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145 Cards in this Set
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Neuroplasticity |
The ability of the nervous system to form new synaptic connections and reconfigure old connections in response to experience or injury.
The ability of the human brain to physically rearrange itself in response to outside stimulus. |
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Recovery requires |
that the brain grow new connections, new synapses, to encode information that has been lost |
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Neurons that fire together, wire together |
When two neurons are active at the same time they will strengthen the connection so that one is activated the other one will tend to be active too |
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Neuroplasticity again |
Different parts of the brain can be "recruited" to take over some of the impaired functions
especially cortical regions that participated when the task got harder |
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Principles of Neuroplasticity |
Repetition Intensity Simultaneity Relatedness Use it or lose it Use it and improve it Timing Attention Emotion Specifity Age Interference |
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Repetition |
sufficient repetition is needed to induce plasticity |
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Intensity |
intense experiences are consolidated in long-term memory |
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Duration |
learning is a process |
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Use it or loose it |
failure to drive a specific brain function can lead to degradation |
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Use it or improve it |
therapy that drives a specific function can improve that function |
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Salience |
therapy must be meaningful or interesting to the client |
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Attention |
neural networks are engaged and oriented to the task |
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Emotion |
pleasant experiences are related well |
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Specificity |
the nature of the therapy dictates the nature of plasticity |
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Age |
younger is better |
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Apraxia of Speech |
neurologic speech disorder that reflects an impaired capacity to plan or program sensorimotor commands necessary for directing movements that result in phonetically and prosodically normal speech. It can occur in the absence of physiologic disturbances associated with the dysarthrias and in the absence of disturbance in any component of language |
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Dysarthria |
group of neurogenic speech disorders that reflect abnormalities in the strength, speed, range, steadiness, tone or accuracy of movements required for breathing, phonatory, resonatory, articulatory or prosodic aspects of speech productions of speech productions.
Due to one or more sensorimotor abnormalities which most often includes weakness, spascity, incoordination, involuntary movemens or excessive reduced or variable muscle tone |
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Motor Speech Disorders |
speech disorders resulting from neurologic impairments affecting the planning, programming, control or execution of speech MSDS include the dysarthrias and apraxia of speech |
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Types of NP |
Homologous area adoption Map extension Cross modal reassignment Compensatory masquerade- alternative means of performing function- teach one body part to do the function of another body part |
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Memory |
Is the product of NP results from experience- can be negative or positive memory is stored in patterns of interneuronal connections 100 billion neurons memory foundation requires change in the nervous system |
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neurons 2 or more |
when two or more neurons are simultaneously stimulated neurochemical events are triggered
neurochemical events create long-term enhancement in signal transmission |
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LTP |
long term potentiation improves the postsynaptic cell's sensitivity to signals received from the pre-synaptic cell |
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neurotransmitter molecules |
repeated stimulation hard wiring the brain to have stronger connections |
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PKMzeta |
one molecue appears necessary and sufficient for creating & maintenance of LTP at synapses
studies to target specific enzymes for memories about experiences to erase them for PTSD example
when PKMzeta aggregates in the post-synaptic region, the synapse ends up with about twice as many receptors |
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PKMzeta. what does this mean? |
the next time the sender neurons releases a neurotransmitter, the receiver neuron will have a stronger, larger electrochemical response |
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Memory formation |
cascading of events all these things happen Stimulation chemical changes L-T potentiation increased receptors dendric aborization
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regeneration |
growing more dendrites, increasing the strength and in some cases regenerating |
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Spontaneous recovery |
is usally from the time the stroke happens to about one year after the stroke. it doesn't matter if the brain receives therapy or not the brain will get better.
