Transcript Paraneoplastic Syndrome and Mimics: What the

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: [email protected]
DISCLOSURES
• NONE
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
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
Herpes Simplex Virus
(Most often Implicated);
HHV, CJD; Lyme
PATHOGENSIS
Infectious
• Paraneoplastic neurologic syndromes are believed to result when an immunologic
response is directed against shared antigens that are ectopically expressed by the tumor
Antibodies against Membrane Antigens:
that are normally expressed by the nervous system
Anti-NMDA
Anti-AMPA
Anti-GABAßR
Encephalitis
• Antibodies can be detected in the serum and cerebrospinal fluid (CSF) of many
Paraneoplastic
• NOTE: not all patients with paraneoplastic
syndromes
(classically
havehave + Ab titers
intra-cellular
antigens)
Antibodies against
Antigens:
• Recent studies suggest that the immune system can mount a T-cell response
toIntracellular
a “ normal
Anti-Hu
AntiCV2/CRMP-5
Anti-Ma2
protein” when it is expressed in a cancer cell
Autoimmune PE
• 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
“NonAnti-GAD
Antibodies against
leads to the Paraneoplastic syndrome Paraneoplastic”
antigens of voltage-dependent potassium
(antigen located on
cell membrance)
channel complex (LGI1, CASPR2, contactin-2)
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
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
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.
CLINICAL SPECTRUM OF CENTRAL AND PERIPHERAL
NERVOUS SYSTEM PARANEOPLASTIC SYNDROMES
Paraneoplastic syndromes of the central nervous system
Encephalomyelitis*
Myelitis*
Limbic encephalitis*
Brainstem encephalitis*
Cerebellar degeneration*
Opsoclonus myoclonus ataxia*
Stiff-person syndrome*
Subacute sensory neuronopathy*
Visual syndromes
•
Cancer associated retinopathy*
•
Melanoma associated retinopathy*
•
Optic neuritis
Necrotizing myelopathy
Motor neuron syndrome
•
Subacute motor neuronopathy
•
Other syndromes
Paraneoplastic syndromes of the peripheral nervous system
Chronic sensorimotor neuropathy
•
Association with plasma cell dyscrasias
Autonomic neuropathy*
Vasculitis of nerve and muscle
Acute sensorimotor neuropathy
•
•
Guillain-Barré syndrome
Plexitis (eg, brachial neuritis)
Paraneoplastic syndromes of the neuromuscular junction and muscle
Myasthenia gravis*
Lambert-Eaton myasthenic syndrome*
Dermatomyositis/polymyositis
* Denotes syndromes where specific antibodies have been identified
Neuromyotonia*
Acute necrotizing myopathy
CA1:A32achectic myopathy
Dalmau J, Rosenfeld M. Overview of Paraneoplastic syndromes of the nervous system. www.uptodate.com. Accessed Oct 25 th 2014
PARANEOPLASTIC SYNDROMES ASSOCIATED WITH
LUNG CANCER
Systemic
Anorexia, cachexia, weight loss Dermatomyositis/polymyositis
Fever
Systemic lupus erythematosus
Nonbacterial thrombotic
endocarditis
Orthostatic hypotension
Renal
Tubulointerstitial disorders
Glomerulopathies
Cutaneous
Acquired hypertrichosis
lanuginosa
Acrokeratosis (Bazex's syndrome)
Clubbing
Dermatomyositis
Erythema gyratum repens
Exfoliative dermatitis
Hypertrophic pulmonary
osteoarthropathy
Deep venous thrombosis
(Trousseau's syndrome)
Tripe palms
Acanthosis nigricans
Neurologic
Peripheral neuropathy
Lambert-Eaton myasthenic syndrome
Cushing's syndrome
Hypercalcemia
Necrotizing myelopathy
Hyponatremia
Cerebral encephalopathy
Hyperglycemia
Visceral neuropathy
Acromegaly
Hematologic
Acquired ichthyosis
Acquired palmoplantar
keratoderma
Erythema annulare centrifugum
Florid cutaneous papillomatosis
Pemphigus vulgaris
Endocrine/Metabolic
Hyperthyroidism
Anemia
Hypercalcitoninemia
Polycythemia
Hypercoagulability
Thrombocytopenic purpura
Gynecomastia
Galactorrhea
Carcinoid syndrome
Pityriasis rotunda
Dysproteinemia (including amyloidosis)
Hypoglycemia
Pruritus
Leukocytosis/leukoerythroblastic reaction
Hypophosphatemia
Sign of Leser-Trelat
Eosinophilia
Lactic acidosis
Sweet's syndrome
Vasculitis
Identifies most common Paraneoplastic syndromes
Hypouricemia
Hyperamylasemia
Dalmau J, Rosenfeld M. Overview of Paraneoplastic syndromes of the nervous system. www.uptodate.com. Accessed Oct 25 th 2014
Antibody
Antibodies, paraneoplastic syndromes and associated cancers
Syndrome
Associated cancers
Well characterized paraneoplastic antibodies
Anti-Hu (ANNA-1)
