The comprehension of spoken and written language, though seemingly normal under casual conditions, is usually slightly defective in the full syndrome of Broca’s aphasia and will break down under stringent testing, especially when novel or complicated material is introduced. The naming of objects and particularly parts of objects may be faulty in articulation, but the proper name can be chosen from a list. These are the most variable and controversial aspects of Broca’s aphasia, as in some patients with a loss of motor speech and agraphia as a result of cerebral infarction, the understanding of spoken and written language may be normal. Mohr and colleagues (1978) have pointed out that in such patients an initial mutism is usually replaced by a rapidly improving dyspraxic and effortful articulation (a “mini-Broca’s aphasia,” in his terms), leading to complete recovery. The lesion in such cases is restricted to a zone in and immediately around the posterior part of the inferior frontal convolution (the latter being the Broca area per se). Mohr and colleagues (1978) have stressed the distinction between this relatively mild and restricted type of motor speech disorder and the more complex syndrome that is traditionally referred to as Broca aphasia.
The lesion in the major form of Broca aphasia subsumes a much larger area than the inferior frontal gyrus and includes the subjacent white matter and even the head of the caudate nucleus and putamen (Fig. 22-2), the anterior insula, and frontoparietal operculum (the term operculum refers to the cortex that borders the sylvian fissure and covers or forms a lid over the insula, or island of Reil.) In other words, the lesion in the usual form of Broca aphasia extends well beyond the so-called Broca area (Brodmann areas 44 and 45). Furthermore, persistence of Broca’s aphasia is associated with the larger type of lesion illustrated in Fig. 22-2.
It is interesting historically that in one of Broca’s original patients, whose expressive language had been limited to a few verbal stereotypes for 10 years before his death, inspection of the surface of the brain (the brain was never cut, although scans have since been done) disclosed an extensive lesion encompassing the left insula; the frontal, central, parietal operculum and included even part of the inferior parietal lobe posterior to the sylvian fissure. The Wernicke area was spared, refuting a prediction made at the time by Marie. Inexplicably, Broca attributed the aphasic disorder to the lesion of the frontal operculum alone, and ignored the rest of the lesion, which he considered to be a later spreading effect of the stroke. Perhaps he was influenced by the prevailing opinion of the time (1861) that articulation was a function of the inferior parts of the frontal lobes. The fact that Broca’s name later became attached to a discrete part of the inferior frontal cortex helped to entrench the idea that Broca aphasia is equated with a lesion in the Broca area. However, as pointed out earlier, a lesion confined only to this area gives rise to a relatively modest and transient motor speech disorder (Mohr et al) or to no disorder of speech at all (Goldstein).