1. Paraneoplastic Syndrome and Mimics: What the Radiology and Clinicians Need to Know
Ammar Chaudhry, MD
Maryam Gul, MD
Abbas Chaudhry, BS
Jared Dunkin, MD
eEdE-30
Correspondence:

2. Disclosures
NONE

3. Objectives
1. Review clinical spectrum and pathogenesis of paraneoplastic syndromes with focus on CNS processes 2. Case-based review highlighting common and uncommon causes of paraneoplastic syndrome 3. Discuss differential diagnoses (physiologic process, congenital, infection, inflammation, trauma, vascular and/or malignancy) that can mimic imaging findings of Paraneoplastic syndromes 4. Review treatment and prognosis

4. Introduction
Paraneoplastic neurologic syndromes are a heterogeneous group of disorders caused by mechanisms other than metastases, metabolic and nutritional deficits, infections, coagulopathy or side effects of cancer treatment
These syndromes may affect any part of the nervous system from cerebral cortex to neuromuscular junction either damaging one area (e.g. Purkinje cell, presynaptic cholinergic synapses) or multiple areas (e.g. encephalomyelitis)
Can simultaneously involve central and/or peripheral nervous system

5. Encephalitis
Infectious
Herpes Simplex Virus (Most often Implicated); HHV, CJD; Lyme
Autoimmune PE
Paraneoplastic (classically have intra-cellular antigens)
Antibodies against Membrane Antigens: Anti-NMDA Anti-AMPA Anti-GABAßR
Antibodies against Intracellular Antigens: Anti-Hu Anti-CV2/CRMP Anti-Ma2
“Non-Paraneoplastic” (antigen located on cell membrance)
Anti-GAD Antibodies against antigens of voltage-dependent potassium channel complex (LGI1, CASPR2, contactin-2)
pathogensis
Paraneoplastic neurologic syndromes are believed to result when an immunologic response is directed against shared antigens that are ectopically expressed by the tumor that are normally expressed by the nervous system
Antibodies can be detected in the serum and cerebrospinal fluid (CSF) of many
NOTE: not all patients with paraneoplastic syndromes have + Ab titers
Recent studies suggest that the immune system can mount a T-cell response to a “ normal protein” when it is expressed in a cancer cell
suggesting that normal self antigens may be processed differently in cancer cells than in the normal cells
Increased immune reaction against the “normal protein” expressed in the nervous systems leads to the Paraneoplastic syndrome
Dalmau J, Gultekin HS, Posner JB. Paraneoplastic neurologic syndromes: pathogenesis and physiopathology. Brain Pathol 1999; 9:275.
Rosenfeld MR, Eichen JG, Wade DF, et al. Molecular and clinical diversity in paraneoplastic immunity to Ma proteins. Ann Neurol 2001; 50:339
Savage PA, Vosseller K, Kang C, et al. Recognition of a ubiquitous self antigen by prostate cancer-infiltrating CD8+ T lymphocytes. Science 2008; 319:215
Dalmau J, Gultekin HS, Posner JB. Paraneoplastic neurologic syndromes: pathogenesis and physiopathology. Brain Pathol 1999; 9:275.
Rosenfeld MR, Eichen JG, Wade DF, et al. Molecular and clinical diversity in paraneoplastic immunity to Ma proteins. Ann Neurol 2001; 50:339
Savage PA, Vosseller K, Kang C, et al. Recognition of a ubiquitous self antigen by prostate cancer-infiltrating CD8+ T lymphocytes. Science 2008; 319:215

6. Paraneoplastic Limbic Encephalitis
Paraneoplastic syndromes are mediated by antibodies occur when certain neoplasms outside of the central nervous system express antigens that are expressed coincidentally by neuronal cells and therefore the immune response results in the production of antibodies that have as objective the tumor and specific sites in the brain.
The tumors most frequently associated with paraneoplastic LE are lung carcinoma (50%), mostly small cell lung carcinoma (SCLC), testicular tumors (20%), breast carcinoma (8%), non-Hodgkin lymphoma, teratoma and thymoma.
Antibodies associated with Paraneoplastic LE
Antibodies against membrane antigens: Anti-NMDA, Anti-AMPA, Anti-GABAbR
Antibodies against Intracelullar Antigens: Anti-Hu, Anti-CV2/CRMP-5, Anti-Ma2

