused by the extravasation of this fluid from the subarachnoid space through a traumatic tear in the arachnoid mater (Fig. 2.23). The acute form is particularly frequent in children and less so in adults (6, 23). Subacute and chronic forms can be seen following sur- gery performed to treat severe head injuries. In such cases, the hypodense subdural collection is either located in the region of the operation or alternatively on the opposite side due to an ex vacuo mechanism following the evacuation of a contralateral haematoma. The differential diagnosis includes chronic, hypodense SDH. Traumatic vascular lesions Traumatic cerebrovascular lesions are somewhat rare, but are probably less infre- quent than reported in the medical literature (3, 9, 20). In certain cases these lesions can be asymptomatic or have a clinical onset sometime after the initial traumatic incident and can therefore be overlooked on routine imaging studies in patients having undergone trauma. In other cases the presence of other craniocerebral lesions related to trauma can conceal the presence of related underlying vascular lesions, as both clinical symptoms and imaging findings may be attributed to other dominant traumatic parenchymal pathology such as DAI, intraparenchymal haematomas or extraaxial haematomas. CT is a most useful technique for identifying pa- tients with an increased risk of vascular le- sions such as those with fractures at the base of the skull extending into the bony internal carotid canal, the sphenoid bone, and the petrous pyramid of the temporal bone and the basiocciput. Of course, it should be pointed out that the presence of fractures in such sites does not necessarily indicate the presence of associated vascular lesions (7, 29). The internal carotid artery, which is the most frequently affected vessel in cranial trauma, can undergo dissection due to the forced extension and torsion of the neck or due to the direct lac- eration of the arterial wall by a skull base frac- ture; this is especially true with trauma to the region directly adjacent to the anterior clinoid processes and the bony internal carotid canal (9). In certain cases the adventitia of the carotid artery wall can remain intact and thereby de- velop a pseudo-aneurysm (3, 9, 20). Other pos- sible cerebrovascular lesions related to the trau- ma include dissections, lacerations and frank vessel occlusions, which may or may not be as- sociated with perivascular haematomas. Another pathological entity connected with brain trauma is the formation of arteriovenous fistulae. The most typical site is a fistula be- tween the internal carotid artery siphon and the cavernous venous sinus, usually a consequence of the fracture of the central skull base. In such 156 II. HEAD INJURIES Fig. 2.23 - Posttraumatic subdural hygroma. The axial CT shows a left sided frontal posttraumatic subdural hygroma. cases, one suggestive indirect sign on imaging is the CT finding of an enlarged, arterialized su- perior ophthalmic vein. CT is very accurate in demonstrating frac- tures of the base of the skull, whereas greater diagnostic sensitivity in demonstrating traumat- ic vascular lesions can be obtained with MR or MR angiography examinations (3, 20). In se- lected cases where such traumatic cerebrovas- cular lesions are suspected on the basis of non- invasive imaging studies and clinical informa- tion, selective cerebral angiography is required to clearly define the diagnosis and to suggest optimal treatment options. S ECONDARY LESIONS Internal cerebral herniation Bony and dural structures grossly subdivide the cranial cavity into functional supra- and in- fratentorial compartments. Internal cerebral herniations are a mechanical shift of the cere- bral parenchyma, cerebrospinal fluid and the attached blood vessels from one compartment to another. These alterations are the most com- mon secondary effects of expanding intracra- nial processes. Based on the site and direction of the shift, they can be divided into subfalcian, transtentorial (ascending and descending), cerebellar tonsillar and transphenoid (ascend- ing and descending) in type. Patients with in- ternal cerebral herniations are usually in com- promised clinical states that only permit the use of axial CT acquisitions, which are not the most suitable for viewing craniocaudal shifts of the cerebral parenchyma. Therefore, due attention 2.2 CT IN HEAD INJURIES 157 Fig. 2.24 - Posttraumatic cerebral swelling. The CT demon- strated diffuse posttraumatic cerebral swelling is seen with