Exam 3: Motor Speech Disorders, Language, Higher-Order Functions

dysarthria

deficit in the control or EXECUTION of speech (related to strength, speed , range, accuracy of speech movements)

generally neurologic in orgin

can be categorized further into specific subtypes

apraxia of speech

deficit in PLANNING or programming speech movements

generally neurologic in origin

usually co-occurs with other conditions (aphasia or generic dysarthria)

flaccid dysarthria (what is it?, localization, neuromotor, etiology/cause of disease)

reduced ability to move —small, weak movements

localization/lesion: LMN (lower motor neuron)

• injury or malformation of the LMN “final pathway” to the neuromuscular junction

neuromotor: weakness

etiology/cause of disease = NMJ disease, Mysathenia Gravis, MS, Bell’s Palsy

phrenic nerves

nerves involved in respiration are spread from the cervical through thoracic divisions of the spinal cord
control the muscles needed for breathing

innervates diaphragm 3-5th cervical segments

• injuries to phrenic nerves —> can cause resp paralysis —> can lead to dysarthria

flaccid dysarthria clinical characteristics

clinical:

• weakness (paralysis)

• hypotonia

• diminished reflexes

• atrophy

• fasciculation (spontaneous muscles contractions)

• fibrillations (rapid, irregular heart rate)

flaccid dysarthria perceptual characteristics

perceptual:

• hyper nasality

• breathiness (continuous)

• nasal emission

• audible inspiration

• short phrases

spastic dysarthria (what is it?, localization, neuromotor, etiology/cause of disease)

• bilateral pyramidal UMN damage to pathways of CNS leading to LOSS OF INHIBITION

• loss of skilled movements, reduced range of motion

localization: bilateral UMN

• damage to the direct & indirect activation pathways+ pyramidal & extrapyramidal pathways

neuromotor: spasticity

etiology/causes of disease: Cerebral Palsy, infarcts of internal carotid/MCA/PCA, ALC, corticospinal or corticobulbar lesion

UMN: Pyramidal/Direct Pathways

consist of corticospinal & corticobulbar tracts

• corticospinal = control of limbs/trunk; decussation at the pyramids of the medulla

• corticobulbar = control of face, head, neck; decussation depending on CN

activation leads to discrete, skilled movements

lesions cause:

• weakness, loss of skilled movements

• babinski sign (loss of proper reflex, toes spread out instead of coming together)

UMN: Extrapyramidal/Indirect Pathways

major contributions from premotor areas

crucial connections with basal ganglia, cerebellum, retic form, vestibular nuclei

generally inhibitory— regulates reflexes for maintaining posture and tone

lesions cause:

• spasticity (inc resist to stretch)

• inc reflexes

• weakness

what patterns result from lesions to UMNs?

pyramidal & extrapyramidal damage (UMN)

• paralysis

• loss of skilled movement

• spasticity, loss of inhibition (specifcally extrapyramidal damage)

• increased and/or pathological reflexes

spastic dysarthria clinical characteristics

clinical/non- speech characteristics:

• dysphagia

• excessive, slow facial expressions

• pathological laughing and crying

• drooling

• facial posture fixed (unchanged)

• partial smile

*damage from pyramidal tract; bilateral

spastic dysarthria perceptual characteristics

speech/perceptual characteristics:

• harshness

• imprecise consonants

• low pitch

• slow rate

• strained-strangled quality

• short utterances

• pitch breaks

what is ataxia?

neurological condition characterized by the loss of coordination and control of muscle movement

due to damage in cerebellum

how does cerebellum modulate speech? how does damage to the cerebellum affect the body?

cerebellum:

• coordinates skilled movement (speed, range of muscular movements)

• part of the indirect pathway to LMNs (extrapyramidal support)

• receives input from the body and cortex; acts as an error controller (provides to the cortex)

impacts of damage:

• errors of force, speech, timing, and range —> difficulty in the coordination of movement

• IPSILATERAL control

  • R cortex, L cerebellum, L side of body

  • L cortex, R cerebellum, R side of body

ataxic dysarthria

results from cerebellar control circuit dysfunction; errors in coordination

localization: cerebellum

neuromotor: incoordination

etiology/causes of disease: cerebellar hemorrhage, Anoxia, Multiple Sclerosis

ataxic dysarthria clinical characteristics

clincal (non-speech):

