Tc-99m-HMPAO (Ceretec^©), Tc-99m- ECD (Neurolite^©), Tc-99m DTPA, Tc-99m Pertechnetate.

Generator produced in the form of Tc-99m Pertechnetate (TcO₄ ¹⁻) from Mo-99. t _phys 6 h. Emits gamma 140 keV (89 %).

Lipophilic structure, crosses BBB, first-pass extraction of roughly 80 %. Not dependent on blood pressure, temperature, or cessation of phenobarbital.

Flow agents – lipophobic: Do not cross BBB.

Tc–99m HMPAO/Tc–99m ECD: Blood pool → crosses BBB (lipophilic) → intracellular (cortical cell, via glutathione) → convert to hydrophilic complex → trapped → taken up by the mitochondria and the nucleus. Blue dye is used to stabilize the Tc-99m HMPAO molecule. It prevents the conversion of the Tc-99m HMPAO to a stereoisomeric form that rapidly washes out from the brain tissue. This may also be used as a quality control; blue color indicates the use of a brain agent. Useful when flow images were not obtained properly and carotids flow cannot be evaluated → no need to repeat exam if no brain uptake is noted by the end of the exam.

Tc–99m DTPA and Tc–99m pertechnetate: IV bolus → flow to the internal carotid arteries → Circle of Willis to the anterior, middle, and posterior cerebellar arteries.

Bladder: Tc-99m ECD, Tc-99m DTPA, Tc-99m pertechnetate. Lacrimal gland: Tc-99m-HMPAO.

Lipophilic tracer: Uptake within brain parenchyma. Lipophobic tracer angiographic phase: Visualization of “trident sign” (anterior and middle cerebellar arteries); blood pool phase: Visualization of venous sinuses.

(brain death):

Absence of angiography phase with lipophobic tracers. Use tracer that does not cross BBB (obtaining flow phase is important even with lipophilic tracers).

Scalp perfusion on lateral images mimics brain perfusion – apply tourniquet (absolute contraindication in small children).

Tc–99m DTPA/Tc–99m pertechnetate: No flow noted on angiography phase, with a sagittal sinus sign on delay phase images (may also be false negative). Tc – 99m HMPAO / Tc – 99m ECD “Helmet sign” – no perfusion to brain stem and cerebellum. Persistent cerebral perfusion.

Patient progressed from a negative to a positive brain perfusion scan. Fig. A – flow study demonstrates visualization of “trident sign” on arterial flow phase. Ten-minute delay image demonstrates appearance of a sagittal sinus. Fig. B – on a repeated study 3 days later, a complete loss of brain perfusion is noted on flow images, as well as loss of sagittal sinus uptake on 10 min delay images.

Generator produced in the form of Tc-99m pertechnetate (TcO₄ ¹⁻) from Mo-99. t _phys 6 h, emits gamma 140 keV.

Lipophilic structure, crosses BBB, first-pass extraction of roughly 80 %.

Cerebral flow: Blood pool → crosses BBB (lipophilic) → intracellular (cortical cell, via glutathione) → convert to hydrophilic complex → trapped → taken by the mitochondria and the nucleus. Tc–99m ECD has a longer shelf life, which permits longer delay in administration while waiting on ictal activity to be demonstrated on EEG.

Cyclotron produced. t _phys 109.8 min. Decay: Positron emission; gamma ray energy = 511 keV. Decays to O-18.

FDG-6P → trapped in cell (missing 2’OH group needed for metabolism). After full decay from F-18 to O-18 (heavy oxygen), it will combine with H⁺ ion to create 2’OH group that will be metabolized in glycolysis.

Cerebral flow: 20 mCi. Metabolism 10–15 mCi.

Tc–99m HMPAO/Tc–99m ECD: IV (Ceretec^©) or Tc-99m ECD (Neurolite^©) → 15 min- 2 h postinjection SPECT as close as possible to the head. Ictal: done with SPECT under EEG monitoring → inject at the time of seizure. (FDG t_phys is too short and preparation is needed).

