A severe dysarthria that is difficult to classify, but resembles that of cerebellar disease, may occur with a left hemiplegia, usually the result of capsular or right opercular infarction. It tends to improve over several weeks but initially may be so severe as to make speech incomprehensible (Ropper).
In Parkinson and other extrapyramidal diseases associated with rigidity of muscles, one observes a rather different disturbance of articulation, characterized by rapid mumbling and cluttered utterance and slurring of words and syllables. The voice is low-pitched and monotonous, lacking both inflection and volume (hypophonia), and trailing off in volume at the ends of sentences. Words are spoken hastily and run together in a pattern that is almost the opposite of the slowed pattern of spastic dysarthria. In advanced cases, speech is whispered and almost unintelligible. It may happen that the patient finds it impossible to talk while walking but can speak better if standing still, sitting, or lying down. In the extrapyramidal disorder of progressive supranuclear palsy, the dysarthria and dysphonia tend instead to be spastic in nature.
With chorea and myoclonus, speech may also be affected in a highly characteristic way. Talking is loud, harsh, improperly stressed or accented, and poorly coordinated with breathing (hyperkinetic dysarthria). Unlike the defect of pseudobulbar palsy or Parkinson disease, chorea and myoclonus cause abrupt interruptions of the words by superimposition of involuntary inspirations and movements of bulbar muscles. The abnormality has been described as “hiccup speech,” in that the breaks are unexpected, as in singultation. Accompanying grimacing and other movement abnormalities must sometimes be depended upon for diagnosis. The Tourette syndrome of multiple motor and vocal tics is characterized both by startling vocalizations (barking noises, squeals, shrieks, grunting, sniffing, snorting) and by speech disturbances, notably stuttering and the involuntary utterance of obscenities (coprolalia).
Elements of both corticobulbar (spastic) and extrapyramidal speech disturbances are combined in Wilson disease, acquired hepatocerebral degeneration, in Hallervorden-Spatz disease (PKAN, the new and preferable designation based on the kinase that is affected in the disease), and in the form of cerebral palsy called double athetosis. The speech is loud, slow, and labored; it is poorly coordinated with breathing and accompanied by facial contortions and athetotic excesses of tone in other muscles. In diffuse cerebral diseases such as syphilitic general paresis, slurred, tremulous speech is one of the cardinal signs.
Ataxic Dysarthria (See Chap. 5)
This condition is a component of acute and chronic cerebellar lesions. It may be observed in multiple sclerosis and various degenerative disorders involving the cerebellum, or as a sequela of anoxic encephalopathy or heat stroke. The principal features are slowness of speech, slurring, monotony, and unnatural separation of the syllables of words. The coordination of speech and respiration is erratic. There may not be enough breath to utter certain words or syllables, and others are expressed with greater force than intended (explosive speech). Scanning dysarthria, speaking metronomically as if scanning poetry for meter, is another distinctive cerebellar pattern and is most often a result of mesencephalic lesions involving the brachium conjunctivum. However, in some cases of cerebellar disease, especially if there is an element of spastic weakness of the tongue from corticobulbar involvement, there may be only a slurring dysarthria, and it is not possible to predict the anatomy of the lesions from analysis of speech alone. Myoclonic jerks involving the speech musculature may be superimposed on cerebellar ataxia in a number of diseases such as Creutzfeldt-Jakob prion infection and Lance-Adams postanoxic encephalopathy.