• hypotonia (low muscle tone)

• slow voluntary movements

• jerky movements

• wide-based gait

• tremors

• paucity of movement

• muscular incoordination

• impairments of equilibrium

ataxic dysarthria perceptual characteristics

perceptual characteristics:

• slurring/stumbling over words (lack of error correction)

• “drunk” sounding speech

• irregular articulatory breakdowns

• irregular vowel distortions

major inputs and outputs of the basal ganglia (circuit)

caudate & putamen: input from cortex, output to globus pallidus

globus pallidus: input from caudate & putamen, output to the thalamus

thalamus: input from globus pallidus, output to cortex

major features of Parkinson Disease

• bradykinesia (slowness of movement; difficulty initiating movement)

• postural instability

• tremor

• rigidity

• cognitive deficits

• hypokinetic dysarthria

hypokinetic dysarthria clinical characteristics

• tremor at rest

• rigidity “cogwheel”

• bradykinesia (slow movements)

• hypokinesia (small movements)

• masked faces: loss of facial expression

• akinesia (lack of voluntary movement)

• swallow infrequently, drooling

• dysphagia (difficulty swallowing food)

hypokinetic dysarthria perceptual characteristics/non-speech related

• monopitch

• reduced stress

• monoloudness

• inappropriate silences

• short rushes of speech

• increased rate overall

dyskinesia

a movement disorder characterized by involuntary, uncontrolled muscles movements (general term)

types of dyskinesia

• hyperkinetic dysarthria

  • with etiologies of: athetosis, chorea, myoclonus

akinesia

inner sense of restlessness but lack of movement/freezing, difficulty initating movement

• hypokinesia (dec amplitude or poverty of movement)

• facial rigidity (stiffness in facial muscles)

• delayed responses

ballism

movement disorder characterized by involuntary, flinging, and often violent movements of the extremities

• large amplitude movements

• flinging/ throwing movements

• repetitive and varying

• usually unilateral (affects one side of the body)

tremors

involuntary movement

rhythmic, oscillatory movement (shakiness, trembling)

tics

involuntary movements

sudden, brief, and repetitive movements or sounds (not necessarily rhythmic like tremors)

hyperkinesia

EXCESSIVE involuntary movements, characterized by an overabundance of muscular activity

(hypokinesia refers to decreased/reduced movements)

hyperkinetic dysarthria? perceptual characteristics?

associated with diseases of the basal ganglia circuit, cerebellar circuit, indirect (extrapyramidal) system

abnormal, rhythmic, or irregular and unpredictable (rapid or slow) involuntary movements

perceptual

• visible abnormal orofacial, head, and respiratory movements

• variable rate

• inappropriate silences

• excess loudness variation

• prolonged intervals & phonemes expiration/inspiration

• transient breathiness

etiologies/causes of hyperkinetic dysarthria

• chorea (Huntington’s or non-Huntington’s)

• tics

• dystonias

• myoclonus

Huntington’s Disease

one type of hyperkinetic dysarthria etiology

characterized by chorea, dementia

• constant jerky movements, including facial movements, restless/fidgety hands

Chorea (not Huntington’s)

one type of hyperkinetic dysarthria etiology

“dance"- like purposeless, unpredictable movement

• due to reduced GABA

• multiple etiologies (Wilson’s Disease, Sydenham’s Chorea)

• speech (excessive range of movement, sustained vowel fluctuations)

Gilles de la Tourette’s Syndrome

one type of hyperkinetic dysarthria etiology

example of vocal tics

brief involuntary movements or sounds that occur over a background of normal motor activity

• simple or complex (simple or complex)

• echolalia (repeating what is heard)

• palilalia (compulsive repetition of phrases)

under partial voluntary control

dystonias (meige, oromandibular, spasmodic dystonia)

one type of hyperkinetic dysarthria etiology

slow hyperkinesia characterized by involuntary abnormal postures resulting from excessive co-contraction of antagonistic muscles

• Meige Syndrome= oromandibular dystonia + forceful, spasmodic closure of the eyes

• spasmodic dysphonia= focal dystonia with strained voice quality & stoppages

• slow initiation of speech

palatopharyngolaryngeal myoclonus

abrupt RHYTHMIC unilateral or bilateral movements of the soft palate, pharyngeal walls and laryngeal muscles

(not like chorea which is more random)

speech:

• intermittent hypernasality

• tremor- like variations

• momentary rhythmic arrests

athetosis

condition where muscle contractions cause involuntary writhing (twisting/squirming) movements of the limbs, neck, tongue and others muscle groups

inability to maintain a body part in a single position

damage to basal ganglia can cause which movement related diseases?