Tc–99m HMPAO lacrimal glands. F–18 FDG Bladder.

Tc–99m HMPAO: By decay in the brain (trapped). Kidneys and hepatobiliary (not trapped). F-18 FDG: kidneys, ureters, and bladder.

Distribution Tc-99m HMPAO Trapped in the brain (intracellular, trapped); muscle and soft tissue (not trapped). F–18 FDG: Brain >> kidneys, ureters, and bladder >> liver. Variable: Heart, GI, salivary glands, uterus, spleen, ovaries, and testes.

Clearance Tc-99m HMPAO By decay in the brain (trapped). Kidneys and hepatobiliary (not trapped). F–18 FDG: kidneys, ureters, and bladder.

Evaluation of patients presenting with dopaminergic symptoms to differentiate parkinsonian syndromes from essential tremors.

Cyclotron-produced t_phys 13.3 h. Emits gamma photons 159 KeV.

Thyroid uptake and scan, whole-body scan for thyroid cancer and I-123 MIBG scan.

Dopamine Transporter (DaT) visualization agent. Cocaine analog. Phenyltropane compound.

Isoflurane has high binding affinity (reversible) for presynaptic dopamine transporters (DaT) in the striatal region of the brain. Loss of DaT significantly correlates with loss of nigrostriatal neurons in Parkinson disease.

Headache, vertigo, increased appetite, and tactile hallucinations. Accepted medical use with strict inventory. Classified as DEA Schedule II controlled substance due to abuse and dependence potential.

3 to 5 mCi IV.

3–6 h postinjection, brain SPECT images (approx 30 min).

Normal: Human striatal anatomy, comma shape. Abnormal: Right or left asymmetry within the putamen or caudate nucleus structures, or bilateral decrease/change of normal comma shape.

Bladder.

Consistent with human striatal anatomy (peak uptake 3–6 h with 30 %).

By 48 h postinjection, 60 % will be excreted via urine, 14 % GI.

Cerebral spine fluid (CSF) circulation: (1) Hydrocephalus, (2) CSF leak, (3) ventriculoperitoneal (VP) or ventriculoatrial (VA) shunt patency.

Cyclotron produced from cadmium (Cd-112) target. t _phys 2.83 days (67 h). Decays: Electron Capture (EC). Emits: gamma 173 keV (89 %) and 247 keV (94 %).

Intrathecal injection of the radiopharmaceutical; will slowly be absorbed in the subarachnoid space which allows tracking of CSF flow dynamics.

0.5 mCi in 10 % dextrose. Lumbar puncture (LP) and intrathecal injection of the radiotracer.

Concept of normal CSF production and flow CSF will be produced predominantly by the choroid plexus of the lateral, 3rd, and 4th ventricles which will determine the dynamics of normal flow. At any time point, there will be no reverse flow toward the lateral ventricles in a normal individual. Normal CSF flow: Lateral ventricle (CSF production) → 3rd vertical via the foramen of Monro (CSF production) → flow via the cerebral aqueduct of Sylvius → 4th vertical (CSF production) → spinal cord subarachnoid via the foramen of Magendie and two Luschka foramina → basal cisterns → subarachnoid over the convexities.

Abnormal flow: Brain atrophy due to age: Delay migration of the tracer over the convexities – no lateral ventricles are seen. Communicating hydrocephalus (normal pressure hydrocephalus) → visualization of the lateral ventricles without migration of tracer over the convexities.

Protocol: Intrathecal injection followed by insertion (usually by ENT) of 6 nasal meatus pledgets labeled as superior, middle, and inferior nasal meatus, bilaterally (1–6). Image protocol may vary per location of the radiotracer with time – image at 1 h, followed by 4 and 24 h as needed. Once full migration of the tracer is seen → remove the pledgets → place each in a test tube → measure and record counts of each pledget with a well counter. Draw 10 ml of blood, measure, and record counts. Interpretation: Pledgets counts/plasma counts > 2.5–3 are abnormal. Use pledget labels for accurate localization. Ear CSF leak: Look for asymmetry in the images.

