NEURORADIOLOGIA DE EMERGENCIA

Frannk Christian Veggro Rios

NEURORADIOLOGIA DE EMERGENCIA

Frannk Christian Veggro Rios

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Abstract
AI

This text discusses the role of neuroradiology in emergency situations, particularly focusing on cerebrovascular emergencies like stroke. It emphasizes the importance of timely imaging to differentiate between ischaemic and haemorrhagic events. The chapter highlights the necessity for neuroradiologists to provide comprehensive morphological and functional information to aid in acute clinical decision-making, especially with the advent of fibrinolytic treatments that enhance the potential for effective interventions.

Figures (500)

Fig. 1.1 - Evolution over time of certain aspects of CT semeiotics: density, CE and mass effect of the ischaemic lesion. The site of the lesion has considerable impor- tance in diagnosis as it reflects a vascular blood supply territory (Fig. 1.2). One or more large ar- terial vessel territories can be partially or totally affected (depending in part on the efficiency of any collateral circulation present) (Figs. 1.3, 1.4, 1.5, 1.6, 1.7); alternatively a reduction of cardiac output can affect the border zones between the various vascular territories or between the deep and superficial districts of the same territory (the so-called “watershed” areas), or the end point of a vascular territory (the so-called “last mea- toms depends on both its age and site and can therefore only be held responsible for symp- toms in progress that are in keeping; if this is not the case it must merely be considered as an incidental finding, expression of the same stroke-causing cerebrovascular pathology (18). Regardless of clinical criteria, there are a num- ber of semeiotic CT findings to be considered in order to identify the nature of a given ischae- mic lesion, namely: 1) site and morphology, 2) evolution of lesion density, 3) presence of mass effect, and, 4) enhancement following endova- scular injection of contrast agents (i.e., pattern of contrast enhancement, CE) (Fig. 1.1).

Fig. 1.3 - Infarct of the middle cerebral artery territory; a-b) partial infarct with involvement of the superficial left district only; c-d) complete infarct on the left with mass effect on the adjacent lateral ventricle, which appears compressed; on the right, other smal er ischaemic hypodensities can be seen.

Fig. 1.4 - Partial infarct of the left anterior cerebral artery ter- ritory.

Fig. 1.5 - Infarct in the territories of a) the right posterior and b) bilateral cerebral arteries.

Fig. 1.7 - Vast infarct of the right anterior, middle and posteri- or cerebral artery territories.

Fig. 1.6 - Infarct of the right anterior and middle cerebral ar- tery territory, with clear mass effect on the shifted midline structures contralaterally.

Fig. 1.9 - Ischaemic lesion at the head of the left caudate nu- cleus; there is also a lacunar infarct of the contralateral external capsule. the main alteration is best described as cyto- toxic oedema represented by the shift of water in neurons. Because this is a relatively modest change, the CT in this stage is usually negative. In this phase, the clinical and CT findings may not agree. In this early stage, despite the fact that the patient may present with complete he- miplegia and unconsciousness, the CT scan of- ten remains normal (Fig. 1.13a). However, with the passage of time, the CT becomes positive.

Fig. 1.10 - Infarct in the vertebrobasilar territory. Large, non-homogeneous hypodense area involving the brain- stem, the anterior and external faces of the brain hemispheres as well as the medial and posterior faces of the temporal lobes. The hyperdensity is associated as with thrombosis of the basi- lar stem (b) and the ectasia of the supratentorial ventricles (c).

Fig. 1.11 - Infarcts in the posterior fossa and in particular in the pons (a), midbrain (b) and left cerebral hemisphere (a-b).

Fig. 1.12 - Thalamic infarcts: on the left (a) and bilaterally (b).

Fig. 1.14 - a) Thrombosis of the left middle cerebral artery (ar- row head). b-c) CT check shortly after onset: ischaemic lesion in the corresponding vascular territory. sceptible to brain haemorrhages if such treat-

Fig. 1.15 - Ischaemic lesion of the lenticular nucleus (15 days from clinical onset) with nodular and homogeneous CE. a) direct examination: small hypodense lacunar area in left thal- amic location; b) examination after contrast medium administration: marked CE in the right putamen.

Fig. 1.16 - Widespread infarct lesion in the left middle cerebral artery territory, with non-homogeneous CE: a) direct examina- tion; b) examination after contrast medium administration.

Fig. 1.17 - Right parietal-occipital infarct with gyral enhance- ment: a) direct examination; b) examination after contrast medium administration.

Fig. 1.19 - Ischaemic lesion of the right capsulothalamic area on direct examination (a); lesion visibility is reduced after contrast medium administration (b).

Fig. 1.18 - Fogging effect of an ischaemic lesion in the left frontal region (12 days from clinical onset); a) the direct exam- ination is negative; b) CE of the lesion.

Fig. 1.20 - Multiple infarcts in the right basal ganglia region. Haemorrhagic arterial infarcts

Fig. 1.21 - Infarct of the right hemisphere with hyperdense haemorrhagic component (a); in b) massive and non-homoge- neous impregnation of the ischaemic-haemorrhagic region.

appear as non-contrasted areas: the so-called rect and indirect signs of dural venous sinus occlusion. The former appear as small hyper- densities within the intravenous space (Fig. 1.22a). Following bolus contrast medium infu- sion, dural venous sinus thromboses generally appear as non-contrasted areas: the so-called

tern of evolution over time and the clinical fin- dings. With infarcts, the mass effect can be mo- dest and subsides within 3 weeks; a late appea- rance of ipsilateral ventricular enlargement and cortical atrophic alterations can also be fre- quently observed in cases of ischaemia. In the case of neoplastic pathology, on the other hand, vasogenic oedema is confined to the white mat- ter only and gradually spreads over time. Mo- reover, in tumours that show some degree of contrast enhancement, non-homogeneous pe- ripheral enhancement or a “ring enhancement” can be observed, which is often not continuous but is markedly irregular. At equal lesion volu-

Fig. 1.24 - Modified from (12). 445° hem’ ~ AVAIL 11Uili Vic). This diagram shows the different percentages of intra- parenchymal haemorrhage distribution: 88% affect the cere- bral hemispheres (75% the paranuclear structures and 13% the white matter); 8% the cerebellum and 4% the brainstem. Deep-seated haemorrhages are included inside the sector of the circle (delimited by the corpus callosum above, the external capsule to the side and the brainstem below). Superficial intra- parenchymal haemorrhages develop outside this boundary. So- called “advanced” haemorrhages originate from the basal gan- glia and spread through the adjacent white matter, crossing this peripheral border.

Fig. 1.25 - The presence of fluid levels is not rare (blood levels stratify in the sloping part). In (a) a large putaminal haematoma presents with a deep, more recent and compact component and another, superficial one characterized by a clear fluid-fluid lev- el (arrowhead). A level can also be observed in the irregular and widespread multifocal intraparenchymal haemorrhage of a pa- tient treated with anticoagulants for a heart attack (b). cause of its relatively long scanning times. These extended examination times often make it inappropriate for use in emergency situa- tions, as these patients are not always able to re- main immobile, and continuous clinical checks are required is such cases. Moreover, on the few occasions in which it is used, the MRI signal of the haemorrhagic focus is not usually sufficient

Fig. 1.26 - Relations between CT and MR. A recent haematoma affects the left paramidline portion of the cerebellum (a). It is not subject to surgical removal (because it does not cause a «narrow» posterior fossa). It is checked one week later using MR (b), here represented in a coronal T1 weighted spin-echo sequence. MR is superior during the sub- acute phase as it better documents haemoglobin breakdown products; in particular around the posterior fossa, due to the absence of artefacts from the cranial theca that are inevitable with CT; in each phase and position due to its superior (three dimensional) spatial localization (7).

Fig. 1.27 - IPH caused by the rupture of a cavernous angioma. In this 22 year-old female, a localized haemorrhagic lesion af- fects the rear arm of the internal capsula (a). With its various sequences (in b it is represented by a PD-weighted SE se- quence), MR demonstrates that it is consequential to the rup- ture of a cavernous angioma.

Fig. 1.28 - Large parenchymal bleed in a chronic alcoholic, with more recent, irregular hyperdense foci, alternated with areas of widespread colliquation in the white matter. The concomitance of cerebral atrophy and the somewhat limited «mass effect» caused by the lesion should also be noted.

Fig. 1.29 - Thalamic haematomas. In (a) thalamic haematoma with limited extent, resolved by conservative treatment alone (note the hypodense wedge- shaped lesion in contralateral parietal location, outcome of a previous ischaemic accident). In (b) a coarser haematoma with marked mass effect (deformation of the 3" ventricle) and in- traventricular inundation with fatal outcome. mesogliomas, angioblastic meningiomas and hy- pophyseal adenomas.

Fig. 1.30 - A «globous-midline» IPH (2), with dimensions (2.5 cm) larger than those usually observed for such formations, which completely obliterates the putamen (compare delin- eation with that of the healthy contralateral). The peripheral crown-shaped hypodensity is also larger than normal. dtls pidotita AL 45° LSU). IPH is also commonly observed in chronic al- coholics, being caused by a number of different pathogenic factors, especially the frequent falls to which such subjects are prone due to im- paired coordination; clotting disorders, most commonly that of reduced platelet function; and cerebral atrophy that exposes brain surface ves- sels and bridging vessels (i-e., from brain surface to parietal dura mater) to greater risk of trau- matic injury. Bleeding can be quite widespread, and usually originates in the subcortical white

Fig. 1.31 - Two examples of putaminal haematomas spread to the external capsule, with the classic elongated shape in an an- terior-posterior direction. That on the right (a) is smaller and surrounded by a clearer hypodense border. These forms ac- count for 11% of all putaminal IPH’s and usually have a good prognosis. matter. For this reason the haemorrhage can thereby be differentiated from more serious post-traumatic contusive haemorrhage, which tend to be smaller and often multiple, and occu- py a more superficial position (Fig. 1.28). Due to the accompanying atrophy, even when extreme- ly widespread, the haemorrhaging gives less sig- nificant mass effect than might be expected in other forms of haemorrhage with similar dimen-

Fig. 1.34 - Recent, voluminous IHP involving the so-called tem- poral-parietal-occipital junction. Fig. 1.33 - «Great cerebral haemorrhage». Recent occurrence of widespread bleed massively involving the left thalamic and putaminal basal ganglia. Concomitance of: a marked mass effect (with conspicuous contralateral shift of the midline structures) and a blocking of the ventricular cavities (the homolateral ventricle is completely obliterated, the right one only in the occipital horn). However, the amount of peri- focal oedema is, as usual, restricted to a peripheral border on- ly. The patient died a few hours later.

Fig. 1.32 - Typical example of putaminal haematoma that spreads to the internal capsule (a) and to the semioval centre (b). These forms account for 32% of all putaminal locations.

Fig. 1.35 and 1.36 - Lobar and white matter haematomas. The left frontal haematoma (Fig. 1.35) is secondary to the rupture of an aneurysm of the anterior communicating artery and is ac- companied by subarachnoid bleeding, intraventricular inunda- tion and hydrocephalus. The right parietal haematoma (Fig. 1.36) is of the «spontaneous» kind in a hypertensive patient. blood vessels, and partly to the oedematous re- action of the surrounding neural tissue to the blood clot. generally cause mass effect with midline shift,

Fig. 1.37 - Voluminous IPH of the left hemisphere causes a de- formation and deviation of the 4th ventricle and a closed pos- terior fossa condition.

Fig. 1.38 - An eight year-old girl falls into a sudden coma. The CT picture shows a coarse IPH of the vermis with a subarach- noid haemorrhagic shift, obviously a non-spontaneous form. All the conditions (age, site and concomitant SAH) point to secondary forms. CT documents two further findings: the widespread ischaemic hypodensity of the brainstem and hydro- cephalus (signalled by the ectasia of the temporal horns). There is no time to perform an angiographic check or other neurora- diological investigations. The vermis is one of the most com- mon sites for «cryptic» angiomas (18). Diagram 1.40 shows the changes that the var- ious IPH parameters undergo over time as judged by CT. Density tends to decrease, pass- ing from a hyper- to an iso- and finally to an area of hypodensity (Fig. 1.41), as a result of a series of phenomena including the phagocytosis of blood pigments, the persistence of necrotic brain tissue and a mingling the whole with xan- thochromic fluid (e.g., expressed serum). This

Fig. 1.39 - A large haematoma with a fragmented appearance massively occupies the brainstem (a) and spreads upwards to- wards the thalamic nuclei.

Fig. 1.40 - Modified from (4). This chart shows the variations that the density of blood collections and other collateral parameters undergo during the phases sub- sequent to acute haemorrhagic accidents.

unchecked eventually results in a severe neu- rovegetative state (1). Ree eee ees a ME eee & It is therefore possible to formulate a progres- sive grading of thalamic and putaminal haemor- rhages. Together with clinical grading (e.g., pa- tient awake; drowsy with or without neurological deficit; sluggish with slight to severe neurological deficit; semi-comatose with severe neurological deficit or early signs of herniation; deep coma with decerebration), it enables an immediate prognostic assessment, which is useful in decid- ing upon subsequent possible courses of treat- ment (16). The debate between the supporters of conservative medical treatment on the one hand, and surgery on the other is still open. Whereas it seems universally accepted that surgical evacua- tion is the preferable treatment for lobar haem- orrhages (especially when they are larger than 35- 44 cm’ and therefore have a greater probability of causing brainstem compression and hernia- tion), the management of haemorrhages occur- ring in more common locations is still somewhat controversial. Te abaald alew Ka BAAR Ait FASE SiseSaRS Te

Fig. 1.41 - Evolution of IPH over time. CT is commonly used in IPH follow-up. In (a) the haematoma is documented a few hours from the stroke (note the deep po- sition, the jagged edges and the presence of small satellite foci). On a check carried out 14 days later (b), the haematoma pres- ents modest reductions in volume and density; it is however, surrounded by a vaster hypodense area (with a prevalence of the oedematous component developing in the white matter). Three months later (c), the haematic hyperdensity is replaced by an irregular porencephalic cavity with a star shape, which produces discreet ectasia of the homolateral ventricle.

Fig. 1.43 - The use of contrast media in the subacute phase. Twenty-five days from the stroke, this haematoma presents with (a) a target-shaped form and a blurred central hyperdensity. The contrast medium (b) impregnates a thin and uniform pe- ripheral rim. This ring is clearly distinguishable, despite the fact that the patient had received long-term steroid treatment, therefore in this «late» phase it is essentially supported by the hypervascularization of granulation tissue.

Fig. 1.42 - The use of contrast medium in atypically positioned acute haematomas. A voluminous lobar haematoma with a prima- rily occipital expansion (a) is constituted by a more hyperdense component (*), an expression of recent bleeding, and by another subacute, more widespread, and partially levelled component. The site and the lack of association with hypertension suggested a secondary haemorrhage and therefore an examination was per- formed after intravenous administration of contrast medium (b). There was no documentation of pathologically significant impreg- nations adjacent to the haematomas, nor alterations in density. The spontaneous haemorrhagic picture, with clots in various phases of evolution, was confirmed during surgery.

245° BOTY ~ WVillidot 1ICUsluili Ust ili lite Midget teste Ui iU01iits &lin countered in the subacute phase only. For approximately two weeks the patient has been suffering from worsening symptoms of intracranial hypertension, with progressive hemiplegia of the left side. Clinical suspicion points to a neoplastic pathology. The lesion documented by CT (a) is hyperdense as with IPH, but with atypical site (and symptoma- ology); it is accompanied by abundant oedema of the white matter and exerts a marked mass effect. The subsequent exam- ination after CE, with the demonstration of the «ring» en- hancement, would therefore strongly suggest a haemorrhagic nature (as confirmed by subsequent checks). It should be not- ed that, despite its circumvolute appearance, also in this phase he ring is thin and regular; which arouses further doubts, be- cause the patient has not yet been treated with steroids.

