Magnetic Resonance Imaging: Serial Observations in

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1 495 Magneti Resonane Imaging: Serial Observations in Multiple Slerosis M.. Johnson' D.K.. U 2 D. J. ryane J.. Payne 3 Three patients with four or more follow-up magneti resonane imaging (MRI) examinations over a month period are desribed to illustrate the differing pattems of follow-up seen with MRI in multiple slerosis (MS). These ases illustrate patterns of remission, exaerbation and remission, and rapid progression. The value of MRI in the follow-up of MS is disussed. Magneti resonane imaging (MRI) has been shown to be a very sensitive method of deteting lesions in multiple slerosis (MS) [1-3]. We illustrate the use of MRI in follow-up by presenting three patients with linially definite MS examined on four or more oasions eah over a month period. Subjets and Methods Three patients with four or more follow-up studies are desribed; eah had a different linial pattern of MS. Their linial histories are presented in detail to orrelate with MRI findings. The MRI sanner and basi pulse sequenes used in this study have been desribed [3, 4]. The prinipal pulse sequenes used during the study are listed in table 1 and desribed aording to merian College of Radiology nomenlature [5]. xamination times were min depending on the number of slies sanned. Up to 15 individual slies were obtained at eah examination. Present slie thikness is 10 mm. ll examinations onformed to the guidelines for linial MRI established by the National Radiologial Protetion oard [6]. The examinations were performed with the permission of the this Committee of the Royal Postgraduate Medial Shool, and informed onsent was obtained from eah patient. No preparation or exogenous ontrast agents were required, and no adverse effets were noted during or after the MRI examination. Case Reports Reeived January 4, 1984; aepted after revision Marh 29, M.. Johnson is a Medial Researh ellow of the lberta Heritage oundation., Department of Diagnosti Radiology, NMR Unit, Royal Postgraduate Medial Shool, Hammersmith Hospital, Du Cane Rd., London W12 OHS, ngland. ddress reprint requests to M.. Johnson. 2 Department of Diagnosti Radiology, University of ritish Columbia, Vanouver V6T 25, ritish Columbia, Canada. 3 Hirst Researh Laboratory, Wembley, London H9 7PR, ngland. JNR 5: , September/Otober /84/ merian Roentgen Ray Soiety Case 1 25-year-old man had aute left hemiplegia that progressed over 1 week and subsequently reovered ompletely. During the aute phase, he developed reflex and postural hanges of an upper motor neuron lesion. uditory- and visual-evoked potentials were normal. Lumbar punture revealed slight inrease in the number of lymphoytes (6/mm 3 ) as well as oligolonal banding in the erebrospinal fluid (CS). Initial omputed tomography (CT) with and without ontrast enhanement revealed a lowattenuation, nonenhaning lesion in the right supra- and periventriular region. n MRI inversion-reovery (IR) san demonstrated a large lesion with long T1 in the orresponding loation (fig. 1). smaller lesion with long T1 was also noted in the posterior limb of the right internal apsule. ollow-up examinations 2 months later when the linial symptoms had ompletely resolved revealed the right periventriular lesion to be smaller on CT and MRI sans (fig. 1 ). The third follow-up MRI san (17 months after the initial san) inluded both IR and spin-eho (S) pulse sequenes and showed further diminution of the right periventriular lesion, with long

2 496 JOHNSON T L. JNR :5, Sept/Ot 1984 T2 as well as long T1 (figs. 1 C and 1 D). The long T1 lesion in the internal apsule was smaller, but more easily identified beause of improved image quality. rim of long T2 surrounding the lateral vertriles was noted. inal IR and S sans 22 months after initial presentation were unhanged, apart from improved image quality (figs. 1 and 1 ). The patient remained linially well with no new symptoms. Case 2 49-year-old woman had right leg ramps and unsteadiness of gait. Physial findings inluded positive jaw jerk, exaggerated deep tendon reflexes, bilateral leg spastiity, bilateral ankle lonus, and