Spinal cord.

CSF flow dynamics.

Absorption of labeled CSF into the blood by the arachnoid villi and by the cerebral and spinal leptomeninges in a lesser extent. Within the first 24 h, approximately 65 % of the dose will be excreted by the kidneys and 85 % at 72 h postinjection.

Tc-99m pertechnetate or Tc-99m sulfur colloid.

Evaluation of lacrimal drainage patency (epiphora – overflow of tears onto the face).

Generator produced in the form of Tc-99m pertechnetate (TcO₄ ¹⁻) (+7 valence) from Mo-99. t _phys 6 h Emits gamma 140 keV (89 %).

0.1 mCi.

Direct application of tracer to the eye will demonstrate the normal pattern of tear drainage. (Optimal with special dispenser).

Tracer instilled in the inferior fornix simultaneously or near simultaneously via a micropipette, preferably, or a syringe. The volume per eye ranges from 10 to 25 μl (with smaller volumes, it is less likely to cause overflow of tracer onto the cheek).

Patient seated/supine with their cornea less than 2 cm from the collimator (LEAP or LEHR typically, pinholes have been used). Dynamic images (1 min frames for 10–15 min or 10–30 s frames for several min). Static images up to 45 min after instillation.

Lens.

Pre-lacrimal sac (pre-sac) delay → tracer fails to reach the sac by 2–3 min, pre-ductal delay → no sac emptying is seen by 3–5 min, and ductal delay if tracer has not entered the nose by 6 min. Delay to drainage defined as mild (6–15 min), moderate (16–30), and severe (31–45).

Hyperthyroidism, thyroid nodule, neonatal hypothyroidism.

Cyclotron-produced t _phys 13.3 h Emits gamma photons 159 keV.

Mo-99 generator-produced t _phys 6 h. Emits gamma 140 keV.

I-123 Na Iodide Rapid GI absorption of iodine in the extracellular fluid → active uptake in the thyroid follicles by Na/I symporter → protein-bound iodine (organification). Chemical form T₃ and T₄. All drugs which affect the thyroid hormone synthesis pathway (Synthroid, PTU, Tapazole, Armour Thyroid) will affect iodine uptake (highly regulated by TSH). Additional uptake (non-protein-bound uptake mechanism) by salivary glands, stomach cells (no trapping), and hepatocytes (thyroglobulin metabolism).

will be transported via the I/Na Symporter channel to the thyroid follicles without organification → No trapping; will wash out with time.

Adult: I–123 NaI (0.1–0.3 mCi). Tc–99m pertechnetate (2–10 mCi). Children: I–123 NaI (0.1–0.2 mCi). Tc–99m pertechnetate 1–5 mCi.

Thyroid.

Once TSH < 0.1 mIU/L → no uptake will be demonstrated in a normal regulated thyroid cell due to negative pituitary-thyroid feedback.

Iodine-containing tissue (thyroid tissue, salivary gland, and stomach) + GI lumen (oral admin), 7 days post-scan – liver uptake due to thyroid hormone metabolism.

Renal, metabolized in the liver.

Parathyroid adenoma, elevated PTH with hypercalcemia.

Cardiac stress scan, breast cancer.

Generator produced in the form of Tc-99m pertechnetate (TcO₄ ¹⁻) (+7 valence) from Mo-99. t _phys 6 h emits gamma 140 keV (89 %).

IV injection of Tc-99m sestamibi. Early images – anterior static images at 10–15 min of neck and upper chest → delay anterior static images at 1–2 h with or without SPECT/CT, institution dependent.

20 mCi.

Intrathyroidal, along the thyroid bed toward the thymic bed, thymus, carotid artery sheath, mediastinum, along the esophagus, and retropharyngeal space.