Fig. 1.44 - The influence of steroids on the outer ring. 17 days after the ictus, this IPH presents a reduction in its cen- tral density, an ample quantity of perifocal oedema and discreet mass effect. After CE it is demarcated by a ring, which because of cortisone treatment is incomplete and blurred (arrowhead).

Fig. 1.46 - Haemorrhagic infarct. An extensive ischaemic infarct that massively affects the terri- tory of the left middle cerebral artery, four days from onset presents an unexpected worsening of clinical conditions. CT documents irregular circumvolute hyperdensities, which can refer to overlapping bleeding phenomena.

Fig. 1.47 - Although rarely, IPH’s can also present with bilater- al multiple localizations. In (a) an example of a deep form, in (b) lobar forms. The haematomas of (a) are both putamino-thalamic; that on the left has a non-homogeneous core and, due to its larger dimensions, prevails in the shift effect on the contralateral ventricular cham- bers. The IPH’s in (b) are due to the recent bleeding of breast cancer metastases.

Fig. 1.48 - CT in differential diagnosis between infarct and haemorrhage. It is rare for ischaemic and haemorrhagic pathologies to pres- ent associated. This case serves to demonstrate the difference between the CT pictures for the two. On the right the sequelae of an extensive infarctual lesion (hy- podense), which affects the territory of the middle cerebral ar- tery and, immediately adjacent, a recent rounded formation (hyperdense) of haemorrhagic type, which expands in depth to the basal grey nuclei.

Fig. 1.49 - CT is also valid in postsurgical follow-up. a) documents a coarse putaminal IPH, spread to the cerebral cortex (note the concomitant haemorrhagic extravasation in he ventricular cavities, with scattered clots in the frontal horns and a minimal amount of fluid sloping in the occipital horns). Three days later (b), the haematoma was surgically re- moved. The CT picture is characterized by the presence of a arge hypodense area and a small gas bubble; more externally here is a malacic appearance of the parietal lobe (however the practically unaltered intraventricular haemorrhagic compo- nent persists). On check-up ten days later, there is a residual ir- regular deep hypodensity that subsequently, one month after the ictus, is surrounded by a granulation tissue with an intense, albeit thin, ring of contrast medium impregnation (d). The fol- lowing week this cavity is subject to drainage; and the tip of the deviation catheter is clearly visible. The periencephalic flu- id-filled spaces and the ventricular cavities contain air (which also occupies the non-sloping parts of the ventricles).

Fig. 1.50 - CT pictures of SAH’s subsequent to the rupture of an aneurysm of the anterior cerebral artery, a few hours after the ictus. a and b: in both cases, the widespread haemorrhagic extravasa- tion demarcates the perimesencephalic and supra-sellar cis- terns, the initial part of the Sylvian fissures and the interhemi- spheric fissure with its hyperdensity. In b the blood collections are clearly less thick in the perimesencephalic location, but they are accompanied by the blocking of the 34 ventricle. Both cause a discreet early ectasia of the ventricular chambers.

Fig. 1.51 - Curcumscribed SAH signalled by focal blood ex- travasations in some of the cortical sulci (arrows). With the exception of these findings, the current improvements in sensitivity are due largely to the progress made in the technology with regard to higher spatial and contrast reso- lution; from the 55% sensitivity of first genera- tion equipment, we have now reached numbers approaching 100% sensitivity for modern day CT appliances (26). It should also be noted that the reduction in the time elapsing between the event and the moment in which the CT scan is performed can be attributed to the greater dis- tribution of equipment throughout the world. Lastly, progress has been made in the interpre- tation of subtle changes, which are usually caused by more focal blood collections (Fig. 1.51). In stable patients, CT is suitable for de-

Fig. 1.53 - (a) large right frontal haematoma (*) and widespread subarachnoid bleeding mainly at the root of the Sylvian fissure are the most striking aspects of this small aneurysm which rup- tured in the stretch between Al and A2 (b). This is accompa- nied by a small haematic layer in the fourth ventricle and the perimesencephalic cisterns.

Fig. 1.54 - Validity of CT in defining the site of the bleed. The presence of a haematoma of the septum pellucidum hollow (*) in its typical midline position between the frontal horns constitutes an accurate localizing element, as it is almost invari- ably associated with the rupture of an aneurysm of the anterior cerebral artery. In (a) the following are present: widespread bleed inside the Sylvian fissures, the cortical sulci and the ante- rior interhemisperic fissure and massive inundation of the ven- tricular chambers. In (b): a blood collection in the right Sylvian fissure, blocking of the 3"¢ ventricle and involvement of the sloping part of the lateral ventricles.

Fig. 1.55 - (a) the irregular haemorrhagic collection inside the Sylvian fissure (*) and above all, the presence of an adjacent comma-shaped haematoma suggest the rupture of an aneurysm of the middle cerebral artery. The angiograph (b) confirmed the presence of a «giant» aneurysm in this position. terns; in these cases, obstruction of the outlets of the 4" ventricle may occur.

Fig. 1.56 - CT’s role in the prognostic definition of SAH. CT scans concerning two cases of aneurysm ruptures of the anteri- or communicating artery. In both the haematoma of the septum pellucidum hollow is typical. The different entity of the bleed is clearly shown by the thickness of hyperdensity in the anteri- or interhemispheric fissure and in the adjacent cortical sulci (very in a thin and thick in b), by the diffusion of the bleed (widespread in b), by the type of ventricular involvement (in a restricted to a clot in the frontal horn, massive in b). The pa- tient in case (a) was in discreet neurological conditions and was subjected to surgery without subsequent complications. Patient b was in a coma when the examination was carried out and died a few hours later.

Fig. 1.57 - Postsurgical CT may not always prove accurate due to the overlapping of artefacts produced by the metal clips. It is usually required to distinguish between the main surgical complications (hydrocephalus, vasospasm, rebleeding). In this case there is widespread hypodensity adjacent to the cran- iotomy, presumably exclusively due to subsequent malacic se- quelae.

Fig. 1.58 - Acute phase ischaemia (30 hours) in the territory of the left middle cerebral artery in a 20 year-old patient without appar- ent risk factors. Axial T1- (a) a,d PD- (b) dependent scans. AP (c) and axial (d) projections TOF MRA reconstructions. In T1, signal hypointensity in the grey matter of the caudate and left lenticular nuclei, with mass effect on the frontal horn of the homolateral ven- tricle; signal alteration, as hyperintensity, is clearer in the PD-dependent images. The MRA examination shows a clear reduction in calibre of the left internal carotid artery, from the origin to the siphon, with visualization of the sole M1 tract of the middle cerebral artery, which appears filiform.

Fig. 1.59 - Acute phase ischaemia in the territory of the perforat- ing arteries. Axial PD-dependent scan. Note the loss of the bound- aries of the anatomical structures affected (lenticular nucleus, cau- date nucleus, claustrum, internal, external and extreme capsule.

Fig. 1.60 - Acute phase ischaemia (20 hours) in the anterior superficial territory of the left middle cerebral artery. Axial PD-depend- ent scans: increase in signal of the cortex with increase in volume of the gyri. The white matter is spared. accompanied by a necrotizing effect upon the endothelial cells and the neurons due to the liberation of free radicals. The importance of Based on pathoanatomical findings and on micro- and macroscopic clinical, rather than accompanied by a necrotizing effect upon the endothelial cells and the neurons due to the liberation of free radicals. The importance of

fig. 1.61 - Acute phase (36 hours) left parietal ischaemia associated with contralateral ischaemia in stabilization phase. Coronal T1- a) and T2-dependent (b) scans. The recent ischaemia appears as a hypodense cortical area in T1, with an increase in volume of the yyrus circumvolution. The finding is less clear in T2, where the difference in signal between acute focus and resolution phase is how- ver evident.

Fig. 1.63 - Hyperintense, haematic rim in T1, in an acute phase ischaemic lesion: note the spiral shape. Fig. 1.62 - Acute phase ischaemia in the left anterior cerebral artery territory. Axial PD-dependent scan: note the increase in signal with obliteration of the adjacent cortical sulci.

Fig. 1.64 - Hyperacute ischaemia in the supply territory of the left middle cerebral artery. Diffusion weighted MR images show (a) the pathological hyperintensity of the ischaemic area; CT (b) findings were negative.

Fig. 1.65 - Acute ischaemia of the right middle cerebral artery territory. At clinical onset, the conventional (T2-weighted FSE sequence) (a) and diffusion (b) MR findings were negative. CT (c), performed 3 days later, showed a vast cortical-subcortical hypodensity with associated mass effect.

Fig. 1.66 - Lacunar ischaemia (millimetric dimensions) of the right lower cerebellar peduncle.

Fig. 1.68 - Hyperacute ischaemia of the left middle cerebral ar- tery territory visible only in the weighted diffusion MR images (a) and not in CT (b) or EPI-FLAIR sequence (c) in which it is possible to see a chronic paraventricular vascular sufferance sustained with hypodensity and hyperintesity, respectively.

Fig. 1.67 - Previous multiple lacunar infarcts in the periventric- ular, bi-hemispheric white matter. The lesions appear hyperin- tense in the EPI-FLAIR sequence (a), whilst the weighted dif- fusion images (b) are isointense.

Fig. 1.69 - Perfusion study of an acute ischaemia. The intensi- ty/time graph shows 3 different curves indicating a drop in sig- nal intensity that varies with the entity of the cerebral perfusion of the ischaemic core (absence of drop in signal intensity due to the absence of perfusion), of the ischaemic penumbra area (re- duction of the drop in signal intensity due to reduced perfu- sion), of the intact surrounding parenchyma (normal reduction in signal intensity due to normal perfusion).

Fig. 1.70 - Spectroscopic study (a) of subacute ischaemia with morphological MRI (T2-W FSE). The drastic reduction of NAA concentration is evident. treatment, and irreversibly ischaemically dam- aged tissue. MR spectroscopy and, in particular, spec- troscopic imaging can be of use in this sense, however it requires relatively long examina- tion times. Perfusion MR studies provide di- rect information on the status of cerebral parenchyma perfusion (depending on the ade- quacy of collateral circulation) and on tissue vitality and reversibility that is required for a

Fig. 1.71 - Hyperacute phase right intracerebral sub-Sylvian haemorrhage (12 hours). Coronal T1-dependent scan (a) and axial T2-dependent scan (b). The lesion presents as hy- pointense in T1 and non-homogeneously hyperintense in T2, where the notably hyperintense oedema halo in formation is al- so visible.

Fig. 1.72 - Acute phase intracerebral haemorrhage (38 hours from onset) in a left thalamo-capsular location. Axial PD (a) and T2 scans: the lesion presents as non-homogeneously hy- pointense with a vast oedematous halo. bin’s oxygen saturation, with the eventual for- mation of deoxyhaemoglobin. Deoxyhaemo- globin, characterized by high magnetic suscep- tibility and enclosed in the finite intracellular space of the erythrocyte, causes non-homo- geneity of the local magnetic field, thus result- ing in a loss of phase coherence of the resident protons. This translates into a preferential field strength -dependent enhancement of T2 relax- ation. Although deoxyhaemoglobin is para- magnetic, it does not influence T1 relaxation because its heme groups are contained in apo- lar pockets that prevent contact with water pro- tons. The presence of deoxyhaemoglobin in the haemorrhagic lesion translates into (Figs. 1.72, 1.73): relative hypo-isointensity on T1-weight- ed images, iso-hypointensity on PD-weighted images and rather marked hypointensity on T2- weighted images. because its heme groups are contained in apo-

Fig. 1.73 - Acute phase intracerebral haemorrhage in left tem- poral location: coronal T1- (a) and T2-dependent (b) scans: note the marked hypointensity of the lesion and the perilesion- al oedema.

Fig. 1.75 - Sagittal PD-dependent MRI scan: note the thin hy- pointense rim that surrounds the lesion, due to the presence of haemosiderin.

Fig. 1.74 - Left parietal haemorrhage in chronic phase (28 days). Axial CT scan after contrast agent (a): hypodense le- sion with thin hyperdense rim. Axial PD-dependent MR scan: the lesion shows the characteristic hyperintense haema- tic signal.

Fig. 1.76 - Right temporal-occipital haemorrhage in subacute phase with arteriovenous malformation. Coronal PD-depend- ent scan: the haemorrhagic lesion is very clear, as is the malfor- mation nidus with its characteristic signal void.

Fig. 1.78 - 65 year-old male patient with hemiplegia of the left side with acute onset. Fibroatheromasic plaque at the origin of the right internal carotid artery (a) with reduction in the vessel diameter of more than 50% (b - short axis). Information obtained from indirect explo- rations does not only concern the vessel ex- plored with the probe, but also haemodynamic variations that take place up- and downstream of it. Indirectly, using compression manoeu- vres, it is possible to evaluate the condition of the circle of Willis and of the intracranial seg- ment of the internal carotid artery. In particu- lar, it is also possible to explore, for example, the condition of the anterior communicating

Fig. 1.79 - 79 year-old man with hypertension, diabetes and fib- rillation. Severely atheromasic common carotids with plaques bulging into the lumen and marked wall alterations (a-b).

Fig. 1.81 - 45 year-old male patient with left-side hemiplegia. Thrombosis of the right internal carotid artery. Fig. 1.80 - 70 year-old male hypertensive patient, with dizziness following fall. Cerebral CT: left hemisphere ischaemic lacunae. Ulcerated fibrocalcific plaque on the rear wall of the left carotid bifurcation.

Fig. 1.79 - (cont.) Fibroatheromasic plaque with irregular sur- faces in the right carotid bulb and the right internal carotid along the entire extracranial stretch explored with max. reduc- tion in the vessel diameter greater than 65% (c - long axis, d - short axis).

Fig. 1.82 - 68 year-old female patient with left side hemiparesis and dizziness. Kinking of the left internal carotid artery with velocitometric acceleration findings both in the internal carotid artery and downstream (left supraorbital artery).

Fig. 1.83 - 78 year-old female patient, hypertensive, diabetic with left side hemiparesis with a duration of a few seconds. Coiling of the right internal carotid artery. stricted to the extracranial vessels (7). I his si- One particular application of the pulsed Doppler technique is the transcranial Doppler (including transcranial ECD and PD, Fig. 1.85) (1), with which it is often possible to penetrate the bony barrier of the skull to ex- plore the large arteries of the circle of Willis. This is done by using compression manoeu- vres to evaluate the intra- and extracranial col- lateral circuits. It can also register severe in- tracranial vascular spasm even when it is asymptomatic and can follow the course of arterial narrowing with serial recordings; in this manner, invasive selective angiography may be avoided and surgery can be under- taken in the critical phase of high flow ve- locity. Bilateral recordings of the flow veloc- ity in the anterior, middle and posterior cere- bral arteries can also aid in the comprehen- sion of flow modes in the collateral arteries and in stenoses and occlusions of the intra- and extracranial carotid arteries. With a simple echotomosraphy or one

Fig. 1.85 - Transcranial Echo-Colour-Doppler. Intracranial cir- culation viewed through the temporal window. tion on the morphology of the vessel wall. It can identify both the surface of flat, non- haemodynamically significant atheromatous plaques (Fig. 1.78), and complicated plaques (haemorrhagic, ulcerated, calcified) (Figs. 1.79, 1.80), which are usually stenosing and associated with occlusive and preocclusive thrombus formation (Fig. 1.81). In this last case, PD has a higher sensitivity, specificity and diagnostic accuracy than does ECD, as it is able to detect the presence of a still accessi- ble lumen, even with an extremely slowed flow that cannot be detected by ECD (Fig. 1.86). ECD therefore provides detailed evalu-

Fig. 1.86 - Pseudo-occlusion of the internal carotid artery. The Power Doppler is able to show a slight flow at an extremely re- duced speed.

