Decoding the Deep Gray-Anatomy Basal Ganglia

BRAIN

Decoding the Deep Gray: A Review ofthe Anatomy, Function, and ImagingPatterns Affecting the Basal GangliaChristie M. Lincoln, MD, Jacqueline A. Bello, MD, and Yvonne W. Lui, MD

ABSTRACTThis article reviews normal anatomy and function of the basal ganglia, organizes basalganglia pathology into patterns of disease based on imaging findings and introduces animaging algorithm to help in formulating a differential diagnosis for basal ganglia disease.

INTRODUCTIONThe basal ganglia are a collection of deepgray matter nuclei that play a major role inthe extrapyramidal system and contributeto higher emotional, sensorimotor, asso-ciative, and cognitive functions.1 CT andMR imaging allow in vivo visualization ofthe complex anatomy of the basal ganglia.We review the imaging anatomy, neuronalcircuitry, and imaging appearance ofpathologic processes that affect these im-portant deep gray nuclei.

AnatomyThe basal ganglia are paired structures,with 1 set of nuclei within each cerebralhemisphere and hemi-brain stem. In eachhemibrain, the basal ganglia are composedof 5 subcortical nuclei, including the cau-date nucleus, lentiform nucleus (putamenand globus pallidus), subthalamic nucleus,and substantia nigra. There are severalclassification schemes that variably includethe claustrum, amygdaloid, and olfactorytubercles, as part of the basal ganglia.These additional structures will not be fea-tured in this review.1

In the classification of basal gangliastructures, the corpus striatum refers to thecaudate nucleus, putamen, and globus pal-lidus. The caudate, putamen, and nucleusaccumbens are referred to as the striatum

or neostriatum.2 The putamen and globuspallidus are referred to as the lentiform nu-cleus (Fig 1A).

Caudate NucleusThe caudate takes its name from the Greekword meaning tailed.3 This nucleus isderived from the telencephalon, composedof a head, body, and tail (Fig 1A, -B). Thecaudate follows the lateral wall of the lat-eral ventricle with its tail terminating at theamygdala. The inferior part of the caudatehead is connected to the putamen at thelevel of the nucleus accumbens. Bridginggray matter structures, incompletely sepa-rated by developing axons, connect thecaudate and putamen and are referred to aspontes grisei caudatolenticularis (Fig1C). Bilateral or unilateral lesions of thecaudate may present with abulia, an apa-thetic affect with loss of initiative, sponta-neous thought, and emotional response.2

On the physiologic level, the bulk of stria-tal input from the cerebral cortex and thal-amus is integrated by the striatum andprojects to the globus pallidus and substan-tia nigra. Most important, the germinalmatrix, fromwhich neuronal and glial cellsmigrate during development, is located inthe caudothalamic groove. Premature birthand low birth weight are associated withgerminal matrix hemorrhage.

ABBREVIATION KEY

ACA anterior cerebral arteryFLAIR uid attenuated inversion

recoveryGABA gamma-aminobutyric acidGPi globus pallidus internaHIV human immunodeciency

virusMCAmiddle cerebral arteryNBIA neurodegeneration with

brain iron accumulationPKAN pantothenate kinase-

associated neurodegenerationT2WI T2-weighted imaging

Received September 22, 2011;accepted after revision December26.

From the Baylor College ofMedicine, Department of Radiology(C.M.L.), Houston, Texas;Monteore Medical Center, AlbertEinstein College of Medicine,Department of Radiology (J.A.B.),Bronx, New York; NYU LangoneMedical Center, New YorkUniversity School of Medicine,Department of Radiology (Y.W.L.),New York, New York.

Please address correspondence toChristie M. Lincoln, MD, Depart-ment of Radiology, Baylor Collegeof Medicine, One Baylor Plaza,Houston, TX 77030; e-mail:[email protected].

http://dx.doi.org/10.3174/ng.3120033

92 Neurographics 2:92102 Sep 2012 www.neurographics.com

Lentiform NucleusThe lentiform nucleus comprises 2 parts, the putamen andthe globus pallidus, which, grouped together, have a lens-like shape. However, there is no similarity in function be-tween these parts. The putamen, a telencephalic derivative,takes its origin from the Latin word for shell because ofits convex curvature over the globus pallidus. The globuspallidus, a diencephalic derivative, is also referred to as thepaleostriatum or pallidum. It contains the highest concen-tration of iron and/or ferritin in the brain. This concentra-tion increases with age and is not present in neonates. Theconcentration of iron in milligrams/100 g of tissue is higherin the brain than the iron concentration found in the liver.4

The globus pallidus is further divided into internal and ex-ternal segments by the internal medullary lamina (Fig1D).The globus pallidus serves as a major output nucleus ofthe basal ganglia. Patients with lentiform nuclei lesionspresent with complex dystonias and behavioral and motordisturbances.