Bile to GI and kidney.

Distribution

Acute pulmonary embolism. Also, chronic pulmonary embolism due to pulmonary hypertension.

Obtained usually before perfusion. Xe-133/Tc-99m MAA: Prevents down scatter energy of higher energy (140–80 keV). Tc/Tc exam: lower dose ratio for ventilation (1 mCi Tc-99m DTPA vs. 3–6 mCi of Tc-99m MAA).

Nuclear Reactor (Fission of U-235), Lipophilic. t _phys 5 days, t _biol 30 s. Decays: Beta minus. Emits: 81 keV gamma dose 10–30 mCi. Target Organ: Lungs. Operation requires a negative-pressure room.

Gas is inhaled via a closed system using face mask/mouthpiece:

Tc–99m: Generator produced in the form of Tc-99m pertechnetate (TcO₄ ¹⁻) (+7 valence) from Mo-99. t _phys 6 h. Emits gamma 140 keV (89 %).

t _biol is 60–100 min in healthy people and ~ 25 min in smokers.

Distribution

Tc-99m-labeled solid graphite particles (0.005–0.2 μm) in argon carrier gas (gas and particle properties).

Preparation Technegas generator: In a crucible, Tc-99m-pertechnetate is heated to high temperatures in the presence of argon gas to create labeled Tc-99m-carbon particle encapsulated within a layer of graphite carbon.

Protocol Radiopharmaceutical delivered to the patient via Technegas generator contains Tc-99m-labeled graphite particle in argon gas. (1) Supine position, (2) nose clip + mouthpiece on, (3) deep breathe and hold for 3 s, (4) exhale, (5) repeat two to three times.

Distribution

Xenon: Liver uptake – Fatty liver, fatty marrow. Aerosols: Oral cavity, esophagus. Stomach – swallow of particles.

Obtain after ventilation. Xe-133/Tc-99m MAA – Prevents down scatter of higher energy (140–80 keV). Tc/Tc exam – lower dose ratio for ventilation (1 mCi Tc-99m DTPA vs. 3–6 mCi of Tc-99m MAA).

Generator produced in the form of Tc 99m pertechnetate (TcO₄ ¹⁻) (+7 valence) from Mo-99. t _phys 6 h. Emits gamma 140 keV (89 %).

Size: 90 % between 10–90 μm and 0 % > 150 μm; actual range: 20–40 μm. Particles in a size of 1 to ~7 μm are taken up by the reticuloendothelial system (RES). MAA Kit – contains four to eight million MAA particles and stannous ion (to reduce TcO₄ ¹⁻ oxidation state from +7 to +4). Each vial should be reconstituted with up to 100 mCi of Tc-99m pertechnetate.

(known as “capillary blockade”): t _biol 2–3 h. MAA particles are larger than the capillaries. Hence, once injected via the venous system, they will be trapped within the pulmonary alveolar capillary bed.

Dose: Healthy adult: 1–6 mCi, 200–700K MAA particles; ideal number: 350 K with a minimum of 200 K particles. Pulmonary hypertension patient: maximum of 150 K particles. Dose modification 1–3 mCi pregnant (preferred perfusion only with 150 K MAA); known right to left shunt and chronic pulmonary hypertension (1–3 mCi, 150 K particles MAA V/Q). Pediatric 25–50 μCi/kg. Newborn 200–500 μCi.

Lung.

Pulmonary alveolar capillary bed.

Abnormal distribution (no PE) (A) right-to-left cardiac shunt: lung, brain, kidneys (B). SVC occlusion: lung, hepatic caudate lobe. (C) Atrial-venous collaterals: lung, kidneys, no brain. (D) Edge scalloping: microemboli due to fat, sepsis, air, tumor, amniotic fluid.

MAA particles are fragile and will undergo degradation to be phagocytized in the RES (reticuloendothelial system in the liver and spleen).

Well’s criteria