Fig. 1.84 - Power Doppler of the carotid bifurcation.

Figs. 1.87-1.88 - Dynamic MRA scan of the epiaortic vessels acquired in the coronal plane with high definition ultrafast T1 sequences (AT: 28 seconds); note the excellent demarcation from the emergence of the epiaortic vessels. To avoid problems with the progressive satura- tion of the spins when using 2D- and 3D-TOF techniques, one should preferably use an acqui- sition plane perpendicular to the longitudinal axis of the vessel being examined; consequent- ly, both the carotid and the vertebral arteries must be examined in the axial plane (Fig. 1.90). The 3D-TOF technique can also be used with a bolus injection of a contrast agent (gadolini- um), using rapid volumetric acquisitions in the coronal plane (Fig. 1.91). The disadvantage of this technique is in its slightly invasive nature (linked to the intravascular administration of gadolinium) and in its limited spatial resolution as compared to the traditional 3D-TOF method utilizing a transverse plane acquisition.

Fig. 1.89 - Dynamic CE MRA: presents a serrated stenosis of the right subclavian artery and a stenosis on the bifurcation of the right carotid artery.

Fig. 1.91 - Dynamic MRA scan of the epiaortic vessels: a) steno- sis on the bifurcation of the right carotid artery and occlusion at the start of the left internal carotid artery; b) the specific study using the 3D-TOF technique better demarcates the pres- ence and entity of the stenosis at the start of the right external carotid artery.

administration of contrast media (gadolinium) dy Means Of an appropriate arrangement otf the

Fig. 1.91 - (cont.) — c) Another case, medium grade stenosis on the right carotid bifurcation and serrated stenosis with presence of plaque at the beginning of the left internal carotid artery; d and e) selective reconstruction of the carotid bifurcations.

Fig. 1.94 - Hyperacute phase ischaemia. a) and b) TSE-HASTE images, a blurred swelling caused by the oedema of the cortex in a right parasagittal frontal position with small hyperintensities near the signal; c and d) DW images: widespread ischaemic focus in the territory of the right anterior cerebral artery.

Fig. 1.94 - (cont.) e and f) MRA of the vessels of the circle of Willis: occlusion at the start of the right anterior cerebral artery and serrated stenosis in segment M2 of the right Sylvian artery.

Fig. 1.95 - Left insular-temporal-parietal ischaemic lesion: a) ba- sic SE T2 MRI, b) 3D-TOF MRA of the vessels of the circle of Willis; occlusion in segment M2 of the left Sylvian artery.

Fig. 1.96 - Left temporooccipital ischaemia: a) basic SE T2 MRI, b) MRA of the vessels of the circle of Willis: occlusion in the P1 segment of the left posterior cerebral artery.

3D-TOF MRA has recently been used in studying aneurysms treated with Guglielmi’s Fig. 1.97 - Right parietal ischaemia: a) basic SE T2 MRI; b) 3D- TOF MRA of the vessels of the circle of Willis: absence of flow signal in the right carotid siphon with partial revascularization of the right Sylvian artery through the circle vessels. underestimation of the dimensions of the lu- men of the aneurysm.

Fig. 1.97 (cont.) - c) MRA of neck vessels: occlusion at the be- ginning of the right internal carotid artery.

Fig. 1.98 - a) Basic SE T2 MRI; blurred signal hyperintensity in right occipital location; b) SE T1 image after gadolinium: non- homogeneous contrast enhancement due to blood-brain barri- er damage caused by the presence of an acute ischaemic area; c) MRA of the vessels of the circle of Willis: stenosis in the proximal segment of the right posterior cerebral artery.

Fig. 1.99 - 3D TOF MRA of the vessels of the circle of Willis: presence of an aneurysm on the anterior communicating artery.

Fig. 1.100 - AVM: a) basic SE T2 MRI: numerous serpigenous images with signal void in the left temporoparietal region; b) 3D TOF MRA: presence of a large AVM, supplied by branches orig- inating from the Sylvian artery and left posterior cerebral artery. CONCLUSIONS for studying the brachiocephalic and cerebral

ee ae ee Treatment must be begun within 6-8 hours from onset of the ischaemic ictus, once an- giography has demonstrated the obstructive nature of the ischaemia. A microcatheter is in- troduced via the transfemoral route into the occluded artery; the distal tip of the catheter is positioned in contact with the thrombus and injecting from 200,000 to 1,000,000 Urokinase; 1/3 of the total amount of the dose is administered as a bolus, and the remainder as a continuous infusion over the subsequent 1-2 hours. The main hindrance to the wider use of this technique is the extreme sensitivi- ty of the cerebral tissue to anoxia, which leaves a very small time margin between on- set and the start of treatment, and the poten- tial risk of peripheral non-cerebral and cere-

Fig. 1.102 - (a-c) Intraparenchymal haemorrhage. a) CT: volu- minous intraparenchymal haematoma in right temporoparietal position of recent onset, with intraventricular expansion. (b-c) Selective catheterism of the right internal carotid artery, early and late arteriographic phase of same case: arteriovenous mal- formation (arrow) sustained by branches of the middle cerebral artery and the rear choroid arteries, with venous drain through ascending superficial veins (arrowheads).

Fig. 1.103 - (a-d) Subarachnoid haemorrhage. a) CT: subarachnoid blood expansion, at the occipital region of the cortical sulci (a1 rows). b) selective catheterism of the left vertebral artery (same case): small aneurysm of the left posterior cerebral artery, near to th start of the temporooccipital artery (arrow). ¢) selective catheterism of the left internal carotid artery: small sac-shaped aneurysm the anterior communicating artery (arrow). d) selective catheterism of the left internal carotid artery: aneurysm of the anterior com municating artery (arrowhead); spasm of the anterior cerebral artery (arrow).

Fig. 1.104 - (a, b) Intraarterial fibrinolysis. a) selective catheter- ism of the left vertebral artery: acute thromboembolic occlu- sion of stretch V3, with impossibility of viewing the basilar stem and the posterior circulation (arrow tips). b) check-up af- ter fibrinolytic treatment: complete recanalization of the verte- bral artery with opacification of the basilar stem and posterior circle (arrowheads)

Fig. 1.106 - (a, b) Angioplasty of the internal carotid artery. Selective catheterism of the right internal carotid artery. 33 year-old pa- tient with history of cerebral ischaemia. a) Segmentary stenosis at the passage between the extra- and intracranial tract, probably of a fibrodysplasic nature (arrow). b) Check-up after angioplasty (same case): complete resolution of stenosis.

Fig. 1.107 - (a, b) Angioplasty of the middle cerebral artery. a) Selective angiography of the right internal carotid artery: serrated spasm post SAH of the M1 stretch of the middle cerebral artery (arrow) in patient operated for an aneurysm on the posterior communicat- ing artery. b) Check-up after papaverine + PTA: complete resolution of the spasm with patent vessel of a good calibre (arrow tip).

Fig. 1.108 - (a, b) Aneurysm embolization with Gugliemi’s detachable coils. a) Selective angiography of the left vertebral artery: 1 cm aneurysm of the apex of the basilar artery (arrow). b) Check-up after embolization: complete occlusion of the aneurysmatic sack with well-compacted spirals (arrow tips).

Tab. 2.3 - Secondary traumatic cranioencephalic lesions

Fig. 2.1 - (a-d) Recent head injury. Irregular hypodense cortical-subcortical areas are observed bilaterally in the frontal lobes; hyper- dense haemorrhagic material is noted in the occipital horns of the lateral ventricles (a-b). Also seen is a frontal bone fracture line (c).

Fig. 2.2 - (a, b) Demonstrated is a depressed fracture of the right parietal bone.

Fig. 2.6 - Frontal head injury caused by road traffic accident with fractures of the walls of the right frontal sinus and the for- mation of an air-fluid level. Fig. 2.5 - Fracture of the left petrous bone, with fluid within the mastoid air cells (arrows).

Fig. 2.4 - (a, b) Open head-facial injury caused by road traffic accident. Multiple fractures of the left orbital, ethmoidal and frontal bones are noted, with fluid within the ethmoid air cells and frontal sinus (a, b).

or cortical contusion, trauma patients with sin- gle intraparenchymal haematomas may not lose consciousness; in 30-50% of cases these pa- tients remain lucid for the entire duration of the clinical outcome (3, 15). Signs and symp- toms in parenchymal haematomas and their clinical evolution are similar to those observed in extraaxial haematoma patients, with the ex- ception of large or temporal lobe haemorrhages that have an unpredictable outcome; even when small, these haematomas can cause brain- stem damage due to associated transtentorial herniation (3, 7, 29)

Fig. 2.7 - (a-c) Diffuse axonal injury (damage). Multiple hyper- dense foci are observed with haemorrhage and compression of the white-grey matter junction bilaterally (arrow heads).

Tab. 2.4 - Comparison between subdural and epidural haematomas mentioned in the preceding sections and repre- sent approximately 5-10% of primary traumat- ic pathology (3, 20, 22). They are associated with severe clinical states, and usually have un- favourable prognoses. Depending upon the clinical severity, CT can be entirely negative or may show relatively minor findings, including small haemorrhages in the areas of the brain- stem surrounding the cerebral aqueduct and in the basal grey nuclei. As compared to CT, on MRI these types of lesions appear relatively more clearly. stem tissue through the tentorial incisura, or even the possibility of herniation of the cere- bellar tonsils through the foramen magnum later in the process of haemorrhagic expan- sion. Clinically it is not always easy to distin- guish intraparenchymal haemorrhage from DAI or parenchymal contusion; this differen- tial diagnostic difficulty probably accounts for the marked variability in the clinical evolution statistics as reported in the literature (3). The prognosis for isolated intraparenchymal haema- tomas is fairly good, but worsens considerably with increasing degrees of mass effect or when it is associated with DAI or haemorrhages in- te the kaeal wsanelia. Traumatic intraventricular haemorrhage is somewhat uncommon and is only present in 1- 5% of closed head injuries; it is usually a con- sequence of particularly severe trauma and tends to be associated with DAI and traumatic lesions of the deep grey matter and brainstem. The clinical prognosis is generally poor (3, 13, 20, 22). CT shows hyperdense intraventricular collections, which may or may not have associ- ated fluid-fluid levels. Intraventricular haemor- Traumatic lesions of the deep grey structures and the brainstem rhages are occasionally seen in combination with choroid plexus haematomas, haematomas of the deep grey or white matter and subarach- noid haemorrhage (Fig. 2.22c).

Fig. 2.8 - (a-f) Temporal evolution of contusive haemorrhagic focus. (a-b) CT examination a few hours following trauma: ir- regular haemorrhagic foci are seen in both frontal lobes and in right temporal-parietal region with the obliteration of the ipsi- lateral Sylvian fissure cistern. nous epidural haematomas are typically seen when resulting from the rupture of one of the larger dural venous sinuses. The CT density of the extraaxial blood collection depends in part upon the phase in which the haematoma is im- aged. In the acute phase, epidural haematomas appear as homogeneously hyperdense lesions, with a biconvex or lens shape; the varying mass effect can be observed in the contralaterally dis- placed ventricular and extraventricular CSF

Fig. 2.8 (cont.) - (c-d) Follow up after 3 weeks: The hyperdense haemorrhage has been almost completely resolved, whereas the hypo- dense component is still clearly visible; a subdural hygroma has accumulated on the left side. (e-f) Follow up after 6 weeks: There is par- tial resolution of the hypodense component, a residual of which persists in a right frontal region; the hygroma on the left side remains.

Fig. 2.9 - An acute post-traumatic intraparenchymal haematoma in observed in the right temporal-occipital area.

Fig. 2.10 - (a-b) A large epidural haematoma is seen in left tem- poral-parietal region (a) associated with an overlying skull frac- ture (b). Tab. 2.5 - Post-traumatic sequelae of head injuries

Fig. 2.11 - Axial CT shows an epidural haematoma with bicon- vex lens shape, in right parietal region with compression of the cerebral parenchyma and midline shift.

Fig. 2.12 - Axial CT reveals a small right frontal subacute epidural haematoma with mixed hypodense and hyperdense component, concomitant extracranial haematoma.

Fig. 2.14 - Bilateral subdural haematomas. There is a biloculat- ed acute-subacute subdural haematoma on the right side (a), a heterogeneous appearance of the two haematomas with fluid- fluid levels (b), and presence of haemorrhagic components of different ages. The left sided subacute subdural haematoma is almost isodense as compared to the underlying brain and is therefore somewhat difficult to visualise. [a), b) axial CT].

Fig. 2.13 - Axial CT demonstrates an acute subdural haematoma along the left hemisphere convexity with right shift of the mid- line structures and compression of the left lateral ventricle. [a), b) axial CT].

Fig. 2.15 - Subdural haematoma. Axial CT shows a subacute right frontal subdural haematoma is noted that is isodense and associated with obliteration of the cortical sulci, displacement of the corticomedullary junction away from the overlying skull, leftward shift of the midline structures and compression of the adjacent lateral ventricle.

Fig. 2.16 - Subdural haematoma. Axial CT reveals and unusual appearing left frontoparietal subdural haematoma with a hy- perdense acute haemorrhagic component layering posteriorly. The left lateral ventricle is compressed by the haematoma and the contralateral lateral ventricle is dilated. [a), b) axial CT].

convex lateral margin; however, in the presence of an SDH this margin becomes flattened, con- cave or irregularly distorted. If the cortico- medullary junction is not visible, a bolus injection of contrast medium administered during the scan may be useful in identifying the cortical surface and delineating the border of an isodense SDH. This image enhancement method can document Fig. 2.18 - Subdural haematomas. Axial and coronal CT shows small, chronic subdural haematoma over the convexity of the brain is observed which is better seen on coronal scans. [a) ax- ial CT; b) coronal CT].

Fig. 2.17 - Bilateral subdural haematomas. Axial CT shows bi- lateral hypodense subdural haematomas. [a), b) axial CT].

Fig. 2.19 - Subdural haematoma. The axial CT shows a right frontoparietal subdural haematoma with associated mass effect upon the adjacent cerebral parenchyma, which causes a subfal- cian herniation of the cingulate gyrus and the compressed right lateral ventricle. The left lateral ventricle is dilated due to a CSF obstruction at the level of the left foramen of Monro.

Fig. 2.20 - Bilateral subdural haematomas. The CT study shows lateral ventricles that are thinned, elongated and parallel to one another. The left sided subdural haematoma is almost isodense as compared to the underlying brain.

Fig. 2.21 - Subarachnoid haemorrhage. Hyperdensity is noted within the cortical sulci over the left cerebral hemisphere. Small haemorrhagic cortical contusions are also seen, the largest of which can be observed in the right temporal region (arrow- head). [a), b) axial CT]. SDH’s do not cross the midline because the subdural spaces on the two sides of the crani- um do not communicate. These haematomas are occasionally observed beneath the tempo- ral lobe within the middle cranial fossa and un- der the occipital lobes extending along the ten- torium cerebelli, and are often difficult to see with axial slices alone. In these instances, sup- plemental coronal slices are helpful for visuali- zation.

Fig. 2.22 - Posttraumatic intraventricular haemorrhage, pneumocephalus, and cerebral oedema. Bilateral eyelid haematomas are seet associated with subcutaneous emphysema (a). Intracranially are observed subarachnoid (b) and intraventricular haemorrhage (a), ai bubbles in the CSF spaces (c) and the widespread oedema within the right cerebral hemisphere (d). [a)-d) axial CT].

Fig. 2.23 - Posttraumatic subdural hygroma. The axial CT shows a left sided frontal posttraumatic subdural hygroma. 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).

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" 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].

