Aphasia can follow any type of neuropathology capable of causing structural alterations in the language area of the brain. It is the neuroanatomical site of damage, rather than the etiology, that determines the individual symptoms of language impairment.

(1) Broca’s Aphasia

In Broca’s aphasia left hemisphere damage of the anterior part of the peri-Sylvian language zone involving the third frontal convolution (i.e., Broca’s Area) is often found. However, much controversy exists over the exact location of the lesion necessary to result in this aphasia.

For example, there is evidence that Broca’s aphasia may arise from a lesion in the lenticular zone, anterior portions of the insular cortex, precentral gyrus, or lesions in the fibers of both the corpus callosum and the left internal capsule (see Levine and Sweet, 1983, for a review). Different types of neuropathology may be involved in this aphasia. For example, a CVA in the orbitofrontal branch of the middle cerebral artery is a possible aetiology, as well as trauma such as an open- or closed-head injury resulting in damage to the specific areas described above. Likewise a tumor may also produce the aphasia by growing in the specific regions, by increasing intercranial pressure, or by disrupting blood supply. Similarly, infectious diseases can also build up cranial pressure and result in damage to the language areas. Degenerative disorders may also be involved if the atrophy extends to the language areas.

Broca’s aphasia is also known as an expressive or non-fluent aphasia, and is predominantly a motor aphasia. The manifestations of this syndrome are awkward articulation, restricted vocabulary, restriction of grammar to the simplest, most over learned forms, and abnormal prosody. However, there is relative preservation of auditory comprehension. There is also an awkwardness and distortion of phonemes including literal paraphasias. Output often contains an excess of semantically significant words with a reduction or absence of syntactical structures or affixes. Although comprehension of spoken language is better than verbal output, comprehension is rarely normal, particularly in regard to grammatically significant structures. Repetition of spoken language is also abnormal. Naming is poor but may be aided by contextual or phonetic prompting. In addition, omissions, iterations, and simplifications of syllabic clusters often occur. These types of deficits are also evident in written language and reading out loud, however, reading comprehension is not impaired.

Broca’s aphasia causes significant problems for its sufferers. Firstly, the abrupt loss of language will severely jeopardize the stability of the patients existence in areas such as work, social life, and relationships. The rich substantive output enables one with this aphasia to communicate ideas, however, in general communication will be very poor.

Secondly, some time after onset of the disorder most nonfluent aphasic patients become aware of their problems. They often know what to say but have a verbal output that is restricted and barely intelligible. The inability to explain wishes or thoughts is frustrating for the patient, and many patients with nonfluent aphasia suffer both frustration and depression. Patients often may show lack of interest and motivation and a helpless attitude and suicidal thoughts may occur (Benson & Ardilla, 1996).

The prognosis of Broca’s aphasia depends on several factors. Like most aphasias there will be an early spontaneous recovery stage. Patients often respond automatically to their language problem by developing alternate successful strategies for communication. Several neurological factors are crucial to the prognosis. Generally the greater the lesion the worse the prognosis for recovery. Patients with damage to adjacent areas to Broca’s area, especially the inferior portion of the precentral gyrus and anterior parietal region have a poorer prognosis than those in whom the areas are spared.

Broca’s aphasia tends to improve in either two ways. Firstly, in some cases sentence length and syntax improve along with normalisation of articulation, phonemic production and repetition (i.e., to extrasylvian motor aphasia and then to anomic aphasia). In other cases, sentence length and syntax recovers without improved articulation, phonemic production, and repetition (i.e., to a conduction aphasia) (Benson & Ardilla, 1996). Obviously one of the greatest factors which influences prognosis is that of etiology. Progressive disorders will result in deteriorating language functions, whereas acute-onset, static disorders (e.g., CVAs, trauma, and tumors) will have a better potential for recovery. Trauma and hematoma cases recover better than CVAs or tumors (although this may be due to age influences). Most intracerebral tumors have a poor prognosis, whereas extracerebral tumors generally have a good prognosis. These prognostic factors are evident in all types of aphasia, not just Broca’ s aphasia (Sarno, 1981).

(2) Wernicke’s Aphasia

This aphasia generally arises from damage to the posterior part of the peri-Sylvian language area, usually a lesion involving the posterior superior portion of the temporal lobe of the dominant hemisphere (i.e., Wernicke’s area). This damage may extend into the supramarginal/angular gyrus region and/or the lateral-temporal-occipital junction area.

Again there is much controversy in the literature on the exact localisation of the necessary lesion. For example in some cases the anterior prerolandic areas, temporal isthmus, anterior portion of the putamen, and even Broca’s area has been implicated (see Kertesz, 1983 for a review). Like Broca’s aphasia it is the localisation of the lesion that results in the syndrome rather than a specific etiology. However, this disorder commonly arises from left hemisphere strokes from blockages or hemorrhages of the left tempero-parietal region. Direct injury from closed head or open head wounds are possible, as well as tumors, degenerative disorders (e.g., Alzheimer’s disease), and infectious diseases, as long as the infarcts occur in the specified areas.

This syndrome manifests itself as an impairment in auditory comprehension, and fluently articulated but paraphasic speech. The impairment of comprehension can even be evident at the single word level. The paraphasia may include literal paraphasia, verbal paraphasia, and neologisms. Further symptoms include word-finding difficulties as well as severe impairments in reading and writing. Verbal output is fluent with a normal number of words per minute. Patients often augment their verbal output adding additional syllables to the ends of words, or additional words at the end of sentences. Little effort is needed for verbal output and often the output is excessive. No problems exist with articulation, or prosody, however, there is sometimes an excessive use of grammar (paragrammatism). Reading both outloud and for comprehension, as well as writing are all often disturbed. What characterizes Wernicke’s aphasia is that the verbal output is often deficient in meaning and is often termed “empty speech”.

Patients with Wernicke’s aphasia or a nonfluent aphasia often have different problems compared to those with a nonfluent aphasia. They not only have difficulties in comprehending spoken language but also often remain unaware of their comprehension problem. This produces a true anosognosia. Many patients cannot monitor their own verbal outputs and therefore fail to realise their output is incomprehensible. Patients also tend to blame their communication difficulties on others, complaining that the person they are talking to is not speaking clearly. Patients also have difficulties in doing simple everyday activities such as reading the newspaper and watching television. Clearly disorders of comprehension will affect relationships and make it extremely difficult to be productive in most jobs. In addition, since aphasia involves loss of braining functioning due to lesions, the patient’s ability to monitor, manage, and control cognitive operations tends to be decreased. Thus, the brain injury may also produce alterations in personality and mental competence (Sarno, 1981).

In Wernicke’s aphasia poor prognosis has been correlated with middle temporal gyrus, supramarginal gyrus, postcentral gyrus, temporal isthmus or insula involvement. This aphasia may recover along two paths. Firstly, there may be better auditory comprehension and improvement in phonemic accuracy and repetition (i.e., toward anomic aphasia). Secondly, there may be better comprehension but poor repetition (i.e., toward conduction aphasia). Prognosis also depends on other factors previously described, such as the size of the lesion and the types of etiology of the aphasia.

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