COMPLEMENTARY VALUES OF STATIC AND DYNAMIC SCINTIGRAPHY, COMPUTERIZED TOMOGRAPHY AND ANGIOGRAPHY IN THE DIAGNOSIS OF A PARTIALLY THROMBOSED GIANT INTRACRANIAL ANEURYSM J. T. Wilrnink* and L. M. Vencken SUMMARY The case history is presented of a 17 year-old male admitted with right hemiplegia and motor aphasia. Static and dynamic scintigraphy allowed prediction of a giant aneurysm in the deep left frontotemporal region, and this supposition was confirmed by CT and carotid angiography. CT also revealed the aneurysm to extend farther medially than the other two examinations had indicated, the medial portion of the aneurysm being thrombosed. Evaluation of the diagnostic information obtained from the three procedures, combined with the clinical data, makes possible a reconstruction of the probable course of events. The presenting signs were probably caused by a newly formed thrombus within the aneurysm. Death, which occurred after five days, was apparently due to subarachnoid hemorrhage. CASE HISTORY A 17 year-old male without a history of previous neurological disease was discovered on a holiday-cruise lying next to his bed, unable to speak or to move his right arm or leg. On the previous evening he had complained of a vague headache, for which he had taken a salicylate. The patient was first admitted to a regional hospital, where neurologic examination revealed motor aphasia, right hemiparesis and a slight echo-shift to the right. On the basis of these findings the patient was transferred to the Neurological Department of the University Hospital of Groningen, The Netherlands. On arrival the patient was found to be mildly obtunded. There was a complete motor aphasia, questions and instructions, however, being readily understood. There was a right facial palsy of the central type, and a near-total flaccid paresi s of fight arm and leg, with abolished superficial reflexes and an extensor plantar response. The various modalities of sensation could not be extensively tested due to the aphasic disorder, but did not appear grossly disturbed. The remaining neurological and general physical examination was normal. Echo-encephalography confirmed the slight displacement of the median structures to the right, earlier reported. Laboratory screening revealed no significant abnormalities. * Department of Neuroradiology, University Hospital, Groningen, The Netherlands. Clin. Neurol. Neurosurg., 1979, Vol. 81-2 88 a b Fig. 1. Technetium brain scintisram with area of increased uptake in deep left frontotemporal region, planeconvex in anterior view (a) and round in left lateral view (b). Round appearance of lesion is unusual for arteriovenous malformation. The technetium brain scintigram performed approximately 24 hours after onset of symptoms demonstrated a rounded area of abnormal uptake deep in the left frontotemporal region (Fig. 1). Serial scintigraphy showed rapid visualization of the lesion, consistent with intravascular blood pooling (Fig. 2). CT (EMI 5005) performed on the same day confirmed the scintigraphic findings of a lesion deep in the left frontotemporal region. The lesion on CT was hyperdense but inhomogenous in the unenhanced CT study, the lateral portion being less dense than the medial part (Fig. 3a). After injection of contrast medium, however, the lesion became homogenous (Fig. 3b). These features are illustrated in a density analysis performed on the computer print-out of the lesion before and after contrast injection (Figs. 3c and 3d). These findings were interpreted as representing a giant aneurysm containing a thrombus (not influenced by contrast injection) in its medial portion, and circulating blood (increasing in CT attenuation values after contrast injection) in the lateral part. There was minimal displacement of the third ventricle to the right. In addition there was a lucent zone visible medial to and above the supposed aneurysm (not visible on CT sections in Fig. 3). This hypodense area was not influenced by contrast injection, and was thought to indicate either edema or infarction. 12"-15" 15~18" 18~21" 21%24" 27~30" 33%36 . ~erlal sclnugrapny in lelt Lateral projection. ~ote early visualization Ol lesion, simultaneous with carotid arteries at 12"-15" after injection. Lesion does not decrease in intensity after arterial phase, early filling veins are not seen. This is unusual for arteriovenous malformation. a b Fig. 3. CT sections demonstrating lesion without (a) and with contrast enhancement (b). Note faint difference m attenuation between medial and lateral portions of lesion in a, abolished in b. These features are high-lighted in density analysis of computer print-outs of the lesion without (c) and with enhancement (d). Num[~ers indicate EMI values. Thin line is drawn around areas having EMI values of 15 or higher. 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Neurosurgical intervention was not considered advisable at this stage, and appropriate conservative measures were instituted. On the third day there was a short period of restlessness with heavy perspiration, arterial hypertension and bradycardia, without other changes in the neurological status. The following morning the patient displayed slight cervical rigidity and it was assumed that there had been some leakage from the aneurysm. On the fifth day there was a sudden deterioration of the level of consciousness, with dilation of the right pupil and arterial hypertension, but with a normal pulse rate. Some minutes later the patient became unresponsive to stimuli and apnoea set in. Artificial ventilation was initiated, but after five more minutes the left pupil also dilated and became fixed. By this time no reflexes could be elicited. Attempts at resuscitation failed and the patient died shortly afterwards. Post-mortem suboccipital puncture revealed xanthochromic spinal fluid containing many erythrocytes. Permission