Spastic Dysarthria Flashcards
What is Spastic Dysarthria?
Distinct MSD produced by BILATERAL damage to direct & indirect activation pathways of the CNS (where it occurs)
- UPPER MOTOR NEURONS
May affect ALL of the respiratory, phonatory, resonatory, and articulatory components of speech
** Issue with final common pathway- PNS
Communication between the brain and musculature
**All of the information is in the corticobulbar tract, makes spastic global in nature
What pathways are the Upper Motor Neurons?
Direct Activation Pathway
Indirect Activation Pathway
Direct Activation Pathways
Pyramidal Tracts
- Corticobulbar- cortex to cranial nerve
- Corticospinal- cortex to spinal nerve
Indirect Activation Pathways
Extrapyramidal Tracts
- Corticoreticular
- Corticorubral
Indirect- tone, posture, keep muscles on and ready to move.
What is the function of the Direct Activation Pathway or Pyramidal System in the Upper Motor Neurons?
Responsible for: skilled movements
Damage leads to weakness & slowness of speech musculature
What is the function of the Indirect activation pathway or Extrapyramidal System in the Upper Motor Neurons?
Responsible for:
- Maintaining posture
- Regulating reflexes
- Monitoring muscle tone
Damage leads to increased muscle tone, spasticity, & abnormal or exaggerated reflexes
** Muscle tension comes from the indirect activation.
** Indirect activation pathway damage start sending the wrong amount of muscle tone
What is the one word for SPASTIC DYSARTHRIA?
TIGHTNESS
**With tightness you are fighting against the muscle
What are the general clinical characteristics?
Weakness due to muscle spasticity
- Reduced force of movement due to muscle tightness
Hypertonia (spasticity)
Increased or abnormal reflexes
- Hyperactive gag, Palmomental (have lip movement), Sucking, Snout, Jaw Jerk
- Hyper reflexive reflexes related to CNS damage
Slowness of movement (caused by fighting the musculature)
What are the NON SPEECH clinical characteristics?
- Dysphagia
- Drooling
- Emotional Lability (aka pseudobulbar affect)
- Jaw clonus – shivering or rapid tremor-like appearance
- Bilateral facial weakness – not as pronounced as with LMN lesions
- Slowed movement
- Hyperactive reflexes
**Pseudobulbar affect – very extensive emotional response to minor triggers. Damage to both sides of the lobes.
What are the SPEECH clinical characteristics?
Prosodic excess
- Slow rate- pervasive & perceptually salient feature, especially AMRs
Prosodic insufficiency
-Monopitch, Monoloudness
Articulatory/Resonatory Incompetence
- Hypernasality
- Consonant imprecision and vowel distortion
Respiration
-Reduced vital capacity, shorter phrases
Phonation (vocal folds are heavily adducted together)
- Strained-strangled voice, pitch breaks
Flaccid and Spastic
Share many of the same speech characteristics:
-Hypernasality
-Imprecise consonants (articulatory issues, vowel distortion)
-Slow speech
BUT spastic dysarthria is more about generalized, global impairment to movement, rather than specific muscle groups
Isolation to just ONE cranial nerve- FLACCID
Distinguishing Flaccid vs Spastic
Site of Lesion (Look in the medical chart!)
- Spastic - Bilateral UMN
- Flaccid - LMN
Hypernasality
- Generally not as severe for spastic dysarthria
- No nasal emissions with spastic dysarthria
Phonation
- Spastic Dysarthria can have a tight, strained-strangled vocal quality (flaccid= hypophonia- soft speech, diplophonia- 2 pitches in voice)
Pseudobulbar affect (emotional lability)
Hyperactive or pathologic reflexes
- Hyporeflexia (absent reflexes) in flaccid
Flaccid- PNS
Bilaterally- spastic
Strider affect- sounds like taking in a quick breath. Vocal fold not in midline. Phonatory
What are the etiologies of Spastic Dysarthria?
