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Hyperintensity of the Basal Ganglia and Cortex on FLAIR and Diffusion-Weighted Imaging

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Hyperintensity of the Basal Ganglia and Cortex on FLAIR and Diffusion-Weighted Imaging AJR Integrative Imaging LIFELONG LEARNING FOR RADIOLOGY Radiological Reasoning: Hyperintensity of the Basal Ganglia and Cortex on FLAIR and Diffusion-Weighted Imaging Eric E. Beltz1, Mark E. Mullins2 Objective the basal ganglia. The findings on the remaining brain im- The educational objectives of this article are to learn an ages were unremarkable. approach to analyzing studies involving abnormalities of the basal ganglia in the acute setting. The approach is based Expert Discussion on using medical history and imaging features to narrow Initial Discussion the differential diagnostic considerations. An emphasis on Abnormalities on imaging of the bilateral basal ganglia understanding the pathophysiology is provided to reinforce are often nonspecific. Therefore, a focused approach to limit the causality of the imaging abnormalities. the differential diagnosis is based on whether the patient presents with acute or chronic symptoms. Subsequent to Conclusion that clinical correlation, imaging characteristics then may Abnormalities on imaging of the basal ganglia are often be useful to further refine the differential diagnosis. nonspecific. Therefore, a focused approach to limit the dif- Metabolism—To better understand the imaging character- ferential diagnosis is based on whether the patient presents istics of the basal ganglia, a brief review of the physiology with acute or chronic symptoms. The most sensitive sequence and pathophysiology is provided herein. The basal ganglia in the acute setting to detect abnormalities within the basal form the core of the extrapyramidal system and regulate ganglia is diffusion-weighted imaging (DWI). The differen- motor activity. This process requires chemical energy in the tial diagnostic considerations in the acute setting should in- form of adenosine triphosphate (ATP) [1]. To produce ATP, clude hypoglycemia, cerebral hypoxic encephalopathy, car- the basal ganglia require a rich blood supply, which typically bon monoxide poisoning, encephalitis, osmotic myelinolysis, provides oxygen, glucose, and a high concentration of miner- toxin exposure, vascular causes, and illicit drug use. als [1]. ATP is produced through aerobic respiration and oxi- dative phosphorylation within the mitochondria [1]. An Case History acute deprivation of oxygen, glucose, or both results in insuf- A 24-year-old man presented to our emergency depart- ficient and inefficient production of ATP [1]. In addition to ment via ambulance in a comatose state. Brain MRI was providing oxygen and minerals, a rich vascular supply to the performed after urgent clinical assessment and stabilization basal ganglia is necessary to remove metabolic by-products in the emergency department. that may be harmful if left in situ [1]. The basal ganglia con- tain inherently high concentrations of trace minerals such as Brain MRI iron, copper, and manganese, many of which are important Unenhanced MRI examination of the brain was per- cofactors for metabolic activity [1]. formed using a routine (standard) protocol; the following The basal ganglia have a high metabolic rate, which sequences were included: T1-weighted, T2-weighted, DWI makes them particularly susceptible to damage from hy- with generation of apparent diffusion coefficient (ADC) poxia or anoxia [1]. Injury may occur with any process that maps, FLAIR, and blood-sensitive T2*. interrupts the normal steps in ATP production including, The FLAIR images showed hyperintensity of the bilat- but not limited to, decreased oxygen, blood flow, or glucose eral caudate nuclei, putamina, globus pallidi, and thalami [1]. In addition, conditions altering the normal mitochon- (Fig. 1A). Cortical swelling was seen in a temporal–occipi- drial structure or resulting in elevated mineral deposition tal–parietal distribution (Figs. 1A and 1B). DW images can potentially injure the basal ganglia and thus impair showed restricted diffusion of the basal ganglia and of the their function [1]. Furthermore, the typically rich vascular temporal–occipital–parietal cortex (Figs. 1C and 1D). T1- supply to the basal ganglia makes them susceptible to tox- weighted images (not shown) depicted hypointensity within ins and infectious agents [1]. The typically high metabolic Keywords: basal ganglia, brain MRI, carbon monoxide, cerebral hypoxic encephalopathy, encephalitis, hypoglycemia, illicit drugs, toxins DOI:10.2214/AJR.07.7089 Downloaded from www.ajronline.org by Dartmouth - Hitchcock Med Ctr on 08/08/14 IP address 130.189.10.62. Copyright ARRS. For personal use only; all rights reserved Received April 10, 2008; accepted after revision June 11, 2009. M. E. Mullins receives honoraria for invited lectures and professorships at the University of Kentucky and the Grand Rapids Medical Education & Research Center. 