7. Autoimmune Paraneoplastic encephalitis
Autoantibodies are directed against two antigen categories: intracellular antigens (referred to as “classical paraneoplastic antigens”) and cell membrane antigens (“non-paraneoplastic”)
Classically described that the antigens in the paraneoplastic encephalitis are intracellular and opposite to this in the non-paraneoplastic are membrane antigens, recent literature reviews reveal that there may be either types of antigens with or without associated tumor
Immune response against intracellular antigens usually associates a cytotoxic T-cell mechanism and a limited response to immunomodulator therapy
Immune response to membrane antigens is mediated by antiboidies and respondes better to treatment.

8. Clinical spectrum of central and peripheral nervous system Paraneoplastic syndromes
Paraneoplastic syndromes of the central nervous system
Encephalomyelitis*
Visual syndromes
Myelitis*
Cancer associated retinopathy*
Limbic encephalitis*
Melanoma associated retinopathy*
Brainstem encephalitis*
Optic neuritis
Cerebellar degeneration*
Necrotizing myelopathy
Opsoclonus myoclonus ataxia*
Motor neuron syndrome
Stiff-person syndrome*
Subacute motor neuronopathy
Subacute sensory neuronopathy*
Other syndromes
Paraneoplastic syndromes of the peripheral nervous system
Chronic sensorimotor neuropathy
Acute sensorimotor neuropathy
Association with plasma cell dyscrasias
Guillain-Barré syndrome
Autonomic neuropathy*
Plexitis (eg, brachial neuritis)
Vasculitis of nerve and muscle
Paraneoplastic syndromes of the neuromuscular junction and muscle
Myasthenia gravis*
Neuromyotonia*
Lambert-Eaton myasthenic syndrome*
Acute necrotizing myopathy
Dermatomyositis/polymyositis
CA1:A32achectic myopathy
Dalmau J, Rosenfeld M. Overview of Paraneoplastic syndromes of the nervous system. Accessed Oct 25th 2014
* Denotes syndromes where specific antibodies have been identified
* Denotes syndromes where specific antibodies have been identified
Dalmau J, Rosenfeld M. Overview of Paraneoplastic syndromes of the nervous system. Accessed Oct 25th 2014

9. Paraneoplastic syndromes associated with lung cancer
Systemic
Neurologic
Endocrine/Metabolic
Anorexia, cachexia, weight loss
Dermatomyositis/polymyositis
Peripheral neuropathy
Cushing's syndrome
Fever
Systemic lupus erythematosus
Lambert-Eaton myasthenic syndrome
Hypercalcemia
Orthostatic hypotension
Nonbacterial thrombotic
endocarditis
Necrotizing myelopathy
Hyponatremia
Renal
Cerebral encephalopathy
Hyperglycemia
Glomerulopathies
Tubulointerstitial disorders
Cutaneous
Visceral neuropathy
Acromegaly
Acquired hypertrichosis lanuginosa
Acquired ichthyosis
Hematologic
Hyperthyroidism
Acrokeratosis (Bazex's syndrome)
Acquired palmoplantar keratoderma
Anemia
Hypercalcitoninemia
Clubbing
Erythema annulare centrifugum
Polycythemia
Gynecomastia
Dermatomyositis
Florid cutaneous papillomatosis
Hypercoagulability
Galactorrhea
Erythema gyratum repens
Pemphigus vulgaris
Thrombocytopenic purpura
Carcinoid syndrome
Exfoliative dermatitis
Pityriasis rotunda
Dysproteinemia (including amyloidosis)
Hypoglycemia
Hypertrophic pulmonary osteoarthropathy
Pruritus
Leukocytosis/leukoerythroblastic reaction
Hypophosphatemia
Deep venous thrombosis (Trousseau's syndrome)
Sign of Leser-Trelat
Eosinophilia
Lactic acidosis
Tripe palms
Sweet's syndrome
Hypouricemia
Acanthosis nigricans
Vasculitis
Hyperamylasemia
Identifies most common Paraneoplastic syndromes
Identifies most common Paraneoplastic syndromes
Dalmau J, Rosenfeld M. Overview of Paraneoplastic syndromes of the nervous system. Accessed Oct 25th 2014