obliteration of the basal subarachnoid cisterns and superficial cortical sulci, compression of the 3 rd ventricle and reduction in size of the lateral ventricles. The midline structures are not shifted, and there are no focal haemorrhages are present. [a), b), c) axial CT]. a b c must be paid to gleaning the indirect signs of internal cerebral herniation (3, 20). Subfalcian and descending transtentorial herniations are the most common subtypes. A subfalcian herniation is defined by a shift of the cingulate gyrus across the midline, traversing below the free margin of the falx cerebri. As the shift progresses, the compressed ipsilateral cerebral ventricle becomes thinner, while the contralateral ventricle dilates as a consequence of CSF obstruction at the level of the foramen of Monro (Fig. 2.19). In addition, distal branches of the anterior cerebral artery are also shifted towards or across the midline, and, in the most severe cases these vessels can be com- pressed against the free edge of the falx cerebri; this in turn may result in secondary ischaemia or infarction due to pressure-occlusion of the pericallosal or callosomarginal arteries. Descending transtentorial herniations consist of a medial and caudal shift of the uncus and the parahippocampal gyrus of the temporal lobe beyond the free margin of the tentorium cere- belli. This results in an asymmetric appearance of the peripontine cisterns and the cerebello- pontine angle, which are widened on the side of the mass lesion due to a contralateral shift of the brainstem; the contralateral cisterns are conso- nantly narrowed by both the lateral shift as well as the downward herniation of cerebral tissue. The anterior choroid, posterior communicating and posterior cerebral arteries are also dis- placed medially and downward and can be compressed against the free edge of the tentori- um cerebelli with resulting ischaemia or infarc- tion of the occipital lobe if severe. In rare cases, compression of the perforating vessels emerging from the arterial circle of Willis can cause is- chaemia and infarction in the basal cerebral nu- clei. Other possible complications of transtento- rial herniations include periaqueductal brain- stem necrosis, brainstem haemorrhage (i.e., Duret haemorrhages) and direct contusion of the cerebral peduncle(s) due to traumatic im- pact against the free edge of the tentorium cere- belli (i.e., Kernohan’s notch) (20). Ascending transtentorial herniations are more rare, and are defined by the cranial shift of the cerebellar vermis and parts of the superi- or-medial aspects of the cerebellar hemispheres through the tentorium incisura. This in turn re- sults in compression of the superior cerebellar and superior vermian cistern and the upper fourth ventricle. If severe, hydrocephalus may develop due to the compression of the aque- duct of Sylvius. Tonsillar herniations are usually caused by an increase in mass effect within the posterior fossa, which causes a downward displacement of the cerebellar tonsils through the foramen magnum. It is estimated that up to half of all descending transtentorial herniations and ap- proximately two-thirds of ascending transten- torial herniations are associated with tonsillar herniations at some point in the evolution of the herniative process. Descending transphenoid herniations are produced by a posterior and downward (cau- dal) shift of the frontal lobe beyond the margin of the greater wing of the ipsilateral sphenoid bone, with backward displacement and com- pression of the Sylvian fissure, the middle cere- bral artery and the temporal lobe on the same side. Conversely, in ascending transphenoid herniations, the frontal lobe is pushed upwards and anteriorly, to extend above the margin of the greater wing of the sphenoid. Posttraumatic diffuse cerebral oedema Diffuse cerebral oedema with generalized swelling of the brain occurs in up to 10-20% of all severe head injuries; this is encountered more commonly in children and can be either unilateral or bilateral (Figs. 2.24, 2.25). Uni- lateral diffuse cerebral oedema is associated with ipsilateral subdural haematoma forma- tion in 85% of cases and with epidural haematoma in 9% of cases; it is an isolated finding in only 4-5% of cranial trauma pa- tients (3, 20). Despite the fact that it can de- velop in just a few hours in the most serious cases, it usually evolves over a period of 24- 48 hours. Posttraumatic diffuse cerebral oede- ma is caused by an increase in the water con- tent of the brain and/or an increase in in- travascular