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
Positron (+)


511 keV
511 keV
Electrón
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
Tracers
11C-Choline
Prostata cancer, brain tumors
y
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 23390
Parkinson (D1 receptors)
11C-PK11195
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
11C-
18F-Acetate
Neurology
Dementia:
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, CreutzfeldtJakob’s disease and corticobasal degeneration

Early Diagnosis and follow-up in Alzheimer's
disease.
Hypothetical steps in the disease progression
Diagnosis FDG
Diagnosis PIB
Cognition
Critical point
FDG
PIB
Cognition
FDG
PIB
Time (years)
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
Tracers
* Characterization of neuronal degeneration
[18F]-FDG (glucose transport)
* Characterization of astrocytosis
[11C]-Deuterodeprenyl (MAO - B binding)
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
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.
Astrocytoma:PET evaluation
11C-methionine
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-PontoCerebellar Atrophy and Shy-Drager syndrome.
•
To differentiate between Parkinson's disease
and Dystonia.
•
Diagnosis in Huntington’s and Wilson’s disease.
MSA
SND : No repons to
L-Dopa treatment
OPCA: Ataxia
SDS:
Autonomic dysfunction
Orthostatism
Parkinson’s disease
Progressive
Supranuclear
Palsy
Ophthalmoplegia
Dysphagia
Neck stiffness
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
The distinction between IDP
and other akinetorigid
extrapyramidal diseases is of
prognostic and
therapeutic value
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)
Neurodegeneration
Substantia nigra
Putamen
Presynaptic neuron
Dopamin
RAC FDG DOPA/
CIT
D2-r
Normal
Engler, 2001
Engler
20001
Neurodegeneration
Substantia nigra
Putamen
Presynaptic neuron
Dopamin
RAC FDG DOPA/
CIT
D2-r
Normal
Parkinson’s disease
without treatment
Engler, 2001
Neurodegeneration
Substantia nigra
Putamen
Presynaptic neuron
Dopamin
RAC FDG DOPA/
CIT
D2-r
Normal
Parkinson’s disease
without treatment
Parkinson’s disease
after treatment
Engler, 2001
Neurodegeneration
Substantia nigra
Putamen
Presynaptic neuron
Dopamin
RAC FDG DOPA/
CIT
D2-r
Normal
Parkinson’s disease
without treatment
Parkinson’s disease
after treatment
Striato-Nigral degeneration
Engler, 2001