Bilateral lesions to Broca's area

A couple weeks ago a reader raised the question of whether unilateral lesions to Broca's area constitute a strong enough test of the motor theory of speech perception. I suggested they were because they sometimes severely disrupted speech production with minimal effects on the recognition (comprehension) of speech. The question continued to nag me though, so I started looking for cases in the literature of bilateral lesions to Broca's area. It turns out there are a handful. Here is the most interesting case report by Levine & Mohr in 1979.

Case 3

A 20-year-old woman suffered a large left perisylvian stroke including Broca's area and developed chronic severe Broca's aphasia. Nine years later she suffered another stroke, this one involving the right homologue to Broca's area.


Here is Levine and Mohr's description of the patient's language abilities:

The patient's speech production was absent, and she was unable even to vocalize. Her speech comprehension was very slightly impaired; she obeyed two-commission but not three-commission verbal commands, and performed approximately 1 standard deviation above the average aphasic patient in the auditory comprehension subsection of the BDAE. p. 932

Clearly, the patient is able to comprehend words quite well; her only difficulty being the comprehension of rather complicated sentences, consistent with Broca's aphasia.

So,

large unilateral lesions that destroy speech production ability do not cause substantial speech recognition deficits (Cases 7, 11, 16, 17; Naeser et al. 1989);

complete deactivation of the entire left hemisphere during Wada procedures does not cause substantial speech recognition deficits (Hickok et al. 2008);

bilateral lesions to the frontal operculum that cause Foix–Chavany–Marie syndrome (anarthria/severe dysarthria and loss of voluntary muscular functions of the face and tongue including speech) do not cause substantial speech recognition deficits (Weller, 1993);

failure to develop the ability to speak does not cause substantial speech recognition deficits (Lenneberg, 1962; Christen, et al. 2000);

and, bilateral lesions to Broca's region does not cause substantial speech recognition deficits (Levine & Mohr, 1979).

Now can we all agree that there is a small problem with the motor theory of speech perception?

References

Christen HJ, Hanefeld F, Kruse E, Imhäuser S, Ernst JP, Finkenstaedt M. (2000). Foix-Chavany-Marie (anterior operculum) syndrome in childhood: a reappraisal of Worster-Drought syndrome. Dev Med Child Neurol., 42, 122-32

Hickok, G., Okada, K., Barr, W., Pa, J., Rogalsky, C., Donneley, K., Barde, L., & Grant, A. (2008). Bilateral capacity for speech sound processing in auditory comprehension: Evidence from Wada procedures Brain and Language, 107 (3), 179-184 DOI: 10.1016/j.bandl.2008.09.006

Lenneberg, E. (1962). Understanding language without ability to speak: a case report. Journal of Abnormal and Clinical Psychology, 65, 419-425.

Levine DN, Mohr JP. (1979) Language after bilateral cerebral infarctions: role of the minor hemisphere in speech. Neurology, 29(7):927-38.

Naeser, M.A., Palumbo, C.L., Helm-Estabrooks, N., Stiassny-Eder, D., and Albert, M.L. (1989). Severe nonfluency in aphasia: Role of the medical subcallosal fasciculus and other white matter pathways in recovery of spontaneous speech. Brain 112, 1-38.

Weller M. (1993) Anterior opercular cortex lesions cause dissociated lower cranial nerve palsies and anarthria but no aphasia: Foix-Chavany-Marie syndrome and "automatic voluntary dissociation" revisited. J Neurol, 240(4):199-208