MSD Paramby Exam 2

Motor speech disorder is a neurogenic motor speech disorder

True

Direct activation pathway originates in the cortex

True

LMN and FCP are two names for the same structure

True

Impairment in LMN is Spastic

False

The FDA is not a standardized assessment

False

Determining localization is important for diagnosis of motor speech disorders

True

It is rare for aphasia and AOS to co-occur with UUMN Dysarthria

True

Foreign accent syndrome is a MSD

False

Ataxic must be neurogenic

True

Voice tremor: shakiness and tremulousness

True

Strengthening exercises are for Flaccid Dysarthria

True

Lesion at or after the brainstem nuclei results in?

ipsilateral weakness

Patient cannot close jaw. What CN?

CN V

________ contraction lengthens the vocal folds for pitch adjustments

cricothyroid

Direct activation pathway includes:

corticospinal and corticobulbar tract

Direct activation pathway facilitates _____ movement

skilled

Bilateral lesions on the cortex =

spastic dysarthria

Patient with slurred speech, tongue deviated to left side, stroke in the medulla

flaccid left CN XII

Voice gets weaker after 5-6 months, fasciculation on tongue, general facial weakness

flaccid dysarthria

Localization of flaccid

LMN

Specific neuromotor of flaccid

weakness

Myasthenia Gravis is a ___________

neuromuscular junction disease

Upper and lower facial weakness, reduced ROM of tongue, breathy voice =

CN VII, CN X, CN XII

Neurological disorder affecting the motor planning, programming, neuromuscular control, or execution of speech =

motor speech disorder

Collective name for a group of neurological speech disorders resulting in abnormalities in strength, speed, range, steadiness, or tone or accuracy of movements required for control for speech production. The responsible pathophysiological disturbances are due to central and peripheral nervous system abnormalities and most often reflect weakness; spasticity, incoordination; involuntary movements; or excessive, reduced or variable muscle tone.

dysarthria

Left upper and lower facial weakness

left CN 7 lesion

Myasthenia gravis

speech stress testing

Apraxia

normal AMR but abnormal SMR

AMR

puh puh puh

SMR

puh tuh kuh

Confirmatory signs

reflexes

Clinical characteristics of flaccid

atrophy, fasciculations, fibrillations, hypotonia (all of the above)

Bilateral trigeminal nerve lesions do not result in

respiration, phonation, or resonance weakness (2 false answers)

Bilateral trigeminal nerve lesions DO result in

imprecise articulation

FCP (matching)

cranial nerves and spinal nerves

Control circuit (matching)

basal ganglia and cerebellum

Direct activation pathway (matching)

corticobulbar and corticospinal tract

Indirect activation pathway (matching)

corticoreticular tract, reticular formation, red nucleus, corticorubral tract

Tongue strengthening (matching)

IOPI

Relaxation exercises (matching)

spastic dysarthria

Palatal lift (matching)

treatment for hypernasality

Teflon injection (matching)

vocal fold weakness

Localization of ataxic

cerebellum control circuit

Localization of hyper/hypokinetic

basal ganglia control circuit

Localization of spastic

bilateral UMN

Specific neuromotor of spastic

spasticity

Mild and transient is what dysarthria?

UUMN

Titibulation (matching)

rhythmic rocking of head or body

Dysmetria (matching)

a disturbance in the trajectory of a moving body part or an inability to control movement range; it is often characterized by overshooting or undershooting of targets and by abnormalities in speech, giving movements a jerky appearance

Hypotonia

reduced muscle tone

Dysdiachokinesis

a manifestation of decomposition of movement because of errors in the timing and speed of movement, with resultant poor coordination; inability to perform rapid alternating movements

Imprecise articulation, slow rate, low pitch, strained voice

spastic dysarthria

Cognitive-linguistic load

all of the above

Left lower facial weakness and mild deviation of tongue to left side of protrusion

right UMN lesion

Picture of 2 lesions (b&w photo)

facial palsy and UUMN

I Olfactory

Function: smell

Origin: cerebral hemisphere

II Optic

Function: vision

Origin: diencephalon

III Oculomotor

Function: eye movement and pupil constriction

Origin: midbrain

IV Trochlear

Function: eye movement down

Origin: midbrain

V Trigeminal

Function: jaw movement

Origin: pons

VI Abducens

Function: lateral eye movement

Origin: pons

VII Facial

Function: facial sensation and hyoid elevation

Origin: pons

VIII Vestibulocochlear

Function: hearing and balance

Origin: pons and medulla

IX, Glossopharyngeal

Function: tongue sensation and taste

Origin: medulla

X Vagus

Function: pharyngeal, palatal, laryngeal movement and control of visceral organs

Origin: medulla

XI Accessory

Function: shoulder and neck movement

Origin: medulla and spinal cord

XII Hypoglossal

Function: tongue movement

Origin: medulla

Flaccid

LMN, execution, weakness

Spastic

Bilateral UMN, execution, spasticity

Ataxic

Cerebellum, control, incoordination

Hyperkinetic

Basal Ganglia control circuit, control, involuntary movements

Hypokinetic

Basal Ganglia control circuit, control, rigidity

UUMN

unilateral upper motor neuron, execution/control, weakness + spasticity + incoordination

Mixed

>1, >1, execution or control, >1

Apraxia of Speech

Left dominant hemisphere, motor planning/programming, planning/programming errors