blood volume, both of which can 158 II. HEAD INJURIES be precipitated by a number of factors. This is a severe clinical condition and is fatal in ap- proximately 50% of cases (20). The CT pic- ture is characterized by a generalized obliter- ation of the cerebral cortical sulci and the in- tracranial subarachnoid spaces of the suprasel- lar and perimesencephalic cisterns (e.g., am- biens and quadrigeminal), and the cerebral ventricles appear thinned and compressed. The brain appears diffusely hypodense, with a loss of the distinction of the grey-white matter interface. The cerebellum is generally spared and can appear relatively hyperdense as compared to the cerebral parenchyma which is isodense. In the later stages of evolution in se- vere cases, diffuse cerebral oedema is often ac- companied by transtentorial internal cerebral herniation (3, 20, 22). Posttraumatic cerebral ischaemia and infarction The herniation of brain parenchyma across the falx cerebri and through the tentorium cerebelli is the most common cause of post- traumatic infarction. The occipital lobe is the territory most frequently affected by ischaemic events, which are usually associated with herni- ation of the temporal lobe through the tentori- al incisura, with consequent compression-oc- clusion of one or both of the posterior cerebral arteries (3, 20). The second most common area of infarction associated with cranial trauma is the vascular territory of the anterior cerebral branches contralateral to the traumatic mass le- sion, to include the pericallosal and callosomar- ginal arteries, consequent to subfalcian hernia- tion of the cingulate gyrus. More rarely, infarcts may occur in the basal ganglia due to the com- pression of the choroid, lenticulostriate and thalamoperforating arteries against the struc- tures at the base of the skull (7, 29). Another category of important secondary manifestations of brain injuries is that of post- traumatic haemorrhages related to direct injury of larger arteries and veins. The caudal shift of the upper portion of the stem in transtentorial herniations can cause a compression of the per- forating vessels in the interpeduncular cistern. This in turn causes small haemorrhagic foci, which can be confluent, in the tegmen (i.e., Duret haemorrhage), which must not be con- fused with the rarer primary haemorrhagic con- tusion lesions in the dorsolateral portion(s) of the midbrain resulting from collision of the brainstem with the free edge of the tentorium cerebelli. As an additional factor in descending transtentorial herniations, the impact of the cerebral peduncle contralateral to the traumat- ic mass lesion(s) against the free edge of the 2.2 CT IN HEAD INJURIES 159 Fig. 2.25 - Posttraumatic cerebral oedema. The CT reveals posttraumatic cerebral oedema is observed associated with dif- fuse hypodensity of the white matter and obliteration of the Sylvian and perimesencephalic cisterns, a reduction in the size of the ventricular system and small intraparenchymal right haemorrhages in the right frontal region. a b tentorium cerebelli may cause oedema, is- chaemia and/or haemorrhagic necrosis of this structure which results in focal atrophy that may take the gross form of a notch (i.e., Ker- nohan’s notch). Clinically this may result in hemiparesis ipsilateral to the side of the pri- mary traumatic effects; this is known by the term “false localizing sign” because it occurs in the peduncle contralateral to the supratentorial traumatic mass effect (20). POSTTRAUMATIC SEQUELAE The most common sequelae of severe cranial trauma include cortical atrophy, encephaloma- lacia, pneumocephalus, CSF leaks (i.e., fistu- lae), leptomeningeal cysts, cranial nerve lesions and diabetes insipidus (Tab. 2.8). Encephalomalacia is characterized by foci of cerebral parenchyma loss in the area of the con- tusion and by diffuse cortical atrophy (3, 20). Encephalomalacic foci appear on CT as hypo- dense areas, often associated with varying de- grees of dilation of the adjacent cerebral ventri- cles and overlying cortical sulci. Skull base fractures with interruption of the dura resulting in direct communication of the cranium with the paranasal sinuses, can lead to intracranial air collection(s) (i.e., pneumo- cephalus). This is easily detected using CT be- cause of the extremely low attenuation coeffi- cient of air (Figs. 2.3, 2.22) (8). Air limited to the epidural space tends to remain localized and does not vary in position with the place- ment of the head; conversely, air localized to the