Nonlanguage disorders of speech reflect complex neurologic apparatus.
The mute or nearly mute patient who is alert and has good understanding of speech and a right hemiparesis could have Broca's aphasia, akinesia of speech (transcortical motor aphasia), or aphemia. The patient who has Broca's aphasia does not write well, and his speech does not improve greatly with repetition. The speech of a patient with akinesia of speech improves with repetition. The aphemic patient writes normally, but his speech does not improve with repetition. The mute patient whose eyes are open but who is poorly responsive and moves little or not at all could be an akinetic mute (with either a cingulate or a thalamomesencephalic lesion) or have a locked-in syndrome. The latter is diagnosed by asking the patient to look up and down or to open and close his eyes. If he obeys these commands, the physician questions him using a code of eye movement responses. If the patient fails to respond at all, he is an akinetic mute; intense stimulation may result in speech or movement. If the patient is drowsy and has third nerve involvement, the lesion is in the thalamomesencephalic reticular formation. If the patient appears alert and has episodes of agitation, he probably has bilateral lesions in the gyri cinguli. Patients with weakness of the bulbar musculature (facial, palatal, and tongue weakness and dysphonia) may have either upper motor neuron or lower motor neuron lesions. Only bilateral upper motor neuron lesions produce permanent dysarthria. As a typical example, a patient has a transient left hemiparesis with dysarthria and almost completely recovers. Later, however, a right hemiparesis develops and the patient experiences severe bilateral facial weakness, drooling, dysphagia, and severe dysarthria. The absence of atrophy of the bulbar musculature, a hyperactive jaw jerk and gag reflex and, sometimes, inappropriate laughing or crying episodes indicate that the lesion is located above the medulla in the corticobulbar tracts. Flaccid paralysis, absence of the jaw jerk or gag reflex, and absence of other upper motor neuron signs, such as upgoing toes, indicate a lower motor neuron or neuromuscular junction problem. Appropriate tests to rule out myasthenia gravis should be done. The other conditions discussed here are often obvious from their clinical presentation. Although the specific disorder of speech sometimes is helpful in localizing the cause, in most patients, the associated deficits on neurologic examination are of greatest value.
D001288:Attention; D001479:Basal Ganglia / Q000503:physiopathology; D001906:Botulism / Q000150:complications / Q000503:physiopathology; D001927:Brain Diseases / Q000150:complications* / Q000503:physiopathology; D001933:Brain Stem / Q000503:physiopathology; D002531:Cerebellum / Q000503:physiopathology; D003391:Cranial Nerves / Q000503:physiopathology; D004525:Efferent Pathways / Q000503:physiopathology; D006801:Humans; D007046:Hysteria / Q000150:complications; D001523:Mental Disorders / Q000150:complications*; D009135:Muscular Diseases / Q000150:complications; D009157:Myasthenia Gravis / Q000150:complications / Q000503:physiopathology; D009469:Neuromuscular Junction / Q000503:physiopathology; D010523:Peripheral Nervous System Diseases / Q000150:complications*; D012131:Respiratory Insufficiency / Q000150:complications; D013064:Speech Disorders / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology