Bilateral basal ganglia abnormalities - MRI
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DIFFERENTIAL DIAGNOSISFOR BILATERAL ABNORMALITIES
OF THE BASAL GANGLIAAND THALAMUS
Dr Roshan Valentine
PG Resident
St Johns Medical College
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INTRODUCTION• Abnormalities of basal ganglia seen in various conditions.• MR – IOC• CT - emergency situations – altered sensorium / acute seizures.• In this article , we review the MRI anatomy of basal ganglia and
pathology conditions of these brain structures
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ANATOMY• Deep gray matter include paired
BG and thalamus• Here we restrict to abnormalities
of lentiform nucleus and caudate nucleus
• Lentiform N : GP(D) + Putamen(I)• Caudate N (I)• Basal ganglia involved in
production of movement and in memory , cognition and emotion.
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ANATOMY• LFN is rich in mitochondria , vascular supply , neurotransmitters –
high metabolic activity and oxygen uptake - vulnerable to metabolic abnormalities
• Thalamus is paired structure on either side of third ventricles. • Responsible for relaying sensory and motor signals to and from the
cerebral cortex• Disorders of thalamus affects consciousness and abnormalities of
sensation
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ANATOMYBLOOD SUPPLY• BG : Medial and lateral
lenticulostriate arteries• Thalamus : PCA and PCOM• Venous drainage : deep venous
system ; internal cerebral veins - basal vein of Rosenthal - great vein of galen
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TOXIC POISONING• CAUSE : MC - CO , methanol and CN• Impairs mitochondrial enzyme in electron transport chain .• CLINICAL FEATURES : Acute cognitive impairment /coma , optic
neuritis (methanol) DIAGNOSIS• Toxicology and Lab tests , imaging ( assess brain damage)
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TOXIC POISONINGIMAGING FINDINGS• CO – GP(MC) : T1 & T2 hyperintense + DWI RD , Delayed
leukoencephalopathy • CN , Meth : Hemorrhagic necrosis of putamen• Meth : White matter edema
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LIVER DISEASE• CAUSATIVE AGENT : Due to nitrogenous waste crossing BBB• CLINICAL FEATURES : cirrhosis with portal htn /iatrogenic (TIPSS)• IMAGING FINDINGS : - GP and SN : hyper on T1( due to Mn deposn) - Reversible post transplantation. - Acute hyperammonemia : bilaterally symmetric swelling, T2 prolongation restricted diffusion in the basal ganglia, insular cortex, and cingulate gyrus - MRS : Detection of glutamate-glutamine
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NON KETOTIC HYPERGLYCEMIA• CLINICAL FEATURES : poorly controlled diabetes with chorea ,
hemiballismus +/- altered mental status.• Treatable condition which shows resolution of findings when
performed 2-12 months laterIMAGING FINDINGS⁻ CT: B/L or rarely U/L hyperattenuation of GP or CN⁻ MR : hyperintensity on T1 and variable intensity in T2
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HYPOGLYCEMIA• CLINICAL FEATURES : Diabetic pts, Seizures , focal neurological
deficits and coma.• Extent of brain damage depends on severity and duration of
hypoglycemia.IMAGING FINDINGS:• T2 hyperintensity in cerebral cortex , hippocampi and BG• Mild reversible hypoglycemia – transient and isolated WMI with true
diff restriction involving splenium , internal capsule and corona radiata.
• BG INVOLVEMENT : POOR PX
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HYPOXIC ISCHEMIC ENCEPHALOPATHY• CAUSE : Result of cardiac arrest /drowning/asphyxiationIMAGING FINDINGS: • Mild HIE : water shed zones• Severe HIE : grey matter structures like cerebral cortex , BG and hippocampi.
• Brainstem and WM are typically spared.
• CT : Diffuse edema , decreased attenuation of the cortical gray matter with loss of normal gray matter–white matter differentiation, BG and Thalamus
• WHITE CEREBELLUM SIGN : diffuse cerebral damage results in lower attn. of cerebral parenchyma , compared to cerebellum and BG which are spared – POOR PX
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HYPOXIC ISCHEMIC ENCEPHALOPATHY• Earliest finding(after 2 hrs) : Increased SI of the affected areas on
DW• T2W : hyperintensity and swelling of affected areas ( after 24 hrs) • Delayed : T2 hyperintensity in subcortical WM
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LEIGH DISEASE• Subacute necrotizing encephalopathy• CAUSE : Disorder in ATP synthesis at ETC• CLINICAL FEATURES : Central hypotonia , developmental
regression/arrest , ophthalmoplegia , resp and bulbar dysfunction and ataxia.
IMAGING FINDINGS: • T2 hyperintensity in BG , periaquedeuctal region , cerebral peduncles
and putamen.• MRS : High lactate levels in BGDIAGNOSIS : Imaging + Elevated serum and CSF lactate levels.