subdural space tends to move its principal focus with head movements (20). Subarachnoid air is typically multifocal, non-confluent, has a “bubble-like” appearance and is often localized within the cerebral sulci. Posttraumatic intra- ventricular air occurs in association with frac- tures at the base of the skull with lacerations of the dura mater. Intravascular air is only rarely observed and is usually detected only in cases of fatal trauma. CSF leaks are a consequence of fractures of the base of the skull in 80% of cases (20). Typ- ically they are frontally positioned with CSF draining via a fistula into the ethmoid or the sphenoid paranasal sinus, and in 20% of cases they are complicated by meningitis, which if untreated can in turn lead to the formation of cerebral abscess or extraaxial empyema (20). Clinical onset of a posttraumatic CSF leak usu- ally occurs within a week of the initial trauma, but can develop as late as several years after the event. High resolution coronal acquisition CT is the examination of choice to identify the as- sociated skull base fracture, although the visu- alization of the fistula is often difficult or im- possible to achieve. Positive contrast CT or MR cisternography may be required to prove the presence and pinpoint the location of the fistu- la preoperatively. Cranial fractures can later cause lepto- meningeal cysts. These cysts are typically limit- ed to children, occurring months to years after the cranial trauma. They are associated with underlying meningeal lacerations and theoreti- cally result from an interposition of meningeal tissue within the space of the fracture line of the overlying calvaria at the time of the trau- matic event. Sometimes known as an “expand- ing posttraumatic fracture”, CSF pulsations have been hypothesized to be the mechanism of cyst accumulation as well as fracture expansion. Diabetes insipidus is an infrequent sequela of cranial trauma, most commonly seen in in- fants as a result of birth trauma. Diabetes in- sipidus can be a direct result of either descend- ing transtentorial herniation causing hypothala- mic infarction or pituitary stalk transection oc- curring at the time of the traumatic event. Posttraumatic paralysis of one or more of the cranial nerves, especially the second, third, fourth and sixth nerves and the second division of the fifth cranial nerve, are typically due to cranial base fractures that involve the cav- ernous venous sinus and the apex of the orbit. The third cranial nerve can also be affected in- dividually by transtentorial herniation of the temporal lobe, whereas the fourth cranial nerve can be injured by compression against the free margin of the tentorium cerebelli during vio- lent shaking movements of the head. One final sequela to cranial trauma is hydro- cephalus, usually secondary to intraventricular 160 II. HEAD INJURIES haemorrhage or traumatic adherence of the meninges over the cerebral convexity, the basal cisterns or the aqueduct of Sylvius. This is caused by an inflammatory meningeal reaction to the effects of the trauma and the presence of blood products with consequent defective CSF resorption. CONCLUSIONS The advent of CT and its progressive tech- nological improvement have revolutionized the diagnosis and clinical management of acute cra- nial trauma patients, resulting in early accurate analysis and swift evidence-based treatment of potentially fatal head injuries. Unenhanced CT is the examination technique of choice in these cases as it is quickly accomplished, readily available and does not require ancillary studies using other imaging technologies in most cases. The spiral (helical) CT technique is princi- pally useful in those cases in which the exami- nation must be performed within an extremely limited time frame and in cases in which three- dimensional acquisition is necessary for multi- planar reconstruction of fractures of the orbit and the facial skeleton or CT angiographic studies of the intracranial vessels. Otherwise, standard CT acquisitions are preferred for their accuracy and absence of artefacts. The use of IV contrast media is restricted to those rare cases in which a CT angiographic ex- amination is needed when posttraumatic vascu- lar pathology is suspected. Intrathecal positive contrast cisternography coupled with either CT or MRI may be required to analyse the pres- ence and focus of a CSF fistula preoperatively. One important limitation of the use of CT is the difficulty in detecting small parenchymal le- sions located in the posterior fossa