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.

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).

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), ¢) axial CT; d), f) axial T2-weighted MRI; e) axial T1-weighted MRI].

Fig. 2.27 - Multiple contusive and lacerative haemorrhagic cere- bral foci in the acute phase. The T2-weighted sequence (a) shows multiple areas of signal hyperintensity within which haemor- rhagic components cannot be distinguished. The long scan time often results in motion artefacts. The echo-planar sequence (b), which is more sensitive to T2*-weighted tissue, enables the iden- tification of areas of hypointense signal caused by the presence of subacute haemorrhage (deoxyhaemoglobin). Motion artefacts can also be reduced by obtaining the acquisition in approxi- mately 500 msec. [a) T2-weighted MRI; T2*-weighted MRI].

Fig. 2.28 - Cerebral contusions. T2 fast spin echo (FSE) and FLAIR sequences demonstrate that the latter prove more sensitive in identifying contusive foci, even of very small dimensions. The superior identification of the subdural haematoma with FLAIR se- quences is also noted. [a), c), d) T2-weighted MRI; b) FLAIR MRI].

Fig. 2.29 - Hyperacute cerebral haemorrhage. CT and T2- weighted MRI images show that in the hyperacute phase only CT is capable of showing the haemorrhagic component of the right temporal-insular shear-contusive focus. [a) axial CT; b) axial T2-weighted MRI].

Fig. 2.32 - Haemorrhagic shearing injuries. Unlike FSE T2- weighted sequences, gradient recalled echo sequences which are more sensitive to T2* effects, are able to distinguish the presence of a haemorrhagic components within very small grey- white matter junction shearing injuries. [a) T2-weighted MRI, b) T2*-weighted MRI].

Fig. 2.33 - Shearing injury. Identified on this T2-weighted FSE sequence is a small posttraumatic lesion of the posterior medul- la oblongata, following attempted suicide by hanging. Subarachnoid haemorrhage consists of local- ized or diffuse haemorrhage within the sub- arachnoid space. These haemorrhages rarely oc- cur as isolated lesions but instead are more fre- quently associated with extraaxial haematomas or cerebral laceration-contusions (3, 4, 28). A distinction can be made between primary and secondary subarachnoid haemorrhage. Primary subarachnoid haemorrhage results from the subarachnoid rupture of small pial-cortical sur- face vessels, from the tearing of bridging veins traversing the subarachnoid space or from the posttraumatic rupture of arteriovenous malfor- mations or cerebral aneurysms. Secondary sub- arachnoid haemorrhage, on the other hand, is caused by the rupture of a subdural haematoma or a cerebral laceration-contusion into the sub- arachnoid space. arr ie: 1 1 +W 1

Fig. 2.35 - Left-sided cerebellar contusion. An MRI examination conducted in the hyperacute phase shows the presence of oedema in a left-sided cerebellar contusion (a, b). The MRI follow up conducted 15 days later documents the partial resolution of the oede- ma within the cerebellar contusion on the left. (a, b) (reprinted from M. Gallucci, et al., 9)

gard to the identification of extradural haematomas, the sensitivity MRI is similar to that of CT, but MRI is more accurate. This is principally due to the ability of obtaining mul- tiplanar acquisitions on MRI that inherently have a greater probability of visualizing even

A tear of the leptomeninges and inner or meningeal layer of the cranial dural mater dur- ing head trauma can result in the passage of CSF into the subdural space. The resulting for- mation of a fluid collection, that is isointense with the fluid in all MR acquisitions, is known as a subdural hygroma (8). Subdural hygromas typically are not large and therefore produce little mass effect upon the underlying cerebral tissue, although exceptions are occasionally en- countered.

Fig. 2.36 - Posttraumatic right-sided cerebellar infarct. T2- weighted MRI shows the presence of a cerebellar infarct in the territory of the right posterior inferior artery. The frontal MRA examination reveals a thinned, string-like incomplete MRI flow signal within the right vertebral artery. A T1-weighted scan of the neck, carried out 4 days after the traumatic event, shows a dissection of the right vertebral artery with intramural hyperin- tensity (open arrows) due to the presence of methaemoglobin. (reprinted from M. Gallucci, et al., 9)

Fig. 2.37 (cont. of 2.36) - Basal ganglia cytotoxic oedema. T2- weighted MRI shows hyperintensity within the basal ganglia and cerebral cortex signal consistent with cytotoxic oedema in a case of brain death. (reprinted from M. Gallucci, et al., 9).

Fig. 2.38 - Cervical spine fracture. a) A scout view of the cervi- cal spine. b) The CT scanogram identifies a C5 fracture.

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 medi- an point of A-B with the sphenoid jugum (neuro-ocular plane). b) The line that passes through the ocular lens, optic nerve, op- tic canal and occipital cortex in the neuro-ocular plane. ¢) Note that the neuro-ocular plane virtually coincides with that of the hard palate.

1. Simultaneous craniofacial imaging is pos- sible: the facial skeleton, to include the orbits, can be scanned at the same time as the brain. As traumatic lesions of the face are frequently associated with concomitant injuries to the brain, this technique avoids having to delay a detailed study of the facial skeleton to the days subsequent to the initial patient imaging evalu- ation in the emergency room. As traumatic lesions of the tace are frequently

Fig. 2.40 - Broken nose as part of a complex facial fracture. A 2 mm axial CT image (a-b) yields a reasonable resolution re- constructed sagittal image (c) from which the axial (d, e) and coronal (f, g, h) images of the nasal bones are reconstructed. This results in optimal demonstration of the fractures. sition within the face and its relatively delicate constitution. The fractures of this region can be divided into isolated fractures of the zygomatic arch or so-called “tripod” fractures.

Fig. 2.41 - Tripod fracture of the left cheekbone, with medial and inferior displacement of the orbital-malar-zygomatic complex. Ax- ial CT images (a, b), reconstructed coronal CT section (c) and three-dimensional reconstructions (d, e, f) show the mildly depressed, fractured zygomatic arch and lateral orbital-maxillary sinus walls.

Fig. 2.42 - Orbital study technique. 2 mm (a) or Imm-slices (b). The optic canal (c) may be documented well with high resolution oblique-coronal reconstructions (d, e). zygomatic-maxillary, zygomatic-trontal and zy-

Fig. 2.43 (cont.) - d) A reconstructed coronal CT section shows the soft tissue within the roof of the maxillary sinus adjacent to the inferior rectus muscle. e), f) Direct coronal sections better show the orbital floor and the herniation of orbital material into the sub- jacent maxillary sinus. g) A second case showing a larger orbital floor fracture on the right side with depression of bone and soft tis- sue into the roof of the maxillary sinus.

Fig. 2.45 - Complex facial fracture. The CT study shows a comminuted hard palate fracture (a), a fracture of the vomer (b), posteri- or extension of the fracture as far as the medial wall of the cavernous venous sinus on the right (c) and a right paramedian sagittal fracture of the ethmoid bone, extending into the optic canal (d).

Fig. 3.2 - Vasogenic oedema caused by malignant cavitary glial neoplasm. The MRI study shows extensive oedema involving the white matter surrounding the neoplasm. Note the mass effect upon the lateral cerebral ventricles and the irregular mural contrast enhance- ment. [a), b) T2-weighted, c) unenhanced T1-weighted, d) and T1-weighted MRI following IV gadolinium (Gd) administration].

Fig. 3.3 - Hemispheric cerebral infarction. Unenhanced axial CT demonstrates a large hypodense area in the vascular distri- bution of the right anterior and middle cerebral arteries associ- ated with mass effect. abetic ketoacidosis, purulent meningitis, severe hypoglycaemia and methanol intoxication.

Fig. 3.4 - Neoplasm of the cerebellar vermis with obstructive hydrocephalus. The MRI examination shows a contrast enhancing mass (a) likely originating within the cerebellar vermis that compresses the 4" ventricle and has resulted in obstructive hydrocephalus (b). The T2-weighted images reveal transependymal extravasation of CSF into the periventricular white matter (c, d).

Fig. 3.5 - Mesencephalic tuberculoma with obstructive hydro- cephalus. The MRI shows a contrast enhancing mass lesion of the posterolateral midbrain resulting in stenosis of the aque- duct of Sylvius and obstructive hydrocephalus. [a) axial T2- weighted and b) sagittal T2-weighted MRI; c) coronal T1- weighted MRI following IV Gd].

the skull is absent or at most modest. In adults

Fig. 3.6 - Type II Arnold Chiari malformation with obstructive hydrocephalus The MRI examination demonstrates cerebellar tonsillar ectopia, fourth ventricular outlet obstruction and hy- drocephalus. In addition, there is right occipital encephaloma- lacic porencephalic cyst and cervicothoracic syringohydromyelia. [a) sagittal T1- weighted cranial MRI; b) sagittal T1-weighted cervical MRI; c) axial T2-weighted cranial MRI]. After a certain time, chronic inadequate flu- id reabsorption can produce an enlargement of the ventricles without an attendant increase in fluid pressure (normotensive hydrocephalus). In acute hydrocephalus, the CSF is reabsorbed vicariously by the minor resorption systems, firstly by the transependymal pathway, with the appearance of typical findings of hypodensity on CT and hyperintensity on T2-weighted MRI in the periventricular white matter (Fig. 3.8). This absorption pathway is more permeable than the normal one and permits the passage through the periventricular white matter of even large protein molecules.

Fig. 3.7 - Trapped 4" ventricle with hydrocephalus. T1-weighted MRI showing a trapped 4" ventricle associated with obstructive hydrocephalus in a patient with tuberculous meningitis. Lastly, in ex-vacuo ventricular enlargement there is a passive increase in the ventricular and extraventricular CSF spaces without an in- crease in the intraventricular fluid pressure. This type of ventricular enlargement is due to a generalized atrophy of the brain parenchy- ma (Fig. 3.9). Generalized atrophy results in a symmetric dilatation of the ventricular system, which may principally involve the lateral ven- tricles although the 34 ventricle may also be affected. If there is atrophy of the structures of the posterior fossa, the 4‘ ventricle will al- so be passively enlarged. The angle between the frontal horns is always greater than 110 de- grees. The basal subarachnoid cisterns and the superficial cerebral sulci can be normal, how- ever they more frequently are widened in syn- chrony with the overall atrophy.

Fig. 3.8 - Normotensive communicating hydrocephalus. The MRI images show a thin margin of hyperintensity representing chronic gliosis surrounding the lateral ventricles in a patient with clinically diagnosed chronic normotensive communicating hydrocephalus, not transependymal extravasation of CSF. [a, b) proton density-weighted MRI; c, d) T2-weighted MRI].

Fig. 3.9 - Ventriculomegaly with passive cerebral atrophy. Axi- al CT shows passive cerebral atrophy associated with ventricu- lomegaly.

Fig. 3.11 - Glioblastoma multiforme. The CT and MRI studies show a large, necrotic left hemispheric glioblastoma associated with extensive perilesional vasogenic oedema resulting mass effect and lateral subfalcian herniation. [a, b) unenhanced axial CT; ¢, d, b) PD-, FLAIR, T2-weighted MRI; f, g) T1-weighted axial and coronal MRI following IV Gd].

cially in cases of metastases and malignant gliomas (2, 10, 12, 19, 23). There are a num- ber of possible intraneoplastic causes of haemorrhage; among these are: primitive tu- moral neovascularization with a disorderly endothelial proliferation and formation of ar- teriovenous shunts, rapid tumour growth with subsequent ischaemic necrosis, release of plasminogens and vascular infiltration by the tumour (2, 6, 11, 23, 24). The metabo- lism within haemorrhagic neoplasia is vari- able, but is generally lower than that ob- served in “benign” haemorrhages (1, 2). Daneohaarminolahin. which de aeralke wale

Fig. 3.12 (cont.) - h, i) axial and coronal T1-weighted MRI following IV Gd].

Fig. 3.13 - Pilocytic astrocytoma. Identified is a mass lesion of the right cerebellar hemisphere characterised by a cystic core and thick rim of solid tissue. The neoplasm compresses the 4% ventricle and brainstem resulting in obstruction of the aque- duct of Sylvius aqueduct and obstructive hydrocephalus. This structures caudally into the foramen magnum and cranially through |-wejohted spin echo MRI: d) coronal inversion recoverv T1-weigcht-

Fig. 3.15 - Postsurgical infection of surgical site. The surgical cavity demonstrates air with irregular contrast enhancement along the resection margins; hypodensity persists in the adjacent white matter due to persistent vasogenic oedema. The CT findings described are of uncertain significance, as they are still compatible with expected postsurgical alterations, however the associated clinical find- ings (headache and high fever) suggest a probable infection of the surgical site. [a, b) unenhanced axial CT; c, d) axial CT following TV contrast].

Fig. 3.16 - Postsurgical cerebritis. The CT examination shows diffuse hypodensity of the subcortical and deep white matter of the right cerebral hemisphere consistent with oedema, with inhomogeneous contrast enhancement and marked mass effect. The mass re- sults in compression of the ipsilateral ventricle, subfalcian herniation of the midline supratentorial structures and early dilation of the contralateral ventricle caused by obstruction at the level of the foramen of Monro on the left side. The ipsilateral perimesencephalic cistern is obliterated due to downward internal herniation of the uncus of the temporal lobe. [a, b) unenhanced axial CT; c, d) axial CT after IV contrast].

, Fig. 3.17 - Meningioma of the left pterion. The imaging studies reveal a left frontoparietal homogenously enhancing, broad dural based mass with perilesional oedema and neovascularity originating from the left middle meningeal artery. [a) unen- hanced CT; b, c) left external carotid, left middle meningeal ar- teriogram].

Fig. 3.18 - Invasive left frontal region meningioma. The skull x-ray demonstrates a large osteolytic lesion of the left frontal region. The CT shows a hyperdense lesion invading the overlying skull and extracranial soft tissues. The angiogram of the left external carotid ar- tery reveals prominent neovascularity originating from branches of the left superficial temporal and middle meningeal arteries. [a) frontal radiograph; b), ¢) axial CT imaged with bone and soft tissue windows; d) left external carotid arteriogram].

ical circulation fed principally from meningeal

Fig. 3.19 - Olfactory groove meningioma. The right internal carotid arteriogram demonstrates neovascularity associated with a persistent parenchymal blush within a lesion in the ante- rior aspect of the skull base on the right side originating prin- cipally from ethmoid arterial branches. In addition, the right ophthalmic artery in hypertrophied as a result of the increased flow in transit to the neoplasm. [a) frontal projection right in- ternal carotid arteriogram; b) lateral projection right internal carotid arteriogram].

Fig. 3.20 - Left temporoparietal glioblastoma multiforme. An- giogram of the left internal carotid artery reveals a prominent parenchymal blush and arteriovenous shunting typical of ma- lignant cerebral neoplasms.

vascular guomas nave areas that are avascular

Fig. 3.22 - Right parietal lobe astrocytoma. Contrast enhanced CT shows mural enhancement within a right parietal lobe sub- cortical mass lesion surrounded by much perilesional oedema. The angiogram of the right internal carotid artery demonstrates no hypervascularity. [a) axial CT following IV contrast; b) lat- eral projection right internal carotid arteriogram] OTHER CEREBRAL NEOPLASMS

Fig. 3.24 - Right temporoparietal parenchymal metastatic neo- plastic disease. Contrast enhanced coronal CT demonstrates an enhancing mass lesion adjacent to the skull on the right side. The right internal carotid arteriogram in the lateral projection reveals an intensely hypervascular cortical lesion associated with a tumor blush and arteriovenous shunting. [a) coronal CT following IV contrast; b, c) lateral projection right internal carotid arteriogram].

