• The right rib lesion has increased uptake from SUVmax 3.5 to 5, with subtly increased sclerosis on CT.
• Increasing sclerosis in a previously involved bone lesion can reflect osteoblastic healing/remodeling, particularly if the patient is clinically well and PSA/ALP are improving.
• With androgen-receptor pathway treatment such as abiraterone, PSMA expression can transiently rise after treatment initiation, causing increased tracer uptake despite antitumor activity. This effect is generally described early, often within weeks after starting or changing systemic treatment. A review of flare in prostate cancer notes that evidence for a sustained PSMA-PET flare with abiraterone is inconsistent, and one small study found no flare at a median of 3 months (review of flare evidence).

• If abiraterone was started or changed only recently, especially in the previous 4-12 weeks, this isolated rise could plausibly be flare/pseudoprogression.
• If the patient has been on stable abiraterone for several months and the scan is a year after the prior scan, a new or progressively PSMA-avid lesion is more concerning for active/progressing metastasis, even though increasing sclerosis may still indicate a healing component.

1. PSA trend, preferably serial values
2. ALP and other biochemical trend
3. New bone pain or worsening analgesic requirement
4. Number and distribution of new/increasing PSMA-avid lesions
5. CT morphology, particularly whether sclerosis is increasing without a destructive soft-tissue component
6. Whether both scans used the same tracer, scanner/protocol, and similar uptake time

“Mild interval increase in PSMA avidity of the right rib mixed lytic-sclerotic lesion with subtle increase in sclerosis. In the setting of ongoing systemic therapy, this may represent treatment-related PSMA-expression flare and/or osteoblastic healing response; however, metabolically active residual/progressive osseous metastasis cannot be excluded. Correlate with PSA, serum ALP, clinical status, treatment timing, and consider follow-up imaging.”

• Do not call progression solely from SUVmax 3.5 to 5.0. SUV is affected by technical differences between scans and, on abiraterone/androgen suppression, by altered PSMA expression.
• The subtle increase in sclerosis supports an osteoblastic healing response. Bone healing can coexist with persistent or temporarily increased PET tracer uptake.
• The very low PSA strongly argues against active bulk adenocarcinoma progression, assuming the PSA has remained suppressed on serial measurements and the patient is clinically stable.
• Current proposed PSMA-PET response criteria emphasize that change in lesion avidity alone does not define progression. Progression is driven principally by confidently new lesions, usually in an appropriate clinical context (PCWG4 recommendations).

Single right rib metastasis demonstrates mildly increased PSMA avidity with increased sclerosis. Given undetectable PSA and sclerotic evolution, findings favor healing-related osseous flare/therapy-related modulation of PSMA expression or stable treated disease. Isolated metabolically active residual disease cannot be entirely excluded. No convincing PSMA-PET evidence of systemic disease progression.

1. Continue abiraterone and ongoing androgen deprivation unless there is other evidence of progression.
2. Check serial PSA, alkaline phosphatase, clinical symptoms, and ensure castrate testosterone if relevant.
3. Compare whether both scans used the same PSMA tracer, scanner, uptake time, and reconstruction protocol.
4. If clinically needed, repeat imaging in about 8-12 weeks or at the next planned restaging interval rather than declaring progression now.
5. If there is focal rib pain, fracture risk, or equivocal CT morphology, targeted CT or MRI can help distinguish healing sclerosis from structural progression.