patients who receive tx earlier have better outcomes than patients who don't receive tx |
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Cognitive stimulation |
is essential to positive NP brain areas for various functions decrease or increase according to their use
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Simultaneity |
when two things happen, simultaneously, they become linked "what you practice is what you get" "neurons that fire together wire together" |
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Relatedness |
concepts, events, words that are linked in the brain Semantic feature analysis (mapping) context makes all the difference in the world word finding- |
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Attention |
The tool that triggers NP Attention is a function of reward & punishment reward-- attention-- memory |
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repetition |
sufficient repetition is needed to stimulate NP -- family members and provide opportunities for hw with more repetitions the connections between the sending and receiving neurons strengthens in some instances memorization is critical |
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intensity |
intense experience is needed for significant brain organization to occur intense enough that the patient notices it and it changes the way the brain reorganizes
it has to be intense enough the client needs enough stimulation to make a difference |
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Specificity |
types of training dictates the nature of the plasticity the type of training decides how the brain reorganzes |
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representation areas |
in the CNS for various functions (motor, language etc) increase or decrease according to their use |
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Emotion |
modulates the strength of memory consolidation
emotional arousal- increase neural excitation; stimulates consolidation of new with old learning |
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emotional state |
influences therapy outcome depression adversely affects learning fear interferes with retrieval positive emotional state enhances learning |
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learning is |
very affective (facial expression, over laid body tone) think of "affect as the channel that cognition is happening inside of" demonstrates your emotion shame is potent and if induced disadvantages performance |
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NP: Age |
plasticity is greater in youth the more you are able to adapt and change- young brains adapt more readily
at birth 2500 synapses age 3- 15,000 (twice that of adults- synaptic pruning) |
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synaptic pruning |
as you age you prune the synapses, the ones that aren't used disappear
appropriate stimulation is very important
aging brain has less synaptogenesis |
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synaptogenesis |
fewer new growth and less cortical information less cortical map reorganization |
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synaptic pruning |
eliminates those neuronal networks less used remaining networks become more interconnected more efficiency for the connections that remain
pay attention to patient strengths |
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use or lose |
failure to engage specific brain functions can cause functional degradation
cause the areas to loose the connections |
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use and improve |
driving a specific brain function enhances the function you can enhance how the brain reorganizes |
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Principles of NP sleep |
memory consolidation (learning) occurs during sleep- sleep is critical to memory enhancement skills learned by repetition improve
memories are stored temporarily in the hippocampus- at night they are put into permanent storage in the hard drive of the neocortex |
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NP principle interference |
learning that occurs in response to one experience can interfere with the acquisition of other behaviors
some compensatory behaviors that develop in the absence of therapy training can impede acquisition of new learning |
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major types of dysarthria |
flaccid spastic ataxic hypokinetic hyperkinetic mixed |
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flaccid dysarthria |
flaccid -- LMN -- weakness the LMN are the cranial nerves that innervate the muscles themselves
when you have damage it's like you've pulled the plug they aren't getting any signal (weak signal) |
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Spastic |
spastic -- bilateral UMN -- spasticity
sounds strained or harsh, weakness, underlying muscle weakness with too much tone
exchange and improve balance of synergy, bilateral upper neuron damage,
the muscles are eventually getting the message but there is interference in the line (static) |
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Ataxic |
ataxic-- cerebellum -- incoordination
staggering gate, disease causes incoordination in speech and walking
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hypokinetic |
hypokinetic -- basal ganglia-- rigidity/ ROM reduced range of motion hypo more common |
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hyperkinetic |
hyperkinetic-- basal ganglia-- involuntary movements
too much movement, involuntary movements excessive movement, tight movements breathiness |
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unilateral UMN |
unilateral UMN -- unilateral UMN-- weakness/ incoordination
unilateral upper motor neuron, usually is mild and gets better |
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mixed |
mixed -- more than one -- more than one
waste basked etiology depends on the disease process & where the brain damage occurs |
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examples of mixed dysarthria |
ALS- mixed dysarthria more than one area of the brain that is damaged |
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major types of MSD: apraxia of speech |
damage to the pre-motor area in the frontal lobe (left hemisphere) results in an impairment to plan the movements for speech the muscles work just fine motor programming problem |
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AOS |
AOS -- Left hemisphere -- motor programming
usually have aphasia and dysarthria |
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cause of spastic dysarthria |
stroke, CP, tumor, trauma, encephalitis |
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flaccid dysarthria |
stroke, CP, tumor, trauma, bell's palsy |
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mixed |
spastic, flaccid dysarthria stroke, trauma, ALS, |
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Motor system: four major functional divisions |
the direct activation pathway the indirect activation pathway the final common pathway the control circuits |
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Direct Activation Pathway (UMN) |
UMN influences consciously, controlled, skilled voluntary
structures corticobulbar tract (cortex to brainstem) corticospinal tract (spinal cord) |
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corticobulbar |
cortex to brainstem |
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corticospinal tract |
spinal cord |
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DAP: pyramidal motor system pathway |
motor cortex: cortical origin for 60% of neurons pre-motor and sensory cortex: cortical origin for the remaining neurons (right in between broca's area) |
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pyrimidal motor system |
axons of the cortical neuron (UMN) pass down to the level of the medulla 90% of these axons will cross over (decussate) in the medullary pyramids axons synapse with a 2nd neuron (LMN) which runs to the muscles |
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after decussate |
after the neurons decussate they become LMN -- run to muscles |
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motor strip |
axons run from the motor strip pass down through the brain to the medulla (inferior, bottom) at the level of the medulla these fibers decussate (cross over)
before the fibers cross they are UMN after they are LMN (1st order, 2nd order) |
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LMN |
the LMN run from the medulla to the muscles Not all fibers cross over 15-20% remain on each side
the cortex has contralateral control over the body
always has some sort of protective mechanism that allows for some retention of function |
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corticobulbar tract |
corticobulbar tract provides innervation for muscles of speech and swallowing runs from the cortex to the brainstem synapses with CN nuclei |
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Internal Capsule |
located between the lenticular and caudate nuclei "bottleneck" fibers into the internal capsule group of myelinated fibers tract that connect the cortex to another part of the CNS |
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DAP 2 main tracts |
corticobulbar internal |
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CSF |
when there is trauma to the brain, it swells the fluid cushions and protects the brain within the skull cavity |
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Official corticobulbar tract |
is comprised of UMNs originates in the motor cortex (lower third) crosses to the opposite side of the brain at various levels of the brainstem (medulla, pons, midbrain) inntervates CN nuclei cortical projections to most CN nuclei is bilateral but corticobulbar projections to some cranial nerve are contralateral |
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Decussation |
upper half of your brain has bilateral innervation the lower half has unilateral contralateral (one side opposite side) travels through the internal capsule |
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Pseudobulbar Palsy |
a bilateral spastic paralysis of the speech musculature results from bilateral involvement of the corticobulbar pathways difficulty controlling facial muscles for delicate and discrete motor control like speech |
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corticospinal tract |
runs from the cortex to the spine provides innervation of the skeletal muscles most fibers begin in the frontal lobe at least 75% decussate at the level of the medulla (pyramidal decussation) |
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Neural pathways of motor control |
Pyramidal motor pathway (direct activation pathway) Extrapyramidal motor pathway (indirect activation pathway) |
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motor strip |
information from the motor strip directly innervates the muscles of speech
at the same time those fibers get input or information from the indirect activation pathways including the basal ganglia |
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basal ganglia |
influences movements that you make damage to the basal ganglia- no paralysis too many movements and have tremors
or too little movements and have rigidity ROM |
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brainstem info |
brainstem info is sent from the cerebellum to the thalamus. all of this is happening in real time, to make movements smooth and continuous |
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movement |
problems with basal ganglia |
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damage to cerebellum |
movement that is ataxic (uncoordinated) |
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Indirect activation pathway |
UMN mediates subconscious, automatic muscle activities including posture, muscle tone, and movement that support and accompany voluntary movement |
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structures of indirect activation pathway |
corticorubrual tracts rubrospinal, reticulospinal, vestibulospinal, and related tracts to relevant cranial nerves |
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Reticular activating system (RAS) |
thalamus hypothalamus basal ganglia (respiration & swallowing)
functional system responsible for arousing the cortex and perhaps for focusing cortical regions to heightened awareness |
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Final common Pathway |
LMN function- stimulates muscle contraction and movement
Structures: cranial nerves spinal nerves lower motor neuron system p. 32 textbook chart |
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cranial nerves |
12 pairs of cranial nerves found in the final common pathway p.19 in textbook chart |
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CN I (0) |
olfactory function: smell location: central hemispheres |
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CN II (0) |
Optic function: vision location: diencephalon |
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CN III (0) |
oculomotor function: eye movement pupil constriction location: midbrain |
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CN IV (T) |
Trochlear function: eye movement location: midbrain |
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CN V (T) |
trigeminal function: jaw movement, face, mouth, jaw sensation location: pons |
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CN VI (A) |
abducens function: eye movement location: pons
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CN VII (F) |
facial function: facial movement, hyoid elevation, stapedius reflex, salivation; lacrimation; taste location: pons |
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CN VIII (A) |
Acoustic ( cochleovestibular) function: hearing, balance location: pons, medulla |
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CN IX (G) |
Glossopharyngeal function: pharyngeal movement; pharynx, and tongue sensation; taste location: medulla |
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CN X (V) |
Vagus function: pharyngeal, palatal and laryngeal movement; pharyngeal sensation; control of visceral organs function: medulla |
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CN XI (A) |
Accessory function: shoulder and neck movement location: medulla, spinal cord |
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CNXII (H) |
hypoglossal function: tongue movement location: medulla |
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CN involved in speech production |
CN V trigeminal CN VII facial CN IX Glossopharyngeal CN X vagus CN XI accessory CN XIi hypoglossal |
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tractus solitarius |
taste for anterior 2/3 tongue, soft palate |
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lesion localization cortical lesion |
lesion of the cortex contralateral symptoms = aphasia, apraxia |
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Control circuits (IAP) |
responsible for integration or coordination of sensory information and activities of direct and indirect activation pathways to control movement |
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control circuits: basal ganglia |
function: plan and program postural and supportive components to control movements |
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Structures involved (control circuits) |
basal ganglia substantia nigra (dopamine) subthalamic nucleus cerebral cortex
these cell bodies are responsible for the background movement |
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function of basal ganglia |
control of background movement initiation of movement patterns regulation of motor cortical output and muscle tone
cognitive functions with multiple projections to prefrontal lobe
in real time makes your movements non-impaired |
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subcortical lesion |
lesion deeper in the brain |
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indirect activation pathway |
(control circuits) sent from cortex to the caudate of BG then down to substantia nigra, back to caudate) then cortex down the DAP to the BS, then all of this is UMN once it leaves the brain stem it's LMN, then muscle innervates the muscle |
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DAP responsible |
are responsible for the big voluntary movements, background control movements not impaired |
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limbic system |
amagydala (fear) hippocampus (memory) |
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fibers down the brainstem |
all fibers come down the brainstem (UMN) then once they decussate at the level of the medulla they become LMN |
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control circuit: cerebellar |
function: integrates and coordinates execution of smooth, directed movements
structures: cerebellum (back of brain) cerebellar peduncles reticular formation red nucleus, pontine nuclei, olive, thalamus, cerebral cortex |
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damage to the cerebellum |
ataxia (coordination) |
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a closer look at cerebellum |
coordinates all relevant input and output systems during movement
most relevant types of movements 1. rapid 2. alternating 3. sequential |
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cerebellar feedback |
if an error is found, the cerebellum can speed up, slow down, or stop the movement at any time via feedback (corrective information)
cerebellum provides REAL TIME feedback, correcting as you go
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ascending feedback |
modifications for muscle preparation is sent to the cortex |
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descending feedback |
regulates and adjusts muscle tone |
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cerebellum contributions |
muscle synergy- coordination and smootheness in ongoing movement muscle tone movement range velocity strength maintenance of body equilibrium |
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innervation of the cerebellum |
the cerebellum must provide extremely fast feedback from incoming signals
cerebellum is connected to the ipsilateral (same) side of the cortex
if a lesion occurs in the cerebellum, the side of the body affected will be the same side
lesion often results in tremors |
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afferent |
sensory (to the brain) |
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efferent |
motor (exiting the brain) |
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direct |
corticobulbar (brain to brainstem, motor strip to cranial nerves) & corticospinal pyrimidal direct activation |
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indirect |
makes movement normal reticular formation, the basal ganglia, extra pyrimidal (thalamus, cerebellum, BG, motor strip) |
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movement |
every movement we make requires collaboration between the direct AND indirect pathways,
can't have one without the other
all UMN |
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flaccid dysarthria |
LMN LMN present with flaccid dysarthria weakness |
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spasticity |
weakness and high tone bilateral UMN
somewhere affecting the pathways damage to direct and indirect pathways |
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unilateral UMN |
weakness in one quadrant very mild speech impairment |
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patient has spasticity |
not just the face it's also pharyngeal and laryngeal muscles, bilateral innervation |
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bilateral innervation |
also contributes to the problems, spasticity and weakness that contribute to both side of the face (bilateral damage) SPASTICITY |
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LMN |
weakness |
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cerebellum |
indirect activation pathway see in coordination in their speech (more than just corticobulbar, usually corticospinal) - usually their whole body not just head and neck |
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basal ganglia |
rigidity/ reduced ROM or too much movement and have tremor |
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hypokinetic dysarthria |
very little movement of their face reduced ROM/ rigidity damage to BG |
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left hemisphere |
damage to your left hemisphere fibers in the left hemisphere (LH stroke)
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UMN damage |
can result in potentially lower quadrant right side face damage (bad signal) |
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Cerebral Palsy |
causes damage to both sides L&R hemisphere bilateral spasticity (don't get anything) |
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fibers that cross over |
85-90% of fibers from each side cross over 10-15% do not decussate
they all have to go through the medulla but don't cross |
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ALS |
LMN you can have mixed UMN and LMN damage all over muscle weakness (de-myelinating disease) |
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damage to the UMN lesion |
representing the brainstem fibers decussate- it is innervating lower and upper quadrants to the face
only causing damage to the lower quadrant from the ipsilateral side
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UMN damage |
is damage to the lower quadrant the top half also has innervation to the opposite side |
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Brain stem |
crosses over the fibers (no information to the side) final common pathway, have converged and then you cut it |
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contralateral lower quadrant weakness |
usually first clinical sign of voice, fluency problem |
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damage to RF |
going to result in lower consciousness, less control, heightened awareness or arousal
being conscious enough to be able to produce speech and respiration |
