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Show JOUI7UlI of Clinical Neuro-ophtludmology 7(2): 112-113, 1987. Neuroradiological Clinical Pathological Correlation Brain Stem Infarct Lawrence Dubin, M.D., and Robert M. Quencer, M.D. © 1987 Raven Press, New YOl'l CASE HISTORY A 68-year-old man who was previously in good health suddenly lost consciousness while exercising. Upon awakening, he complained of numbness in his mouth, chin, the left side of the face, and the left arm. He then lapsed into a deep coma for 72 h. After regaining consciousness, he presented with several neurological deficits, including abduction of the left eye, distorted double vision, inability to elevate the head or eyes, lack of awareness of the extremities on the left side, and dysarthric and inarticulate speech. He recovered partially over the following 5 years but was still bothered by vertical and horizontal double vision and difficulty reading. On examination, he was found to have Horner's syndrome on the right side, classic macrosquare wave jerks, mild bilateral internuclear ophthalmoplegia, and skew deviation with hypertropia of the right eye when he looked to the right and hypertropia of the left eye when he looked to the left. Abnormal optokinetic responses were especially noted when the patient was asked to follow a target to the left or upward. A computed tomographic (CT) scan obtained 5 years later was read as normal and magnetic resonance (MR) was obtained. DISCUSSION The MR abnormality was located in the dorsal pons (Figs. 1 and 2). The T2 weighted axial images (Fig. 2) were suggestive of old hemorrhage. The appearance of a hematoma on MR will vary ac- From the Department of Radiology R-130, University of Miami School of Medicine, Miami, Florida. Address correspondenee'1ql4 tePool~uests to Lawrence Dubin, M.D., Departm.ent of RamoIogyBt130, University of ~vharnl!Jackson Memonal Medical Center, P.O. Box 016960 Hi.\M:, .'! .HI01., C.S.A. . , 112 AG. 1. Sagittal MR, TR 600ITE 38. MR of the brain in the midsagittal plane (5 mm thick sections) shows ail isointense lesion (arrow) in the posterior pons sur· rounded by a ring of decreased signal (arrowheads). The lower intense rim represents hemosiderin. cording to its age. While a subacute hematoma shows predominately high signal intensity on T1 and T2 weighted images (1) due to methemoglobin, older hematomas are conspicuous by the presence of the low intensity signal of hemosiderin. Depending on the type and amount of break-- . down of blood products, there will be some or nO residual methemoglobin in these chronic hema.. tomas. Acute infarcts that involve the pons, medulla, and cerebellum are associated with a high mo~ tality rate. In a series of 31 patients (2) with acu~;· posterior fossa infarct, nearly all presented witlt~ dizziness, lethargy, and weakness. Four patien~i BRAIN STEM INFARCT 113 FIG. 2. Axial MR, TR 2000/TE 60. This T2 weighted axial image demonstrates a small central isointense signal (arrow) surrounded by a very low signal rim (arrowhead). The very low signal represents hemosiderin, and the central high signal may still represent hemorrhage remaining in the methemoglobulin phase. had sudden onset of coma without preceding symptoms. One prognostic factor is the degree of swelling of the posterior fossa structures. Patients demonstrating obliteration of the basal cisterns on CT have a high mortality rate. Magnetic resonance is superior to CT for imaging the brain stem. In CT the brain stem is often obscured by artifacts (Hounsfield artifacts) caused by the thick petrous temporal bones. These artifacts are not present in MR. In addition, the brain stem can be easily studied in axial, coronal, or sagittal projections, and early brain stem hemorrhages and infarcts can be visualized with MR. The pathophysiology of stroke lends itself well to MR. Following an ischemic event edema is present. Cytotoxic edema, the earliest form of edema, results from anoxia and a subsequent change in the ATP content of the cell membrane. As a result there is a loss of the sodium- potassium pump and excess fluid accumulates inside the cell. Following this, vasogenic edema occurs, which is due to a breakdown of the blood-brain barrier. In both instances, there is increased water in the ischemic or infarcted region. This is manifested by a prolongation of Tl (hypointensity) on Tl weighted images and a prolongation of T2 (hyperintensity) on T2 weighted images. Magnetic resonance is very sensitive in detecting small and early infarcts. The earliest changes in ischemia have been detected at 30 min in cats (3). Other studies have demonstrated ischemic changes in as early as 2 h in rats (4). When compared to CT, MR defines infarcts more clearly (5). Often, MR shows the damaged area to be more extensive than demonstrated by CT (6). In the case presented here, we postulate that because of the type of signal abnormalities seen on MR there was a hemorrhagic event in the pons (either a spontaneous hemorrhage or a hemorrhagic infarct) rather than a simple ischemic infarct. The explanation for findings on MR in hematomas is as follows. Methemoglobin, a product of blood breakdown, has five unpaired electrons and is therefore a paramagnetic substance and, because of this molecule's proximity to nearby hydrogen atoms, there is a change in the longitudinal and transverse relaxation times (short Tl, long TI). If a hemorrhage is subacute in nature, the Tl image will show an area of hyperintensity, but if the hemorrhage occurred many years in the past (as in our case) only the effect of hemosiderin will be seen. As opposed to the effect of methemoglobin, hemosiderin changes the magnetic suspectibility of the sample. In this situation the iron in the hemosiderin actually changes the local magnetic fields, resulting in a signal loss (rapid proton dephasing) from that area. Because recent and old events that have occurred in the brain stem are so well depicted by MR, it is the preferred imaging modality when a neurological event suggests an abnormality in that area. REFERENCES 1. Gomoni J, Grossman R, Goldberg H, Zimmerman R, Bilaniuk L. Intracranial hematomas: imaging by high field MR. Radiology 1985;157:87-93. 2. Bydder G, Steiner R, Young I, et aI. Oinical NMR imaging of the brain: 140 cases. Am J RoentgenoI1982;139:215-36. 3. Brant-Zawadzki M, Pereira B, Weinstein P, et aI. MR imaging of acute experimental ischemia in cats. Am J NeuroradioI1986; 7:7-11. 4. Buonanno F, Pickett I, Brady T, et aI. Proton NMR imaging in experimental ischemia infarction. Stroke 1983;14:178-84. 5. Sipponen J, Kaste M, Ketonen L, Seppohen R, Katevuo F, ~ivula A.. Serial nUclea~ magn~tic resonance imaging in patients With cerebral mfarctlon. J Comput Assist Tomog 1983;7:585-9. 6. Britan R, Willcott M, Schiders N, Ford J, Derman H. NMR evaluation of stroke. Radiology 1983;149:189-92. I Clin Neuro-ophthillmol, Vol. 7, No.2, 1987 |