Fig. 4.1 - Extrapontine myelinolysis in an alcoholic patient. The MRI demonstrates multiple areas of hyperintensity within the hemispheric subcortical hemispheric white matter, the deep hemispheric white matter and the midbrain. [a) coronal FLAIR MRI; b, c, d) axial T2-weighted MRI].

Fig. 4.2 - Two cases of pontine myelinolysis in alcoholic pa- tients. T2-weighted MRI shows a single hyperintense lesion of the pons in each case. [a, b) axial T2-weighted MRI]. The involvement of the mamillary bodies has been demonstrated in 98% of autopsies per- formed on Wernicke sufferers. Using MRI it is possible to demonstrate the involvement of the mamillary bodies primarily in acute cases in which contrast enhancement of the mamillary bodies is observed. However, this finding is not constant and is probably only present in cases in which there is endothelial necrosis with atten-

Fig. 4.3 - Wernicke’s encephalopathy in alcoholic patient. CT only rarely shows an area of hypodensity in the midbrain in cas- es of Wernicke’s encephalopathy, as in this case.

Fig. 4.4 - Wernicke’s encephalopathy in an alcoholic patient. Enhanced MRI shows contrast enhancement within the mamil- lary bodies bilaterally. More craniad T2-weighted scans shows abnormal hyperintensity within the posteromedial aspect of the thalami bilaterally and the hypothalamus. [a), b) T1-weighted MRI following IV Gd; c-e) PD- and T2-weighted MRI].

Fig. 4.5 - Wernicke-Korsakoff syndrome in alcoholic patient. T2-dependent SE a) and PD-dependent sequences b). Wide- spread signal alteration in the dorsal-medial region of the thal- amus bilaterally and in the hypothalamus.

Fig. 4.6 - Wernicke’s encephalopathy in a malnourished 8-year old child. T2-weighted MRI shows hyperintense periaqueduc- tal MRI signal alteration. from convulsions to hallucinations and deliri-

Fig.4.7 - Marchiafava-Bignami disease in alcoholic patient. Sagittal T2 weighted MRI shows marked thinning of the corpus callosum associated with abnormal signal hyperintensity along its entire course. Acquired hepatocellular degeneration syn- drome is a complex illness characterized by changes in consciousness, behaviour and per- sonality often associated with acute or chron- ic kidney disease or liver cirrhosis. It would appear to be linked to alterations in the me- tabolism of nitrogenated substances and alter- ations of the glutamate-glutamine ratio, with an increase in the synthesis of aromatic amino acids and false neurotransmitters. The alter- ations visible on MRI are closely correlated with plasma ammonia levels, but do not seem to be linked to the degree of neuropsychiatric

Fig. 4.8 - Hepatocerebral degeneration in patient with cirrho- sis. The MRI demonstrates an abnormal area of high MRI sig- nal intensity in the globus pallidus bilaterally. [a) axial, b) sagit- tal T1-weighted MRI]. There are a number of sources of methanol, which can be present in solvents, industrial liq- uids, perfumes and counterfeit spirits, thus making methanol intoxication relatively com- mon amongst alcoholics. It manifests clinically as general malaise and headache and may progress to stupor and coma. Necrotic areas are visible in the putamen as hypodense on CT scans and as high signal intensity on T2-de- pendent sequences in MR studies (Fig. 4.9). The appearance of these areas can also be af- fected by the presence of haemorrhagic infarc- tion. Other related necrotic areas can be identi- fied in the subcortical white matter and in the frontal cortex (12, 28, 29).

Fig. 4.9 - Alcoholic patient following consumption of a large quantity of methanol. Coronal T2-weighted MRI reveals high signal intensity within the putamena and in the frontal subcor- tical white matter bilaterally.

Fig. 4.10 - Glycol-ethylene intoxication. Axial CT shows marked hypodensity of the thalami bilaterally.

Fig. 4.11 - Delayed post-hypoxic leukoencephalopathy,. MRI examination performed approximately three hours following admission shows widespread MRI signal hyperintensity of the white matter of the centrum semiovale. Follow up MRI approximately 1 month later shows necrosis within the abnormal hemispheric white matter foci identified on earlier scans. This evolution is consistent with delayed post-hypoxic leukoencephalopathy. As in this case, this phenomenon has been described in heroine addicts following expe- riencing acute cardiorespiratory depression. [a), b) axial T-2 weighted MRI on admission; b) axial T1-weighted MRI on admission; c), one month follow up axial T2-weighted MRI, d) one month follow up T1-weighted MRI]. Intoxication from Methotrexate

Fig. 4.13 - Acute carbon monoxide intoxication with cerebral necrosis. CT undertaken in the acute phase documents bilateral globus pallidus hypodensity and within the anterior frontal white matter on both sides. CT follow up approximately three weeks later reveals bilateral globus pallidus necrosis; MRI performed the same day as confirms globus pallidus necrosis and the frontal subcortical de- generative alteration. [a, b) acute phase axial CT; c) three week follow up CT; d) three week follow up T2-weighted MRI].

Fig. 4.14 - Acute carbon monoxide intoxication with clinicora- diologic resolution. T2-weighted MRI on patient admission shows swelling of the frontal lobe cortex, more prominent on the right side, resulting from cytotoxic oedema. Follow up MRI performed after clinical resolution reveals regression of the frontal swelling. [a, admission T2-weighted MRI; b) follow up T2-weighted MRI].

Fig. 4.15 - Epidural haematoma. The CT examination shows a biconvex blood collection over the right temporoparietal region asso- ciated with marked mass effect. Note the displacement of the surrounding parenchymal structures associated with leftward midline subfalcian herniation and compression of the right lateral ventricle. In the more caudal scan, ipsilateral downward herniation of the uncus is also clearly visible. In addition, there is a fracture in the right temporal bone, with minor fragment displacement. CT follow up three months later documents encephalomalacia of the posterior temporal lobe, perhaps as a result of infarction secondary com- pression-occlusion of the posterior cerebral artery caused by the uncal herniation. [a,,) initial axial unenhanced CT with brain win- dows; b,,) initial axial CT with bone windows; c) three month follow up axial CT].

— CT is the preferred method of imaging in co- ma patients due to its very rapid examination acquisition speeds, with single or multiple slice scanning times faster than one second in latest generation appliances; in addition to its gener- al diagnostic capabilities, it is also very sensitive in recognizing acute and hyperacute phase in- tracranial haemorrhages, in localizing the cra- nial compartment of the bleed (e.g., subdur- al/epidural, subarachnoid, intraparenchymal); finally it is almost universally available in the Fig. 4.17 - Acute hydrocephalus in a case of spontaneous subarachnoid haemorrhage. Unenhanced cranial CT shows an intra- ventricular blood clot at the level of the foramina of Monro and the symmetrical subarachnoid haemorrhage. Also note the di- latation of the lateral ventricles, including the temporal horns, as a consequence of the obstructive hydrocephalus. [a-c) unen- hanced axial CT]

Fig. 4.18 - Subacute cerebral infarction within the right middle cerebral artery territory. Unenhanced cranial CT shows wide- spread cortical-subcortical hypodensity in the right tem- poroparietal region. Moderate mass effect is present, as a result of vasogenic oedema, represented by the effacement of the re- gional superficial subarachnoid spaces and the compression of the right lateral ventricle.

Fig. 4.19 - Diffuse axonal injury (damage). Unenhanced cranial CT shows the presence of multiple, small cortical-subcortical junction haemorrhagic foci. These haemorrhages are an ex- pression of axonal shearing, some of which are not visible due to the absence of bleeding. The parenchymal, and therefore functional, damage is often greater than predicted on the basis of CT alone. [a, b) unenhanced axial CT].

Fig. 4.20 - Cytotoxic oedema. Unenhanced cranial CT reveals a subtle absence of the normal hyperdensity of the left putamen as compared to the contralateral structure, indicating the pres- ence of ischaemic cytotoxic oedema.

Fig. 4.21 - Brain death. Unenhanced cranial CT demonstrates bilateral subdural and subarachnoid blood collections. There is also diffuse brain swelling, with loss of the grey-white matter differentiation, and bilateral compression of the cerebral ven- tricular system due to parenchymal oedema. totoxic oedema. Cytotoxic oedema, an expres- sion of cellular injury, principally involves the cerebral cortex and the basal nuclei of the cerebral hemispheres. edema generally shows a relative reduction in density on CT, a reduction in signal on T1-weighted MR and hyperintensity in T2-weighted sequences. Clin- ical practice has recently witnessed the intro- duction of T2-dependent FLAIR sequences (Fig. 4.22), on which abnormal signal alter- ations adjacent to the superficial and deep sub- arachnoid spaces are more immediately recog- nizable, thanks to the choice of parameters that cancel out the CSF signal; these sequences are currently the most sensitive in demonstrat- ing oedema and pathological tissue in general in the acute phase of patient deterioration. Oedema can also be recognized by its mass ef- fect, however, this may be very modest in the cytotoxic phase; in this early time period, the oedema may appear on CT not as hypodensity, but simply as a loss of the slight normal physi-

Fig. 4.22 - Global hypoperfusion. Unenhanced cranial CT performed 24 hours after a cardiac arrest during heart surgery documents relative isodensity of the lenticular nuclei bilaterally. Axial T2-weighted MRI 48 hours after the event reveals MRI signal hyperinten- sity within the lenticular nuclei. Axial T2-weighted and FLAIR MRI 3 weeks later demonstrates minor dilation of the ventricular sys- tem as a result of resolution of cerebral swelling, and an increase in the hyperintensity of the MRI signal of the lenticular nuclei. The FLAIR image at 3 weeks shows hyperintense cortical-subcortical MRI signal alterations. [a) initial axial CT; b) axial T2-weighted MRI at 48 hours; ¢) axial T2-weighted MRI at 3 weeks; d) axial FLAIR MRI at 3 weeks].

Tab. 4.1 - Prognostic evaluation of cerebral lesions by SPECT.

Tab. 4.2 - Prognostic evaluation of brain lesion using SPECT. In our practice we use a rotating gammacam- era with a single dedicated head (GE 400 AC, Milwaukee, Wisconsin, USA) a few minutes af- ter an intravenous injection of freshly prepared 950 MBq of 99mTc -HM-PAO (Ceretec, Amer- sham-Sorin, Saluggia, Italy).The following ac- quisition parameters are used: 64 planar images with a 1.6x zoom, 64 x 64 pixel matrix, radius of rotation = 15 cm (on average), 20% symmetric window on photopeak of 140 keV of the 99mTc, acquisition time 25-30 minutes and a general purpose parallel hole collimator. TYyraeune then aAYVTAMmMIIinNnatinn i ttratiant 1c rant

Fig. 4.23 - Normal SPECT examination. SPECT examination of the brain utilising 99mTC HM-PAO in a healthy subject for comparison.

Fig. 4.24 - Post-traumatic coma. Unenhanced CT shows no abnormality. The CT examination (Fig. 4.24) was nega- tive for focal lesions; the BAEP’s determination (Brainstem Auditory Evoked Potentials) was normal. The scintigraphic study of cerebral perfusion in this patient showed (Fig. 4.25) multiple small perfusion defects in both cere- bral hemispheres, with good perfusion of the cerebral cortex. The patient came out of coma approximately one month from the injury. He was subsequently referred to a functional reha- bilitation centre in order to complete the re- covery of neuromuscular activity. To reiterate, in studies of rCBF in cere- brovascular disease, SPECT is able to docu- ment flow alterations at an early stage, within a few hours after the trauma. This is observed be- fore CT becomes positive, which in this stage occurs in less than 1 case every 5. Serial rCBF studies have considerable prognostic impor- tance: patients with limited perfusion defects subsequently generally show complete or near complete recovery, whereas almost 50% of pa- occurs in less than 1 case every 5. Serial rCbr

Fig. 4.25 - Same case as in Fig. 4.24. Left hand images: SPECT images reveal multiple small perfusion defects. Right hand images: Another normal case is shown on the right for comparison.

Fig. 4.26 - Acute cerebrovascular pathology. Unenhanced CT demonstrates a large intraparenchymal haemorrhagic focus associated with rupture into the ventricular system and ventricular dilatation. The first scintigraphic study in this patient documented a marked reduction in blood sup- Tab. 4.3 - Relationship between CBF, O, transport (DO,) and cerebral oxygen consumption (VO,).

Fig. 4.27 - Same case as in Fig. 4.26. Note that the SPECT im- ages reveal extensive perfusion defects and evidence of cere- bellar diaschisis.

Fig. 4.29 - Post-anoxic coma. The SPECT study demonstrates diffuse, bilateral marked reduction in perfusion of the cerebral cortex. Fig. 4.28 - Same case as in Figs. 4.26 and 4.27. The follow up SPECT examination shows an improvement in brain perfusion.

Fig. 4.30 - Same case as in Fig. 4.29. A SPECT follow up ex- amination conducted seven days later shows that the global hy- poperfusion of the left cerebral hemisphere persists. The CT study in this patient was negative (not shown).

Fig. 4.31 - Same case as in Figs. 4.29 and 4.30. Two weeks after the first examination, the SPECT images show good cerebral perfusion recovery.

Fig. 4.32 - Diffuse cerebral cytotoxic oedema in a patient with subarachnoid haemorrhage. Unenhanced CT shows swelling of the brain with compression of the ventricular and subarach- noid spaces of the supratentorial compartment and posterior fossa. Note also the disappearance of the grey-white matter dif- ferentiation indicating diffuse cytotoxic oedema.

Fig. 4.33 - Brain death. Selective right carotid arteriogram reveals an absence of flow of contrast past the base of the cranium via the internal carotid artery. Similar findings were observed in the left carotid and vertebral arteries (not shown).

Fig. 4.34 - Brain death. SPECT scans reveal a complete absence of cerebral and cerebellar perfusion. [a) axial a), sagittal b) and c) coronal SPECT]. doubts have been voiced concerning the use of conventional cerebral angiography for verifying BD (20).

Fig. 4.35 - Same case as Fig. 4.34. The CT images show only the presence of a deep intraparenchymal haematoma.

Fig. 4.36 - SPECT, CT and MRI comparison of brain death. See text. Fig. 4.37 - SPECT, CT and MRI comparison of brain death. See text.

Fig. 4.40 - SPECT, CT and MRI comparison of brain death. See text.

Fig. 4.38 - SPECT, CT and MRI comparison of brain death. See text.

Fig. 4.41 - SPECT, CT and MRI comparison of brain death. See text.

Fig. 4.39 - SPECT, CT and MRI comparison of brain death. See Text.

Fig. 4.42 - SPECT, CT and MRI comparison of brain death. See text. ols are adopted in all hospitals were BD certi-

Fig. 4.43 - Craniotomy alterations. Unenhanced axial CT shows expected alterations of a recent prior craniotomy procedure to remove a left temporoparietal neoplasm.

Fig. 4.45 - Spontaneous pontine haemorrhage. Unenhanced ax- ial CT demonstrates an acute pontine haematoma in a patient with plasmacytopenia following the surgical removal of a neo- plastic metastatic deposit in the right temporal region. Extraaxial haemorrhage may occur in the form of subgaleal, epidural and subdural haematomas. The pathogenic mechanism most commonly underlying subgaleal haematomas is inadequate haemostasis during the reconstruc- tion phase of the muscular and subcutaneous planes, which results in a blood collection be- low the surgical flap.

Fig. 4.44 - Postoperative intra-axial haemorrhage. Axial CT (a) shows extensive intraparenchymal haematoma in patient recent- ly operated on for large frontal meningioma (b). [a) postopera- tive unenhanced axial CT; b) preoperative T2-weighted MRI].