to perform autopsy was refused. DISCUSSION Although it was not possible to obtain verification by autopsy, we nevertheless feel that the three neuroradiological procedures employed permit a reliable diagnosis of the lesion under investigation. Rapid filling of a lesion in the arterial phase of the serial scintigram, as seen in our patient, is consistent with intravascular pooling of blood such as in arteriovenous malformation (AVM) or giant aneurysm. An AVM, however, rapidly decreases in scintigraphic intensity after the arterial phase (PENNING and FRONT, 1975) while the lesion in question does not exhibit this characteristic (Fig. 2), thus suggesting rapid filling, but slow emptying. This is unusual for an AVM. The absence of signs of early filling of the venous sinuses points in the same direction. Moreover, the rounded configuration of the lesion in the lateral projection is not typical of an AVM, as these malformations usually present a more irregular appearance. These features make the existence of a giant aneurysm more likely. The diagnosis of meningeoma was considered, but thought less likely because of the intense early visualization of the lesion. Angiography confirms the presence of a giant aneurysm arising from the most distal portion of the left internal carotid artery. The circulation within the aneurysm is slow (contrast medium is still visible within the aneurysm 12 seconds after injection) thus explaining the findings at serial scintigraphy, nUBER and RIVOIR (1971) have mentioned similar angiographic findings. 91 ~. , _Ja. / f Fig. 4. Left carotid anglogram in AP and lateral projection at 2,2 sec. (a, b) and at 3,3 sec. (c, d). Configuration of aneurysm did not change after 3,3 sec. Aneurysm was still faintly visible at 11,5 sec. Aneurysm arises from supraclinoid portion of internal carotid artery (arrow head), branches of middle cerebral artery seem to arise from lateral portion of aneurysm (arrow). Note smooth lateral surface of contrast image but blurred medial surface, probably representing lateral edge of thrombus, 92 The CT scan demonstrates that the lesion extends farther medially than the scintigram or the angiogram indicate. As Fig. 5 illustrates, on CT the lateral portion of the lesion corresponds with the picture at angiography and scintigraphy. The medial, denser portion of the lesion on CT is not visualized with the other two techniques. We believe that the medial portion of the aneurysm contains a thrombus having higher attenuation values than unenhanced blood, a difference which is abolished when the attenuation values of the circulating blood are elevated by contrast injection. Ir Fig. 5. Composite illustration of, from top to bottom, coronal reconstruction of CT, CT slice in canthomeatal plane, angiogram and scintigram in anterior view. Lateral, less dense portion of CT lesion corresponding with circulating blood, is well demonstrated on angiogram and scintigram while denser medial portion, corresponding with thrombus mass, is not visible with the other two techniques. An alternative explanation is that the lateral portion of the CT lesion represents the whole aneurysm, that there is no thrombosis and that the hyperdense medial portion represents an intracerebral hemorrhage adjacent to the medial wall of the aneurysm. We consider this unlikely, mainly because of the shape of the lesion on CT. Although intracerebral hemorrhages with a smooth outline have been described (SCOTXet aL, 1974), in our patient the medial and the lateral portion of the lesion form one smooth globoid mass. This is a highly unlikely configuration for a vascular malformation with an adjacent hemorrhage. The medial surface of the lesion at angiography also presents an irregular appearance. This seems more likely to correspond with the surface of a thrombus than the aneurysm wall. Finally, an intracerebral hemorrhage might be expected to have caused a greater displacement of intracerebral structures. 93 With regard to the sequence of events in this patient, a number of speculations can be made. 1. The presenting symptoms (rapid outset of motor aphasia and hemiparesis, with a relatively well-preserved level of consciousness and without cervical rigidity) are unusual for a giant aneurysm. There is considerable disagreement concerning the risk of rupture of giant aneurysms. MORLEYand BARR(1968) review the literature in this respect, and in their own 28 cases point to hemorrhage as the presenting symptom in 6 out of the 17 cases with intracranial (extracavernous) aneurysms, with two other patients bleeding at a later date. The other patients presented symptoms of a mass lesion due to the giant aneurysm, the nature of the neurological deficit being determined by the localisation of the aneurysm. The three patients with aneurysms of the middle cerebral artery all had epilepsy as a presenting symptom; in none of the other patients was this found. Other authors reporting on nonbleeding giant middle cerebral aneurysms (SADIKet al., 1965; CANTU and LEMAY, 1966; rIUBER and RIVOIR, 1971; LUKIN et al., 1975; SEGAL and MCLAURIN, 1977) usually describe histories of often vague complaints, with findings such as hemiparesis, disorders of speech and papilledema. In none of these patients was the neurological deficit as severe and as rapid in outset as in our patient. In other words, while the clinical findings in the patients mentioned above are compatible with a supratentorial mass lesion, the evolution of the symptoms in our patient appears to indicate a cerebrovascular etiology. The findings at CT and angiography which demonstrate only minimal displacement ofmidline cerebral structures, also indicate that the aneurysm in our patient had. no significant mass effect. Many of the authors mentioned above describe marked displacement of cerebral vessels in their patients. It seems very unlikely that the presenting