extensor plantar responses. Lumbar punture revealed an elevated CS level of immunoglobulin G (lgg) (24% of total protein), suggestive TL 1: MRI Pulse Sequenes Ml Pulse Sequene Time Interval (mse) epetition Inversion ho Inversion-reovery Spin-eho of MS. tentative diagnosis of spasti paraparesis from MS was made, and treatment with dantrolene sodium was begun to relieve the leg spasms. Three years later, she developed tingling of the left fae, left side of the body, and left hand, with subsequent loss of power in her hand and shoulder and loss of sensation in her hand. high ervial relapse of MS involving the lowest sensory trigeminal fibers was diagnosed. This resolved, leaving residual paresthesia of the left hand. The patient was well, apart from ontinuing leg spasms, for another 21 months until she developed numbness of the right fae and slurred speeh. CT revealed two ontrast-enhaning lesions adjaent to the left lateral ventrile, suggesting aute MS lesions. Initial IR and S sans demonstrated multiple lesions with long T1 and long T2; the largest of these lesions orresponded to the ontrast-enhaning lesions on CT (figs. 2 and 2). t least six more lesions were identified on MRI. On repeat IR and S sans 10 days later, the two largest lesions were enlarged, while the rest of the lesions were unhanged. The aute symptoms resolved over 12 days, leaving leg spasms as well as minimal ataxia. Repeat CT 6 months after the initial san revealed redution in size and degree of ontrast enhanement of the left periventriular lesions. Corresponding IR and S sans revealed diminution of the previously noted lesions (figs. 2C and 2D). Subsequently, the patient was linially stable with oasional minor relapses. 1 year follow-up MRI san was unhanged, allowing for differenes in positioning and improved image quality. n MRI san 14 months after initial sanning revealed enlargement of several right periventriular lesions, espeially one lesion at the posterior horn (figs. 2 and 2). o ig. l.-case 1. Supraventriular level., IR 1400/400 san. Large lesion with long T1 in entrum semiovale., 2 month follow-up. IR 1400/400 san. Lesion has diminished. C and 0, 17 month follow-up. IR 1400/400 (C) and S 1080/80 (D) sans. urther diminution. Improved image quality. and, 22 month follow-up. IR 1400/400 () and S 1580/80 () sans. Lesion unhanged. Image quality improved.

3 JNR:5, Sept/Ot 1984 MRI O MULTIPL SCLROSIS 497 D ig. 2.-Case 2. and, InitiallR 1400/400 () and S 1080/80 () sans. Multiple long T1 () and long T2 () lesions in peri ventriular white matter. C and D, 6 month follow-up. IR 1400/400 (C) and S 1080/80 (D) sans. Diminution of lesions. and, 14 month follow-up. IR 1400/400 () and S G H 1080/80 () sans. Inreased size of lesions. G and H, 17 month follow-up. IR 1400/400/44 (G) and S 1580/80 (H) sans. Diminution of lesions. Improved image quality. inallr and S sans 17 months after initial sanning revealed the previously noted lesions to be smaller (figs. 2G and 2H). ewer levels were sanned, however, due to tehnial diffiulties. Case 3 36-year-old woman had had five attaks of paresthesia and numbness involving the extremities. During one of these attaks, vertigo and diplopia on right horizontal onjugate gaze was noted. Physial examination revealed dereased light touh in the right hand with poor fine movements. Lumbar punture showed the presene of 15 lymphoytes and elevated IgG at 20% of the total protein (normal, less than 12%) in the CS. tentative linial diagnosis of MS was made. Over the next 5 years the patient experiened numerous relapses. and demonstrated signs of retrobulbar neuritis as well as upper motor neuron and erebellar involvement. Treatment during this period inluded several doses of Synathen. The patient's first CT and MRI sans were obtained during a linial relapse when she noted vertigo, right hand paresthesia, internulear ophthalmoplegia on gaze to the left, and dysonjugate eye movements. CT demonstrated four low-attenuation lesions, inluding a single lesion in the entrum semiovale and a lesion adjaent to the posterior horn of the lateral ventrile bilaterally. Initial IR and S sans learly demonstrated at least 16 lesions with