or at base of the skull, principally because of beam harden- ing artefacts typically present. However, this problem is of little practical significance clini- cally in the acute stage of trauma, as such pathology seldom requires surgical interven- tion. It should be noted that MRI is more sensi- tive than is CT in detecting small cortical con- tusion lesions at the grey-white matter inter- face, DAI, extracerebral haematomas (especial- ly when hypodense) and primary and second- ary brainstem lesions. However, these changes are relatively minor and do not usually demand operative therapy in the emergency time frame. On the other hand, MRI can be a useful com- plement in the acute phase of cranial trauma in patients with significant clinical findings but no or few CT observations. And finally, MRI is the technique of choice in the evaluation of the subacute and chronic phases of symptomatic head injury. REFERENCES 1. Bahner ML, Reith W, Zuna I et al: Spiral CT vs incremen- tal CT: is spiral CT superior in imaging of the brain? Eur Radiol. 8(3): 416-20, 1998. 2. Frankowski RF, Annegers JF, Whitman S: Epidemiological and descriptive studies. Part I: The descriptive epidemiology of head trauma in the United States. In: Becker DP, Poli- shock J, eds. Central Nervous System Trauma Status Report. Bethesda, MD National Institute of Health, 33-51, 1985. 3. Gentry LR: Head trauma. In: Atlas SW:Magnetic resonan- ce of the brain and spine.(2 nd ed.), Lippincott-Raven, Phi- ladelphia, pp 611-647, 1996. 4. Gentry LR: Imaging of closed head injury. Radiology 191:1-17, 1994. 5. Grumme T, Kluge W, Kretzschmar K et al: Head trauma. In: Cerebral and spinal computed tomography. Blackwell Science, Berlin pp 49-69, 1998. 6. Hymel KP, Rumack CM, Hay TC et al: Comparison of in- tracranial computed tomographic (CT) findings in pedia- tric abusive and accidental head trauma. Pediatr Radiol. 27(9):743-7, 1997. 7. Johnson MH, Lee SH: Computed tomography of acute ce- rebral trauma. Radiol Clin N Am 30:325-352, 1992. 8. Keskil S, Baykaner K, Ceviker N et al: Clinical significan- ce of acute traumatic intracranial pneumocephalus. Neu- rosurg Rev. 21(1):10-3, 1998. 9. Klufas RA, Hsu L, Patel MR: Unusual manifestations of head trauma. AJR 166:675-681, 1996. 10. Kuntz R, Skalej M, Stefanou A: Image quality of spiral CT versus conventional CT in routine brain imaging. Eur J Ra- diol. 26(3): 235-40, 1998. 11. Lanksch W, Grumme T, Kazner E: Computed tomography in head injuries Springer, Berlin, 1979. 12. Lee SH, Rao KL: Cranial computed tomography. MC Graw-Hill, New York, 1983. 13. Lee TT, Aldana PR, Kirton OC et al: Follow-up compute- rized tomography (CT) scans in moderate and severe head injuries: correlation with Glasgow Coma Scores (GCS) and complication rate. Acta Neurochir Wien. 139(11): 1042-7; discussion 1047-8, 1997. 14. Leidner B, Adiels M, Aspelin P et al: Standardized CT examination of the multitraumatized patient. Eur Radiol. 8(9):1630-8, 1998. 2.2 CT IN HEAD INJURIES 161 15. Lerner C: Detecting acute extraaxial blood with bone al- gorithm CT images. AJR 17:1707, 1998. 16. Lloyd DA, Carty H, Patterson M et al: Predictive value of skull radiography for intracranial injury in children with blunt head injury. Lancet. 22; 349(9055): 821-4, 1997. 17. Mogbo KI, Slovis TL, Canady AI et al: Appropriate ima- ging in children with skull fractures and suspicion of abu- se. Radiology. 208(2): 521-4, 1998. 18. Nagurney JT, Borczuk P, Thomas SH: Elderly patients with closed head trauma after a fall: mechanisms and out- comes. J Emerg Med. 16(5): 709-13, 1998. 19. Nagy KK, Joseph KT, Krosner SM et al: The utility of head computed tomography after minimal head injury. J Trau- ma. 46(2): 268-70, 1999. 20. Osborn A: Craniocerebral trauma. In Osborn A: Diagno- stic neuroradiology. St Louis, pp 199-247, 1994. 21. Parizel PM, Ozsarlak P, Van-Goethem JW et al: Imaging findings in diffuse axonal injury after closed head trauma. Eur Radiol. 8(6): 960-5, 1998. 22. Pellicanò G, Bartolozzi A: La TC nei traumi cranioencefa- lici. Edizioni del Centauro, Udine ,1996. 23. Petitti N, Williams DW 3 rd : CT and MR imaging of no- naccidental pediatric head trauma. Acad Radiol. 5(3): 215- 23, 1998. 24. Rhea JT, Rao PM, Novelline RA: Helical CT and three-di- mensional CT of facial and orbital injury. Radiol Clin North Am 37:489-513, 1999. 25. Shane SA, Fuchs SM: Skull fractures in infants and pre- dictors of associated intracranial injury. Pediatr Emerg Ca- re. 13(3):198-203, 1997. 26. Weisberg L., Nice C: Cerebral computed tomography. W.B. Saunders, Philadelphia, pp 321-343, 1989. 