Perturbation-based Regional Interpretability through Subtraction Mapping (PRISM): naming-error dissociations in language models and post-stroke aphasia

Interpretability methods for large language models (LLMs) describe internal state but do not directly test whether that state is causally sufficient to produce the observed behavior. In earlier work, we lesioned LLMs to produce error profiles in picture naming, a central task for assessing aphasia, and found that specific lesions produced errors resembling those of individual stroke survivors. Here we ask the inverse question: given an error profile, can the lesion parameters that produced it be recovered, and what does this inverse problem reveal about transformer computation? Lesions in LLaVA-Vicuna 13B were parameterized by layer index, modification percentage, and noise sigma across 4,840 configurations, and error profiles were characterized by a seven-category clinical taxonomy (correct, semantic, unrelated, formal, mixed, neologism, no-response). We trained a multi-task neural network to map error profiles back to perturbation parameters. The problem admitted a partial solution: across 10 independently trained inverse models, modification percentage and noise sigma were recoverable, whereas layer index was recoverable only within a neighborhood. In counterfactual validation, a fresh model instance perturbed with the recovered parameters reproduced the target behavior in 81.4% of cases. This dissociation between low layer recovery and high counterfactual fidelity is consistent with functional redundancy across transformer layers, a property not captured by standard interpretability methods. As an out-of-distribution test, we applied the trained model to picture-naming error profiles from 278 stroke survivors; recovered parameters were syndrome-discriminative, most strongly for perturbation intensity, indicating generalization beyond the training distribution. Counterfactual validation provides a general framework for LLM interpretability claims beyond inverse mapping.

Aphasia following stroke commonly produces systematic naming errors with characteristic profiles, but whether general-purpose language models not designed for clinical simulation can reproduce these patterns remains untested. We investigated (1) whether lesions or controlled perturbations to a multimodal language model can reproduce different types of errors in picture naming, and (2) whether the framework can reproduce the complete error profile of individual persons with aphasia (PWAs). Using LLaVA 1.6, we evaluated perturbation configurations that varied the layer, proportion, and amount of noise applied to model units. We examined 278 PWAs on the Philadelphia Naming Test, classifying responses into seven categories using a validated neural classifier. Six of seven response categories (correct, semantic, mixed, unrelated, neologism, no response errors) emerged at clinically-comparable proportions across distinct parameter space regions, with formal paraphasia being the exception. Searching the perturbation space revealed configurations that reproduced the individual error profile in at least six of seven categories for 97.8% of PWAs and in all seven categories for 79.5% of PWAs. Monte Carlo baselines confirmed that this matching reflects joint inter-category structure rather than marginal overlap. These results establish a quantitative framework for reproducing individual aphasic error patterns in picture naming. They suggest the potential for language models to serve as digital twins of individuals with post-stroke aphasia.

Aphasias, selective language impairments which can arise from brain damage, reveal the functional organization of human language by providing causal links between affected brain regions and specific symptom profiles. Drawing on this literature, we introduce an aphasia-inspired technique to characterize the emergent functional organization of language models (LMs). We ``lesion'' (zero-out) model parameters and measure the effects of this intervention against clinical aphasia symptoms, as diagnosed by the Text Aphasia Battery (TAB). When applied to 112,426 outputs from five 1B-scale LMs, the full range of evaluated symptoms surface, but in distributions largely distinct from those of humans. Our method uncovers broad symptom-profile differences between attention components (query, key, value, output) and feed-forward components (up, gate, down), with weaker evidence for differences among components within the same mechanism. We also find an effect of depth, where lesions in early layers disproportionately cause syntactic and semantic symptoms while late-middle layers yield higher rates of phonological and fluency deficits. Although some LM lesions induce quantitatively more similar profiles to some human aphasia types than others, qualitative differences in symptom patterns between LMs and humans suggest that aphasia syndromes are heavily influenced by the details of learning and processing rather than being a domain-invariant consequence of disrupted language processing.