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WILSON DISEASE• CAUSE : Accumulation of Cu due to ceruloplasmin deficiency.• CLINICAL FEATURES : dysarthria, dystonia, tremors, ataxia,
Parkinsonian symptoms, and psychiatric problems.IMAGING FINDINGS: • MR : T2 hyperintensity in Putamen(MC)• GP , caudate nucleus , thalamus• Less common : cortical and subcortical region , mesencephalon , pons , vermis
and dentate nuclei• DWI restriction in early stages
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OSMOTIC MYELINOLYSIS• CAUSE : electrolyte imbalance, chronically alcoholic pts, chronically
debilitated organ transplant pts , rapid overcorrection of hyponatremia.
• Oligodendroglial cells are more susceptible to osmotic stresses.
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OSMOTIC MYELINOLYSISIMAGING FINDINGS:• MRI : T1 and T2 hyperintensity in affected areas• Central pontine myelinolysis : Symmetric trident shaped / bat wing
shaped T2 /FLAIR hyperintensity in central pons • Ventrolateral pons and pontine portion of CST are spared
• Extrapontine myelinolysis : T2 hyperintensity in GP , putamen , thalamus and cerebellum.• DWI R in early stages – not typical though
DIAGNOSIS : Imaging + serial Na measurement
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WERNICKE ENCEPHALOPATHY• CAUSE: Vit B1 def , Chronic alcoholics , GI or hemat neoplasm ,
chronic dialysis , prolonged TPN without vit supplementation.• CLINICAL FEATURES : altered consciousness, ocular dysfunction, and
ataxiaIMAGING FINDINGS: • MRI : Symmetric T2 hyperintensity in medial thalamus ,
periaqueductal area , mammillary body and tectal plate. • Petechial hemorrhage , diffusion restriction and contrast
enhancement of affected areas
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NEURODEGENERATION WITH BRAIN IRON ACCUMULATION (NBIA)• Heterogenous group of disorder with brain degeneration and
excessive iron deposition in basal ganglia(PAN K 2 gene mutation.)• 2 types • Classic early onset , rapidly progressive(halloverden spatz)• Atypical late onset and slowly progressive
• CLINICAL FEATURES : pyramidal or extrapyramidal signs, dystonia, and dysarthria
IMAGING FINDINGS: • MR : B/L T2 hypointensity in GP with high signal intensity center -
EYE OF THE TIGER appearance
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Creutzfeldt –jakob Disease• Transmissible fatal neurodegenerative disorder caused by prions• CLINICAL FEATURES : rapidly progressive dementia, myoclonus, and
multifocal neurologic dysfunction.• DIAGNOSIS: Brain Biopsy /autopsy, periodic charp wave complexes
at EEGIMAGING FINDINGS: • MRI : DWI R of cerebral cortex and basal ganglia• Variant CJD : Bovine spongiform encephalopathy • B/L lesions in pulvinar nuclei of thalamus(pulvinar sign/hockey stick sign)
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FAHR DISEASE• Bilateral striopallidodentate calcinosis• B/L symmetric deposition of Ca and other minerals in BG ,Thalamus ,
Dentate nuclei and centrum semiovale in absence of HYPOPARATHYROIDISM.
• CLINICAL FEATURES : Headache , vertigo , movt disorders , syncope , seizures , coma, dementia , parkinsonism , chorea, dystonia etc.
IMAGING FINDINGS: • MRI/CT : B/l symmetric dense calcifications in BG , dentate nuclei ,
thalamus , subcortical white matter .
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DEEP CVT• CAUSE : hypercoagulable states , OCPS , vasculitis , intracranial / systemic infectionsIMAGING FINDINGS: • Superficial CVT: cerebral edema and venous infraction of cerebral
cortex near vertex.• Deep CVT: Venous HTN , b/L involvement of thalamus and basal ganglia.• MRI/CT: Venous HTN and cerebral edema results in T2 hyperintensity
in thalamus , BG , internal capsule and DWM • Hemorhhagic transformation common
• MR venogram : evaluation of thrombus
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ARTERIAL OCCLUSION • CLINICAL FEATURES : Agitation , obtundation , coma , memory
dysfunction and various ocular changesIMAGING FINDINGS: • Acute infarcts : T2 hyperintensity and DWI R with occlusion seen on
MRA based on the artery occluded.• Artery of Percheron infarct : B/l symmetric paramedian parts of
thalamus and midbrain on both sides.
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Figure 19. Basilar artery occlusion in a 61-year-old man with ocular signs and severe obtundation. (a) Diffusionweighted MR image shows bilateral hyperintense areas in the paramedian thalamus (arrows). (b) Timeof- flight MR angiogram clearly depicts occlusion of the rostral portion of the basilar artery (arrow). (c, d) Noncontrast CT scans obtained 3 days later show bilateral subacute infarcts of the thalamus (arrows in c) and an infarct in the right cerebellar hemisphere(arrow in d).