10. Antibodies, paraneoplastic syndromes and associated cancers
Antibody
Syndrome
Associated cancers
Well characterized paraneoplastic antibodies
Anti-Hu (ANNA-1)
Encephalomyelitis including cortical, limbic, brainstem encephalitis, cerebellar degeneration, myelitis, sensory neuronopathy, and/or autonomic dysfunction
SCLC, other
Anti-Yo (PCA-1)
Cerebellar degeneration
Gynecological, breast
Anti-Ri (ANNA-2)
Cerebellar degeneration, brainstem encephalitis, opsoclonus-myoclonus
Breast, gynecological, SCLC
Anti-Tr (DNER)
Hodgkin's lymphoma
Anti-CV2/CRMP5
Encephalomyelitis, cerebellar degeneration, chorea, peripheral neuropathy
SCLC, thymoma, other
Anti-Ma proteins• (Ma1, Ma2)
Limbic, hypothalamic, brainstem encephalitis (infrequently cerebellar degeneration)
Germ-cell tumors of testis, lung cancer, other solid tumors
Anti-amphiphysin
Stiff-person syndrome, encephalomyelitis
Breast, lung cancer
Anti-recoverinΔ
Cancer-associated retinopathy (CAR)
SCLC
Partially-characterized paraneoplastic antibodies
Anti-Zic 4
mGluR1
No tumor or Hodgkin's lymphoma
ANNA-3
Sensory neuronopathy, encephalomyelitis
PCA2
Encephalomyelitis, cerebellar degeneration
Anti-bipolar cells of the retina
Melanoma-associated retinopathy (MAR)
Melanoma
Antibodies that occur with and without cancer association
Anti-VGCC
Lambert-Eaton myasthenic syndrome, cerebellar dysfunction
Anti-AChR
Myasthenia gravis
Thymoma
Anti-NMDAR
Multistage syndrome with memory and behavioral disturbances, psychosis, seizures, dyskinesias, and autonomic dysfunction
Teratoma
Anti-AMPAR
Limbic encephalitis, psychiatric disturbances
Variable solid tumors
Anti-GABA(B) receptor
Seizures, limbic encephalitis
Anti-LGI1 (previously attributed to VGKC)
Limbic encephalitis, seizures
Thymoma, SCLC
Anti-CASPR2 (previously attributed to VGKC)
Morvan's syndrome and some patients with neuromyotonia
Thymoma and variable solid tumors
Anti-nAChR
Subacute pandysautonomia
SCLC, others
GlyR
Encephalomyelitis with muscle spasms, rigidity, myoclonus, hyperekplexia
Often without cancer
Dalmau J, Rosenfeld M. Overview of Paraneoplastic syndromes of the nervous system. Accessed Oct 25th 2014

11. diagnosis
Patients suspected of having a paraneoplastic neurologic syndrome should be examined for paraneoplastic antibodies in their serum.
NOTE: low level of antibodies can be positive in cancer patients w/o paraneoplastic syn.
NOTE: same neurologic symptoms/syndrome can be caused by one or more antibodies known to cause paraneoplastic syndrome
NOTE: high titers of paraneoplastic antibodies with or without symptoms should warrant careful search for underlying neoplasm
Neuroimaging studies, lumbar puncture, and electrophysiology tests can be helpful in characterizing the neurologic syndrome