Fig. 4.46 - Postoperative extra-axial haemorrhage. Unenhanced axial CT reveals an acute epidural haematoma over the frontal convexity in patient following surgery for ipsilateral tem- poroparietal meningioma. Cerebral oedema may be caused by a num- ser of factors, such as surgical manipulations Infections

Fig. 4.47 - Infection of the surgical site in patient previously op- erated on for intracranial meningioma. Axial CT after contrast medium administration shows extensive swelling and enhance- ment of the superficial soft tissues overlying the temporal sur- gical site which ultimately proved to be active infection. Following craniotomy, the bone flap is devascularized and therefore devitalized. For this reason, bacterial proliferation and conse- quently bony infection is facilitated (16). Stan- dard treatment of bone flap infection involves the removal of the infected bone and the drainage of any associated suppurative collec- Infarction

Fig. 4.48 - Postoperative cerebral infarction. Unenhanced axial CT shows an extensive right hemisphere infarction associated with mass effect in patient recently operated on for aneurysm of the right internal carotid artery.

Fig. 4.49 - Fracture of surgical spinal appliance. A lateral radi- ograph of the cervical spine shows a fracture of the upper ver- tebral body screw in a patient with cervical myelopathy operat- ed on for spinal cord decompression and anterior fusion.

Fig. 4.50 - Collapse of spinal interbody bone graft in patient undergoing for diskectomy and spinal fusion. A lateral radi- ograph of the cervical spine shows postoperative intervertebral disc space collapse at the C6-7 level following diskectomy and attempted bone graft placement.

Fig. 4.51 - Dislocation of surgical appliances following verte- bral collapse in patient with multiple myeloma operated on for posterior stabilisation. [axial CT].

Fig. 4.52 - Over insertion of transpedicular screw with im- pingement upon the aorta. Axial T1-weighted MRI shows pen- etration of the transpedicular screw on the left side through the anterior cortex of the vertebral body associated with impinge- ment upon the abdominal aorta.

Fig. 5.1 - Acute cervical spine trauma. a), b) Axial CT of the cervical region includes the distance extending from the entire thickness of the skull base to at least the bottom of C2, scanned with 2mm thickness or less slices. ¢), d) Contiguous axial sections show a com- minuted fracture of the anterior arch of the C1 with associated involvement of a lateral mass. The posterior arch of C1 is intact.

Fig. 5.2 - Acute cervical hyperextension trauma. a) Lateral x- ray of the cervical spine shows a hangman fracture associated with anterior subluxation of C2 and bilateral fractures of the posterior arch of C1. b) Lateral scanogram and c) d) axial CT confirms the x-ray findings of the C1 and C2 fractures.

Fig. 5.2 (cont.) - c), d) oblique scanograms highlight the distal por- tion of the cervical spine at the cervicothoracic junction. e), f) Axial CT is performed initially with no angulation utilising 4 mm thick slices covering the entire cervical spine; this is then followed by a second set of axial CT scans utilising thinner slices (2 mm or less) extending from C1 to C3, angled generally to the cross-sec- tional plane of the longitudinal axis of the cervical spine. g) 2 mm- thick axial CT scans demonstrate the C1 and C2 fractures.

Fig. 5.2 (cont.) - h), i) Sagittal reconstructions of the 4 m (h) and the 2 mm (i) thick slides. Note the relative difference in spatial definition. j) A three-dimensional reconstruction clearly shows the bilateral fractures of the posterior arch of C1 and confirms the integrity of the anterior arch.

Fig. 5.3 - Acute cervical spine trauma. a) Lateral x-ray of the cervical spine shows a fracture of the anterior-inferior corner of C3 associated with a very minor retrolisthesis of C3 on C4. There is also a malalignment of the body of C2 with relation- ship to C1. b) Lateral CT scanogram proscribed to acquire ax- ial images extending from C1 to C4. tions in the sagittal and coronal planes in order to show the subluxation of the articular facet processes.

Fig. 5.3 (cont.) - c) Axial CT showing a comminuted fracture of the right occipital condyle, d) rotation of the odontoid process with relationship to C1 and e) a comminuted fracture of C2 at the base of the odontoid process. f) Coronal CT reconstruction poorly demonstrates the fracture at the base of the odontoid process. g) Sagittal CT reconstructions show the fracture at the odontoid base of C2 and the posterior dislocation of the C3 vertebral body on that of C4.

Fig. 5.4 - Acute cervical spine trauma. a) Lateral cervical CT scanogram suggests the presence of rotation-subluxation in the mid cervical spine. b) Right anterior-oblique scanogram show- ing the malalignment of the posterior aspect of the C6-7 verte- brae (arrows). c) Left anterior-oblique scanogram shows nor- mal alignment of the bony structures. d) Lateral x-ray confirms the finding of rotation of the distal cervical spine and shows the presence of a fracture of the anterior-superior corner of C7 and retrolisthesis of C6 on C7.

fracture-dislocations. CT must be performed using thin slices, extending from the foramen magnum through C4 and must be comple- mented by reconstructions in the sagittal and coronal planes. CT is necessary when the pa- tient feels pain in the upper neck, when cervi- cal spine x-rays are negative or when radiogra- phy shows thickening of the perivertebral soft tissues.

Fig. 5.4 (cont.) - j), k), 1) Coronal reconstructions showing a fracture of C7 (j), fractures of the lateral masses (k) and lateral displacement of the spinous process of C6 (I). m), n), 0), p) Sa- gittal reconstructions: the reconstruction on the left side (m) demonstrates comminuted fractures of the posterior articular spinal facet processes; the reconstruction on the right side (p) shows normal relationships of the posterior articular spinal fa- cet processes; n-o) adjacent parasagittal reconstructions show the fracture of the body of C7 and the greater intersegmental rotational subluxation to the right of midline (n).

Fig. 5.5 - Acute cervical spine trauma. a) Lateral radiograph conducted shows anterior subluxation of C5 on C6, an increase in the interlaminar distance and dislocation of the posterior ar- ticular facets. b) Anteroposterior radiograph shows deviation of the spinous process of C5 to the right indicating a probable rotational dislocation. c, d) Right-oblique projection radi- ographs confirms the anterior dislocation of the articular facets associated with probable fracture of the pedicle of C5. d) Left- oblique projection radiograph shows a similar finding, but with a smaller displacement than that of the contralateral side. Note the malalignment of the contralateral vertebral pedicles.

Fig. 5.5 (cont.) - e) Lateral CT scanogram . f) Axial CT shows asymmetric dislocation of the body of C5 with relationship to C6. g) Axial CT shows a fracture of the right pedicle of C5. h) Image summation technique including the bodies of C5 and C6 showing the C5-6 anterior subluxation. i) Oblique-sagittal re- construction method from preceding axial image set.

Fig. 5.5 (cont.) -j), k) Parasagittal right and left reconstructions that show the asymmetric dislocation of posterior articular spi- nal facets. essential to supplement the examination with high resolution multiplanar reconstructions and with conventional tomography.

Fig. 5.7 - Acute lumbar hyperflexion trauma. a) Lateral CT scanogram shows a wedge fracture of L1. b, c) Axial CT sec- tions demonstrating a comminuted fracture of L1 and some retropulsion of bony fragments into the central spinal canal in- dicating a burst fracture. (1: anterior column; 2: middle col- umn; 3 posterior column) d, e) Sagittal reconstructions show the posteriorly displaced fragment (e).

Fig. 5.7 (cont.) - £) Three-dimensional (3-D) CT sagittal plane sectional reconstruction in the sagittal plane shows a relative increase in the density of the vertebral marrow in three adjacent vertebrae (darker vertebral body shading), indicating that there is marrow com- pression and concentration of bony trabeculae. g) 3-D CT reconstruction demonstrating a superficial overview of the vertebral trauma. h), i) 3-D CT reconstruction of L1 shows the posterior vertebral body fracture, the central spinal canal stenosis and the widening of the posterior spinal facet joint articular space on the left side (arrows). by this posterior displacement of bone with di- rect trauma to the spinal nerves/roots and spinal cord. Trauma of the thoracic and lumbar segments of the spinal column

Ligamentous trauma can be detected direct- ly or indirectly on medical imaging studies. However, while MRI is capable of visualizing the spinal ligaments, it may not be able to dif- ferentiate between ruptured ligaments and ad- jacent tissue injury, all of which may be hy- pointense.

Fig. 5.8 - Acute thoracic spine trauma. The MRI images show a burst fracture of the T12 vertebral body, with posterior dis- placement of bony fragments into the central spinal canal and resulting stenosis. There are no visible signal alterations of the spinal cord. [a) Sagittal T1-weighted MRI; b, sagittal T2- weighted MRI; c) axial T2-weighted MRI].

Fig. 5.9 - Acute lumbar spine trauma. The MRI reveals an L2 burst fracture with posterior displacement of the upper portion of the vertebral body into the central spinal canal and conse- quent canal stenosis. [a) sagittal Tl-weighted MRI, b) sagittal T2-weighted MRI].

Unquestionably, MRI is the imaging exami- nation technique of choice in the evaluation of spinal cord injury (1, 2). In the acute phase, this facilitates the identification of those conditions that may benefit from emergency surgical treat- ment, while also enabling an immediate prog- nostic judgement to be made. MR examina- tions should aim in particular to detect oedema,

Fig. 5.11 - Acute cervical spine trauma. MRI in a patient with bilateral C2 pedicle fractures (Hangman fracture). a), b) Sagit- tal, axial T2-weighted MRI. Fig. 5.12 - Acute thoracic spine hyperflexion trauma. The MRI study shows a fracture of the T9-10 vertebrae with anterior wedging of the vertebral bodies. There is also evidence of oede- ma of the involved vertebral bone marrow. The spinal cord, al- though deflected by posterior displacement of the T9 vertebra, does not show intrinsic signs of MRI signal alteration. [a) sagit- tal T1-weighted MRI, b) c) sagittal, axial T2-weighted MRI].

Fig. 5.13 - Acute cervical spine trauma. The images show < posttraumatic C4-C5 disk herniation and anterior subluxatior of C4 on C5, with minor impingement upon the anterior sur face of the cervical spinal cord. A minor C4 compression frac ture is also noted. a) Sagittal T1-weighted MRI; b) sagittal T2. weighted MRI.

Fig. 5.16 - Acute cervical spine flexion trauma. The MRI ex- amination shows anterior dislocation of C6-C7 associated with marked stenosis of the central spinal canal. The spinal cord is severely compressed at this level, revealing oedema and swelling of the cord above and below the compression. [a) sagittal T1-weighted MRI; b) sagittal T2-weighted MRI].

Fig. 5.17 - Acute cervical spine trauma. The MRI images reveal straightening of the physiologic cervical lordotic sagittal spinal curvature. In addition, there is a compression fracture of the C6 vertebral body. The spinal cord is swollen and is hyperintense on T2*-weighted MRI due to oedema associated with cord con- tusion, but no evidence of acute haemorrhage can be identified. [a) sagittal T1-weighted MRI; b) Sagittal T2*-weighted MRI].

Fig. 5.18 - Acute cervical spine trauma. The MRI examination shows a loss of the physiologic cervical lordotic sagittal spinal curvature and pre-existent central spinal canal stenosis. A focal area of spinal cord contusion (i.e., oedema and swelling) can be seen on the right side at the C4 level as well as a presumed trau- matic posterior disk herniation associated with underlying spinal cord compression. [a, sagittal T2-weighted MRI; b) axi- al T2-weighted MRI].

Fig. 5.19 - Acute thoracic spine trauma. The MRI acquisitions reveal a compression fracture of the body of T12 associated with T12-L1 anterior subluxation and central spinal canal nar- rowing. In addition, there is a small anterior epidural haematoma at T11. MRI signal hypointensity is present within the spinal cord on the T2* acquisition due to acute haemor- rhagic contusion (deoxyhaemoglobin). a) [sagittal T1-weighted MRI; b) sagittal T2*-weighted MRI].

Fig. 5.20 - Chronic spinal cord trauma. MRI images in a case of late follow up of a burst fracture of L1 revealing diffuse spinal cord atrophy and a focal area of myelomalacia within the conus medullaris. [a) sagittal T1-weighted MRI; b) sagittal T2- weighted MRI].

Fig. 5.21 - Chronic spinal cord trauma. MRI in the chronic phase following spinal cord trauma reveals a posttraumatic sy- ringomyelia cavity extending from C6-T1. [a) sagittal T1- weighted MRI; b) sagittal T2-weighted MRI, c) axial T2- weighted MRI].

Fig. 5.22 - Chronic spinal cord trauma. MRI examination sev- eral years following flexion injury and spinal cord contusion shows postsurgical changes and a multisegmental syringohy- dromyelia cavity of the lower thoracic spinal cord. [a) sagittal Tl-weighted MRI; b sagittal T2-weighted MRI, c) axial T2- weighted MRI]. Fig. 5.21 (cont).

malacia and frank syringomyelia formation, the latter of which may be progressive. Spinal cord atrophy appears as a reduction in the calibre of the cord both at the level of trauma as well as caudally. Non-cystic/cystic myelomalacia ap- pears as an area that is hyperintense on T2- weighted images in the chronic phase following trauma. This alteration is often poorly visual- ized if at all on T1-weighted sequences, and is associated with cord atrophy (Fig. 5.20). Sy- ringomyelia is easily demonstrated on both T1- and T2-weighted sequences, may be well de-

Fig. 5.23 - Acute spinal trauma. Sagittal T1l-weighted MRI re- veals anterior C4-C5 subluxation associated with a multilevel anterior epidural haematoma deflecting the spinal cord poste- riorly,

CT typically reveals a diminution in number but thickening of the individual trabeculae Some rarer forms of benign tumour include osteochondromas, osteoid osteomas, osteoblas-

Fig. 5.24 - Vertebral haemangioma. The lateral radiographic examination shows the typical vertical striations consistent with a bone marrow haemangioma at the L3 level. The T1-weighted MRI reveals bone marrow hyperintensity typical of vertebral haemangioma. [a) Lateral radiograph of lumbar spine; b) sagittal T-1 weighted MRI.

Fig. 5.26 - Osteoblastoma of the posterior arch of C5. The MRI examination reveals a hypointense lesion within the posterior arch of C5 on the right. The CT study shows a sclerotic mass lesion of the posterior arch of C5. [a) oblique-sagittal T1- weighted MRI; b) axial T1-weighted MRI; c) axial CT].

Fig. 5.29 - Iatrogenic epidural abscess. The MRI study shows a mass forming posterior epidural lesion that displaces the nerve roots of the cauda equina forwards. There is inhomogeneous enhancement of this process following IV Gd administration. [a) sagittal T2-weighted MRI; b) unenhanced sagittal T1-weighted MRI; ¢) sagittal T1-weighted MRI following IV Gd; d) coronal T1-weighted MRI following IV Gd].

Fig. 5.31 - Subacute spondylodiskitis caused by brucella species. The MRI study shows a simultaneous pathologic involvement of two adjacent vertebrae and the intervening intervertebral disk. There is irregular contrast enhancement in all involved struc- tures following IV Gd administration. The perivertebral soft tis- sues demonstrate limited involvement. [a) unenhanced sagittal T1-weighted MRI; b) sagittal T1-weighted MRI following IV Gd; c) coronal T1-weighted MRI following IV Gd].

Concerning the intradural component of the neurinoma, myelography provides typical findings of spinal cord displacement and compression, and cup-shaped blockage of the contrast medium by the neoplasm; myel- ography provides no information on the ex- tradural component of the lesion. CT fol- lowing the myelogram, however, reveals the entire extent of the tumour together with the bony remodelling when present. Neurinomas generally show heterogeneous enhancement on CT after IV iodinated contrast medium administration. Neurinomas originate from Schwann cells and favour the posterior spinal nerve roots as sites of origin. They are more frequently observed at cervical and thoracic spinal lo- cations, but can involve the roots of the cauda equina. These neoplasms can be mul- tiple in Recklinghausen’s disease (Fig. 5.37). Neurinomas present in an intradural-ex- tramedullary location, can extend into the neural foramen and even grow outside the spinal canal (i.e., hourglass-shaped mass). In such cases on x-rays it is possible to observe widening of the neural foramen and, if suf- ficiently large, the presence of a paraverte- bral mass. If voluminous, neurinomas can al-

Fig. 5.32 - Spondylotic myelopathy. Multilevel degenerative discovertebral alterations result in central spinal canal stenosis and asso- ciated cervical spinal cord compression. In addition, a focal area of hyperintense MRI signal is observed on the T2-weighted image at the C5 level consistent with myelomalacia. [a) sagittal T1-weighted MRI; (b) sagittal T2-weighted MRI.

