Neurological manifestations of systemic and chronic disease, such as paraneoplastic disorders
Description
- Two separate problems that present identically:
- Paraneoplastic neurological syndromes (PNS) - remote immune effect of a tumour, not metastasis, not treatment toxicity
- Neurological complications of systemic disease - inflammatory, metabolic, endocrine, nutritional, infective
- The shared clue is a subacute (weeks to a few months) neurological syndrome that does not fit a single vascular territory or a single nerve
Why paraneoplastic syndromes matter disproportionately
- Precede the cancer diagnosis in ~60-80% - often by months to years
- Often more disabling than the tumour itself
- Tumour treatment is the most effective neurological treatment
- Deficits, once established, are usually irreversible - neuronal death, not inflammation
Two antibody classes - the distinction that predicts everything
| Intracellular (onconeural) antigen | Cell-surface antigen | |
|---|---|---|
| Examples | Hu, Yo, Ri, CV2/CRMP5, Ma2, amphiphysin, GAD65 | NMDAR, LGI1, CASPR2, AMPAR, GABA-B, glycine receptor |
| Mechanism | Cytotoxic T cell mediated | Antibody directly pathogenic |
| Tumour association | High (>70%) | Variable (LGI1 low; NMDAR teratoma ~half in young women; GABA-B SCLC high) |
| Response to immunotherapy | Poor | Good, often dramatic |
| Prognosis | Poor, deficits fixed | Often good with early treatment |
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