27. Wilson AJ: Gunshot injuries: what does a radiologist need to know? Radiographics 19:1358-1368, 1999. 28. Wysoki MG, Nassar CJ, Koenigsberg RA et al: Head trau- ma: CT scan interpretation by radiology residents versus staff radiologists. Radiology. 208(1):125-8, 1998. 29. Zee CS, Go JL: CT of head trauma. Neuroimaging Clin N Am. Aug; 8(3):525-39, 1998. 162 II. HEAD INJURIES 163 INTRODUCTION Trauma is the most common cause of death among children and infants, of which head in- juries account for some 60%. The mortality and morbidity rates concerning primary lesions and posttraumatic sequelae in patients with head in- juries have been considerably reduced by the advent of computed tomography (CT), which is still the examination technique of choice in the acute phase, thanks to the rapidity with which it can be performed, the ready availability of the imaging equipment and the absence of con- traindications (6, 25, 29). The drawback of this technique is the difficulty encountered in de- tecting smaller lesions, which are often located at the grey-white matter junction or in the vicin- ity of bone (e.g., temporal and frontal lobe poles, posterior fossa). In certain cases, the pa- tient’s clinical condition can be quite in contrast with the information yielded on their respective CT examinations (4, 7). Due to its greater sensitivity in detecting these types of lesions, magnetic resonance im- aging (MRI) can be used as a complement to or even a substitute for CT in some instances (5, 10, 14, 16, 18, 19, 24, 26). This said, perform- ing an MR examination in the acute phase of trauma can prove somewhat difficult and en- tails a number of risks. These drawbacks, which will be discussed briefly below, make MR a technique of secondary importance in the overall imaging evaluation of head injuries (12). DRAWBACKS Intrinsic limits The intrinsic limits of the MR technique con- sist in the absolute contraindication of examining subjects having ferromagnetic foreign bodies or electronic device implants (e.g., cardiac pace- makers). This problem becomes important in polytrauma patients, who may have acquired metal splinters from the traumatic event itself, and even more so in subjects with disorders of consciousness in whom it is not possible to re- construct an accurate medical history with regard to previous surgical or prosthetic implant proce- dures (22, 9). It is therefore necessary if possible to determine the compatibility of any metallic foreign materials that are known or suspected to be present before exposure of the patient to the strong magnetic fields inherent in MRI. Semeiological limits The semeiological limits of MRI during the acute phase of cranial trauma include its lower 2.3 MRI IN HEAD INJURIES M. Gallucci, G. Cerone, M. Caulo, A. Splendiani, R. De Amicis, C. Masciocchi sensitivity as compared to CT in identifying bony fractures of the skull, especially small ones, and acute intracranial bleeds (1, 30). Whereas in CT the densitometric value of the blood is due primarily to the quantity of the haemoglobin protein component, in MRI the intensity of the signal depends in large part on the magnetic properties of the iron contained in blood, or rather, on the electronic configura- tion that the hemoglobin iron assumes during evolution of the haemoglobin breakdown process (2). Therefore, although CT is clearly able to detect a hyperacute phase haemorrhage as an obvious area of hyperdensity due to the 164 II. HEAD INJURIES Fig. 2.26 - Hyperacute mesencephalic haemorrhage. CT (a) shows the haemorrhage as a hyperdense area in comparison with the sur- rounding brain tissue. The MRI examination conducted in the acute phase shows the haemorrhage to be isointense on T1-weighted sequences (b) and hyperintense on T2-dependent, FLAIR and turbo spin echo (TSE) (c, d) sequences because blood cannot be dis- tinguished from oedema in this phase on the basis of MRI (i.e., oxyhaemoglobin). a b c d high concentration of haemoglobin, MRI in this same phase has characteristically poor sen- sitivity, as the blood (oxyhaemoglobin) has not yet undergone metabolic transformation to a paramagnetic species (Fig. 2.26). It is only in the acute period, after approxi- mately 12 hours after the event responsible for the bleed, that the first of a series of haemoglo- bin breakdown products starts to form in amounts that will alter the MR signal. This new species, deoxyhaemoglobin, causes a shorten- ing of T2 time, and, to a greater extent T2*, thus creating