12. Paraneoplastic syndrome radiological findings
The findings of limbic involvement are similar regardless of the type of antibody found. Some patients do not show any alteration in MRI, espceially those with anti- NMDA (up to 50% had normal MRI)
In patients with abnormalities, most common findings include hyperintense signal on FLAIR/T2-weighted sequences most notably affecting the mesial region in temporal lobes, hippocampi, frontobasal and insular regions
Other patterns of brain involvement can be found, especialy in patients with anti-NMDA, where the cerebellum, basal ganglia and brainstem can be affected

13. Dx: Anti-GAD Limbic Encephalitis
CASE: 69 YEAR OLD MALE WITH expressive aphasia and seizure-like episode
Ill-defined FLAIR hyperdensity in the left temporal lobe with loss of sulci suggestive of edema. There is no evidence of restricted diffusion, post-contrast enhancement or susceptibility artifact
CSF + pleocytosis;
Infectious work up was negative
Dx: Herpes encephalitis
Ill-defined FLAIR hyperdensity in the left temporal lobe with loss of sulci suggestive of edema. There is no evidence of restricted diffusion, post-contrast enhancement or susceptibility artifact.
Dx: Anti-GAD Limbic Encephalitis

14. Case: 54 year old male with seizure
Anti-LGI1+ Paraneoplastic syndrome

15. CASE: 61 YEAR OLD FEMALE WITH SLURRED SPEECH AND WEAKNESS

16. Paraneoplastic limbic encephalitis associated with anti-Ma2
Paraneoplastic limbic encephalitis associated with anti-Ma2. Patient with progressive 3-month history of memory loss, anxiety attacks, conduct disorder and ophthalmoplegia. Crainal MRI (A) axial and (B) coronal FLAIR which show signal hyperintensity in hippocampus and temporal amygdales (arrows). (C) axial image sequence showing a discrete diffusion restriction in the medial temporal region (arrows). PCR of HSV in CSF and body CT were negative. Determination of Anti-Hu antibody positive associated to a breast cancer.

17. CASE: 47 year old woman presented with seizures and choreiformmovements. Initial CT scan was read as normal. On retrospective review, there is a very subtle area of hypodensityinvolving the medial right temporal lobe (arrow). MRI demonstrates increased FLAIR signal involving the bilateral temporal lobes and thalamus without contrast enhancement or restricted diffusion. Additional imaging revealed a breast mass with axillary lymphadenopathy, confirming the diagnosis of paraneoplastic limbic encephalitis
Anti-amphphysin +
DIFFERENTIAL POINTS: 1) enhancement is rare. 2) can involve thalamus, midbrain, and brainstem. (although rarely HSV can involve these areas as well, particularly in immunocompromised patients) 3) no hemorrhage or restricted diffusion

18. Case: Patient with seizures, had negative routine MRI; however, on PET-MRI, + right frontal lobe hypometabolic focus likely the source of seizure
Anti-GABA + paraneoplastic encephalitis
Anti-GABA + paraneoplastic encephalitis

19. Mimics: Infection
Wide spectrum of viral, bacterial and fungal germs with the most frequent etiology herpes simplex virus type 1 (HSV-1)
70% of infectious encephalitis in immunocompetent patients are due to HSV-1
In immunocompromised patients, esp if infected with human immunodeficiency virus (HIV) or s/p stem cell transplant should be considered for herpes simplex such as herpes virus tpe 2 (HSV-2), human herpes virus 6 and 8 (HHV6 and HH7)
Clinical manifestations typically consist on subacute presentation of seizures, fever, memory loss, confusion to a rapid deterioration in level of consciousness that usually progress faster than in paraneoplastic encephalitis.
The diagnostic method of choice is the HSV genome amplification by PCR in sample cerebrospinal fluid, with sensitivity and specificity of 94% and 98% respectively, but with the disadvantage that this test may be negative in the first hours of onset of symptoms and after 10 days.
CSF + pleiocitosis and CSF protein elevation