Vascular Disease
- Bilateral stroke
- Lacunar Infarcts
- Binswanger’s disease (subcortical vascular dementia)
- Viral or Bacterial Infections:
- Primary Lateral Sclerosis (PLS)
- Multiple Sclerosis (1-2% are flaccid dysarthria)
- Diffuse TBI damage to the cerebrum and cortical white matter
- Cerebral anoxia
- Cerebral Palsy
(BPMCC)
Vascular Disease: Bilateral stroke
Brainstem strokes near the UMN -> LMN synapse (~25% of all strokes)
Vascular Disease: Lacunar Infarcts
Subcortical strokes affecting the thalamus, white matter, and/or brainstem
Vascular Disease: Binswanger’s Disease
Vascular dementia, usually associated with hypertension
Viral or Bacterial Infections:
Examples:
- Meningitis
- Encephalitis
Infection may be restricted to a specific part or parts of the brain
- Causes wide-spread effects
- Spasticity occurs when it affects UMNs Bilaterally
Primary Lateral Sclerosis (PLS)
Motor Neuron Disease (ALS) subtype (mixed flaccid-spastic)
Signs begin to appear in 50s or 60s
UMN signs are prominent, with no LMN signs for at least 3-4 years
When dysarthria and/or dysphagia are present early, it may be referred to as Progressive Pseudobulbar Palsy
Median lifespan after diagnosis is ~10 years
-Longer than ALS
Multiple Sclerosis (1-2% are flaccid dysarthria)
Autoimmune, demyelinating disease typically affecting the brain and spinal cord (CNS)
Damage to the myelin sheath decreases action potential speed and damages axons leading to disrupted pathways
Affects women more than men
Most diagnoses occur between 20 and 40 years old
Can present with spastic, ataxic or mixed dysarthria depending on location of damage
-Flaccid is rare
**Slower sending action potential- leading to slower movements
Diffuse TBI damage to the cerebrum and cortical white matter
TBI- you can see spastic dysarthria during the swelling stage
Can have chronic phase if there is damage to motor cortex or tearing of axons if brain is stretching in the skull
TBI dysarthrias- more location dependent. Not really a one cause. You have to look at sight of damage is to see what kind of dysarthria it would lead to
Cerebral Anoxia
A complete interruption of the supply of oxygen to the brain
Cerebral Palsy
Specifically the spastic subtype (as opposed to ataxic, athetoid)
Congenital or acquired neurologic disorders that affect motor function
- Stroke, anoxia, epilepsy, neurodevelopmental disorder
Congenital suprabulbar palsy
- Group of disorders associated with UMN abnormalities affecting the bulbar muscles
What are some types of Treatment Options that are CONTRAINDICATED/NOT GOOD?
Some treatments designed to help with weakness are NOT GOOD for people with spastic dysarthria
- Effortful closure techniques for vocal fold adduction
- Oral motor exercises
- Laryngoplasty
These do not work well because they reinforce the hypertonic nature of spastic dysarthria rather than compensate for it.
Spastic- DON’T DO STRENGTHING (ORAL MOTOR EXERCISES)
What are some types of Treatment Options that are GOOD?
Intelligibility drills
Minimal pairs
Exaggerated consonants
Rate control (slow even more till they get precision) (trade speed for clarity and work on speed later)
Easy onset to reduce strain-strangled voice
Contrastive stress drills (prosodic aspects, have them hear how the pitch of their voice is)
Stretching to reduce hypertonicity
Amplifier for insufficient loudness
What are some types of Pharmacological Treatments?
Antispasticity medications often help limbs more than speech
- Benzodiazepines (e.g., Valium)
Laryngeal botox injections have some limited positive results, but should be carefully considered
- Requires repeated injections due to temporary effect
Antidepressants may alleviate emotional lability
SPASTIC CHART
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RESPIRATION
- Reduced vital capacity
- Shorter phrases
PHONATION
- Strained strangled voice
- Pitch breaks
- Reduced pitch range
RESONANCE (refers to the way airflow for speech is shaped as it passes through the pharynx (throat), oral (mouth) and nasal (nose) cavities)
- Hypernasality
ARTICULATION
- Imprecise consonants and vowel distortion
- Slow AMR and SMRs
PROSODY (variation in pitch, loudness, and duration)
- Monopitch
- Monoloudness
- Slow rate, slow speech
- Equal and excess stress
NON SPEECH
- Dysphagia
- Drooling
- Emotional liability (pseudo bulbar affect)
- Jaw clonus (pulsing cramp) shivering or rapid tremor like appearance)
- Bilateral facial weakness
- Slowed movement hyperactive reflexes
NEUROANATOMY
- UMN bilateral damage
- Corticobulbar and corticospinal (direct)
- Corticoreticular and corticorubral (indirect)