long T1 and long T2 in the periventriular white matter, the entrum semiovale, and the brainstem, onsistent with plaques of MS (figs. 3 and 38). Treatment with azathioprine was begun but disontinued 2 weeks later beause of allergy. nother relapse with development of retrobulbar neuritis ourred 8 months later. IR and S sans demonstrated enlargement of several periventriular lesions as well as new lesions (figs. 3C and 3D). Repeat CT sans 1 month later when the patient ontinued to have retrobulbar neuritis demonstrated a left periventriular lesion not seen on the previous CT san but seen on the original MRI san. Repeat MRI 1 month after the previous san was unhanged. Treatment with Synathen and prednisolone at intervals over the next 6 months was attempted, but several relapses ourred. ifteen months after initial MRI, slurring of speeh, gait unsteadiness, and left limb weakness ourred. Left erebellar inoordination was found, and the speeh slurring was believed to be erebellar in origin also. Tone was redued on the left. MRI revealed large new lesions in the

4 498 JOHNSON T L. JNR :5, Sept/Ot 1984 D ig. 3.-Case 3. and, InitiallR 1400/400 () and S 1080/80 () sans. Multiple long T1 () and long T2 () lesions predominantly in periventriular white matter. C and 0, 8 month follow-up. IR 1400/400 (C) and S 1080/80 (0) sans. Inreased side of lesions and new lesions seen best seen on O. and, 15 month follow-up. IR 1500/500/44 () and S 1580/80 () sans. Marked enlargement of lesions. right entrum semiovale as well as adjaent to the posterior horns of the lateral ventriles (figs. 3 and 3). The patient was inapaitated and was transferred to a hroni are faility. Disussion ah of the three patients demonstrated a different linial pattern of MS. Case 1 suffered one aute episode that gradually resolved with no relapse. MRI initially demonstrated two lesions that diminished on sans at 2 and 19 months and were stati on a san at 22 months. Case 2 demonstrated a more hroni ourse with oasional exaerbations. Her first MRI san revealed multiple lesions, two of whih orresponded to ontrast-enhaning lesions on CT. The lesions diminished on sans at 6 months and 1 year, but several lesions were larger on a san at 14 months. ollow-up sans 2 months later showed a diminution of these lesions. Case 3 suffered a hroni progressive ourse despite treatment resulting in inapaitation. Multiple MS lesions were identified initially on MRI sans. Repeat san at 8 months during a linial relapse demonstrated new lesions as well as enlargement of several previously noted lesions. MRI sans at 9 months were unhanged, but at 15 months, during another relapse, several large, new lesions were present. s expeted, these serial follow-up examinations reveal dereasing size, but not disappearane, of lesions after aute episodes. During relapses, new lesions appear and existing lesions beome larger. Problems exist in aurate interpretation of serial examinations. Slie seletion and angulation may not be exatly omparable. quipment improvements may result in different slie profiles and thiknesses along with improvements in image quality and resolution. The tehnique of image reonstrution may alter lesion detetability. Projetion-reonstrution tehniques produe better signal-to-noise ratios than do two-dimensional ourier transformation tehniques [7]. New pulse sequenes may improve lesion detetability. or example, our initial studies on MS did not inlude any S images, sine initial studies with S sequenes failed to demonstrate pathology in a few ases. urther studies with S sequenes using a longer time for spin-spin relaxation showed S images to be very sensitive in deteting abnormalities. Multislie apability [8, 9] is neessary if a omplete multisequene study of the brain, the optimal examination for MS, is to be ompleted in a reasonable period of time. Threedimensional volume aquisition of data and reonstrution would failitate aurate omparison between a series of follow-up examinations on the same patient [10] Despite these diffiulties, follow-up examinations are important in assessment of the natural history of MS, aute exaerbations, and assessment of healing after treatment.

