The orthographic qualities of writing deteriorate in many motor disorders such as Parkinson disease, tremors, dystonias, and spasticity, but careful inspection shows that language content is normal.
Also worth brief comment is mirror writing, in which script runs in the opposite direction to normal with each letter also being reversed. Some individuals have an unusual facility to produce mirror writing (notably, Leonardo da Vinci) though it has also been reported in developmentally delayed left-handed children. Those few instances in which mirror writing is acquired tend to be transient and incomplete with strokes in various parts of the left hemisphere, or rarely, the right hemisphere or bifrontal lesions (see the review by Schott).
A lesion of the dominant thalamus, usually vascular and involving the posterior nuclei, may cause an aphasia, the clinical features of which are not entirely uniform. Typically, there is mutism initially and comprehension is impaired. During the early phases of recovery, spontaneous speech is reduced in amount and is dysfluent; less often, speech is fluent and paraphasic to the point of jargon. Reading and writing may or may not be affected. Characteristically, the patient’s ability to repeat dictated words and phrases is preserved. This configuration has been termed “mixed transcortical aphasia,” a syndrome originally described in bilateral border-zone infarctions or large left-frontal lesions. It may exist in isolation or in combination with the mixed transcortical aphasia. Complete recovery in a matter of weeks is the rule unless the underlying cause is a tumor. Anomia has also been described with ventrolateral thalamic lesions (Ojemann).
Aphasia has also been described frequently with dominant striatocapsular lesions, particularly if they extend laterally into the subcortical white matter of the temporal lobe and insula. The head of the caudate, anterior limb of the internal capsule, or the anterosuperior aspect of the putamen are the structures involved in different patients. The aphasia is characterized by nonfluent, dysarthric, paraphasic speech and varying degrees of difficulty with comprehension of language, naming, and repetition. The lesion is vascular as a rule, and a right hemiparesis is usually associated with it. In general, striatocapsular aphasia recovers more slowly and less completely than thalamic aphasia.
These two subcortical aphasias, thalamic and striatocapsular, resemble but are not identical to the Wernicke and Broca types of aphasia, respectively. For further discussion, the reader is directed to the articles of Naeser and of Alexander and their colleagues.
The effects on speech and language of diffuse cerebral disorders, such as delirium tremens and Alzheimer disease, were mentioned in Chaps. 19 and 20. Pathologic changes in parts of the cerebrum other than the perisylvian regions may secondarily affect language function. The lesions that occur in the border zones between major cerebral arteries and effectively isolate perisylvian areas from other parts of the cerebrum fall into this category (see transcortical aphasias). Other examples are the lesions in the mediorbital or superior and lateral parts of the frontal lobes, which impair all motor activity to the point of abulia or akinetic mutism. The mute patient, in contrast to the aphasic one, emits no sounds. If the patient is less severely hypokinetic, his speech tends to be laconic, with long pauses and an inability to sustain a monologue. Extensive occipital lesions will, of course, impair reading, but they also reduce the utilization of all visual and lexical stimuli. Deep cerebral lesions, by causing fluctuating states of inattention and disorientation, induce fragmentation of words and phrases and sometimes protracted, uncontrollable talking (logorrhea). The nonaphasic language disorders of the confusional states, emphasized by Geschwind, have already been mentioned.