• Parkinson’s Disease (HYPOkinesia)

• Huntington’s Disease (HYPERkinesia)

flaccid dysarthria is due to damage in what area?

lower motor neuron (LMN)

spastic dysarthria is due to damage in what area?

upper motor neuron; pyramidal (volitional mvmt)

ataxic dysarthria is due to damage in what area?

upper motor neuron; extrapyramidal support (cerebellum)

unilateral upper motor neuron (UUMN) dysarthria

unilateral innervation = when one side of the brain controls one side of the body

(usually contralateral hemisphere of brain controls the opposite part of body)

BUT usually gets compensated by the unaffected side of the brain except for CNs controlling lower half of face

often UNDERDIAGNOSED because signs do not usually show with compensation from other side of brain; perceptual characteristics are not well-defined

frequently co-occurs with aphasia, apraxia of speech (planning of speech)

etiologies examples of UUMN dysarthria

• vast majority etiologies are vascular (result of stroke)

• focal lesions to unilateral UMN, occlusion of L or R carotid artery

UMN pathways

corticospinal

• fibers originate from the cerebral cortex, cross at the medulla, and descend to the spinal cord (end destination)

• CONTRALATERAL CONTROL

corticobulbar

• fibers originate from the cerebral cortex, cross midline somewhere along the brainstem at the level of the CN they innervate

• BILATERAL CONTROL (controls both sides of body)

what results in lesions to UMN systems (corticobulbar and corticospinal tracts)?

loss of fine, skilled movements

• hemiplegia — paralysis of one side of the body

• hemiparesis — weakness on one side of the body

atypical, increased reflexes

• hypereflexia, Babinski sign

• absent abdominal reflex

Mixed dysarthria

any combination of 2+ dysarthria types across 2+ dimension of the nervous system

important distinction for guiding diagnostics & treatment plans

etiology examples: ALS, multiple CVAs/strokes, TBI, other infectious/metabolic diseases

Amytrophic Lateral Sclerosis (ALS)

type of mixed dysarthria

• UMN and LMN are affected

progressive loss of motor neurons

speech: flaccid-spastic dysarthria (spastic speech, flaccid resonance of speech)

• wet, gurgled voice

• strained- strangled

• monopitch

• hypernasality

Multiple Sclerosis (MS)

type of mixed dysarthria

demyelination of CNS white matter

speech: ataxic-spastic dysarthria

respiratory problems

may/may not have communication problems

Friedreich’s Ataxia

type of mixed dysarthria

hereditary (autosomal recessive)

speech: spastic- ataxic dysarthria

signs & symptoms= primarily spinocerebellar, cardiac problems are often the cause of death

Wilson’s Disease

type of mixed dysarthria

rare but important to recognize b/c its curable

inadequate processing of dietary copper

• distinguishing sign= GOLDEN RING around cornea (Cu deposits)

speech: hypokinetic, spastic, and/or ataxic dysarthria (can manifest in many ways)

apraxia of speech

deficit in PLANNING or PROGRAMMING speech movements

localization: left hemisphere (dominant for language, even if left- handed)

impaired capacity to program sensorimotor commands for the positioning & movement of speech muscles

• effortful trial-and-error groping with attempts to self-correct

• aware that speech is not executed correctly

• automatic + reactive speech is better than volitional/intentional speech

etiology: trauma, stroke, tumor that damages dominant (left) hemisphere structures involved in motor speech

problems that usually co-occur with apraxia of speech

majority (around 80%) have non-verbal apraxia (limb- apraxia) and aphasia

47% have dysarthria

what are the neural substrates for motor planning and programming?

left (dominant) hemisphere

• broca’s area

• premotor cortex

• supplementary motor area

• insula

controversy about developmental apraxia of speech (DAS)

uncertainties about the appropriate assessment + treatment protocols, characteristics of the disorder, and if it has a neurological basis

aphasia

an impairment of language (general term)