Subthalamic NucleusThe subthalamic nucleus, derived from the diencephalon(Fig 1E, -F), is named for its location. This small lens-shaped structure lies inferior to the thalamus and superior

to the substantia nigra. Clinically, lesions of the subtha-lamic nucleus produce characteristic hemiballismus, invol-untary flinging motions of the extremities.2

Substantia NigraThe substantia nigra is derived from the diencephalon,named for its dark appearance on gross inspection due tothe dopaminergic neurons, which are heavily concentratedin this structure. It was first described by Samuel Thomasvon Sommering (17551830), who also noted that the pig-mentation was not obvious in early development.3 Thereare 2 zones of the substantia nigra. The ventral pale zone,referred to as the pars reticulata, resembles the inner seg-ment of the globus pallidus and is GABA-ergic. The dorsaldark zone, referred to as the pars compacta, comprises do-paminergic neurons and contains reciprocal connectionswith the striatum (Fig 1G). Histologically, the substantianigra pars reticularis resembles the globus pallidus in struc-ture and function.

Vascular SupplyThe high metabolic demand of the basal ganglia is pairedwith a rich vascular supply, which is variable among indi-viduals. The primary contributors to the basal ganglia vas-

Fig 1. A, Axial T1-weighted MR image demonstrates the putamen (short arrow) and globus pallidus (arrow), collectively referred to as the lentiformnucleus. Anasterisk is over the caudate head.B, Sagittal T1-weightedMR image shows thebodyof the caudate nucleus (arrow).C, Sagittal T1MR imagedemonstrates incompletely separated bridging gray matter structures connecting the caudate and putamen and referred to as the pontes griseicaudatolenticularis (arrow). D, The globus pallidus comprises 2 segmentsthat is, internal (black arrow) and external (white arrow) segmentsseparatedby the internalmedullary lamina.Medical illustration courtesy of JerryMicalizzi, MD.E, Coned-downaxial T2-weightedMR image shows thesubthalamic nuclei (arrows), which are located at the level of the midbrain and slightly inferior to the thalamus. F, The drawing depicts the midbrainat the level of the superior colliculus (SC) and quadrigeminal plate cistern (QC), with the subthalamic nucleus (SN) at the level of the red nucleus (RN).Medical illustration courtesy of Jerry Micalizzi, MD.G, The substantia nigra is locatedwithin themidbrain at amore inferior level from the subthalamicnucleus. It comprises 2 partsthat is, the ventral pale zone, referred to as the pars reticulata (thinner arrow), and the dorsal dark zone, referred to asthe pars compacta (thick arrow). D,F,G, Medical illustration courtesy of Jerry Micalizzi, MD, Monteore Medical Center, Bronx, New York.

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cular supply are the medial and lateral lenticulostriate ar-teries, and the recurrent artery of Heubner.

The internal carotid artery terminates in the ACA andMCA. The medial lenticulostriates supply the medial basalganglia, caudate nucleus, and internal capsule. They arisefrom the A1 segment of the ACA (Fig 2A). The recurrentartery of Heubner, the largest and longest of the perforatingbranches, typically arises from the proximal A2 segment ofthe ACA andmakes a characteristic acute turn to supply thesuperolateral caudate head, the anterior limb of the internalcapsule, and the anterior lentiform nucleus (Fig 2A). Thelateral lenticulostriates supply the lateral putamen, caudatenucleus, and external capsule. They arise from the M1 seg-ment of the MCA (Fig 2B).5

The substantia nigra is supplied at its caudal extent bypeduncular branches of the posterior cerebral artery, themedial posterior choroidal artery, and the superior cerebel-lar artery. At its rostral region, the vascular supply to thesubstantia nigra is from the premamillary branches of theposterior communicating artery and the peduncularbranches of the anterior choroidal artery.5

The subthalamic region is supplied by posteromedial ar-teries derived from the posterior communicating and pos-terior cerebral artery as well as the peduncular branchesof the anterior choroidal artery.5

Neuronal CircuitryThe basal ganglia play a major role in the complex extrapy-ramidal motor system. This collection of deep gray matternuclei functions in many neuronal pathways that deal withmotor function, as well as a diverse spectrum of behavioralfunctions, such as emotion, motivation, association, andcognition.