20. Imaging findings in infectious encephalitis
MRI: “gold standard” with alterations in 90% of patients with HSV-1 encephalitis
findings are usually bilateral but asymmetrical
T2-FLAIR: Hyperintense lesions reflects edema, hemorrhage or necrosis and affect the inferomedial region of the temporal lobes and the orbital surface of the frontal lobes with frequent extension to the insular cortex. The basal ganglia are generally respected
Diffusion (DWI): there is restriction due to cytotoxic edema
UPTAKE: There is not uptake in the initial stages, but can show giral uptake as disease progresses, usually 1 week after the onset of symptoms
Small microhemorrhages are exceptional in early stages and is more frequently found in subacute phases

21. 38 year old male presenting with delirium, confusion and headache
38 year old male presenting with delirium, confusion and headache. Initial non-contrast head CT images demonstrate abnormal hypodensityinvolving the right parietal lobe.
Herpes Encephalitis
Mortality is very high, approaching 70% across all cases. Even in young patients with early recognition of symptoms and early therapy, mortality reaches 25% with less than 10% patients recovering with no long-term neurologic sequelae.
MRI demonstrates significantly more involvement than the CT, and we see the characteristic imaging pattern of asymmetric abnormal T2/FLAIR signal intensity involving the temporal lobes and insula.The parietal lobe is also involved as seen on CT, and the T1 image demonstrates hyperintensitymirroring the hyperdensityon CT confirming early subacutehemorrhage. Although we see contrast enhancement here, enhancement is variable, and can be absent early in the course of the disease. Diffusion is typically restricted from cytotoxic edema and is more sensitive than increased T2 signal.

22. Mesial Temporal Sclerosis
38 year old with seizures
Mesial Temporal Sclerosis
Most common cause partial complex seizures
May be acquired or developmental
20% bilateral, 15 % dual path with cortical dysplasia most common dual path
70-95% cured with ant temporal lobectomy
T2 hyper signal and atrophy of hippocampus with loss internal architecture
Secondary signs: Fornix and mamillary body atrophy, enlarged temp horn

23. Seizure epiphenomenon
48 year old male presented with seizure. MRI demonstrates faint increased FLAIR signal involving the right medial temporal lobe. T1 post contrast image demonstrates gyriform enhancement involving the right insula. No restricted diffusion is seen.
Infectious and neoplastic workup was negative.
This finding was therefore felt likely to represent seizure epiphenomenon, a term used to described MRI findings reflecting the effect of, rather than the cause, seizures.
Most commonly, T2 hyperintensity and contrast enhancement are seen. Diffusion abnormalities also occur.
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24. Gliomatosis cerebri
A 34 year old male presented with seizure. MRI demonstrates abnormal T2 and FLAIR signal involving the bilateral temporal lobes, right thalamus, insular cortex, and the brainstem. No contrast enhancement is seen. There was no restricted diffusion. Notably, there is significant mass effect with effacement of the frontal horn of the right lateral ventricle.
Given the clinical presentation and mass-like quality of the abnormality, there was concern for an infiltrating glioma. Open brain biopsy demonstrated a WHO grade III glialtumor.
DIFFERENTIAL POINTS: 1) enhancement is variable, although usually uncommon in infiltrating gliomas. High grade gliomascan enhance. 2) mass effect may or may not be present (seen in this case) 3) diffusion restriction is rare. 4) MR spectroscopy may be helpful, demonstrating increased choline, as well as occasionally increased lactate/lipid in higher grade tumors.

25. Case 4: 40 year old with seizure
Case 4: 40 year old with seizure. MRI reviews enhancing lesion with restricted diffusion with +FDG avidity. Bx: +Left temporal lobe glioma

26. Left MCA Infarct
In a different patient, FLAIR and DWI MR images demonstrate typical appearance of a left MCA infarct involving the left insula and frontal lobe, as well as the anterior temporal lobe. The left putamen is also involved. CT angiography demonstrates a segmental occlusion of the left M1.
FLAIR and DWI MR images demonstrate typical appearance of a left MCA infarct involving the left insula and frontal lobe, as well as the anterior temporal lobe. The left putamen is also involved.
CT angiography demonstrates a segmental occlusion of the left M1.