• affect production and/or comprehension

• can affect any modality— speaking, reading, writing, auditory, comprehension

• due to injury to the brain

dysphasia

congenital/developmental language problem

alexia

impaired reading

agraphia

impaired writing

paraphasic errors

sounds or words are replaced by substitutions so that desired response is only approximated

• literal/formal/phonological= incorrect or incomplete phonemes (grass is g_een)

• verbal= incorrect words (grass is blue)

  • semantic paraphasia — the substituted word is related to the intended word (I spent the day working on the computer, i mean TV)

  • remote paraphasia — the substituted word is, at most, distantly related to the word (You forgot your musketeer, I mean, umbrella)

etiologies/causes of aphasia

• #1 etiology: cerebrovascular accident (CVA) = stroke (ischemic or hemorrhagic)

• traumatic brain injury (TBI)

• tumors

3 parameters used to categorize aphasia

• ability to produce (fluency)

• ability to comprehend

• ability to repeat

Broca’s Aphasia

non- fluent speech, can comprehend, does not repeat

reduced verbal output

• mostly content words

• restricted vocab

• not a lot of function words

lesion: broca’s area, anterior perisylvian , insular cortex

awareness of impairment can lead to depression

transcortical motor aphasia

non-fluent, comprehends, repeats

limited speech output & syntactic errors (not as severe as Broca’s Area)

lesion: frontal lobe (anterior to Broca’s area)/ supplementary motor cortex

global aphasia

non-fluent, doesn’t comprehend, doesn’t repeat

severe impairment in all modalities (speaking, listening, reading, writing)

restricted vocab, no understanding in any modality, no ability to communicate

lesion: middle cerebral artery which causes frontal-temporal-parietal lesion

Wernicke’s Aphasia

fluent, does not comprehend, does not repeat

fluent but still paraphasic verbal output (naming difficulty, not as severe as Broca’s)

impaired auditory comprehension + impaired repetition

most common etiology/lesion: infarct to the inferior division of the middle cerebral artery

transcortical sensory aphasia

fluent, doesn’t comprehend, repeats

auditory comprehension is relatively poor

repetition is intact

fluent, well articulated speech

naming impaired

lesion: left posterior temporal- occipital lobe

transcortical mixed aphasia

not fluent, doesn’t comprehend, repeats

comprehension is severely impaired + no purposeful speech output

may have echolila (repeats heard phrases)

lesion: Broca’s + Wernicke’s area are spared, but damage to surrounding frontal, temporal, and parietal lobe

conduction aphasia

fluent, can comprehend, impaired repetition

may or may not have reading and writing deficits

lesion: left arcuate fasciculus, superior temporal regions, or supramarginal gyrus

anomic aphasia

fluent speech, can comprehend, can repeat

difficulty in naming and word retrieval

aud comprehension, reading, and writing are intact

lesion: temporal or parietal lobe, usually associated with focal trauma (specific location)

subcortical aphasias

related to the site of lesion; disrupts connections to and from language areas of the cortex

• anterior subcortical aphasia

  • head of caudate, anterior putamen (basal ganglia)

  • non-fluent (with dysarthria), mild deficits with naming + aud comprehension

• thalamic aphasia

  • damage to dominant thalamus

  • fluent with paraphasic errors, intact comprehension

progressive aphasia

• due to neurodegenerative processes

• primary progressive aphasia

  • word finding and naming issues

  • many variants, depending on language modalities that are impaired

issues with the classical model (of aphasias)

oversimplified

• most ppl with aphasia have problems with all modalities of language, regardless of aphasia type

• patients don’t all fit the “classical models”

neuroimaging shows

• syndromes don’t map well onto lesions

alexia with agraphia

lesion: left inferior parietal lobule (supramarginal and angular gyri)

cannot read or write

overlaps with wernicke’s aphasia and evolves during recovery

alexia without agraphia (pure alexia)

lesion: left posterior cerebral artery (PCA) territory

patients can write, but not read what they have written

often accompanied by visual field deficit and inability to name colors

5 higher level functions of the brain

1) perisylvian network= language

2) parietofrontal network= spatial cognition

3) occipitotemporal network= face and object recognition

4) limbic network = retentive memory

5) prefrontal network= cognitive and behavioral control

language

symbolic representation of thoughts

spoken, written, and signed

language dimensions

• phonology= rules of how the SOUNDS of language are organized (ex: ks sound only occurs in middle or end of word, not in the beginning)

