1 ts, fluent aphasia and a particularly severe anomia.

2 on for temporal lobe epilepsy had measurable anomia.

3 revealing an associative basis for retrieval anomia.

4 d to explore the factors contributing to the anomia.

5 a, pure word blindness and category-specific anomias.

6 nd after 30 h of aphasia treatment targeting anomia, an impairment in the ability to name common obje

7                     SD patients present with anomia and impaired word comprehension.

8 sease starts with word-finding disturbances (anomia) and frequently proceeds to impair the grammatica

9 rk, leading to impairments of object naming (anomia) and word comprehension.

10 ation-induced speech arrest, 82 patients had anomia, and 23 patients had alexia.

11 d these deficits were modulated by degree of anomia, concept familiarity and item typicality.

12             In patients with the more severe anomias, conceptual maps were more extensively disrupted

13 rior temporal atrophy during which prominent anomia exists without word comprehension or object recog

14 re is progressive semantic deterioration and anomia in the face of relative preservation of other lan

15 ge support the argument that their prominent anomia is due to disrupted temporal lobe connections.

16 nsion deficits but with amnesia and variable anomia, leading some to conclude that semantic memory is

17 causes global impairments such as multimodal anomia, neglect and amnesia, whereas their selective dis

18                                              Anomia/paraphasia data demonstrated foci not only within

19 tor) or negative (speech arrest, dysarthria, anomia, phonological and semantic paraphasias) findings

20 across all of the domains examined, but with anomia, reduced phonemic fluency and slowed speech rate

21 ct word in patients with mild but not severe anomia, reflecting a gradual intensification of the sema

22 s preserved in one patient with postsemantic anomia, who could write the names of objects she could n