1
2 PET: Tomografía de Emisión de Positrones 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 Ciclotrón acelerador de partículas transforma blancos no radiactivos en nucleidos inestables que generan positrones ejemplos: 18F, 11C y 15O The PET scanner is used to produce PET images from the detection of positron annihilation. Because such a radioactive event emits two gamma photons simultaneously in exactly opposite directions, the usual PET scanner architecture is a tunnel detector through which the patient table is moved. The PET/CT scanner is the imaging system used to provide, in a single exam, both PET images and CT images. The PET/CT scanner external shape is similar to those of a conventional PET scanner, but a little bit deeper because of the presence of the additional CT module. 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 3
4 Emisión de positrones Positron (+) 511 keV Electrón 10-05-23PET imaging is based on positron decay. Because of the instability of its nucleus, an atom emits a positively charged particle, the positron. The positron produced travels for a short distance through surrounding tissue, losing energy as it collides with molecules. Then the positron interacts with an electron of another atom in an annihilation reaction that transforms the two particles into energy. This energy is dispersed in the form of two photons of 511 keV, emitted in exactly opposite directions from each other. 4
5
6 FDG La fluordeoxiglucosa marcada con 18F es el trazador más 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-Choline Prostata cancer, brain tumors11C- y 18F-Acetate Prostata cancer 11C-Methionine Brain tumors, parathyroidea tumors 11C- y 18F-Metomidate Adrenocortical carcinomas and adenomas 11C-Raclopride D2 Receptors, prolactinoma; Parkinson, Parkinsonismo 11C-Flumazenil Epilepsy, neurodegeneration 11C-Hydroxytryptophan Neuroendocrin 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 Parkinson (D1 receptors) 11C-PK Microgliosis 18F-FDDPN Amyloidosis and neurofibrillary tangles 11C-NST-ML10 Apoptosis in stroke 15O Oxígen extraction and y consumtionde 15O-CO Cerebral Bood volume 15O-H2O Blood Flow
8 Neurology Dementia: FDG, Deprenyl, PIB Epilepsy: FDG and Flumazenil Neurology Dementia: FDG, Deprenyl, PIB Epilepsy: FDG and Flumazenil Tumours: Methionine, Raclopride, FDG and Deprenyl Parkinson’s disease: DOPA, FDG, Raclopride and CIT
9 Dementia Tracers: FDG, Deprenyl, PIB 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.
10
11
12
13
14
15
16
17
18
19
20
21
22
23 Hypothetical steps in the disease progression Hypothetical steps in the disease progression Diagnosis PIB Diagnosis FDG Critical point Cognition FDG PIB Cognition FDG PIB Engler, 2006 Time (years) 23
24 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.
25 Prion diseases *Sporadic Creutzfeldt-Jakob disease (CJD) *Familial CJD 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 Neuropathologic changes Neuronal loss Astrocytosis Spongiform changes Deposits of Protease resistent prion protein in brain
27 Tracers * Characterization of neuronal degeneration Tracers * Characterization of neuronal degeneration [18F]-FDG (glucose transport) * Characterization of astrocytosis [11C]-Deuterodeprenyl (MAO - B binding)
28 Patients with definite and probable CJD 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 cortices were the more affected regions
29
30 Epilepsy Tracers: FDG and Flumazenil 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.
31
32
33
34
35 Tumours Tracers: Methionine, Raclopride, FDG, Deprenyl 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.
36
37
38
39 Astrocytoma:PET evaluation Astrocytoma:PET evaluation 11C-methionine
40
41 Parkinson’s disease Tracers: DOPA, FDG, Raclopride, CIT 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 Parkinson’s disease MSA SND : No repons to L-Dopa treatment MSA SND : No repons to L-Dopa treatment OPCA: Ataxia SDS: Autonomic dysfunction Orthostatism Parkinson’s disease Progressive Supranuclear Palsy Ophthalmoplegia Dysphagia Neck stiffness 42
43 Neuropathology * 15-20% of patients with diagnosis IPD had APD 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 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 Neurodegeneration Engler, 2001 Substantia nigra Putamen Neurodegeneration Substantia nigra Putamen RAC FDG DOPA/ CIT Dopamin Presynaptic neuron D2-r Normal Engler Engler, 2001 20001
47 Parkinson’s disease without treatment Neurodegeneration Substantia nigra Putamen RAC FDG DOPA/ CIT Dopamin Presynaptic neuron D2-r Normal Parkinson’s disease without treatment Engler, 2001
48 Parkinson’s disease without treatment 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 Parkinson’s disease without treatment 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
50
51
52
53
54