Important possible explanations

1. Multiple-system atrophy, cerebellar type (MSA-C) / olivopontocerebellar degeneration
   • This is a leading neurodegenerative pattern when FDG PET shows combined cerebellar and pontine hypometabolism.
   • Autonomic symptoms such as urinary dysfunction, postural hypotension, erectile dysfunction, constipation, and REM-sleep behavior disorder may be absent early. Normal bladder function does not exclude early MSA-C.
   • The textbook library specifically notes that olivopontocerebellar degeneration/MSA-C can show marked pontine and cerebellar hypometabolism. FDG-PET literature similarly describes distributed cerebellar-pontine hypometabolism in MSA (cerebellar-disease imaging consensus).
2. Hereditary or sporadic cerebellar ataxia
   • Spinocerebellar ataxias, especially SCA1, SCA2, SCA3 and SCA36, can produce cerebellar hypometabolism that extends to the pons and brainstem.
   • Family history may be absent because of late onset, reduced penetrance, or an unrecognized affected relative.
   • Normal hearing makes SCA36 less characteristic, but does not rule out other SCAs. In an established ataxic state, several SCAs demonstrate cerebellar and brainstem hypometabolism (FDG-PET movement-disorder review).
3. Paraneoplastic cerebellar degeneration or immune-mediated cerebellar ataxia
   • In a patient with cancer and a subacute gait disorder, this must be actively excluded.
   • Prostate adenocarcinoma is an uncommon cause, but paraneoplastic neurologic syndromes can occur with many malignancies. Consider antibodies such as anti-Yo, Hu, Ri, Ma2, CV2/CRMP5, amphiphysin, and anti-Tr/DNER, along with autoimmune ataxia antibodies including GAD65, depending on the clinical setting.
   • PET may show cerebellar metabolic abnormality before major structural changes are apparent on MRI.
   • This matters because potentially treatable causes should be identified promptly.
4. Toxic, drug-related, alcohol-related, or nutritional cerebellar dysfunction
   • Review alcohol exposure and all medications carefully, including recent chemotherapy and non-oncology drugs.
   • Relevant potentially reversible causes include thiamine deficiency, vitamin B12 or vitamin E deficiency, copper deficiency, hypothyroidism, hepatic/uremic encephalopathy, and medication toxicity.
   • Chemotherapy-associated peripheral neuropathy may worsen gait, although it would not alone usually explain diffuse pontocerebellar FDG hypometabolism.
   • Abiraterone is not a classic cause of this particular PET pattern.
5. Vascular disease
   • Posterior-circulation ischemia, multiple small infarcts, or chronic vertebrobasilar insufficiency can cause gait ataxia and reduced metabolism.
   • If the gait instability was sudden or developed over hours to a few days, posterior-circulation stroke should be excluded urgently, even if there are no speech, swallowing, or limb symptoms.
6. Structural posterior-fossa pathology
   • Cerebellar/brainstem metastasis, leptomeningeal disease, hydrocephalus, inflammatory disease, or compression need MRI assessment.
   • Brain metastasis would more often cause a focal lesion rather than symmetric diffuse cerebellar, pontine, and medullary hypometabolism, but PET cannot safely exclude it.
7. CANVAS or sensory/vestibular ataxia syndromes
   • CANVAS, caused commonly by biallelic RFC1 expansion, produces cerebellar ataxia with sensory neuropathy and bilateral vestibular impairment.
   • On FDG PET, CANVAS often has cerebellar hypometabolism with relative preservation of the brainstem, so the reported prominent pons/medulla involvement makes MSA-C or an SCA relatively more compatible, though it is not definitive (CANVAS imaging series).

What should be done next

1. MRI brain with contrast, including diffusion-weighted imaging and detailed posterior-fossa sequences. Look for cerebellar or pontine atrophy, the MSA-C “hot-cross-bun” sign, infarction, metastasis, leptomeningeal enhancement, hydrocephalus, or demyelination.
2. Formal neurologic examination: cerebellar signs, eye movements/nystagmus, dysarthria, pyramidal signs, neuropathy, and vestibular function.
3. Document the time course:
   • Hours to days: vascular, toxic, infectious
   • Weeks to months: paraneoplastic/autoimmune, nutritional, drug-induced
   • Slowly progressive over months to years: MSA-C, SCA, sporadic adult-onset ataxia
4. Check orthostatic blood pressure and ask specifically about REM-sleep behavior disorder, constipation, erectile dysfunction, reduced sweating, and subtle urinary urgency/retention for early MSA.
5. Blood tests: CBC, renal/liver profile, glucose, electrolytes, TSH, B12, folate, thiamine, vitamin E, copper/ceruloplasmin, and consider HIV/syphilis testing where clinically appropriate.
6. If onset is subacute or MRI is unrevealing, involve neurology early for serum plus CSF autoimmune/paraneoplastic testing, CSF cytology if leptomeningeal disease is a concern, nerve-conduction studies, and targeted genetic testing such as RFC1/SCA panel when indicated.

Bottom line

Practical interpretation

1. A true peripheral vestibular problem
   • May cause unsteadiness, especially while walking in the dark, on uneven ground, or with rapid head movement.
   • Hearing can remain normal, as in vestibular neuritis, bilateral vestibular hypofunction, vestibular migraine, and some cases of Ménière disease.
   • It does not usually explain a convincing diffuse pontocerebellar hypometabolic PET pattern.
2. An early central gait/ataxia syndrome
   • MSA-C, spinocerebellar ataxia, autoimmune/paraneoplastic ataxia, nutritional/metabolic causes, or less commonly a treatment-associated neurologic problem can produce gait instability before conventional MRI shows atrophy or a lesion.
   • The combined pons-cerebellum pattern means this possibility should not be dismissed purely because MRI is normal.

Next appropriate tests

• Video head impulse test (vHIT): assesses all semicircular canals and vestibulo-ocular reflex.
• Videonystagmography (VNG) with positional testing and caloric testing.
• cVEMP and oVEMP: assess otolith organ pathways.
• Dynamic visual acuity and posturography, if available.

Also important in this patient

• Vibration/proprioception at toes and ankles
• Reflexes
• Romberg test
• Nerve-conduction studies if signs suggest neuropathy
• B12, thiamine, vitamin E, copper, TSH, glucose/HbA1c, renal/liver function, electrolytes including potassium and magnesium

Clinical bedside clues