Congress:
ECR25
Poster Number:
C-14461
Type:
Poster: EPOS Radiologist (educational)
Authorblock:
M. Hovsepian, J. San Roman, C. Collaud, G. B. Amorin, N. Pabstleben; Buenos Aires/AR
Disclosures:
Magali Hovsepian:
Nothing to disclose
Jose San Roman:
Nothing to disclose
Carlos Collaud:
Nothing to disclose
Gabriela Beatriz Amorin:
Nothing to disclose
Nadia Pabstleben:
Nothing to disclose
Keywords:
Hybrid Imaging, Molecular imaging, Neuroradiology brain, PET-CT, Molecular imaging, Dementia, Motility
- Parkinson’s disease (PD) is the second most frequent neurodegenerative disorder, with increased incidence due to the aging population, being a leading cause of disability and high health costs. [1, 2, 3]
- In normal subjects, neurons in the substantia nigra produce dopamine that is transported and released at the striatum through the dopamine pathway. Reduction of dopamine in the striatum (lenticular and caudate nucleus) affects motor control.
Fig 1: Basal ganglia anatomy and function. Brain and basal ganglia anatomy on MRI, T2-weighted image, axial plane. The following structures are considered part of the basal ganglia: caudate and lentiform nuclei, thalamus, subthalamic nuclei and substantia nigra. The basal ganglia are involved in both motor and non-motor functions. The main clinical symptoms of diseases with basal ganglia involvement are movement and muscle tone disorders. - It is known that PD is characterized by the progressive degeneration of dopaminergic neurons in the substantia nigra, causing striatal dopamine deficiency.
- The clinical symptoms include resting tremors, muscle rigidity, bradykinesia (cardinal motor manifestations) and other symptoms including impaired balance, speech and writing problems, smell loss, etc. [1, 2]
- Parkinsonian like syndromes (PS) are a group of conditions including essential tremor, drug-induced, vascular, and psychogenic parkinsonism that share clinical symptoms with PD, mainly motor signs. However, these PS are not associated with striatal dopamine deficiency. [1, 2, 3]
- In many cases neurologists can differentiate PD from other causes of parkinsonism, but it is not always possible and accurate diagnosis is necessary for adequate patient treatment selection.
- 18F-DOPA (dihydroxyphenylalanine) is an amino acid analog to natural L-DOPA, a dopamine precursor. The radiotracer reaches the nigrostriatal pathway and is converted to 18F-fluoro-dopamine, therefore the decrease in its uptake depicts dopamine terminal loss, distinctive of PD. [3, 4] Consequently, evaluating striatal 18F-DOPA uptake with a brain PET scan is a reliable tool to differentiate PD from PS and may change treatment. [1, 2, 4, 5, 6]
Fig 2: Normal versus pathological brain scan. A) 18F-DOPA PET of the brain shows homogeneous and symmetrical uptake of the tracer in the striatum (typical “comma” shape), expressing normal functioning of dopaminergic pathway. B) In a patient with Parkinson’s disease (PD), brain 18F-DOPA PET scan shows reduction of the uptake in both putamen (arrows), due to degeneration of dopaminergic neurons in the substantia nigra, causing striatal dopamine deficiency. In this patient, uptake is slightly asymmetrical with left predominance, which coincides with predominant right-side tremor.
Fig 3: Female patient (45 y/o), with involuntary movements in the left hand and arm. Brain 18F-DOPA PET scan shows decrease in the radiotracer uptake in both lenticular nuclei, particularly in the posterior sector of both putamens (red and yellow arrows, right and left respectively), and to a lesser extent in the head of the right caudate nucleus (red dotted arrow). It is compatible with dysfunction of the dopaminergic pathway, consistent with PD. - Ibrahim et al [1] reported a 95.4% sensitivity and 100% specificity of 18F-DOPA PET for detecting dopamine deficiency. These results agree with other published studies that show that functional imaging is highly sensitive and specific and may be valuable in PD diagnosis. The previously reported sensitivities and specificities for 18F-DOPA PET were 90%-100% and 91% respectively. [1, 6]
- It is also currently indicated to detect early onset PD with mild symptoms, atypical cases and to evaluate patients with no appropriate response to treatment.
Fig 4: Male patient of 70 y/o, with involuntary movements and tremors in the left lower limb for 2 years. He also suffers from anxiety and depression. History of treatment with clebopride due to functional gastrointestinal disorders, which is a dopamine antagonist drug and could explain altered movements of pharmacological origin. Brain PET scan with 18F-DOPA shows evident decrease in tracer uptake in both striatum nuclei with right predominance (red arrows), depicting presynaptic dopaminergic deficit of the nigrostriatal pathway, compatible with Parkinson´s disease. Yellow arrow: incidental tracer uptake in calcified pituitary gland. (Upper row: PET images. Lower row: fused PET-CT images). - 18F-DOPA PET is also recommended to help distinguish between DLB (Dementia with Lewy Bodies) and Alzheimer´s disease (AD). [2]
Fig 5: Fig 5A Female patient (76 y/o), with involuntary movements and tremors in the upper limbs, disorientation and cognitive impairment (memory loss). Brain 18F-DOPA PET scan shows decrease in the concentration of radiotracer in both lentiform nuclei, with particular involvement of the posterior putamen (red and yellow arrows, right and left respectively), with slight right-side predominance. It is compatible with compromise of the dopaminergic pathway.
Fig 55: Fig 5B Female patient (76 y/o), with involuntary movements and tremors in the upper limbs, disorientation and cognitive impairment (memory loss). Brain 18F-FDG PET scan shows significant decrease in cortical metabolism in the temporal lobes (red arrows) and parietal regions (yellow arrows), lobes that are usually affected both in DLB and AD. In this case also involvement of the occipital lobes is seen (green arrows), which is not usually seen in AD. Cortical involvement is slightly asymmetrical, with the right side being more involved. A slight decrease in radiotracer concentration is also observed in the frontal lobes. The pattern of cortical metabolism involvement is compatible with Dementia with Lewy bodies (DLB).
Fig 555: Fig 5C Female patient (76 y/o), with involuntary movements and tremors in the upper limbs, disorientation and cognitive impairment (memory loss). Brain 18F-DOPA and 18F-FDG PET scans show striatal dopaminergic deficit (red arrows) and cortical hypometabolism in temporal, parietal and occipital lobes (yellow and green arrows). The combined and complementary information from both exams is clinically relevant. The fact that there is a reduction in the uptake of DOPA added to the metabolic compromise of the occipital lobes points to DLB as the first diagnostic option. Dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD) overlap in many clinical and imaging features and are currently considered as subtypes of α-synuclein-associated disease spectrum. They are characterized by similar metabolic decrease in cerebral cortex and decreased DOPA binding in putamen.