Before a motor signal intensity descends from the cortexto the brain stem and spinal cord, several cortical and sub-cortical centers, including some within the basal ganglia,help influence and organize the final motor output withrespect to timing, sequencing, and coordination of move-ment.2 The basal ganglia use several different neurotrans-mitters, including GABA, dopamine, acetylcholine, andglutamine. These enable the function of the basal ganglia asan intermediary between the cortex and the thalamus viathe basal gangliathalamocortical circuits.6 These circuitsconsist of 2 main pathways: direct and indirect. The 2 path-ways maintain somatotopic organization of movement forfluidity and coordination. The striatum and subthalamicnucleus are primary excitatory structures, receiving inputfrom the cerebral cortex. In contrast, the thalamus andbrain stem receive inhibitory output from the GPi and sub-stantia nigra pars reticulata. The subthalamic nucleus andthe GPi are important pacemakers in this system. The directpathway involves striatal neurons that contain neurotrans-mitters/neuromodulators that express the dopamine D1 re-ceptor. This pathway has a net stimulatory effect on com-munication between the thalamus and frontal cortex byinhibiting the inhibitor, which is the GPi (Fig 3A). The

Fig 2. A, Conventional frontal-projection cerebral angiogram in themidar-terial phase after injection of the left internal carotid artery shows the me-dial lenticulostriate artery arising from theA1 segment of the anterior cere-bral artery (short arrow) and the origin of the recurrent artery of Heubner,the largest and longest perforating branch, arising from the proximal A2segment of the anterior cerebral artery (arrow). B, Conventional frontal-projection cerebral angiogram in the early arterial phase after left internalcarotid artery injection shows the lateral lenticulostriate artery arising fromtheM1 segment of themiddle cerebral artery (arrow).C, A sketch of the leftintrancranial internalcarotidarterywiththerecurrentarteryofHeubner(H),themedial lenticulostriate artery (MLST), and the lateral lenticulostriate ar-tery (LLST). C, Medical illustration courtesy of Jerry Micalizzi, MD, Monte-oreMedical Center, Bronx, NewYork.


indirect pathway involves the globus pallidus externa andthe subthalamic nucleus (Fig 3B). These neurons express thedopamine D2 receptor. This pathway has a net inhibitoryeffect on communication between the thalamus and frontalcortex by stimulating the inhibitor, the GPi. Depending onthe pathology, one of these pathways may be more involvedthan the other, with variable excitatory and inhibitoryeffects.7

ImagingMost of the basal ganglia are well-demonstrated on cross-sectional imaging. Noncontrast CT shows the caudate, pu-tamen, and globus pallidus as having relatively high atten-uation compared with white matter. The substantia nigra

and the subthalamic nuclei are not as clearly depicted onCT. On MR imaging, the caudate and putamen generallyfollow cortical gray matter signal intensity. In the healthyadult, the globus pallidus, subthalamic nucleus, and sub-stantia nigra often appear relatively hypointense to corticalgray matter on T2WI, due to higher iron concentration. Ina young patient, the substantia nigra is hyperintense onT2WI. With increasing age and higher iron content, there isincreasing susceptibility of the substantia nigra on gradient-recalled echo T2*.3,8

The basal ganglia also contain high concentrations oftrace metals like iron, copper, and manganese. The charac-teristic features of the basal ganglia (ie, increased vascular-ity related to metabolic demand and increased trace metalconcentration) make the basal ganglia susceptible to injury,particularly in childhood.9-12 An alteration in vascular sup-ply to the basal ganglia can be deleterious. Furthermore,although trace metals in the basal ganglia are beneficial ascofactors in normal metabolic activity, they can otherwisebe harmful, particularly in excess. Imaging is useful in theevaluation of basal ganglia abnormalities. CT and MR im-aging are complementary studies, each with unique advan-tages. CT is the most commonly performed brain imagingand demonstrates calcification, acute hemorrhage, priorischemic injury, and volume loss. CT is useful in patientswith non-MR imagingcompatible implantable devices, in-cluding subthalamic and brain stem stimulators in patientswith movement disorders.13-17

MR imaging is advantageous in delineating anatomy anddemonstrating signal-intensity alteration.