1Northwest Radiology Network, 5901 Technology Center Dr., Indianapolis, IN 46278. Address correspondence to E. E. Beltz ([email protected]). 2Department of Radiology, Emory University, Atlanta, GA. AJR 2010; 195:S1–S8 0361–803X/10/1953–S1 © American Roentgen Ray Society AJR:195, September 2010 S1 Beltz and Mullins Fig. 1—24-year-old man who presented in comatose state. A and B, Axial FLAIR images show hyperintensity of caudate nuclei, putamina, globus pallidi, and thalami. Note cortical swelling in temporal–occipital–parietal distribution. C and D, Axial diffusion-weighted images depict restricted diffusion of basal ganglia, thalami, temporal–occipital cortex, and parietal cortex. A B C D demand of the basal ganglia is similar to that of the cere- ited to hypoglycemia, hemolytic uremic syndrome, osmotic bellum and cerebral cortex [1]. Presumably, this character- myelinolysis, encephalitis, carbon monoxide (CO) exposure, istic is why the cortex and basal ganglia are often involved exposure to other toxins, recreational drug use, vascular simultaneously in pathologic conditions along these lines causes, and hypoxic ischemic encephalopathy. The clinical [1]. A common end point leading to cellular injury may re- presentation and imaging characteristics of these disease sult from an insufficient production of ATP, resulting in in- processes and of the abnormalities caused by toxin exposure creased intracellular water [1]. This increase, in turn, causes or illicit drug use are reviewed herein. Chronic conditions are the basal ganglia to show abnormal signal hyperintensities not discussed in this article for the sake of brevity. on FLAIR, T2-weighted, and DW images. If hemorrhage Differential diagnosis: hypoglycemia—The neurologic signs or mineral or protein deposition also occurs within the basal of hypoglycemia (neuroglycopenia) include weakness, confu- ganglia, the basal ganglia may show T1-weighted signal hy- sion, anxiety, and tingling of the autonomic group [2]. Sei- perintensity or hypointensity or may be invisible on essen- zures and coma usually occur in those with blunted responses tially any MR sequence of the brain. to hypoglycemia such as patients with diabetes or tumor-as- sociated hypoglycemia [2]. There are numerous causes of hy- Downloaded from www.ajronline.org by Dartmouth - Hitchcock Med Ctr on 08/08/14 IP address 130.189.10.62. Copyright ARRS. For personal use only; all rights reserved Case Discussion poglycemia, but most are related to diabetes [3]. Other causes Because the patient described here presented with acute include alimentary problems, fasting, tumors (insulinoma), symptoms, the differential diagnosis includes but is not lim- endocrine disorders, hepatic diseases, and sepsis [2, 3]. Hypo- S2 AJR:195, September 2010 Basal Ganglia and Cortex Hyperintensity on MRI A B C Fig. 2—Alcoholic man with ataxia. A and B, Note T2 hyperintensity within pons (A) and basal ganglia and thalami (B), representing abnormal myelin signal in osmotic demyelination. C, Restricted diffusion is observed within pons. glycemia acutely results in “brain energy failure” and in imaging may illustrate hyperintensity within the basal gan- membrane ionic pump failure, the latter of which causes a glia from coagulative necrosis secondary to microthrombosis prominent rise of intracellular water [4]. The regions of af- [7]. T2 hyperintensity may occur within the basal ganglia fected brain are variable but include the temporal–parietal– and cerebral cortex [7]. DW images can show reduced diffu- occipital cortex, hippocampus, and basal ganglia, especially sion in the acute phase [7]. the caudate and lentiform nuclei [5, 6]. Differential diagnosis: osmotic myelinolysis—As discussed The changes in the brain caused by hypoglycemia may previously, the basal ganglia are particularly susceptible to result in T1 and T2 prolongation in the acute phase and T1 electrolyte imbalances because of their high metabolic rate. and T2 shortening in the subacute phase [4–6]. Investiga- Osmotic myelinolysis classically occurs from rapid correction tors have speculated that T1 and T2 shortening are the re- of hyponatremia, often in malnourished alcoholics [8] but also sult of neuronal death, proliferation of glial cells, lipid ac- may occur in transplant patients, secondary to polydipsia and cumulation, paramagnetic substance deposition, or a in the chronically debilitated. Patients typically present with combination of these factors [6]. Restricted diffusion with spastic quadriparesis and pseudobulbar palsy [8]. The imaging decreased ADC values in the cerebral cortex, adjacent white findings are characteristically centered within the pons, but matter, and basal ganglia may be seen in the acute phase the basal ganglia and thalami may be
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