Anti-Yo–associated autoimmune encephalitis presenting with catatonia: a case report

Background

Catatonia, once primarily associated with schizophrenia, is now recognized as a syndrome more commonly linked to mood disorders and a broad range of medical conditions(1). Increasing evidence indicates that catatonia may also emerge secondary to neurological, autoimmune, infectious, or paraneoplastic processes(2). Differentiating primary psychiatric catatonia from secondary causes is essential in clinical practice, particularly in cases with late onset, atypical features, or fluctuating levels of consciousness. Failure to recognize underlying medical etiologies may delay appropriate diagnosis and treatment.

Case Presentation

A 55-year-old woman with a history of bipolar disorder (diagnosed in 2018) and chronic urticaria presented with one-week of immobility, bird-like vocalizations, aggression and suicidal ideation, along with a 2–3 week history of crying spells, decreased sleep, and marked functional decline. She had been receiving quetiapine 150mg/day and lithium 900mg/day. On admission, confusion and disorganized behavior were observed, and lithium was discontinued due to suspected toxicity. The Bush–Francis Catatonia Rating Scale score was 6, supporting the diagnosis of catatonia. Lorazepam 1.5mg/day was initiated with close clinical monitoring(3).

Electroencephalography findings were within normal limits. Neuroimaging revealed cerebellar atrophy, although no clinical cerebellar dysfunction was detected on neurological examination. The Frontal Assessment Battery score was 9, indicating significant frontal lobe dysfunction.

Cerebrospinal fluid(CSF) analysis demonstrated pleocytosis with a blood-tinged appearance. Although interpreted cautiously, this finding suggested a possible inflammatory process. Comprehensive infectious evaluation was negative. Anti-Yo antibody positivity was detected in both serum and CSF in the paraneoplastic panel, while systemic autoimmune vasculitis antibodies were negative. CSF protein and IgG levels were elevated, with a mildly increased IgG index; oligoclonal bands were negative.

Brain PET demonstrated widespread cortical hypometabolism involving the bilateral prefrontal and cingulate cortices, inferior parietal regions, precuneus, and prominently the right lateral temporal cortex. These findings were consistent with diffuse cortical dysfunction.

Further oncological evaluation revealed a previously identified breast lesion suspicious for papilloma, raising concern for an underlying neoplastic process. The patient was referred for surgical evaluation, and management including possible mastectomy was planned.

The coexistence of catatonia, confusion, frontal dysfunction, CSF abnormalities, cerebellar atrophy, anti-Yo positivity, and widespread cortical hypometabolism strongly suggested an underlying organic and possible paraneoplastic process. The case was evaluated by a neuroimmunology council, and further investigations were initiated.

Following lorazepam treatment, a marked clinical improvement was observed. Catatonic symptoms resolved, confusion subsided, and frontal functions improved significantly(FAB: 9→15). Electroconvulsive therapy, initially considered, was deferred due to clinical improvement.

CSF WBC	25/mm³
CSF Protein	67.7mg/dL Elevated
IgG Index	0.789 Slightly elevated
Oligoclonal Bands	Negative
Infectious Panel(CSF)	Negative
Autoimmune/Paraneoplastic Antibodies	Anti-Yo positive(serum(+), CSF(+))
Brain PET(FDG)	Hypometabolism in bilateral prefrontal, cingulate, inferior parietal, precuneus, and right lateral temporal cortex
Brain MR	mild cerebellar atrophy

Conclusions

Catatonia may reflect underlying medical conditions rather than a primary psychiatric disorder(4). Late onset, confusion, cognitive impairment, and CSF abnormalities should raise suspicion for organic etiologies.

Anti-Yo antibodies are associated with breast and gynecological malignancies and paraneoplastic neurological syndromes(5). Psychiatric and catatonic symptoms may also occur in such processes.

In this case, catatonia may represent an early neuropsychiatric manifestation of a paraneoplastic process. Early recognition may enable timely cancer detection and improve outcomes.

References

1. Fink M, Taylor MA. Catatonia: A Clinician’s Guide to Diagnosis and Treatment. Cambridge University Press; 2003.
2. Rogers JP, Pollak TA, Blackman G, David AS. Catatonia and the immune system: A review. Lancet Psychiatry. 2019;6(7):620–630.
3. Bush G, Fink M, Petrides G, Dowling F, Francis A. Catatonia I: Rating scale and standardized examination. Acta Psychiatr Scand. 1996;93(2):129–136.
4. Oldham MA. The probability that catatonia in the hospital has a medical cause: A systematic review. Psychosomatics. 2018;59(4):333–340.
5. Dalmau J, Graus F. Antibody-mediated encephalitis. N Engl J Med. 2018;378(9):840–851.