local inhomogeneities in the mag- netic field generated by the MR unit. On the other hand, red blood cell lysis and the block- age of the respiratory chain in haemorrhages cause an increase in the quantity of free water and therefore an increase in T2 and proton density signal, with consequent balancing of the T2 shortening, effect and a possible con- cealment of the hypointensity linked to the presence of intracellular deoxyhaemoglobin. As the magnetic susceptibility effect and there- fore T2* shortening is directly proportionate to the square of the intensity of the static magnet- ic field, by using high field MR appliances and sequences particularly sensitive to T2* (e.g., gradient echo sequences, echo-planar sampling techniques) it is possible to resolve the problem and achieve dominant T2 shortening effects on imaging (i.e., focal reduction of the MR signal within subacute haemorrhages). Another limitation posed by MRI is the fact that it requires relatively longer examination times than does CT. Time is critical in the diag- nostic management of critical cranial trauma patients. In addition, these patients frequently are unable to consciously cooperate for the long examination times inherent in MRI, there- by often resulting in motion artefacts. Recent progress in technology has largely made it pos- sible to overcome such limits with the use of high field equipment having ultrafast acquisi- tion sequences, that allows to obtain single slice images in less than one second (9, 20) (Fig. 2.27b). However, it should be remembered that in acute head injury patients the fundamental question to be answered is whether emergency surgery is required. In almost all cases this question is answered by CT, which is efficient in depicting significant haematomas or frac- tures of surgical interest. MRI is doubtlessly more sensitive in identifying subtle haemor- 2.3 MRI IN HEAD INJURIES 165 Fig. 2.26 (cont.) - An MRI examination conducted three days later shows an area of hyperintense signal on T1-weighted se- quences (e) and hypointense signal on T2-weighted sequences as a result of haemoglobin breakdown products (i.e., deoxy- haemoglobin). [a), b), c) axial CT; d), f) axial T2-weighted MRI; e) axial T1-weighted MRI]. e f [...]... gradient-echo MR imaging at 1 .5 T Comparison with spin-echo imaging and clinical applications Radiology 168:80 3-8 07, 1988 2 Cirillo S, Simonetti L, Di Salle F et al: La RM in ematologia con particolare riguardo all’emorragia intracranica In: Trattato delle malattie del sangue Ed P Larizza pp 56 356 8 Piccin, Padova, 1990 3 Cirillo S, Simonetti L, Di Salle F et al: La RM nell’emorragia sub-aracnoidea: Parte... TRAUMA Fig 2.39 - Neuro-ocular plane a) A CT scanogram in lateral projection with indication of the neuro-ocular plane A-B = line joining the orbital roof and floor C-D = line joining the median point of A-B with the sphenoid jugum (neuro-ocular plane) b) The line that passes through the ocular lens, optic nerve, optic canal and occipital cortex in the neuro-ocular plane c) Note that the neuro-ocular plane... FLAIR e FFE del carico lesionale in pazien- II HEAD INJURIES 24 25 26 27 28 29 30 ti affetti da gravi traumi cranici chiusi Rivista di Neuroradiologia 10 :5 7-6 0, 1997 Piovan E, Beltramello A, Alessandrini F et al: La Risonanza Magnetica nei traumi sub-acuti e cronici In: Pellicanò G, Bartolozzi A (eds): La TC nei traumi cranio-encefalici Ed del Centauro, 15 3-1 71, Udine 1996 Scotti G, Pieralli S, Righi... 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The echo-planar sequence (b), which is more sensitive to T2*-weighted tissue, enables the identification of areas of hypointense signal caused by the presence of subacute haemorrhage (deoxyhaemoglobin) Motion artefacts can also be reduced by obtaining the acquisition in approximately 50 0 msec [a) T2-weighted MRI; T2*-weighted MRI] Contusions and laceration-contusions represent approximately 45% of all . Acad Radiol. 5( 3): 21 5- 23, 1998. 24. Rhea JT, Rao PM, Novelline RA: Helical CT and three-di- mensional CT of facial and orbital injury. Radiol Clin North Am 37:48 9 -5 13, 1999. 25. Shane SA, Fuchs. Lancet. 22; 349(9 055 ): 82 1-4 , 1997. 17. Mogbo KI, Slovis TL, Canady AI et al: Appropriate ima- ging in children with skull fractures and suspicion of abu- se. Radiology. 208(2): 52 1-4 , 1998. 18 temporal-insular shear-contusive focus. [a) axial CT; b) axial T2-weighted MRI]. Fig. 2.30 - Contusion-shearing injury. T2-weighted MRI se- quences highlight multiple grey-white matter junction