Chapter 5 Spastic Dysarthria (2/19/25 and 2/20/25) UMN LESION!! flaccid=LMN

know all deviant characteristics from jeopardy

Definition: SD is caused by damage to the direct and indirect activation pathways of the central nervous system (CNS).
excessive muscle tone= hypertonicity
Pathway Characteristics:
- Pathways are bilateral, often resulting in bilateral damage to both pathways.
- Damage commonly occurs along the upper motor neuron (UMN) in the direct pathway (from cortex to bulbar or spinal nerve).
Primary Characteristics:
- Spasticity: Muscles stiffen or tighten due to damage.
- Damage nature: Can be focal, multifocal, or diffuse.

UMNs are part of the direct activation pathway (pyramidal tract).
Role of UMNs:
- Connects with lower motor neurons (LMN) to facilitate skilled, specific movements.
- Regulates reflexes and posture through the indirect activation system (extrapyramidal tract).
Structures Involved:
- Synapses are in the: Basal ganglia, cerebellum, reticular formation, vestibular nuclei, red nucleus.

Effects of UMN lesions:
- Initial weakness and reduced muscle tone leading to increased muscle tone and spasticity.
- Hyperactivity of stretch reflexes due to unbalanced excitatory and inhibitory actions of LMNs.
- Increased muscle tone presents resistance to movement, often visible during initiation or quick responses.
Clonus: Rhythmic tremor-like contractions can occur.

reflexes become hyper excitable when damaged

Normal reflexes may diminish initially, but pathological oral reflexes (e.g., snout, suck) can become hypersensitive and increase the muscle tone
Babinski reflex- stroke foot, toes will flare.
UMN normally inhibits these reflexes, but damage results in hyper excitability.
CLONUS= INCREASED MUSCLE TENSION

Each pathway originates in opposite cerebral hemispheres (right and left).
Upper facial muscles have contralateral innervation, while lower facial and tongue muscles are affected differently.

Direct Activation Pathways (Pyramidal Tracts):
- Loss of fine motor skills, hypotonia, weakness (distal more than proximal), absent abdominal reflexes, hyperreflexia.
Indirect Activation Pathways (Extrapyramidal Tracts):
- Increased muscle tone, spasticity, clonus, decerebrate or decorticate postures.

Vascular Disorders (Stroke):
- Lesions can occur in arteries such as internal carotid, middle and posterior cerebral arteries.
Degenerative Diseases:- most common!
- Examples: ALS, primary lateral sclerosis, multiple sclerosis. involves degeneration of the motor neuron or motor neuron disease
Congenital Disorders:
- Conditions like cerebral palsy due to various perinatal issues. disorders from birth
Inflammatory Disease:
- Demyelinating diseases such as leukoencephalitis.
Cognitive Deficits:
- Associated with dementia, TBI, and aphasia. damage can be focal, multifocal, or diffuse

bulbar muscles impacted (slide 15)

Movement Characteristics:
- Slow, effortful speech movements with reduced range and force.
- Spasticity causes excessive muscle tone.
- weakness is due to hypertonicity and spacicity of muscle movement. leads to constant hypertonus or hyperactive muscle movements and they will be tired all the time. stuck in one position for so long makes you tired. this may mean they need frequent breaks during therapy
Primary Complaints:
- Fatigue during speech, and possible swallowing difficulties (dysphagia). slow and effortful movements, fatigue, nasal overtone of speech

Nonspeech Evaluations:
- Findings may include bilateral facial weakness and reduced lip retraction.
Speech Evaluations:
- Assess during conversation, reading, and AMRs (Alternate Motion Rates).
- Speech characterized by increased muscle tone, reduced force, and slowness impacting prosody.
Speech Features:
- Harsh, strained voice quality, nasal resonance issues, imprecise consonants, and reduced prosodic variation.
- when testing look for bilateral weakness of face, decreased range of lip retraction and pursing, tounge movement is reduced along with weakness, jaw clonus and slow jaw
- AMRs (puh puh puh) are slow and reduced but still in rhythm
- palate is symmetrical but may hang lower and cannot close VP port
- gag reflex increased
- cough and glottal coup should be normal
- harder to chew
- may exhibit pathologic laughing and crying = tension in their face causes this
- pathologic reflexes are present
- assess through conversation, reading, AMRs, and vowel prolongation, grandfather passage. look for these characteristics: increased muscle tone or spasticity so movements will have a reduced range, may exhibit repetitive movements, there will be reduced force during movement and speech will be slow, which impacts prosody.
- Hyperadduction of vocal folds= vocal folds are strained like they are being strangled
- slide 24: 2/20/25: imprecise consonants
- prosodic issues include monopitch, longer syllables, low pitch, reduced stress, short phrases

Major Clusters: ranked from most to least common
- Prosodic Excess: Slow rate and equal stress.
- Articulatory-Resonatory Incompetence: Imprecise consonants, distorted vowels.
- Prosodic Insufficiency: Monopitch, monoloudness.
- Phonatory Stenosis: Low pitch, strained-strangled voice, pitch breaks.
- slide 20- most deviant speech characteristics for SPD: imprecise consonants, monopitch, reduced stress, harshness, monoloudness. top one is articulatory bc muscles are so stiff

Case 1: 65-year-old female with slurred speech and dysphagia indicating bilateral UMN involvement affecting bulbar muscles.
tongue is thick= tongue is not mobile, muscles are starting to tighten
verge of crying expression= tension in facial muscles bc they are tightening
WFL= within functioning limits
normal hertz should be between 225-260 Hz
bulbar muscles= head and neck area muscles
Case 2: 80-year-old female with sudden onset dysarthria and weakness post-infarct; the pattern indicates significant spastic dysarthria affecting intelligibility.
hypertension= high blood pressure. not important
imprecise consonants= you will see this

Resulting from bilateral UMN pathway damage, characterized by slow, effortful speech.
Common clinical signs: weakness, spasticity, and abnormal reflex activity.
Common etiology factors include degenerative and vascular issues.
Speech characteristics may include prosodic issues and impaired articulation due to hypertonicity.
Recognizing spastic dysarthria can assist in diagnosing underlying neurologic conditions.