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NEURO – BEHCET DISEASE• Behcet syndrome : uveitis , oral ulcers and genital ulcers.• CNS involvementin 4-49%• CLINICAL FEATURES : Headache , dysarthria , cerebellar signs ,
sensory signs and personality change.IMAGING FINDINGS: • T2 hyperintense and T1 hypointense and CE with vasogenic edema
at brainstem, basal ganglia (bilateral involvement in one-third of cases), and thalamus , WM(LC)
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FLAVI VIRUS ENCEPHALITIS• Eg : Japanese encephalitis, West nile fever , Murray valley feverIMAGING FINDINGS: • Symmetric involvement of deep grey matter JE : T2 hyperintensity in B/L posteromedial thalamus
• Intralesional hemorrhages + DWI R• Less common sites : basal ganglia, substantia nigra, red nucleus, pons, hippocampi,
cerebral cortex, and cerebellum.
• JE and Murray valley fever involve THALAMUS• West nile fever : B/L involvement of thalamus , caudate and lentiform nucleus
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CEREBRAL TOXOPLASMOSIS• CAUSE : Toxoplasma gondii typically in imuncompromised ptsMAGING FINDINGS: • Multiple focal lesions in the basal ganglia and lobar gray matter–
white matter junctions• T2 W : hypo to isointense lesions with prominent mass effect and
vasogenic edema +/- hemorrhagic lesions• Post Contrast : nodular/ ring enhancement• MRS : increased lipid levels without elevated choline levels
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PRIMARY CNS LYMPHOMA• CAUSE : immunocompetent and immunocompromisedIMAGING FINDINGS: • T2 hypointensity and high attenuation in CT involves deep
hemispheric periventricular white matter, corpus callosum, and basal ganglia
• MRS : Elevated choline levels• Immunocompetent : Solid, homogeneously enhancing lesions• Immunocompromised : Ring enhancement and central necrosis
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PRIMARY BILATERAL THALAMIC GLIOMA• Thalamus is affected in 1-1.5% of brain tumors / contiguous spread
from pineal germ cell tumors.• CLINICAL FEATURES : behavioral impairment ranging from
personality changes to dementia. • IMAGING : T2 hyperintense and T1 isointense B/L symmetric mass
with no CE • Low grade tumors characterized by absence of tumor progression
on serial MR images,
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NEUROFIBROMATOSIS TYPE I• MC neurocutaneous syndrome• CLINICAL FEATURES : café-au-lait spots, axillary freckling, Lisch
nodules, neurofibromas, plexiform neurofibromas, optic glioma, bone dysplasias, or pseudoarthrosis.
IMAGING FINDINGS: Focal T2 hyperintense and TI hypointense in GP > brainstem and cerebellum• NO mass effect• No surrounding edema• No CE
• MRS : high NAA-Ch , Naa-Cr and Cr- Cho ratios
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IMAGING
LAB IXCL.HISTORY
DX
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LAB EVALUATIONImmunoassay Toxoplasmosis and Flavivirus
Eeg + CSF analysis CJD
Vit B1 assay Wernickes
Serum glucose Hypoglycemia/Hyperglycemia
Serum Ceruloplasmin Wilsons disease
Serum and CSF Lactate Leigh Disease
Serum Ca , P and PTH Fahrs DIsease
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IMAGING
LAB IXCL.HISTORY
DX
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• CLINICAL HISTORY • Suicide attempt • cardiac arrest • diabetic hypoglycemia • hyperglycemia • Hiv – AIDS • Vit deficiency • Electrolyte imbalance
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IMAGING
LAB IXCL.HISTORY
DX
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IMAGING FINDINGS
B/L symmetric LN andCN Systemic /metabolic
Asymmetric focal/Discrete Infection/neoplasm
Thalamus+ BG Hypoxia , osmotic myelinolysis , wilsons disease , Leighs disease , Fahrs disease , CJD , deep CVT, Infection , Primary CNS lymphoma
BG w/o Th Systemic disease ( toxic poisoning , hypoglycemia , hyperglycemia , liver disease , huntingtons disease , NF)
B/L Th w/o BG Focal ( arterial occlusion ,Flavivirus , infection )
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ASSOCIATED ABNORMALITIES
Diffuse or focal cortical involvement Hypoxia , hypoglycemia and CJD
Diffuse and bilateral white matter abnormality
poisoning , hypoglycemia
Brainstem Leigh disease , Myelinolysis , Neuro behcets disease , Basilar artery occlusion
Perilesional edema + infiltration outside BG + Th
CNS infection + tumors
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ASSOCIATED ABNORMALITIEST2W HYPERINTENSITY Acute diseases of deep grey
matter nuclei T1W HYPERINTENSITY Hepatic dis , Mn deposition ,
Hyperglycemia , NF 1
CT Ca – Fahrs disease, HypoparathyroidismH’age – Poisoning, CNs toxoplasmosis, Venous infarction , JE
DWI Acute cytotoxic brain damage in acute infarction, hypoxia, hypoglycemia, CJD,and Wernicke encephalopathy
MRS lactate in hypoxia or mitochondrial disease
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