symptoms were caused by subarachnoid hemorrhage (SAH). The clinical picture affords no evidence for SAH, and CT failed to demonstrate blood in the subarachnoid space, scoTrI et al. (1977) consider that CT may be 100% reliable in demonstrating extravasated blood if performed within a week of the bleeding episode. For reasons mentioned above, we do not consider intracerebral hemorrhage a likely explanation for the symptoms at admission. An interesting possibility is that of cerebral ischemia in the area supplied by the left middle cerebral artery. This could account for the clinical picture, and angiography demonstrated delayed filling of middle cerebral branches. Possibly there was spasm of these arteries, but it seems more likely that the thrombus within the aneurysm was at fault, either by direct compromise of circulation within the aneurysm, or by release of emboli into the middle cerebral branches. SCOXT and BALLANTINE(1972), reporting on a left middle cerebral giant aneurysm, describe an episode of transient speech disorder, ascribed to embolus from the aneurysm. At a repeat angiogram performed several years later, the aneurysm was not demonstrated, and was thought to have spontaneously thrombosed. The CT and scintigraphic characteristics of the lesion in our patient differ from those mentioned in the literature. Authors reporting on CT findings in partially thrombosed giant aneurysms (PRESSMANet al., 1975; DAVISet al., 1977; JONES and 94 SCHWARZ, 1977; SCOTTI et al., 1977; HANDA et al., 1978) describe, as we do, two 'compartments' within the aneurysm, with the portion which contains circulating blood demonstrating increased enhancement upon contrast injection, while the portion made up of thrombus material is not influenced. However, the lesion is usually described as being more or less isodense before contrast injection, with the portion containing circulating blood becoming relatively hyperdense after the enhancement procedure. This is the opposite to our findings. In other words, the attenuation values of the thrombus in our patient appear to be higher than in patients reported in the literature. It is our opinion that these variations in attenuation values are dependent on the age of the thrombus. In a recent literature report FODSTADet al. (1978) describe the evolution of the CT picture of thrombosis of a giant aneurysm after carotid ligation. Two days after ligation the attenuation values of the lesion had increased markedly, and these values were not significantly influenced by contrast injection. Two months later CT showed that a vascular channel had developed in the aneurysm, but the attenuation values of the thrombosed portion had decreased drastically, and appeared isodense or possibly slightly hypodense with relation to normal brain tissue. The aneurysm was then excised and was found to be largely thrombosed, with signs of organization in the peripheral portions of the thrombus, and small endothelium-lined blood vessels in the remainder. Thus it appears that attenuation values of a fresh thrombus increase markedly, decreasing as the process of organization sets in. Probably in a later stage the attenuation values will rise again if and when calcium is deposited in the lesion. This is the most likely explanation for the single case with a partially thrombosed aneurysm with high attenuation values reported by SCOTT1et al. (1977). Another argument for a thrombus of recent origin in our patient can be derived from the scintigraphic findings. Two of the authors mentioned above (JONESand SCHWARZ, 1977; SEGALet al., 1977) present scintigraphic findings in two of their four patient with partially thrombosed giant aneurysms. In both cases the lesion at scintigraphy is considerably larger than at angiography, and probably represents the thrombosed as well as the unthrombosed portion of the aneurysm. In our case, however, the scintigraphic lesion is approximately equal in size to the angiographic lesion, and the thrombosed portion of the aneurysm is not visualized by scintigraphy (Fig. 5). It is known that intracerebral hemorrhages as a rule are not visualized scintigraphically within the first few days, as scintigraphic visualization probably depends on development of newly-formed capillaries which do not yet possess a blood-brain barrier (SUGITANI et al., 1973). If the same applies to intravascular blood clots, this would confirm that the thrombus within the aneurysm in our patient, being invisible at scintigraphy, was of recent origin. It thus seems probable that the formation of the thrombus in our patient coincided with the appearance of neurological symptoms, and was possibly responsible for the appearance of these symptoms. 95 2. The precipitate demise of the patient and the post-mortem findings of hemorrhagic cerebrospinal fluid indicate subarachnoid hemorrhage as the cause of death. This case reiterates the value of CT studies with and without contrast enhancement in patients with intracranial aneurysms in order to ascertain the true size and composition of the lesion. This is not always possible by means of angiography. Others have pointed out this fact, and in addition the value of CT in the follow-up of patients submitted to procedures such as carotid ligation for giant aneurysm is stressed (DAVIS e l aL, 1977; HANDAet aL, 1978). Undoubtedly more information will become available in the near future on the CT characteristics ofintravascular blood clots in various stages of organization. At the present time we were only able to trace one case in the literature in which serial follow-up CT studies were made of a thrombosed aneurysm. ACKNOWLEDGEMENTS We are grateful to Dr. L. Nederveen, neurologist of the Delfzicht Hospital, Delfzijl, to Prof. Dr. J. M. Minderhoud, head of the Department of Neurology and to Prof. Dr. M. G. 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