Anti-Yo (PCA-1)
Anti-Ri (ANNA-2)
Anti-Tr (DNER)
Anti-CV2/CRMP5
Anti-Ma proteins• (Ma1, Ma2)
Anti-amphiphysin
Anti-recoverinΔ
Encephalomyelitis including cortical, limbic, brainstem
encephalitis, cerebellar degeneration, myelitis, sensory
neuronopathy, and/or autonomic dysfunction
Cerebellar degeneration
Cerebellar degeneration, brainstem encephalitis,
opsoclonus-myoclonus
Cerebellar degeneration
Encephalomyelitis, cerebellar degeneration, chorea,
peripheral neuropathy
Limbic, hypothalamic, brainstem encephalitis (infrequently
cerebellar degeneration)
Stiff-person syndrome, encephalomyelitis
Cancer-associated retinopathy (CAR)
SCLC, other
Gynecological, breast
Breast, gynecological, SCLC
Hodgkin's lymphoma
SCLC, thymoma, other
Germ-cell tumors of testis, lung cancer, other solid tumors
Breast, lung cancer
SCLC
Partially-characterized paraneoplastic antibodies
Anti-Zic 4
mGluR1
ANNA-3
PCA2
Anti-bipolar cells of the retina
Cerebellar degeneration
Cerebellar degeneration
Sensory neuronopathy, encephalomyelitis
Encephalomyelitis, cerebellar degeneration
Melanoma-associated retinopathy (MAR)
SCLC
No tumor or Hodgkin's lymphoma
SCLC
SCLC
Melanoma
Antibodies that occur with and without cancer association
Anti-AMPAR
Anti-GABA(B) receptor
Lambert-Eaton myasthenic syndrome, cerebellar
dysfunction
Myasthenia gravis
Multistage syndrome with memory and behavioral
disturbances, psychosis, seizures, dyskinesias, and
autonomic dysfunction
Limbic encephalitis, psychiatric disturbances
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
Encephalomyelitis with muscle spasms, rigidity, myoclonus,
Often without cancer
hyperekplexia
Anti-VGCC
Anti-AChR
Anti-NMDAR
GlyR
SCLC
Thymoma
Teratoma
Variable solid tumors
SCLC
Dalmau J, Rosenfeld M. Overview of Paraneoplastic syndromes of the nervous system. www.uptodate.com. Accessed Oct 25 th 2014
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
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 antiNMDA (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
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: Anti-GAD Limbic
Encephalitis
CASE: 54 YEAR OLD MALE WITH
SEIZURE
Anti-LGI1+ Paraneoplastic syndrome
CASE: 61 YEAR
OLD FEMALE
WITH
SLURRED
SPEECH AND
WEAKNESS
Paraneoplastic limbic encephalitis associated with antiMa2. 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.
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
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
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 48-72 hours of onset of symptoms and after 10 days.
• CSF + pleiocitosis and CSF protein elevation
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
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 longterm 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.
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
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.
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.
CASE 4: 40 YEAR OLD WITH SEIZURE. MRI REVIEWS ENHANCING
LESION WITH RESTRICTED DIFFUSION WITH +FDG AVIDITY.
BX: +LEFT TEMPORAL LOBE GLIOMA
LEFT MCA INFARCT
• 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.
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
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.
YOUNG FEMALE S/P LEFT CN 8 SCHWANOMA REMOVAL P/W LEFT SIDED CN 6 PALSY
T2
FLAIR
ADC
Brain
Click
toStem
play Infarct Involving CN 6 Nucleus
DWI
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 23mo with 8% mortality
• Smooth enhancement of cauda
equina which may be slightly
thickened
• Preferential contrast accentuation
of ventral roots of cauda
• Conus enhancement variable
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
DDX:
• T2 hypo material subarachnoid
spaces, 50% perivent WM lesions, may cause
• TB
small vessel vasculitis
• Fungal infection
• Contrast >1/3 mult parencymal lesions, >1/3 leptomeningeal involvement,
• Leptomeningeal carcinomatosis
10% solitary intra axial mass, 5% solitary dural based extra axial mass
• Neurosarcoidosis
• Lymphoma
• Pyogenic
BASILAR
MENINGITIS
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
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
REFERENCES
1.
Brierly JB, Corsellis JA, Hierons R, et al. Subacute encephalitis of later adult life mainly affecting the limbic areas. Brain. 1960; 83;356-368.