Fig. 5.33 - Os odontoideum. The MRI images show anterior subluxation of the C1 vertebral body and adjacent odontoid process in relationship to the vertebral body of C2. In addition, the spinal cord is compressed between the posterior bony arch of C1 and the vertebral body of C2, and the intervening spinal cord is hyperintense indicating underlying myelomalacia. Note the partial reduction of the dislocation in extension. [a): neutral T1- and T2-weighted sagittal MRI; b): flexion T1- and T2-weighted sagittal MRI; c): ex- tension T1- and T2-weighted sagittal MRI].

Fig. 5.34 - Spontaneous subacute epidural haemorrhage in patient with plasmacytopenia. The MRI examination shows mass forming posterior epidural haematoma. IV Gd enhanced MRI shows minor peripheral enhancement around the haematoma. The remaining MRI study reveals hypointensity of the margins of the haematoma consistent with early haemosiderin evolution and anterior spina cord deflection-compression. [a) unenhanced sagittal T1-weighted MRI; b) T1-weighted MRI following IV Gd; c) T2-weighted MRI d) sagittal T2-weighted MRI with fat suppression; e) axial T1-weighted MRI; (f) axial T2-weighted MRI]. The rarer mass-forming lesions of the sub- arachnoid space include (in decreasing order of

Fig. 5.35 - Extradural arachnoid cysts. The MRI images show a posterolateral intraspinal mass lesion that has an MRI signal that is slightly higher than that of CSF. There is associated cra- nial and caudal displacement of the supra- and subjacent epidural fat surrounding the mass indicating its epidural loca- tion. There is also minor mass effect upon the thecal sac and ex- tension of the cyst into the contiguous, expanded spinal neural foramen. [a) midline sagittal T2-weighted MRI; b) parasagittal T2-weighted MRI; c) midline T1-weighted MRI; d) coronal T1- weighted MRI; e) midlesion axial T2-weighted MRI; f) subja- cent axial T2-weighted MRI].

dymomas and haemangioblastomas. Astrocy- tomas represent 25-30% of all intramedullary tumours presenting in adults and more than 90% of all spinal cord tumours in children. Typ- ical astrocytomas cause a fusiform expansion of the spinal cord. If a cystic component is present, it is typically intratumoral, although satellite cysts and secondary syringomyelia are observed. Astrocytomas reveal moderate, irregular en- hancement after TV contrast medium adminis- tration. The boundaries of the astrocytoma are usually poorly defined. The evolution of such le- sions into glioblastoma multiforme is occasional- ly seen (Fig. 5.40).

including intradural arachnoid cysts and lateral spinal meningoceles (associated with von Reck- linghausen’s disease).

Fig. 5.36 (cont.). demonstrate intense, rather homogeneous en- hancement after IV gadolinium contrast medium administration. Originating from ependymal cells, they occupy a less eccentric location that astrocytomas. They are most commonly encountered in adolescents and young adults. Not uncommonly they may be located in the cauda equina because of em- bryonic rests of ependymal cells in the filum terminale (Fig. 5.42). oe i a4 commonly encountered in adolescents and

Fig. 5.37 - Multiple spinal schwannomas in a subject with von Recklinghausen’s disease. The MRI imaging study demonstrates multi- ple intramedullary and intradural-extramedullary masses in the cervicothoracic region, which appear hyperintense on T2-weighted MRI, and show contrast enhancement following IV Gd administration. Also note the multiple perimedullary masses and the numer- ous masses within the nerve roots of the cauda equina. [a) sagittal cervicothoracic T2-weighted MRI; b) sagittal cervicothoracic T1- weighted MRI following IV Gd; c) axial cervical T1-weighted MRI following IV Gd; d) sagittal midthoracic T1-weighted MRI follow- ing IV Gd; e) axial upper thoracic T1-weighted MRI following IV Gd; f): sagittal lumbosacral T1-weighted MRI following IV Gd]. MRI is also useful for the diagnosis of acute spinal cord involvement in multiple sclerosis and sudden onset ischaemic medullary disease. Multiple sclerosis (MS) (6, 9) is a demyelinating disease that most frequently affects females, and which presents with variable neurological

Fig. 5.37 (cont.). signs and symptoms often in a relapsing-remit- ting pattern. Spinal cord involvement typically affects the dorsolateral regions of the cervical cord. Although isolated medullary involvement (i.e., in the absence of cerebral disease) can be observed in up to 10% of cases, nevertheless, when a spinal cord lesion of a probable de- myelinating nature is identified using MRI, a

signs and symptoms of progressive myelopathy (venous congestion or arterial steal) or with the onset of an acute neurological deficit secondary to spontaneous intramedullary and/or sub- arachnoid haemorrhage. In such cases MRI demonstrates serpentine flow voids within ab- normal coiled vessels, focal spinal cord swelling, haemorrhage in various stages, and hyperintensity on T2-weighted images adjacent to the nidus of the malformation, representing oedema, ischaemia and/or gliosis. After TV con- trast medium administration, depending upon flow velocity and intravascular turbulence, en- hancement is seen in some of the vascular com- ponent and occasionally within the surround- ing parenchymal component if the latter has undergone insult from spontaneous adjacent parenchymal haemorrhage of the vascular mal- formation or if related cord infarction has oc- curred. ae = - ee os

Fig. 5.38 - Intradural spinal metastasis in a patient with primary intracranial pinealoblastoma. The MRI examination shows that the spinal cord is compressed posterolaterally by an enhancing intradural-extramedullary mass consistent with subarachnoid dissemination of the pinealoblastoma. [a) sagittal T2-weighted MRI, b) sagittal T1-weighted MRI; c) axial T1-weighted MRI following IV Gd].

Fig. 5.39 - Metastatic neoplastic leptomeningeal spread in a case primary pineal region neoplasm. Sagittal T1-weighted MRI following IV Gd administration shows diffuse lep- tomeningeal contrast enhancement consistent with subarach- noid dissemination of the primary intracranial neoplasm.

mations. They do not typically cause haemor- rhage, but instead patients present with either chronic signs and symptoms of progressive myelopathy secondary to spinal cord ischaemia that is generated by venous congestion, or acute clinical findings consistent with sudden myelopathy secondary to spinal cord ischaemia

Fig. 5.42 - Ependymoma of the conus medullaris. The MRI study shows a septated partially cystic mass with a mural nodu- lar area of contrast enhancement. [a) sagittal T2-weighted MRI, b) sagittal T1-weighted MRI following IV Gd].

Fig. 5.41 (conz.). spinal cord infarction. T2-weighted MRI shows an indentation of the posterior surface of the spinal cord by dilated intradural-perimedullary veins (Fig. 5.45), a finding that can often be more clearly visible after TV gadolinium admin- istration; multilevel intramedullary spinal cord hyperintensity is also observed in acutely pre- senting cases as a result of the evolving infarct

Fig. 5.44 - Ischaemia of the thoracic spinal cord associated with spinal dural arteriovenous fistula. T-2 weighted MRI demon- strates high signal intensity within the central region of the conus medullaris associated with central medullary hyperinten- sity and vascular flow voids over the posterior surface of the thoracic spinal cord. [a) sagittal T1-weighted MRI; b) axial T2- weighted MRI; c) axial T-weighted MRI].

Fig. 5.43 - Thoracic intramedullary multiple sclerosis. T2 weighted MRI shows an area of intramedullary high signal in- tensity at the T8-9 level associated with minor focal swelling of the spinal cord. Contrast enhancement is seen within the area of MRI signal abnormality following IV Gd administration. [a) sagittal T2-weighted MRI; a) sagittal T-1 weighted MRI follow- ing IV Gd].

Fig. 5.45 - Thoracic spinal dural arteriovenous fistula. The MRI study reveals subarachnoid space MRI signal irregularity posterior to the spinal cord, which becomes much more evident on the T2-weighted images due to the presence of serpentine vascular flow voids. [a) sagittal T1-weighted MRI; b) sagittal T2-weighted MRI, c) coronal T2-weighted MRI].

Fig. 5.46 - Chronic haemorrhage within thoracic intramedullary cavernous angioma. T2*-weighted sagittal MRI reveals hy- pointensity within the upper thoracic spinal cord as a conse- quence of deposition of haemosiderin associated with thrombo- sis-haemorrhage within an intramedullary cavernous angioma.

Fig. 5.47 - Acute haemorrhage within intramedullary cavernous angioma. The spinal T1-weighted spinal MRI images demon- strate an extensive acute-subacute (deoxyhaemoglobin and methaemoglobin) thoracic intramedullary haemorrhage associ- ated with an intramedullary cavernous angioma showing intrin- sic hypointensity on T2-weighted acquisitions consistent chron- ic peripheral microhaemorrhages (haemosiderin). The MRI of the brain showed several cavernous angiomas demonstrating the multicentric potential of this pathologic process. [a) sagittal T2- weighted spinal MRI b) sagittal T1-weighted weighted spinal MRI; c) sagittal T2*-weighted spinal MRI; d) axial T1-weighted spinal MRI; e) axial T2*-weighted cranial MRI.

fections from adjacent perispinal tissues or from penetrating trauma. T2-weighted MRI demonstrates an intramedullary mass that is hyperintense on T2-weighted sequences and reveals rim enhancement after IV gadolinium administration. Distinguishing this pattern from other spinal cord lesions such as neopla- sia is not always possible on the basis of the images alone.

Spinal cord abscess formation is rare and is usually caused by the direct extension of in-

Fig. 5.48 - Radiation induced thoracic myelitis/spondylitis three years following radiotherapy. T2-weighted MRI with fat suppression shows hyperintense MRI signal within the thoracic spinal cord and within the bone marrow of several contiguous vertebral bodies, both of which are caused in this case by the preceding radiation therapy. Axial T2*-weighted images demonstrate again the intramedullary location of the patholog- ic process. No contrast enhancement of the intramedullary process can be identified. Note the postsurgical alterations. [a) sagittal T2-weighted MRI; b) sagittal T1-weighted MRI follow- ing IV Gd; c) axial T2*-weighted MRI].

Fig. 6.1 - Hypoxic-ischaemic injury in newborn. a, b) Unenhan- ced CT shows widespread hypodensity of the subcortical and periventricular white matter and enlargement of the cerebral ventricular system.

Fig.6.3 - Intraparenchymal haematoma caused by AVM hae- morrhage. a, b) Unenhanced CT demonstrates inhomogeneous right frontoparietal intraparenchymal haemorrhage associated with compression of the right lateral ventricle and contralateral shift of the midline structures.

Fig.6.4 - Ischaemia of the basal ganglia. a) Unenhanced CT shows hypodensity in the head of the caudate nucleus and the frontal aspect of the putamen on the right side, with involve- ment of the anterior limb of the internal capsule. b) Corre- sponding MRI.

Fig.6.6 - Moya-Moya syndrome. a) coronal MR angiogram shows that the flow signal of the internal carotid arteries is not visible in an intracranial vessels above the supraclinoid segments of the internal carotid artery siphons. b) MR angiogram reveals absence of flow signal in the arterial vessels of the circle of Willis, which have been replaced by a number of small, irregular vessels at the base of the brain. c) T2-weighted MRI demonstrates poor visualisation of the anterior and middle cerebral arteries and the presence of nu- merous irregular vascular structures.

This is a rare progressive idiopathic condi- tion typically encountered in children and ado- lescents and adult women. The most common

Fig.6.7 - Cerebral haematoma. a) T1-, b) T2-, c) T2*-, d) T1-weighted MRI shows a large extracranial haemorrhage in the right pa- rietal region.

Fig.6.8 - Acute extradural haematoma. CT shows a biconvex extradural haemorrhage in the right frontoparietal region. Marked mass effect upon the underlying cerebral structures is present.

edges of a skull fracture. Vascular and CSF pul-

Fig. 6.9 - Posterior fossa extradural haematoma. a) CT shows a fracture of the base of the skull involving the occipital bone on th« left with anterior extension into the left petrous bone. b, c and d) CT reveals a posterior fossa extradural haemorrhage with signs o compression on the left cerebellar hemisphere and the 4" ventricle.

Fig.6.10 - Acute subdural haematoma. Unenhanced CT shows a) a left occipital skull fracture and b) an acute right frontal subdural haematoma. following arterial laceration in the space be-

Fig.6.11 - Chronic subdural haematoma resulting from shaking injury in child. Unenhanced CT demonstrates a chronic left he- misphere subdural haematoma with a fluid-fluid level due to the sedimentation of the haemorrhagic content. Also note the signs of compression of the left lateral ventricle and shift of the midline cerebral structures.

Therefore, with the exception of certain sit- uations (e.g., very small extraaxial haematomas nveethe exanial ranwawnr ap the wmoeretart ere MRTis presently assuming a more important role in the evaluation of paediatric patients with acute head injuries. The advantages of the technique include safety, multiplanar imaging capability, excellent anatomical definition, ma- jor blood vessel identification without using contrast agents and critical posterior fossa analysis absent of artefacts typically present on CT. The technique’s main disadvantages are the relatively long acquisition times and the unsuit- ability of the method in critical patients requir- ing continuous extracorporeal monitoring and life support devices. — r r

The headache may present in a frontoorbital

Fig. 6.14 - Acute disseminated encephalomyelitis (ADEM). a, b) CT demonstrates areas of hypodensity of the subcortical white matter. c-e) axial T2-weighted and d) coronal T2-weigh- ted MRI reveals regions of signal alteration in the subcortical white matter with associated mass effect.

Fig. 6.14 (conz.). lution of the illness. In cases where there is a mobile intraventricular mass lesion, the headache has a positional character whereby head movements can alter its intensity. These headaches are refractory to even the most pow- erful analgesics. The vomiting is sudden and “projectile” in character, and is not preceded by nausea; it is often the first sign of illness.

mass with a vermian or hemispheric location. They are frequently cystic and slightly hypo- dense on unenhanced imaging studies. After [V contrast medium administration, there is en- hancement in up to 50% of cases. On MRI the solid components are typically hypointense on T1-weighted images and hyperintense on T2- weighted acquisitions. The signal characteris- tics of the cystic components depend on the content of the cavity. Uncomplicated, simple cysts yield an MR signal similar to that of CSF; intracystic necrotic material on the other hand produces a signal on T1-weighted images that is slightly hyperintense in comparison to CSF, which becomes yet more hyperintense on T2- weighted sequences.

Fig.6.16 - Obstructive hydrocephalus associated with posterior fossa medulloblastoma. a) sagittal, b) axial and ¢) coronal T1- weighted MRI following IV gadolinium administration reveals inhomogeneous enhancement of a midline posterior fossa mass associated with poorly defined borders and with signs of com- pression of the 4" ventricle and brainstem. Note the early ob- structive hydrocephalus.

Fig.6.17 - Papilloma of the choroid plexus. a) CT shows an intraventricular mass lesion associated with obstructive hydrocephalus. b) PD-weighted and c) T2-weighted MRI shows an intraventricular mass lesion with inhomogeneous signal on long TR sequences, in part possibly due to intratumoural macroscopic neoplastic vasculature. Also noted is obstructive hydrocephalus and signs of transe- pendymal resorption of CSE. d) digital angiogram confirms the neovascularisation of the intraventricular neoplasm.