27. Case: 66 y/o female with worsening headaches, altered mental status and paresthesias
CT w/o contrast: Hyperdense brainstem mass with perilesional edema was concerning for acute hemorrhage.
MRI: Heterogenous T1 Hypointense T2/FLAIR hyperintense heterogenous lesion demonstrating postcontrast enhancement and areas of susceptibility artifact.
PET-MRI reveals hypermetabolic lesion in the brain stem with 29.7 SUV most compatible with a neoplastic process.
Biospy revealed metastatic renal cell carcinoma
CT w/o contrast: Hyperdense brainstem mass with perilesional edema was concerning for acute hemorrhage
MRI: Heterogenous T1 Hypointense T2/FLAIR hyperintense heterogenous lesion demonstrating postcontrast enhancement and areas of susceptibility artifact
PET-MRI: reveals hypermetabolic lesion in the brain stem with 29.7 SUV most compatible with a neoplastic process.
Biospy revealed metastatic renal cell carcinoma

28. Case : 56 year old female with breast cancer presents with headaches
Pre-Treatment MRI reveal leptomeningeal T2/FLAIR hyperintense lesion with post-contrast enhancement. There is marked associated FDG-PET activity, suggestive of breast cancer leptomeningeal metastasis,
Post-Treatment: On routine MRI, there is residual FLAIR activity with mild post-contrast enhancement. However, on PET-MRI, there is no residual activity, confirming successful treatment.

29. Young Female s/p left CN 8 Schwanoma Removal p/w left sided CN 6 Palsy
FLAIR
Click to play
DWI
ADC
Click to play
Brain Stem Infarct Involving CN 6 Nucleus

30. Subacute development of ascening paralysis
Autoimmune post-infectious or post-vaccinial acute inflamm demyelination of peripheral nerves, nerve roots, and CN’s
Acute flaccid paralysis or distal paraesthesia followed by rapid ascending paralysis
Most pts somewhat better by 2- 3mo with 8% mortality
Smooth enhancement of cauda equina which may be slightly thickened
Preferential contrast accentuation of ventral roots of cauda
Conus enhancement variable

31. Case: worsening headache
Neurosarcoid
CNS invovlement 5%
Most common symptom CN deficit most often CN 7
Solitary or multifocal CNS masses
Dura, leptomeninges, subarachnoid space
Brain parenchyma hypothalamus>stem> cerebral hemis>cerebellar hemis
T2 hypo material subarachnoid spaces, 50% perivent WM lesions, may cause small vessel vasculitis
Contrast >1/3 mult parencymal lesions, >1/3 leptomeningeal involvement, 10% solitary intra axial mass, 5% solitary dural based extra axial mass
DDX: TB
Fungal infection
Leptomeningeal carcinomatosis
Neurosarcoidosis
Lymphoma
Pyogenic
Basilar Meningitis

32. Case Subacute memory loss
Rapidly progressing, fatal, potentially tranmissible dementing disorder caused by a prion
Dementia with myoclonic jerks and akinetic mutism
EEG periodic high voltage waves on background of low voltage activity
Atrophy with progressive T2 hyper with possible restricted diffusion involving gray matter including BG (caudate, putamina), thalamus, and cerebral cortex (frontal and temporal lobes)
“Pulvinar” sign bilat sym hyper of pulvinar (post) nuclei of thalamus relative to ant putamen
“Hockey stick” sign sym pulvinar and dorsomedial thalami hyperintensity
No contrast enhancement
Creutzfeldt-Jakob Disease

33. CONCLUSION
Paraneoplastic syndrome is not an uncommon cause of encephalitis
Knowledge of its clinical presentation, pathophysiology and immunology is essential in making the diagnosis
Although the differential diagnosis is broad, it can be narrowed utilizing age, clinical features, imaging characteristics (e.g. Location, enhancement pattern, PET-MRI findings, etc) and pathology correlation

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35. Please send correspondence to: Ammarchaudhry84@gmail.com
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