PET: Tomografía de Emisión de Positrones

2. 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

3. 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

4. Positron (+) 511 keV   511 keV Emisión de positrones Electrón

6. 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

7. Tracers 11C-CholineProstata cancer, brain tumors 11C- y 18F-Acetate Prostata cancer 11C-Methionine Brain tumors, parathyroidea tumors 11C- y 18F-MetomidateAdrenocorticalcarcinomas and adenomas 11C-Raclopride D2 Receptors, prolactinoma; Parkinson, Parkinsonismo 11C-Flumazenil Epilepsy, neurodegeneration 11C-HydroxytryptophanNeuroendocrin tumors 11C-Hydroxiefedrine Pheochromocytoma 11C- y 18F-DOPA Presinaptic degeneration : Parkinson, Parkinsonism 11C-Deuterodeprenyl Astrocytosis cerebral, CJD, Alzheimer, etc 11C- y 18F-PIB Amyloidosis, Alzheimer 11C-Nomifensine Parkinson, Parkinsonism 11C-Beta-CIT Parkinson, Parkinsonism 11C-N-Methylspiperone Parkinson, Parkinsonismo, squizofrenia 11C-SCH 23390 Parkinson (D1 receptors) 11C-PK11195 Microgliosis 18F-FDDPN Amyloidosis and neurofibrillary tangles 11C-NST-ML10 Apoptosis in stroke 15O Oxígenextraction and y consumtionde 15O-CO Cerebral Bood volume 15O-H2O Blood Flow

8. Neurology Dementia: FDG, Deprenyl, PIB Epilepsy: FDG and Flumazenil Tumours: Methionine, Raclopride, FDG and Deprenyl Parkinson’s disease: DOPA, FDG, Raclopride and CIT

9. DementiaTracers: 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.

23. Hypothetical steps in the disease progression Diagnosis FDG Diagnosis PIB Critical point Cognition FDG PIB Cognition FDG PIB Engler, 2006 Time (years)

24. This tracer has good specificity for amyloid deposits in vitroand itseems also to be a promising candidate for application as an in vivo agent of processes related to amyloid plaque formation in man.

25. Prion diseases *Sporadic Creutzfeldt-Jakob disease (CJD) *Familial CJD *Fatal familial imnsomnia *Gerstman-Sträussler-Scheinker syndrome *Iatrogenic CJD *Variant CJD (bovine spongiform encephalopathy)

26. Neuropathologic changes • Neuronal loss • Astrocytosis • Spongiform changes • Deposits of Protease resistent prion protein in brain

27. Tracers * Characterization of neuronal degeneration [18F]-FDG (glucose transport) * Characterization of astrocytosis [11C]-Deuterodeprenyl (MAO - B binding)

28. Patients with definite and probable CJD *FDG and DED showed a typical pattern with decreased glucose metabolism (cell dysfunction) and increased DED binding (astrocytosis) *Frontal, occipital and parietal corticeswere the more affected regions

30. 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.

35. TumoursTracers: 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.

39. Astrocytoma:PET evaluation 11C-methionine

41. 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.

42. MSA SND : No repons to L-Dopa treatment OPCA: Ataxia SDS: Autonomic dysfunction Orthostatism Parkinson’s disease Progressive Supranuclear Palsy Ophthalmoplegia Dysphagia Neck stiffness

43. Neuropathology * 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

44. The distinction between IDP and other akinetorigid extrapyramidal diseases is of prognostic and therapeutic value

45. Tracers * Characterization of presynaptic degeneration L-[11C]-DOPA (dopamine synthesis) [11C]-CIT-FE (dopamine re-uptake) * Characterization of postsynaptic degeneration [11C]-RAC (dopamine receptors) [18F]-FDG (glucose transport)

46. D2-r Neurodegeneration Substantia nigra Putamen RAC FDG DOPA/ CIT Dopamin Presynaptic neuron Normal Engler Engler, 2001 20001

47. Neurodegeneration Substantia nigra Putamen RAC FDG DOPA/ CIT Dopamin Presynaptic neuron D2-r Normal Parkinson’s disease without treatment Engler, 2001

48. Neurodegeneration Substantia nigra Putamen RAC FDG DOPA/ CIT Dopamin Presynaptic neuron D2-r Normal Parkinson’s disease without treatment Parkinson’s disease after treatment Engler, 2001

49. Neurodegeneration Substantia nigra Putamen RAC FDG DOPA/ CIT Dopamin Presynaptic neuron D2-r Normal Parkinson’s disease without treatment Parkinson’s disease after treatment Striato-Nigral degeneration Engler, 2001