CTCT hyperattenuation in the basal ganglia is seen in the set-ting of acute hemorrhage andmineralization. The lentiformnucleus is a typical location for hypertensive hemorrhage(Fig 4A). Perforating vessels, which are small end arteries,are susceptible to damage from toxins, microthrombi, oruncontrolled hypertension.18 Contrast leakage across theblood-brain barrier during selective intracranial endovascu-lar injection can mimic acute hemorrhage (Fig 4B). Calcifi-cation of the lentiform nuclei commonly occurs with in-creasing age. In young patients, however, one shouldconsider abnormalities of calcium or phosphate metabo-lism, Fahr disease, HIV, and Down syndrome (trisomy 21).Fahr disease, or familial idiopathic basal ganglia calcifica-tion, is an inherited disorder, manifest by attenuated bilat-eral basal ganglia calcification and calcification of extras-triatal regions. Patients present with variable symptoms,ranging from cognitive and behavioral changes to dystonia,parkinsonism, and ataxia (Fig 5A). zref19 HIV is also asso-ciated with basal ganglia calcification, which preferentiallyoccurs within the globus pallidus, possibly due to a vascu-litic process (Fig 5B).20,21 In Down syndrome (trisomy 21),calcifications occur predominantly in the globus palliduswith greater frequency than in the general population andoccur at a younger age (Fig 5C).22

Fig 3. A, A diagram depicting the direct pathway of the thalamocorticalcircuit, which involves striatal neurons that contain neurotransmitters/neuromodulators that express the dopamine D1 receptor. This pathwayhas a net stimulatory effect on the communicationbetween the thalamusand frontal cortex by inhibiting the inhibitor, namely the GPi. B, Theindirect pathwayof the thalamocortical circuit, wherein the external pal-lidal segment and the subthalamic nucleus are involved with expressionof the dopamine D2 receptor, is depicted. There is a net inhibitory effecton communication between the thalamus and frontal cortex by stimulat-ing the inhibitor, namely the GPi.


CT hypoattenuation in the basal ganglia is seen withedema due to hypoxic injury (Fig 6).9 During early isch-emia, noncontrast CT findings may be normal; however,one of the early CT signs of MCA territory infarct is pu-taminal hypoattenuation (Fig 7).

Chronic ischemia results in lacunar infarcts and volumeloss. Patientswith both acute and chronic intracranial vasculardisease may have choreiform movements and other extrapy-ramidal signs. Imaging is helpful in suggesting ischemic etiol-ogy and differentiating it from neurodegenerative disorders,which tend to exhibit bilateral symmetric abnormalities, as inHuntington disease. In this disorder of the caudate atrophygene repeat expansion in the Huntingtin gene, symmetric at-rophy of the caudate heads produces a characteristic boxcarconfiguration to the frontal horns (Fig 8).23,24

MR ImagingIn diseases affecting the basal ganglia, MR imaging signalintensity aids in formulating the differential diagnosis.

T1 ShorteningDiseases associated with abnormal T1 hyperintensity in-clude hypoxia, hyperalimentation, Wilson disease, and

Fig 4. A, A 70-year-old woman with a history of hypertension presentswith headache. Noncontrast head CT shows acute hemorrhage in the leftlentiform nucleus. B, A 53-year-old man immediately after a conven-tional cerebral angiography has a noncontrast head CT, demonstratingleft lentiform hyperattenuation, which resolved on follow-up imagingthe next day (not shown).

Fig 5. A, A 45-year-old woman with Fahr disease manifesting hyperat-tenuation/calcication of the bilateral lentiform nuclei on noncontrasthead CT. B, A 16-year-old HIV-positive girl also with hyperattenuation/calcicationof thebilateral lentiformnuclei onnoncontrast headCT.C, A21-year-oldmanwithDown syndrome (trisomy21) has noncontrast headCT demonstrating bilateral lentiform calcications.


chronic liver failure.Manganese deposition occurring in theglobus pallidus is seen in conditions such as total parenteralnutrition and chronic liver failure. The relatively short T1relaxation time of manganese results in the observed T1hyperintensity on imaging. Occasionally, this finding maybe reversible if the underlying issue is addressed.25 Manga-nese toxicity and chronic liver failure also result in T1 hy-perintensity within the globus pallidus (Fig 9).26,27

T2 ProlongationT2 hyperintensity is more common in basal ganglia pathol-ogy. The differential diagnosis depends on the location andpattern of signal-intensity abnormality.

T2 Prolongation: Globus PallidusInvolvement of the globus pallidus is seen in hypoxia, hy-poglycemia, and toxic and metabolic abnormalities such ascarbon monoxide toxicity, neurofibromatosis type I, and

Fig 7. A 58-year-old man with left hemineglect has noncontrast head CTusing a narrowwindow showing subtle hypoattenuation in the right len-tiform nucleus (A). Gray scale cerebral blood volume perfusion map (B)clearly shows the perfusion decit.