• morphology= rules governing how words are FORMED (ex: grammatic endings change meaning/diff tenses)

• semantics= rules governing the MEANING of words and combinations (ex: knowing the diff b/w a pen and pencil)

• syntax= rules abt how words are combined to form SENTENCES (proper grammar in a sentence)

• pragmatics= rules abt the use of language in CONTEXT (ex: knowing to take turns in a convo)

what side of the brain is generally associated with language specialization?

left (for most people)

but language lateralization can change after injury

what is the categorical and representational hemisphere?

dominant + non-dominant hemispheres have been replaced with complementary specialization

• CATEGORICAL hemisphere— usually LEFT

  • sequential- analytic processes (language + analytic reasoning)

  • functions: verbal ability, fast temporal processing, details

• REPRESENTATION hemisphere — usually RIGHT

  • visuospatial relations (recog of faces, musical themes)

  • functions: musical ability, emotional recognition, abstract language

Broca’s Area

• formation of words

• ordering of words

• output for spoken language

Wernicke’s Area

• involved in word comprehension (receives fibers from visual cortex + aud cortex)

• surrounds primary aud cortex

arcuate fasciculus

• AKA conduction area

• connects Wernicke’s area to Broca’s area (white matter tract)

• important for REPEATING and SPEAKING a written word

Exner’s Area

• writing output pathway

• above broca’s area

  • broca’s area organizes signals from posterior language areas —> relays them to exner’s area

visual word form area

processes the word as a whole

angular gyrus

perception of written language, as well as other language processing functions

adjacent to visual receptive areas

lesions can result in impaired reading (alexia) + writing (agraphia)

what cognitive functions are affected by lesions to frontal lobes?

executive functions, working memory, planning, inhibition/impulse control, speech production (Broca’s Area)

insula

• beneath the lateral fissure (where temporal, parietal and frontal lobes come together)

• function:

  • relays somatosensory info

  • planning and coordinating speech/language + swallowing

higher order functions

• language

• attention

• memory

• visuospatial functions

• executive functions

• mathematical functions

• social cognition

• reasoning

• problem-solving

• critical thinking

lateralization of brain functions

left hemisphere

• fast temporal processing

• details

• verbal ability + language

• praxis + skilled motor function

right hemisphere:

• spectral processing; acoustic pitch

• visuospatial attention + analysis

• emotional recognition

localized functions

• lesions affecting the frontal lobes and their connections impact executive functions (ex: attentional control, declarative learning)

• lesions on the mesial temporal lobes affect declarative learning

• lesions on subcortical structures (cerebellum + basal ganglia) can affect non-declarative learning

• lesions affecting the thalamus can affect sustained attention

limitations of functional localization

• neurons are highly interconnected

• brain is incredibly plastic in health and disease (localiz wouldnt be that accurate)

• brain functions are highly interdependent

what cognitive functions are affected by lesions to mesial/medial temporal lobes?

new long-term, declarative memories, emotional processing, language

what cognitive functions are affected by lesions to basal ganglia and cerebellum?

basal ganglia= regulating movement, planning/sequencing, motivation/reward

cerebellum= motor coordination, language/speech, visual-spatial memory

what cognitive functions are affected by lesions to thalamus?

sensory integration, memory (episodic memory b/c connects to hippocampus), regulation of attention

four features that brain disorders tell us about healthy brains

• localization of cognitive functions

  • shown by analyzing lesion sites

  • different regions of the brain are specialized for different functions)

• onset and clinical course of the brains’s capacity to adapt to changing circumstances

• individual variability in symptoms and outcome

• recovery and neuroplasticity in health and disease

coup-contrecoup

type of TBI

injury to one side of head (i.e during fall) or injury to opposite side of head as the brain hits against opposite side of injury

acceleration/decelertion

a sudden stop causes head to go forward and then back, as in a car accident

edema

type of brain injury

swelling of brain tissue; causes pressure

hemorrhage

type of brain injury

rupturing of blood vessels

focal injury/lesions

type of brain injury

lesions just beneath the point of direct impact

sheering

type of brain injury

twisting of axons that causes trauma & diffuse white matter/axonal injury

Complications associated with TBI

• polytrauma (other body parts also affected)

• emergent care (life-threatening)

• medications

• cognitive issues

• behavioral issues