Dysarthria refers to abnormal phonic characteristics of speech production due to impairment of the motor processes of speech. This contrasts with aphasia, in which abnormalities of language underlie impaired communication. The neurologic pathways involved in speech articulation include upper motor neurons in the primary motor cortex and other associated regions of cortex, the basal ganglia, the cerebellum, cranial nerves (CN) V, VII, IX, X, and XII, the neuromuscular junction, and the oropharyngeal muscles of speech; disruption anywhere along these pathways can lead to dysarthria. Dysarthria can be categorized based on its particular phonic characteristic, although this can be challenging to assess in routine practice:
Spastic: Typically caused by bilateral dysfunction of the corticobulbar pathways innervating the cranial nerves mentioned above, as may be seen with bilateral strokes, demyelinating disease, or motor neuron disease. Features can include a strained hoarseness with slow and imprecise articulation.
Hypo/hyperkinetic: In Parkinsonism, speech is quiet and often slow, but sometimes rapid and mumbling. Spasmodic dysphonia causes a choked-sounding speech. Vocal tremor is a feature of essential tremor. Irregular rate and volume of speech occur in hyperkinetic disorders such as Huntington disease.
Ataxic: “Scanning” speech, with irregular intonation, pitch, volume, and speed, can be seen with cerebellar lesions.
Flaccid: There may be specific parts of the oropharyngeal musculature affected, identified by eliciting syllables of “ka”, “la”, and “ma”, which involves CN IX/X, XII, and VII, respectively. Fasciculations in these muscles, but especially the tongue, suggests motor neuron disease.
Mixed: More complicated patterns involving features of two or more of the above types.
Ischemic stroke is a frequent cause of acute onset dysarthria, especially if other focal neurologic signs and symptoms are present. Rapid neuroimaging and triage for possible reperfusion therapy are indicated.
Dysarthria without other focal neurologic symptoms in the setting of altered mentation suggests intoxication, with alcohol being the most common offender. Toxic-metabolic encephalopathy is also common in susceptible hospitalized patients with underlying infections, acute kidney injury, or other metabolic derangements.
Acute inflammatory polyneuropathies can affect the cranial nerves in addition to nerve roots and peripheral nerves, causing rapidly progressing bulbar symptoms. This is most common in the Miller-Fisher variant of Guillain-Barré syndrome (GBS), but classic GBS and other variants can also feature prominent bulbar symptoms. Clues to the diagnosis include areflexia (though reflexes may remain early in the disease course) and, particularly with Miller-Fisher syndrome, weakness of the extraocular muscles manifesting as double vision.
Signs of raised intracranial pressure (positional headache, nausea, and vomiting) with or without other progressive deficits may suggest an enlarging mass lesion. Demyelinating disease should be considered especially if there is a history of prior, recurrent attacks of focal neurologic symptoms.
Because all spinal nerve roots and cranial nerves except the olfactory and optic nerves traverse the subarachnoid space, processes involving inflammation within or infiltration of the subarachnoid space or the leptomeninges can cause multiple cranial neuropathies and/or radiculopathies; atypical infections, leptomeningeal carcinomatosis, and inflammatory diseases such as neurosarcoidosis should be considered.
If dysarthria is episodic and fluctuating, neuromuscular junction disorders such as myasthenia gravis should be considered. Other features of fatigable weakness including ptosis with curtaining, double vision, and limb weakness should be sought. If detected, testing for acetylcholine receptor antibodies and electromyography with repetitive stimulation should be done (see Chapter 97).
Very rarely, recurrent brief episodes of isolated dysarthria may occur with transient ischemic attack, usually when there is a large vessel stenosis. Diagnosis typically requires computed tomography or magnetic resonance angiography. While atypical, isolated fluctuating dysarthria can also be due to myasthenia gravis.
Motor neuron disease should be suspected when there is evidence of upper and lower motor neuron signs on examination in addition to dysarthria (see Chapter 96).
Slowly progressive dysarthria can be a feature of numerous neurodegenerative and/or hereditary conditions, such as Parkinson disease, atypical Parkinsonian syndromes, hereditary or acquired ataxias, vocal tremor (as in essential tremor), spasmodic dysphonia, and paraneoplastic cerebellar degeneration. Associated features on examination can suggest further workup, including structural and functional neuroimaging and laboratory testing.
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