Fig 6. A 29-year-oldmanwith hypoxic brain injury after heroin overdosehas hypoattenuation within the lentiform nucleus and caudate on non-contrast CT. Also note the pseudosubarachnoid sign from cerebraledema.

Fig 8. Noncontrast headCT in a68-year-oldwomanwith knownHunting-ton disease shows atrophy of the bilateral caudate nuclei resulting in aboxlike conguration to the frontal horns.

Fig 9. A T1-weighted MR image in a 56-year-old manwith hepatoma andhepatic encephalopathy shows hyperintensity within the bilateral glo-bus pallidi.


neurodegenerative disorders, including Hallervorden-Spatzdisease. Occasionally, prominent and tumefactive perivas-cular spaces mimic pathology.

Neurofibromatosis type I is an autosomal dominant dis-order and one of the most common phakomatoses. T2 pro-longation typically affects the globus pallidus and the brainstem, cerebellum, and thalamus (Fig 10A). These areas ofill-defined signal-intensity abnormality are postulated torepresent hamartomas, heterotopias, or areas of myelinvacuolization. Because they tend to resolve with maturity, itis unlikely that they represent hamartomas or heteroto-pias.28-33 The globus pallidus and pars reticulata of thesubstantia nigra contain the highest concentration of iron inthe brain and are highly susceptible to carbon monoxidepoisoning, due to the affinity of carbon monoxide for theporphyrin ring of the hemoglobin molecule.34,35 SymmetricCT hypoattenuation and T2 hyperintensity due to necrosisin the globus pallidus are characteristic of carbonmonoxidepoisoning (Fig 10B).36

Hallervoden-Spatz (PKAN) or NBIA is an autosomal re-cessive disease of excessive iron deposition within the glo-bus pallidus and substantia nigra, resulting in hyperpigmen-tation of these structures and clinical manifestations ofdystonia, progressive rigidity, dysarthria, and mental im-pairment. MR imaging findings are nearly pathognomonic,described as having an eye of the tiger appearance, withbilateral central T2 hyperintensity representing gliosis, sur-rounded by a rim of T2 hypointensity, representing iron inthe globus pallidus on T2-weighted sequences (Fig 10C).7

T2 Prolongation: PutamenThe putamina are predominantly affected in a variety ofdisorders, including Leigh disease, methanol toxicity, Wil-son disease, and prion disease. They also contain perivas-cular spaces, which may be pronounced.

Leigh disease is a progressive hereditary neurodegenera-tive disorder of mitochondrial energy metabolism dysfunc-tion. The disease involves brain structures highly dependenton glucose metabolism (ie, the lentiform nuclei and caudatenuclei) with additional areas of involvement including thethalamus, periaqueductal gray, tegmentum, red nuclei, anddentate nuclei. Within these structures, there is symmetricT2 signa-intensity abnormality.37-39

Toxic and metabolic insults may also affect the putam-ina. Classically, the toxin that produces bilateral putaminallesions is methanol poisoning. Methanol is contained incommon housecleaning solvents and antifreeze. Patients of-ten present with metabolic acidosis and classic MR imagingfindings of bilateral putaminal necrosis, which may be as-sociated with hemorrhage.40-42

Wilson disease, also known as hepatolenticular disease,is an autosomal recessive disorder with an abnormality ofcopper transport leading to copper accumulation.When thenervous system is affected, patients present with motor andbehavioral dysfunction, including tremor and rigidity. Typ-ical MR imaging findings of Wilson disease include sym-

Fig 10. A, An 18-year-old woman with neurobromatosis 1 also demon-strating characteristic irregular hyperintense signal intensity on T2WI inthe bilateral globus pallidi. B, Noncontrast head CT in a 30-year-oldmanwith carbon monoxide poisoning shows characteristic bilateral globuspallidal necrosis. Case courtesy of Daniel Meltzer, MD, St. Lukes Roos-evelt Hospital, New York, New York. C, A 15-year-old girl with falls andhyperreexia has MR imaging demonstrating hyperintensity on a T2-weighted sequence, corresponding to gliosis in the globus pallidi, andsurrounding low signal intensity resulting in the eye of the tiger ap-pearance, which is a typical imaging nding seen in Hallervoden-Spatz(PKAN) or NBIA.


metric putaminal T2 signal-intensity hyperintensity, whichis likely the result of gliosis and necrosis (Fig 11).43-45 Wil-son disease may also show T1 hyperintensity within theputamina.