Elaine Miller

2009

This scientific statement is intended for use by physicians and allied health personnel caring for patients with transient ischemic attacks. Formal evidence review included a structured literature search of Medline from 1990 to June 2007 and data synthesis employing evidence tables, meta-analyses, and pooled analysis of individual patient-level data. The review supported endorsement of the following, tissue-based definition of transient ischemic attack (TIA): a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction. Patients with TIAs are at high risk of early stroke, and their risk may be stratified by clinical scale, vessel imaging, and diffusion magnetic resonance imaging. Diagnostic recommendations include: TIA patients should undergo neuroimaging evaluation within 24 hours of symptom onset, preferably with magnetic resonance imaging, including diffusion sequences; noninvasive imaging of the cervical vessel...

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Definition and evaluation of transient ischemic attack: a scientific statement for healthcare professionals from the American Heart Association/American Stroke Association Stroke Council; Council on Cardiovascular Surgery and Anesthesia; Council on Cardiovascular Radiology and Intervention; Counc...

Elaine Miller

Stroke; a journal of cerebral circulation, 2009

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Diagnosis and initial management of transient ischaemic attack

Pippa Tyrrell

Clinical Medicine, 2010

Transient ischaemic attack (TIA) is the sudden onset of focal neurological dysfunction of presumed vascular origin that, by definition, resolves within 24 hours (usually much sooner). Its importance as a predictor of completed stroke has only recently been recognised. Updated guidance on the recognition and management of TIA has recently been published as part of the National Clinical Guideline for Stroke. This is a concise version of the TIA component of the full guideline that recommends an urgent response to TIA to prevent subsequent stroke.

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Transient cerebral ischemia

Michael Cusimano

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Transient Ischemic Attack: Clinical Features and Outcome

Dimitar Maslarov

Journal of Biomedical and Clinical Research, 2017

SummaryA Transient Ischemic Attack (TIA) is a state of emergency and an independent risk factor for ischemic stroke. The social significance of the disease is determined, based on the probability of occurrence of subsequent cerebrovascular incidents and their frequency among groups. The purpose of the present study was to perform a comparative analysis of clinical features and outcome in patients with TIA for at least 24 months after onset had been registered, according to the pathogenesis and to ABCD (2) score. Two hundred and fifty-seven patients were monitored at the Neurology Clinic, First MHAT – Sofia after suffering an initial TIA. All subjects were studied using a clinical evaluation of pathogenetic mechanisms and an ABCD (2) algorithm. A diagnosis of TIA was confirmed by neuroimaging. The comparison between specific pathogenetic mechanisms demonstrated a statistically significant difference. Two TIA subgroups were involved – thromboembolic and cryptogenic (p<0.05). Also, ...

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Transient Ischaemic Attack (TIA)

Kujan Nagaratnam

Geriatric Diseases, 2018

TIA frequency increases with age reaching 10.2% in males and 7.4% in females and decreased in subjects of both sexes aged 85 years or over. The symptoms of TIA vary widely depending on the area of the brain involved. Medical history of specific symptoms and thorough neurological and cardiovascular examinations provide the most important information to diagnose a TIA. TIA poses considerable difficulty in diagnosis, and diagnostic uncertainty is common. Patients presenting with TIA or minor stroke are at high risk of early stroke up to 10% in the first 48 h. Current international guidelines have adopted the ABCD2 score in risk stratification of patients with TIA. For a new-onset TIA patient, an ABCD2 can be a guide in the management.

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The review of transient ischemic attack patients; an experience of a clinic about diagnosis and follow-up

Ayşe Yılmaz

SiSli Etfal Hastanesi Tip Bulteni / The Medical Bulletin of Sisli Hospital, 2018

The Review of Transient Ischemic Attack Patients: An Experience of a Clinic about Diagnosis and Follow-up T ransient ischemic attack (TIA) is an entity characterized by short-term symptoms of acute, focal cerebral or monocular dysfunction that develops due to insufficient blood flow. Generally, episodes lasting less than 24 hours are considered as TIA. TIA is present in 10-5% of patients with ischemic stroke. [1-4] Eighteen percent of these patients experience a stroke within the first three months and half of them within the first 48 hours. [5] The importance of this condition is that secondary prophylactic therapies to be initiated can prevent stroke. Therefore, the risk of near-term stroke in patients is determined by ABCD2 scoring (age, blood pressure, type of TIA, duration) after TIA, so possible Objectives: Transient Ischemic Attack (TIA) is due to a temporary lack of adequate blood and oxygen to the brain. TIAs typically last less than 24 hours. 10-15% of ischemic stroke patients have a history of TIA. 18% of them experience an ischemic stroke within 90 days, and the ABCD2 scoring system is used to estimate the risk. Our study aims to investigate the risk factors, the etiology, the lesion occurrence on MRI and the near-term risk of stroke of patients on whom TIA was diagnosed. Methods: In this study, 124 patients were included between January 2012 and January 2018. Sixty-eight of the 124 patients were male. The history of patients was questioned; systemic and neurological examinations were made. The stroke risk factors and TIA duration were noted and ABCD2 scores were calculated. All the patients' blood samples, including glucose and lipid profile, were studied. They received CT, DWI MRI, electrocardiography, transthoracic echocardiography, ultrasound and/or MR angiography of the cervical arteries. Results: One hundred twenty-four patients were included in this study, and 56 patients were female. The mean age was 63.04±16.77. Hypertension was the most common risk factor (50.8%). Twenty-seven patients were on antithrombotic; six patients were on anticoagulant therapy, while 91 patients were not receiving any antiaggregan therapy. ABCD2 scores were significantly higher on the antithrombotic therapy group (p=0.019). In 52 patients ABCD2 score was below 4, and in 72 patients, the score was greater than 4. In 67.7% of patients, no etiology was found. An ischemic lesion was detected in 16.9% of the patients. 58 % of the patients were discharged on anticoagulant therapy. Five patients developed ischemic stroke. Conclusion: The risk factors of ischemic stroke and TIAs are similar factors. The etiology of TIAs cannot be found out in most of the patients. Thus, the patients are discharged with oral anticoagulant treatment.

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Editorial Comment--Transient Cerebral Ischemia Demands Urgent Evaluation

Colin Graham

Stroke, 2003

Background and Purpose-Recent studies suggest that the short-term risk of stroke may be greater after transient ischemic attack (TIA) than after stroke. Methods-We compared risks of neurological deterioration in those with and without TIA in the National Institute of Neurological Disorders and Stroke (NINDS) tissue plasminogen activator (tPA) trial, a randomized trial of intravenous tPA given within 3 hours of onset of cerebral ischemia, after excluding those with cerebral hemorrhage and those dying before 90 days of causes other than new ischemic stroke. TIA was defined as a National Institutes of Health Stroke Scale (NIHSS) score of zero at 24 hours. We chose subsequent deterioration as our outcome, defined as a worsening on the NIHSS at 90 days compared with 24 hours, so that episodes of new ischemia that may have been attributed to other causes would be included. Results-Of 498 subjects meeting entry criteria, 40 (8%) had TIA. Subsequent deterioration occurred in 30% of those with TIA and 10% of others (Pϭ0.001, Fisher exact test). In multivariable models with adjustment for age, sex, ethnicity, 24-hour NIHSS score, tPA administration, presumed stroke subtype, and baseline systolic blood pressure, temperature, and glucose, TIA was an independent predictor of subsequent deterioration (odds ratio, 5.0; 95% CI, 2.0 to 12.5; Pϭ0.001). Subsequent deterioration was not associated with tPA treatment, and there was no interaction between tPA administration, TIA, and subsequent deterioration. Lesser degrees of substantial acute recovery were also associated with greater risk of subsequent deterioration.

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Transient ischaemic attacks: "mini-strokes" with major but preventable consequences

John Gommans

The New Zealand medical journal, 2013

Transient ischaemic attack (TIA) can be defined as symptoms consistent with stroke that resolve within 24 hours. The public and many health professionals refer to TIAs as 'mini-strokes', terminology that belies their potentially serious prognosis. Although people make a full recovery from a TIA, acute ischaemic lesions revealed on MRI scans occur in just under half of patients.

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Clinical evaluation and management of transient ischemic attacks

John Rothrock

The Western journal of medicine, 1987

Transient ischemic attack (TIA) is a common but poorly understood disorder. Although it rightfully has been classified as a major risk factor for stroke, the majority of patients with TIAs do not suffer subsequent stroke, and it is unclear whether aggressive evaluation and treatment of TIA will significantly lower stroke risk. To effectively treat this disorder, the implications of transient cerebral ischemia and the basic pathophysiologic process underlying this condition must be understood, as well as the myriad of specific clinical causes that must be considered in any patient. Any less sophisticated approach will only propagate the confusion that already exists and lead to the use of therapies that may be useless or even harmful.

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Imaging of acute stroke and transient ischaemic attack

Celestine Santosh

Journal of Neurology, Neurosurgery & Psychiatry, 2005

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Management of transient ischemic attack: 2005

Ciaran Donegan

Expert Review of Cardiovascular Therapy, 2005

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Transient ischemic attacks: Part I. Diagnosis and evaluation

Nina Solenski

American family physician, 2004

Transient ischemic attack is no longer considered a benign event but, rather, a critical harbinger of impending stroke. Failure to quickly recognize and evaluate this warning sign could mean missing an opportunity to prevent permanent disability or death. The 90-day risk of stroke after a transient ischemic attack has been estimated to be approximately 10 percent, with one half of strokes occurring within the first two days of the attack. The 90-day stroke risk is even higher when a transient ischemic attack results from internal carotid artery stenosis. Most patients reporting symptoms of transient ischemic attack should be sent to an emergency department. Patients who arrive at the emergency department within 180 minutes of symptom onset should undergo an expedited history and physical examination, as well as selected laboratory tests, to determine if they are candidates for thrombolytic therapy. Initial testing should include complete blood count with platelet count, prothrombin ...

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Hemodynamic and Metabolic Changes in Transient Ischemic Attack Patients A Magnetic Resonance Angiography and 1H-Magnetic Resonance Spectroscopy Study Performed Within 3 Days of Onset of a Transient Ischemic Attack

Robertus Willy

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Preventing strokes: the assessment and management of people with transient ischaemic attack

John Gommans

The New Zealand medical journal, 2009

This review is a summary of the New Zealand guideline for the management of Transient Ischaemic Attack (TIA). TIA is a medical emergency and warrants urgent attention. The risk of early stroke following TIA may be as high as 12% at 7 days, and 20% at 90 days, with half of these strokes occurring within the first 48 hours. All people with suspected TIA should be assessed at initial point of health care contact for their risk of stroke. Diagnosis of TIA is more likely to be correct if the history confirms: sudden onset of symptoms, with maximal neurological deficit at onset; symptoms typical of focal loss of brain function such as unilateral weakness or speech disturbance; and rapid recovery, usually within 30-60 minutes. The ABCD2 score is a tool that assists with diagnosis and identifies people most at risk of stroke after TIA. People at high risk of stroke require urgent specialist assessment as soon as possible but definitely within 24 hours. This includes those with ABCD2 scores ...

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Transient Ischaemic Attack in the Acute Setting – Diagnosis, Management and Treatment

Ted Glynn

European Neurological Review, 2008

More than 700,000 acute strokes 1 and 300,000 transient ischaemic attacks (TIAs) 2,3 occur annually in the US. It is estimated that between 15 and 26% of acute stroke cases have a prior history of TIA. 4 TIAs are important because they are associated with high short-term risk of both stroke and cardiac events. In a widely quoted emergency department (ED) study of over 1,700 TIA cases from California, the three-month stroke risk was found to be 10.5%. 5 A recent meta-analysis of 11 TIA cohort studies found that the summary estimate for the 90-day stroke risk was 9.2%very similar to the Californian study. 6 This meta-analysis also confirmed that most of this stroke risk occurs in the first few days after the TIA event; the risk of stroke was 3.5% at two days and 8.0% at 30 days. 6 Similar findings were found in another recent meta-analysis of 18 cohort studies, which estimated that the seven-day risk of stroke was 5.2%. 7 Patients with TIA are also at high risk of other cardiovascular events. In a meta-analysis of 39 cohort studies, the annual risk of myocardial infarction and non-stroke vascular death following TIA was 2.2 and 2.1%, respectively. 8 These studies, which serve to illustrate the high risk of cardiovascular events following a TIA, suggest that patients suspected of having a TIA event require an expedited clinical work-up.

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Transient ischemic attack (TIA): the initial diagnostic and therapeutic dilemma

Peter Panagos

The American Journal of Emergency Medicine, 2012

Many patients with transient ischemic attacks (TIA) are at high risk of stroke within the first few days of onset of symptoms. Emergency physicians and primary care physicians need to assess these patients quickly and initiate appropriate secondary stroke prevention strategies. Recent refinements in diagnostic imaging have produced valuable insight into risk stratification of patients with TIA. Clinical data regarding urgent initiation of antiplatelet therapy specifically in this patient population with noncardioembolic TIA are limited but promising. This review outlines the diagnostic tools available for rapid assessment of patients presenting with symptoms of TIA and discusses clinical trials that apply to these vulnerable patients.

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The changing face of transient ischaemic attacks

Chamila Mettananda

Journal of the Ceylon College of Physicians, 2020

TIAs predict stroke risk A transient ischaemic attack (TIA) is not a simple 'mini-stroke', but a major warning sign of an impending stroke that demands urgent attention. About 15-30% of all ischaemic strokes are preceded by TIAs 1-4. The estimated recurrent TIA and stroke risk at three months after a TIA is 17.3% 1 ; the risk of stroke is greatest immediately after a TIA, providing only a short window of opportunity for stroke prevention 2. 52% of all strokes during the first 7 days and 42% of all strokes during the first 30 days following a TIA do occur within the first 24 hours 2-5. Early and optimal treatment of TIA has been shown to be effective in prevention of recurrent The changing face of transient ischaemic attacks This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Short-term outcome of patients with possible transient ischemic attacks: a prospective study

Catarina Fonseca

BMC Neurology, 2015

Background: Patients with transient ischemic attack (TIA) have an increased risk of vascular events. There is scarce data regarding the prognosis of patients with transient neurological symptoms less typical of TIA, in whom a vascular origin cannot be excluded, also known as possible TIA. In this study we aimed to compare the short-term prognosis between TIA and Possible TIA patients. Methods: Patients with transient neurological events consecutively referred to a TIA Clinic during five years were classified as TIA, Possible TIA or mimic. Patients were prospectively followed. We compared the outcome at 30 and 90 days after TIA or Possible TIA. The primary outcome was stroke and the secondary outcome was a combination of vascular events (stroke, TIA, myocardial infarction or vascular death).

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New Transient Ischemic Attack and Stroke

D. Matchar

Archives of Internal Medicine, 2000

Background: Patients with transient ischemic attack (TIA) or stroke frequently first contact their primary care physician rather than seeking care at a hospital emergency department. The purpose of the present study was to identify a group of patients seen by primary care physicians in an office setting for a first-ever TIA or stroke and characterize their evaluation and management. Methods: Practice audit based on retrospective, structured medical record abstraction from 27 primary care medical practices in 2 geographically separate communities in the eastern United States. Results: Ninety-five patients with a first-ever TIA and 81 with stroke were identified. Seventy-nine percent of those with TIA vs 88% with stroke were evaluated on the day their symptoms occurred (P=.12). Only 6% were admitted to a hospital for evaluation and treatment on the day of the index visit (2% TIA; 10% stroke; P=.03); only an additional 3% were admitted during the subsequent 30 days. Specialists were consulted for 45% of patients. A brain imaging study (computed tomography or magnetic reso

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