PET: Tomografía de Emisión de Positrones
• Técnica de medicina nuclear
• Ciclotrón y cámaras PET/TAC
• Permite cuantificar la cinética de sustancias trazadoras ionizantes
• En tejidos animales o humanos
• Permitiendo medir los procesos fisiológicos y bioquímicos
Ciclotrón •acelerador de partículas
•transforma blancos no radiactivos en nucleidos inestables
• que generan positrones
•ejemplos: 18F, 11C y 15O
Dada la posibilidad de marcar el carbono y el oxígeno, gran parte de las substancias orgánicas existentes pueden ser marcadas y su trayecto dentro del organismo vivo revelado
Emisión de positrones
Electrón
Positron (+)
511 keV
511 keV
FDG
•La fluordeoxiglucosa marcada con 18F es el trazador más utilizado en la PET
•Tiene múltiples indicaciones en oncología y neurologia
•Muchos creen que la FDG es la PET
•El CUDIM aspira a tener una batería de trazadores que nos permita entrar en una etapa más avanzada de la técnica
Tracers11C-Choline Prostata cancer, brain tumors11C- y 18F-Acetate Prostata cancer11C-Methionine Brain tumors, parathyroidea tumors11C- y 18F-Metomidate Adrenocortical carcinomas and adenomas11C-Raclopride D2 Receptors, prolactinoma; Parkinson, Parkinsonismo11C-Flumazenil Epilepsy, neurodegeneration11C-Hydroxytryptophan Neuroendocrin tumors11C-Hydroxiefedrine Pheochromocytoma11C- y 18F-DOPA Presinaptic degeneration : Parkinson, Parkinsonism11C-Deuterodeprenyl Astrocytosis cerebral, CJD, Alzheimer, etc11C- y 18F-PIB Amyloidosis, Alzheimer11C-Nomifensine Parkinson, Parkinsonism11C-Beta-CIT Parkinson, Parkinsonism11C-N-Methylspiperone Parkinson, Parkinsonismo, squizofrenia11C-SCH 23390 Parkinson (D1 receptors)11C-PK11195 Microgliosis18F-FDDPN Amyloidosis and neurofibrillary tangles11C-NST-ML10 Apoptosis in stroke15O Oxígen extraction and y consumtionde15O-CO Cerebral Bood volume15O-H2O Blood Flow
NeurologyDementia: FDG, Deprenyl, PIB
Epilepsy: FDG and Flumazenil
Tumours: Methionine, Raclopride, FDG and Deprenyl
Parkinson’s disease: DOPA, FDG, Raclopride and CIT
Dementia Tracers: FDG, Deprenyl, PIB
To differentiate between:
Alzheimer's disease, Lewy Bodies disease, frontotemporal dementia, multiinfarctions dementia, limbic encephalitis, Creutzfeldt-Jakob’s disease and corticobasal degeneration
Early Diagnosis and follow-up in Alzheimer's disease.
PIB
Cognition
FDG
Diagnosis PIB Diagnosis FDG
Hypothetical steps in the disease progression
Critical pointCritical point
Time (years)
CognitionFDG
PIB
Engler, 2006
•This tracer has good specificity for amyloid deposits in vitro and it seems also to be a promising candidate for application as an in vivo agent of processes related to amyloid plaque formation in man.
Prion diseases
*Sporadic Creutzfeldt-Jakob disease (CJD)
*Familial CJD
*Fatal familial imnsomnia
*Gerstman-Sträussler-Scheinker syndrome
*Iatrogenic CJD
*Variant CJD (bovine spongiform encephalopathy)
Neuropathologic changes
• Neuronal loss
• Astrocytosis
• Spongiform changes
• Deposits of Protease resistent prion protein in brain
* Characterization of astrocytosis
* Characterization of neuronal degeneration
Tracers
[11C]-Deuterodeprenyl (MAO - B binding)
[18F]-FDG (glucose transport)
*FDG and DED showed a typical pattern withdecreased glucose metabolism (cell dysfunction)and increased DED binding (astrocytosis)
Patients with definite and probable CJD
*Frontal, occipital and parietal cortices were the more affected regions
Epilepsy Tracers: FDG and Flumazenil
• Preoperative investigation when MRT, EEG and SPECT have been inconclusive.
• FDG and Flumazenil can be combined to improve sensibility and specificity in the case of suspect foci outside the temporal lobe.
Tumours Tracers: Methionine, Raclopride, FDG, Deprenyl
• To determinate tumour grade in astrocytomas.
• To differenciate between recidive and radiation necrosis
• To localize the best place for biopsy before operation.
• To follow up the treatment of meningeomas.
• To quantify the level of D2-receptors in Prolactinoma before treatment with D2-agonists.
• To control treatment in hypofysis tumours.
• To differenciate between meningeoma and suprasellar adenoma.
11C-methionine
Astrocytoma:PET evaluation
Parkinson’s disease Tracers: DOPA, FDG, Raclopride, CIT
• To differentiate between Parkinson's disease and Multipel System Atrophy.
• To differentiate between different MSA forms:
Striato-Nigral-Degeneration, Olivo-Ponto-Cerebellar Atrophy and Shy-Drager syndrome.
• To differentiate between Parkinson's disease and Dystonia.
• Diagnosis in Huntington’s and Wilson’s disease.
ProgressiveSupranuclear
PalsyOphthalmoplegia
DysphagiaNeck stiffness
MSASND : No repons to L-Dopa treatment
OPCA: Ataxia
SDS: Autonomic dysfunction Orthostatism
Parkinson’s disease
* 15-20% of patients with diagnosis IPD had APD
* In 23 confirmed cases of MSA, 65% responded to levodopa initially, 35% remained partially responsive until death
Hughes et al, J Neurol Neurosurg Psychiatry 1992
Neuropathology
The distinction between IDP and other akinetorigid
extrapyramidal diseases is of prognostic and
therapeutic value
* Characterization of presynaptic degeneration
* Characterization of postsynaptic degeneration
Tracers
L-[11C]-DOPA (dopamine synthesis)[11C]-CIT-FE (dopamine re-uptake)
[11C]-RAC (dopamine receptors)[18F]-FDG (glucose transport)
20001
Engler
Substantia nigraDopaminPresynaptic neuron
Normal
RAC FDGPutamen
Neurodegeneration
D2-r
DOPA/CIT
Engler, 2001
Substantia nigraDopaminPresynaptic neuron
D2-r
Normal
Parkinson’s disease without treatment
RAC FDGPutamen
NeurodegenerationDOPA/CIT
Engler, 2001
Substantia nigraDopaminPresynaptic neuron
D2-r
Normal
Parkinson’s disease after treatment
RAC FDGPutamen
NeurodegenerationDOPA/CIT
Parkinson’s disease without treatment
Engler, 2001
Engler, 2001
Substantia nigraDopaminPresynaptic neuron
D2-r
Normal
Striato-Nigral degeneration
RAC FDGPutamen
NeurodegenerationDOPA/CIT
Parkinson’s disease after treatment
Parkinson’s disease without treatment