5 JNR :5, Sept/Ot 1984 MRI O MULTIPL SCLROSIS 499 lthough the MRI findings in MS are well defined [1-3, 8, 11-13], the exat histologi and biohemial hanges that produe these abnormalities are unertain. ollow-up MRI studies will demonstrate the natural history of the lesions and an be ompared and orrelated with histohemial hanges in pathologi speimens [14, 15] as well as with orresponding abnormalities of high-dose ontrast-enhaned delayed CT sans. These ontrast-enhaning lesions indiate regions of blood-brain barrier disruption, and there is evidene to suggest that they orrelate with more aute MS lesions [16]. Serial examinations provide a measure of ativity and quiesene of the disease proess and an indiation of the severity and extent of lesions. uonanno et al. [17] suggested that determination of T1 values of MS lesions may provide a quantitative method of haraterization of ativity of individual MS lesions, although quantifiation was not attempted in our study pending validation studies of the auray of T1 and T2 measurements. It is neessary to be able to doument in vivo arrest and/ or healing and remyelination of speifially identified lesions if the effetiveness of therapeuti regimens is to be monitored [18], sine linial signs and symptoms do not orrelate with the extent and ativity of lesions seen at neropsy [19]. Therapeuti trials in MS have been hampered by the lak of a good laboratory indiator of disease ativity, the plaebo effet, the extremely variable linial ourse of the disease, and the lak of knowledge of the etiology of MS [18, 20]. eause it is sensitive, has no known hazards, and does not require exogenous ontrast agents, MRI appears to be an ideal method for monitoring disease ativity in treated and untreated MS patients. RRNCS 1. Young IR, Hall S, Pallis C, Legg NJ, ydder GM, Steiner R. Nulear magneti resonane imaging of the brain in multiple slerosis. Lanet 1981; 2 : ydder GM, Steiner R, Young IR, et al. Clinial NMR imaging of the brain: 140 ases. JNR 1982;3: , JR 1982; 139: ailes DR, Young IR, Thomas DJ, Straughan K, ydder GM, Steiner R. NMR imaging of the brain using spin-eho sequenes. Clin Radio/1982;33: Young IR, url M, Clarke GJ, et al. Magneti resonane properties of hydrogen: imaging of the posterior fossa. JNR 1981;2: , JR 1981 ;137: merian College of Radiology. Glossary of NMR terms. Chiago: merian College of Radiology, National Radiologial Protetion oard. xposure to nulear magneti resonane linial imaging. Harwell, Oxon, ngland: National Radiologial Protetion oard, King K. Signal to noise ratios in nulear magneti resonane imaging (thesis). Madison, WI : University of Wisonsin, Crooks L, Mills CM, Davis PL, et al. Visualization of erebral and vasular abnormalities by NMR imaging: the effets of imaging parameters on ontrast. Radiology 1982;144 : Crooks L, rakawa M, Hoenninger J, et al. Nulear magneti resonane whole-body imager operating at 3.5 kgauss. Radiology 1982;143 : uonanno S, Pykett IL, rady T J, et al. Clinial relevane of two different nulear magneti resonane (NMR) approahes to imaging of a low grade astroytoma. J. Comput ssist Tomogr 1982;6: Young IR, Randell CP, Kaplan PW, James, ydder GM, Steiner R. NMR imaging in white matter disease of the brain using spin-eho sequenes. J Comput ssist Tomogr 1983;7: uonanno S, Pykett IL, Vielma J, et al. In: Witofski RL, Karstaedt N, Partain CL, eds. NMR imaging. Winston-Salem, NC: owman Gray Shool of Mediine, 1982: rant-zawadzki M. Davis PL, Crooks L, et al. NMR demonstration of erebral abnormalities: omparison with CT. JNR 1983;4: , JR 1983;140: Lumsden C o The neuropathology of multiple slerosis. In: Vinkin PJ, ruyn GW, eds. Handbook of linial neurology, vol 9. msterdam: North Holland, 1970: ernstrom J, arron KD. Chemial pathology of multiple slerosis. In: Vinken PJ, ruyn GW, eds. Handbook of linial neurology, vol 9. msterdam: North Holland, 1970: Lebow S, nderson DC, Mastri, Larson D. ute multiple slerosis with ontrast-enhaning plaques. rh Neurol 1978;35: uonanno S, rady T J, Pykett IL, et al. NMR imaging in patients with multiple slerosis: potential of in-vivo lesion haraterization using T, NMR imaging (abstr). Neurology (NY) 1982;32: Marlin D, Marland H. Multiple slerosis. N ngl J Med 1982;307: MDonald WI, Halliday M. Diagnosis and lassifiation of multiple slerosis. r Med ull 1977;33: Marlin D. Treatment of multiple slerosis. N ngl J Med 1983;308: