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what are the 5 higher levels of brain function and what structures are generally associated with them?
parisylvian network for language, parietofrontal network for spatial cognition, occipitotemporal network for face and object recognition, limbic network for retentive memory, and prefrontal network for cognitive and behavioral control
language definition
symbolic representation of thoughts + spoken, written, signed
phonology definition
rules governing the ways in which the sounds of language are organized
morphology definition
rules governing how words are formed
semantics definition
rules governing the meaning of words and combinations
syntax definition
rules governing how words are combined to form sentences
pragmatics
rules governing the use of language in context
what is the categorical hemisphere and what does it do?
(usually) the left hemisphere specializes in sequential-analytic processes like language and analytic reasoning
what is the representational hemisphere and what does it do?
(usually) the right hemisphere specializes visuospatial relations like identification of objects by their form, recognition of faces, and recognition of muscial themes
what side of the brain is usually dominatn for language?
the left hemisphere
how does language dominance happen?
lateralization begins early in prenatal development and can be changed by brain damage, but it’s unclear how much is genetically preprogrammed vs. influenced by environmental factors
broca’s area functions of language
formation of words, ordering of words (syntax), and output for spoken language
wernicke’s area function of language
involved in spoken word comprehension + permits understanding of written and spoken language and enables a person to read a sentence, understand it, and say it out loud
arcuate fasciculus (conduction area) function of language
important for repeating and speaking a written word
exner’s area function of language
writing output pathway that translates and integrates linguistic and motor output commands + form written words and sentences
visual word form area function of language
acts as the brain’s “letterbox” for reading, rapidly identifying written letters and words regardless of font or case
angular gyrus function of language
perception of written language, as well as other language processing functions
insula function of language
relays somatosensory information and planning and coordinating speech/language and swallowing
aphasia definition
an impairment of language that affects production and/or comprehension and is due to injury to the brain
dysphagia definition
covers a wider range of issues regardless of their cause
alexia definition
impaired reading
agraphia definition
impaired writing
paraphasia definition
sounds or words are replaced by substitutions so that desired response is only approximated
literal/formal/phonological paraphasia definition
incorrect or incomplete phonemes (grass is g_een)
verbal paraphasia definition
incorrect words (grass is blue)
semantic paraphasia definition
the substitued word is related to the intended word
remote paraphasia definition
the substituted word is, at most, distantly related to the intended word
neologisms definition
nonsense words (grass is gronus)
what are the common causes of aphasia?
STROKE, traumatic brain injury, brain tumors, degenerative conditions, exposure to neurotoxic agents
what are the three parameters used to categorize aphasia in the ‘classic’ model?
fluency, comprehension, and repetition
broca’s aphasia
nonfluent/effortful, impaired repetition, relatively intact comprehension, due to occlusion of the superior division of the middle cerebral artery
wernicke’s aphasia
fluent but still paraphasic verbal output, impaired repetition, impaired comprehension, infarct to inferior division of middle cerebral artery, to the posterior temporal or angular branches
conduction aphasia
fluent, impaired repetition, intact comprehension, lesion is usually left arcuate fasciculus, superior temporal regions, or supramarginal gyrus
global aphasia
nonfluent/mute initially, impaired repetition, impaired comprehension, large MCA lesion (frontal-temporal-parietal lesion)
transcortical motor aphasia
nonfluent, intact repetition, intact comprehension, ‘anterior watershed zone’
mixed transcortical aphasia
nonfluent/dysarthric, intact repetition, severly impaired comprehension, ‘isolation syndrome’ = pathological function of language network when it is isolated from other regions of the brain
transcortical sensory aphasia
fluent, intact repetition, impaired comprehension, lesion to the left posterior temporal-occipital lobe (‘posterior watershed zone’)
anomic aphasia
fluent/word finding pauses, intact repetition, relatively preserved comprehension, focal lesion to temporal or parietal lobe
what are some problems with the classic model?
it’s oversimplified and some patients don’t ‘fit’ classic models and neuroimaging also shows that sometimes syndromes don’t map well onto lesions
what is the dual-stream model?
divides cortical processing into two pathways
ventral stream role
“what” stream for perception and identification
dorsal stream role
“where” stream for spatial awareness, action, and sensorimotor integration
alexia WITH agraphia
lesion in the left interior parietal lobule and overlaps with wernicke’s aphasia and evolves during recovery
alexia WITHOUT agraphia
lesion in the left PCA territory, often accompanied by visual field deficit and inability to name colors, patient can write, but not read what they have written
what are the two subcortical aphasias?
anterior subcortial aphasia and thalamic aphasia
anterior subcortical aphasia
head of caudate, anterior putamen (basal ganglia), anterior limb internal capsule and non-fluent (with dysarthria), mild deficits with naming and auditory comprehension
thalamic aphasia
typically damage to dominant thalamus and fluent with paraphasic errors, intact comprehension
progressive aphasia
due to neurodegenerative processes and causes word finding and naming issues, many variants depending on language modalities that are impaired, patterns are slightly different than ‘classic’ aphasias
dysarthria definition
deficit in control or execution of speech movements
apraxia of speech definition
deficit in planning or programming speech movements
flaccid dysarthria site of lesion and neuromotor basis
LMN and weakness
spastic dysarthria site of lesion and neuromotor basis
bilateral UMN and spasticity
ataxic dysarthria site of lesion and neuromotor basis
cerebellum and incoordination
hypokinetic dysarthria site of lesion and neuromotor basis
basal ganglia circuit and rigidity/reduced ROM
hyperkinetic dysarthria site of lesion and neuromotor basis
basal ganglia circuit and involuntary movements
UUMN dysarthria site of lesion and neuromotor basis
unilateral UMN and weakness/incoordination
mixed dysarthria site of lesion and neuromotor basis
combination and combination
apraxia of speech site of lesion and neuromotor basis
left (dominant) hemisphere and motor programming
flaccid dysarthria symptoms
reduced ability to move – small, weak movements (paralysis vs. paresis), hypotonia, diminished reflexes, atrophy, fasciculation, fibrillations, fatigue (rapid weakening followed by recovery)
spastic dysarthria symptoms
resistance to passive stretch, weakness, loss of skilled movements, increased tone, increased reflexes, dysphagia, drooling, facial expression reduced, pathological laughing and crying
ataxic dysarthria symptoms
errors of force, speed, timing, and range of movements translate into difficulty with coordination of movement, dysprosody, irregular articulation errors, stumbling over words, prolonged phonemes
hypokinetic dysarthria symptoms
decreased mobility or range of movement, indistinct articulation and difficulty initiating movements, reduced pitch and loudness, lack of emotional prosody, faster and increasing speech rate, rigidity ‘cogwheel,’ bradykinesia (slow), akineasia (lack of involuntary movement), loss of postural reflexes
hyperkinetic dysarthria symptoms
abnormal, rhythmic, or irregular and unpredictable (rapid or slow) involuntary movements, extra involuntary movements of all speech subsystems of speech, uncontrolled variable rate and volume, excess loudness variation, sudden forced inspiration/expiration, transient breathiness
UUMN dysarthria symptoms
symptoms and perceptual characteristics are not well defined, contralateral impairments of fine, skilled movements, atypical/increased reflexes
mixed dysarthria symptoms
any combination of 2+ dysarthria types due to neurologic disease distributed across 2+ dimensions of the nervous system
apraxia of speech symptoms
impaired capacity to plan and/or program sensorimotor commands for the positioning and movement of speech muscles, effortful trial-and-error groping with attempts at self correction, frequent and variable articulatory errors that increase with complexity of speech targets, automatic and reactive speech is better than volitional speech
how do we assess and categorize motor speech disorders?
age and type onset, course, or progression; site and severity of damage or lesion; perceptual, acoustic, or physiologic characteristics; and speech production tasks
chiari malformation
displacement of cerebellum through foramen magnum
bell’s palsy
disease of CN VII, unilateral, sudden onset and temporary, viral/autoimmune/viral/allergic response
what are the phrenic nerves and what do they control?
nerves involved in respiration are spread from the cervical through thoracic divisions of the spinal cord + injuries above C3 can result in respiratory paralysis
how does a lesion in the final common pathway (lower motorneuron) lead to flaccid dysarthria
cuts off the direct nerve impulses from the brainstem/spinal cord to the speech muscles, leading to failure of muscle contraction + this damage disrupts the final motor units, resulting in profound muscular weakness, loss of muscle tone (flaccidity), and reduced speed, range, and accuracy of articulatory movements
what is the pattern of lesion associated with UUMN dysarthria?
unilateral, focal injury within the upper motor neuron system (redundancy assures everything is not ‘wiped out’)
corticobulbar pathway
motor cortex, through internal capsule, pes pedunculi, cross the midline in the brainstem, synapse on LMN
corticospinal pathway
similar path but cross in the pyramids of the medulla
what patterns result from a lesion to the UMN systems?
UMN lesions cause weakness (paresis), spasticity, and hyperreflexia from a loss in inhibitory control over reflex arcs
ataxia definition
a neurological lack of muscle coordination and control caused by damage to the brain (usually the cerebellum), nerves, or spinal cord
how does the cerebelum modulate speech movement and why does damage to a cerebellar hemisphere affects the ipsilateral side of the body?
the cerebellum modulates speech by acting as a predictive, feedforward controller that refines the timing, force, and sequencing of muscular movements to produce fluid, rapid articulation + it corrects errors between intended and actual movement, preventing slurred or jerky speech (dysarthria) + damage causes ipsilateral effects because the cerebellum receives input and sends output to the same side of the body via double-crossing pathways (first crossing down from the motor cortex, then crossing back within the cerebellar tracts)
what are the major conditions/diseases that lead to ataxic dysarthria?
spinocerebellar ataxia, multiple sclerosis, vascular disorder, and tumors
what are non-speech/associated signs of cerebellar damage?
hypotonia, slow voluntary movements, jerky movements, wide-based gait, impairments of equilibrium, intention tremor, terminal tremor, truncal titubation, dysmetria
what are the major speech characteristics that define ataxic dysarthria?
incoordination of speech movements, leading to a "drunken," slurred, or irregular speech pattern + the core deficit is in the timing, force, and range of movement
what are the major inputs and outputs of basal ganglia?
major inputs come from the cortex and substantia nigra to the striatum, while outputs, largely inhibitory, project from the internal pallidum (GPi) and substantia nigra pars reticulata (SNr) to the thalamus
what are the major features of parkinson’s disease?
hypokinesia, postural instability, tremor, rigidity, bradykinesia, sensory impairment, dysarthria, dysphagia, cognitive deficits, depression, gait disturbances
what are non-speech findings associated with hypokinetic dysarthria?
face (unblinking, unsmiling, masked, expressionless at rest, lack of animation), swallow infrequently and drooling, dysphagia in 40-80%
dyskinesia defintion
abnormal, involuntary movements, regardless of etiology
dystonia definition
slow hyperkinesia characterized by involuntary abnormal postures resulting from excessive co-contraction of antagonistic muscles
hyperkinesia definition
excessive, bigger movement
hypokinesia definition
small movement
akinesia definition
inner sense of restlessness but lack of movement/freezing, difficulty initiating movement
chorea definition
‘dance’-like purposeless, unpredictable movement
athetosis definition
inability to maintain a body part in a single position because of superimposed slow, writhing, purposeless movements that tend to flow into one another
ballism definition
gross, abrupt contractions of axial/proximal muscles of extremities that produce flailing
tremor definition
regular, rhythmic (4-7 Hz), periodic movement of a body part
tic definition
involuntary complex movements; rapid, stereotyped coordinated or patterned movements that are under partial voluntary control
myoclonus definition
involuntary single or repetitive brief jerks of a body part (rhythmic or non-rhythmic)
spasm defintion
general term that designates a variety of muscle contractions
what are the major presenting/distinguishing signs of hyperkinetic dysarthria?
abnormal, rhythmic, or irregular and unpredictable (rapid or slow) involuntary movements, extra involuntary movements of all speech subsystems of speech, uncontrolled and variable rate and volume, excess loudness variation, sudden forced inspiration/experation, transient breathiness
what type of damage generally causes hyperkinetic dysarthria?
damage to the basal ganglia control circuit in the brain
huntington’s disease
characterized by chorea, dementia + constant jerky movements, including facial movements, restless/fidgety hands
tardive dyskinesia
involuntary, repetitive movements—such as lip smacking, eye blinking, and tongue protrusion—caused by long-term use of dopamine-blocking medications
oromandibular dystonia
involuntary, forceful muscle spasms in the face, jaw, and tongue, causing difficulties with chewing, swallowing, and speaking