2.
Corselis JA, Goldberg GJ, Norton AR. “Limbic Encephalitis” and its association with carcinoma. Brain 1968; 91;481-496.
3.
Tuzun E, Dalmau J. Limbic Encephalitis and Variants: Classification, Diagnosis and treatment. The Neurologist 2007; 13;261-271.
4.
Soler B, Godoy J, Mellado P. Encefalitis Limbica por anticuerpos anticanales de potasio dependientes de voltaje. Caso clinic. Rev Med Chile 2009; 137; 675-679.
5.
Ramos A, Ballenilla F, Martin P. Uncommon Epiloptogenetic Lesions Affecting the Temporal Lobe. Semin Ultrasound CT MRI 2008; 29; 47-59.
6.
Schott JM. Limbic encephalitis: a clinician’s guide. Practical Neurology 2006; 6; 143-153.
7.
Whitley RJ. Herpes simplex encephalitis: Adolescents and adults . Antiviral Research 2006; 71; 141-148.
8.
Fica A, Perez C, Reyes P, Gallardo S, Calvo X, Salinas AM. Encefalitis herpetica. Serie clinica de 15 casos confirmados por raccoon de polimerasa en cadena. Rev Chili Infect 2005; 22; 38-46.
9.
Dalmau J, Bataller L. Encefalitis limbica: los nuevos antigenos de membrane y propuesta de una clasificacion clinicoimmunologica con implicaciones terapeuticas. Neurologia 2007; 22; 526-537.
10.
Saket RR, Geschwind MD, Josephson SA, Douglas VC, Hess CP. Autoimmune-mediated encephalopathy: Classification, evaluation, and MR imaging patterns of Disease. Neurographics 2011; 01; 2-16.
11.
Gonzalez-Valcarcel J, Rosenfeld MR, Dalmau J. Diagnostico diferncial en la encephalitis por anticuerpos contra el receptor NMDA. Neurologia 2010; 25; 409-413.
12.
Graus F, Saiz A, Lai M, Bruna J, Lopez F, Sabeter L, et al. Neuronal surface antigen antibodies in limbic encephalitis Clinical-immunological associations. Neurology 2008; 71; 930-936.
13.
Dalmau J, Lancaster E, Martinez-Hernandez E, Rosenfeld M, Balice-Gordon R. Clinical experience and laboratory investigations in patients with anti-NMDAR encephalitis. Lancet Neurology 2011; 10; 63-74.
14.
Lee R, Buckley C, Irani SR, Vincent A. Autoantibody testing in encephalopathies. Practical Neurology 2012; 12; 4-13.
15.
Graus F, Boronat A, Xifro X, Boix M, Svigelj V, Garcia A, et al. The expanding clinical profile of Anti-AMPA Receptor encephalitis. Neurology 2010; 74; 857-859.
16.
Boronat A, Sabater L, Saiz A, Dalmau J, Graus F. GABAB receptor antibodies in limbic encephalitis and anti GAD associated neurologic disorders. Neurology 2011; 76; 795-800.
17.
Lai M, Hujibers MG, Lancaster E, Graus F, Bataler L, Balice-Gordon R, et al. Investigation of LGI1 as the antigen in limbic encephalitis previously attributed to potassium channels: a case series. Lancet Neurology 2010; 9; 776-785.
18.
Srinivasan A, Goyal M, Al Azri F, Lum C. State of the Art Imaging of Acute Stroke. Radiographics 2006; 26; S75-S95.
19.
Stadnik TW, Demaerel P, Luypaert R, Chaskis C, Van Rompaey KL, Michotte A, et al. Imaging Tutorial: Differential Diagnosis of Bright Lesions on Diffusion-weighted MR Images. Radiographics 2003; 23; e7.
20.
Bladin CF, Alexandrov AV, Bellavance A, Bornstein N, Chambers B, Cote R, et al. Seizures After Stroke. Archives Neurology 2000; 57; 1617-1622.
21.
Frey LC. Epidemiology of Posttraumatic Epilepsy: A Critical Review. Epilepsia 2003; 44; 11-17.
22.
Duncan JS. Imaging and epilepsy. Brain 1997; 120; 339-377.
23.
Alvarez-Linera J. Resonancia magnetic structural de la epilepsia. Radiologia 2012; 54; 9-20.
24.
Bargallo N, Auger C, Rovira A. Radiologia Esencial. En: Del Cura JL, Pedraza s, Gayete A, editors. Malformaciones congenitas en el adulto. Epilepsia. Hidrocefalia. 1 ed. Madrid: Editorial medica Panamericana; 2010-p. 1235-40.
END
PRESENTATION
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