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Motor Speech > Spastic Dysarthria > Flashcards

Spastic Dysarthria Flashcards

1
Q

What is Spastic Dysarthria?

A

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

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2
Q

What pathways are the Upper Motor Neurons?

A

Direct Activation Pathway
Indirect Activation Pathway

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3
Q

Direct Activation Pathways

A

Pyramidal Tracts
- Corticobulbar- cortex to cranial nerve
- Corticospinal- cortex to spinal nerve

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4
Q

Indirect Activation Pathways

A

Extrapyramidal Tracts
- Corticoreticular
- Corticorubral

Indirect- tone, posture, keep muscles on and ready to move.

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5
Q

What is the function of the Direct Activation Pathway or Pyramidal System in the Upper Motor Neurons?

A

Responsible for: skilled movements

Damage leads to weakness & slowness of speech musculature

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6
Q

What is the function of the Indirect activation pathway or Extrapyramidal System in the Upper Motor Neurons?

A

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

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7
Q

What is the one word for SPASTIC DYSARTHRIA?

A

TIGHTNESS

**With tightness you are fighting against the muscle

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8
Q

What are the general clinical characteristics?

A

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)

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9
Q

What are the NON SPEECH clinical characteristics?

A
  • 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.

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10
Q

What are the SPEECH clinical characteristics?

A

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

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11
Q

Flaccid and Spastic

A

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

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12
Q

Distinguishing Flaccid vs Spastic

A

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

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13
Q

What are the etiologies of Spastic Dysarthria?

A

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)

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14
Q

Vascular Disease: Bilateral stroke

A

Brainstem strokes near the UMN -> LMN synapse (~25% of all strokes)

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15
Q

Vascular Disease: Lacunar Infarcts

A

Subcortical strokes affecting the thalamus, white matter, and/or brainstem

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16
Q

Vascular Disease: Binswanger’s Disease

A

Vascular dementia, usually associated with hypertension

17
Q

Viral or Bacterial Infections:

A

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

18
Q

Primary Lateral Sclerosis (PLS)

A

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

19
Q

Multiple Sclerosis (1-2% are flaccid dysarthria)

A

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

20
Q

Diffuse TBI damage to the cerebrum and cortical white matter

A

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

21
Q

Cerebral Anoxia

A

A complete interruption of the supply of oxygen to the brain

22
Q

Cerebral Palsy

A

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

23
Q

What are some types of Treatment Options that are CONTRAINDICATED/NOT GOOD?

A

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)

24
Q

What are some types of Treatment Options that are GOOD?

A

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

25
Q

What are some types of Pharmacological Treatments?

A

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

26
Q

SPASTIC CHART

A

—–>

27
Q

RESPIRATION

A
  • Reduced vital capacity
  • Shorter phrases
28
Q

PHONATION

A
  • Strained strangled voice
  • Pitch breaks
  • Reduced pitch range
29
Q

RESONANCE (refers to the way airflow for speech is shaped as it passes through the pharynx (throat), oral (mouth) and nasal (nose) cavities)

A
  • Hypernasality
30
Q

ARTICULATION

A
  • Imprecise consonants and vowel distortion
  • Slow AMR and SMRs
31
Q

PROSODY (variation in pitch, loudness, and duration)

A
  • Monopitch
  • Monoloudness
  • Slow rate, slow speech
  • Equal and excess stress
32
Q

NON SPEECH

A
  • Dysphagia
  • Drooling
  • Emotional liability (pseudo bulbar affect)
  • Jaw clonus (pulsing cramp) shivering or rapid tremor like appearance)
  • Bilateral facial weakness
  • Slowed movement hyperactive reflexes
33
Q

NEUROANATOMY

A
  • UMN bilateral damage
  • Corticobulbar and corticospinal (direct)
  • Corticoreticular and corticorubral (indirect)

Motor Speech (9 decks)

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