Chapter 9 Unilateral Upper Motor Neuron Dysarthria

UUMN dysarthria is linked to damage of UMN pathways sending signals to cranial and spinal nerves for speech muscles.
Its classification is anatomical rather than based on function due to limited research on perceptual traits and their physiological correlates, highlighting variability in presentation among individuals.

Traditionally considered a mild and temporary disorder, making it challenging to study.
Frequently co-occurs with other speech disorders such as aphasia or apraxia (left hemisphere lesions), and cognitive deficits (right hemisphere lesions).

Accounts for approximately 12.5% of all dysarthrias and 11.8% of motor speech disorders (MSDs).
Likely an underestimate; commonly appears as a secondary diagnosis in patients with other speech disorders.

Comprises both direct (pyramidal) and indirect (extrapyramidal) pathways.
Bilateral organization: half of the fibers originate from each cerebral hemisphere.

Involves corticobulbar and corticospinal tracts targeting cranial/spinal nerves, generally contralateral to their origin.
Begins in the cerebral cortex and descends through the corona radiata to the internal capsule near the basal ganglia and thalamus.

Predominantly contralateral, synapses in several structures primarily in the reticular formation and brainstem nuclei.

Caused by unilateral damage to UMNs:
- Tumors on one CNS side affecting UMN pathways.
- Surgical trauma leading to focal deficits.
- Most common: strokes due to left or right carotid artery occlusions, often associated with other cognitive-communication issues.

Speech often described as "slurred," "thick," or "slow."
Common complaints include drooling, heaviness on affected side of the face or tongue, leading to difficulty in speech.

Unilateral facial weakness observed in ~80% of cases.
Unilateral lingual weakness in 52% of cases.
Jaw and velopharyngeal functions typically normal; dysphagia often mild with good recovery prospects.

Confidence in diagnosing UUMN can be low, especially if dysarthria presents with severe spasticity or ataxia features, suggesting additional bilateral damage.

Emphasize potential diagnostic ambiguity:
- Speech characteristics potentially indicative of UUMN lesions may mimic other conditions, warranting caution in diagnosis.

Patient profile: 55-year-old man with right-sided weakness and dysarthria linked to a left internal capsule infarct.
Speech characteristics: Imprecise articulation, harsh voice, moderately reduced intelligibility.
Conclusion: Diagnosed with UUMN dysarthria after one session of therapy.

Patient profile: 57-year-old man post-stroke.
Speech characteristics: Mild weakness, imprecise articulation, improved with slower speech.
Conclusion: Mild UUMN dysarthria diagnosed; patient deemed therapy unnecessary due to mild symptoms.

Results from unilateral UMN damage and has comparable frequency to other major dysarthria types, primarily impacting articulation and prosody.
The anatomical definition of UUMN dysarthria relates to lesion location, with a clinical presentation varying in terms of derived weakness, spasticity, or incoordination.
Stroke is the primary cause of UUMN dysarthria, with lesions typically in the posterior frontal lobe or internal capsule.
Accompanying symptoms include lower facial and lingual weakness, drooling, and mild dysphagia.
Severity is usually mild to moderate, with potential for good recovery, though some patients may experience lasting deficits.
Common speech characteristics include imprecise articulation, slow and irregular AMRs, and reduced loudness, with various associated physiologic abnormalities.
Recognition of UUMN dysarthria can aid in the diagnosis of neurologic diseases, alongside the need for clinical correlation due to variable characteristics.