Prion diseases are a collection of neurodegenerative dis-eases caused by an accumulation of abnormally folded pro-teins in the brain. On imaging, the appearance varies withsubtype, but nearly all types share the common finding ofT2 signal-intensity hyperintensity within the basal ganglia,specifically the putamina (Fig 12A).46-50 FLAIR and diffu-sion imaging are the most useful MR images for this entity.FLAIR helps to depict cortical signal-intensity abnormalityand other lesions, which may be obscure on T2-weightedsequences. Similarly, lesions of the cortex and basal ganglia,in particular the caudate, are well-demonstrated on diffu-sion-weighted imaging due to vacuolization caused by gli-osis or astrocytosis of brain tissue, resulting in restrictedwater diffusion (Fig 12B).50

Perivascular spaces or Virchow-Robin spaces containingperforating lenticulostriate arteries course through the infe-rior basal ganglia. In the setting of generalized cerebralvolume loss (Fig 13), metabolic disorders such as mucopo-lysaccharidoses, and central nervous system infection suchas Cryptococcus infection, these perivascular spaces maybecome enlarged. Occasionally, dilated perivascular spacesmay appear tumefactive, with mass effect and small areas ofsurrounding T2 prolongation. In general, perivascularspaces follow CSF on all pulse sequences and do notenhance.51-53

Substantia Nigra and Subthalamic NucleusNigrostriatal denervation, the hallmark of Parkinson dis-ease, leads to overactivity of the globus pallidus interna andthe substantia nigra pars reticulata. The cardinal motorsigns found in Parkinson disease, akinesia, rigidity, andresting tremor, are attributed to loss of dopaminergic input

to the striatum, which results from degeneration of the sub-stantia nigra pars compacta. On imaging, this finding issubtle, but there is a reduction in the size of the substantia

Fig 11. A 31-year-old woman with known history of Wilson disease pres-ents with characteristic MR imaging ndings of lateral putaminal T2 hy-perintensity (arrow).

Fig 12. A 40-year-old woman with progressive multifocal neurologicdysfunctionwho underwent MR imagingwith symmetric T2 signal inten-sity abnormality in the bilateral caudate heads, bilateral putamina, andbilateral subinsular ribbon and bifrontal cortex, which are imaging nd-ings shared by all types of prion diseases (A). Diffusion-weighted imag-ing shows restricted diffusion in the same areas (B).

Fig 13. An MR image of an 87-year-old woman with memory loss whoshows prominent perivascular spaces following the CSF on all pulse se-quences including T2.


nigra (Fig 14A, -B). Movement disorders related to the sub-stantia nigra were first described by Blocq and Marinesco(1893) and Tretiakoff (1919).3

The subthalamic nucleus and globus pallidus are targets fordeep brain stimulation in the treatment of Parkinson diseaseand other movement disorders (Fig 15). The initial treatmentwith bilateral subthalamic nucleus stimulationwas performedby Limousin et al17 on a human subject with chronic debili-tating Parkinson disease; marked improvement in rigidity andakinesia was demonstrated.13-16 In order to assist the radiolo-

Fig 14. A 74-year-old woman with Parkinson disease has frequent MRimaging with 2 T2-weighted sequences, spanning a 2-year period show-ing progressive T2 hypointensity within the pars reticulata (short ar-rows) and decreasing width of the pars compacta (arrows).

Fig 15. Patient with known Parkinson disease has noncontrast CT dem-onstrating deep brain electrodes targeting the subthalamic nuclei andglobus pallidi in the treatment of a movement disorder.

Fig 16.On thebasis ofwhether thepathologyonCT is hyperattenuatedorhypoattenuated, an imaging algorithm is formulated to assist the radiol-ogist in an appropriate differential diagnosis.

Fig 17. With signal intensity (ie, hyperintense or hypointense), an imag-ing algorithm is formulated to assist the radiologist in an appropriatedifferential diagnosis.


gist in a differential diagnosis, a CT algorithm (Fig 16) and aMRI Algorithm (Fig 17) have been provided.

SUMMARYThis review outlines the anatomic, functional, and patho-logic importance of the basal ganglia. CT and MR imagingcharacteristics of disorders that target the basal ganglia arehighlighted, with a focus on how different imaging pat-terns may aid the radiologist in narrowing the differentialdiagnosis.

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Decoding the Deep Gray-Anatomy Basal Ganglia

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