Flashcards
neuro
Cards in this deck (198)
- 1What are the processes that underpin brain development in the embryo.EARLY:
Embryonic nervous system is established
Formation of major brain regions
Generation of neurons from undifferentiated cells (stem cells)
Migration of neurons from sites of generation to final positions
Subsequent formation of axon pathways and synaptic connections. - 2Outline the formation of the nervous system in the embryo.Embryonic processes of gastrulation: generation of layers of cells from the initial single layer to define the ultimate axes of development, including the central longitudinal fold that becomes the notochord
Then neurulation: the ectoderm above the notochord give rise to the entire nervous system (neuroectoderm) neural plate neural tube brain, spinal cord and most of the peripheral nervous system.
Precursor cells, also known as stem cells, give rise to neurons, astrocytes and oligodendroglia - 3What are the 4 stages of neural development?1 Neurogenesis = proliferation of neural cells
2 Cell migration follows to establish distinct cell populations
3 Next stage is full cell differentiation relative to region and gene expression
4 Along with process outgrowth – extensive growth of axons and dendrites and proliferation of synapses - 4Understand the results of abnormal development in several key syndromes of pathological presentationsVariety of
Congenital neurological syndromes
(Spina bifida (failure of neural tube to close completely)
Anencephaly (failure of anterior tube to close at all)
Fetal alcohol syndrome, exposure to other drugs early in pregnancy
Hydrocephalus – some forms related to irregular formation of ventricles
Fragile X syndrome – common reason for mental retardation, genetic problem resulting in irregular formation of dendrites and synapses
Downs syndrome – another genetic anomaly
Developmental disorders
Neurotrophic dysfunction in the adult CNS may underlie degenerative pathologies like Alzheimers and Parkinsons disease. - 5Understand the basis for modification post-natally.The modification of neural circuits is what underpins the variation between people in terms of personality, ability and behaviour.
Brought about by genetic and environmental influences - experience
Activity-mediated influence is greatest for some processes during “critical periods” – temporal windows - when change is more likely
For other functions the possibility for modification remains throughout life – (neuroplasticity) - 6Give examples of critical periods and another process of neural modificationExamples of critical periods may include development of vision in early childhood, language, aspects of dexterity.
Relies on neurotransmitter activity, receptor sensitivity etc
So some functions are difficult to change after this period
another process of neural modification is through changing the ratio of grey and white matter- increasing myelination into late teens and early twenties- partly explains behavioural stereotypes - 7Describe human development broadlythe product of changing relations between the developing person and his/her changing multi-level environmental contexts.
A person is a self-organizing unit consisting of several systems:-
Neurological, musculoskeletal, cognitive, environment - 8Definition of development?Process of change in the individual’s level of functioning across the entire lifespan
- 9define hereditary?23 Pairs of chromosomes carry 1000’s of genes that influence our characteristics e.g. muscle fibre type, hair color, eye color, personality, body build……..
Genotype –genetic material of chromosomes & gene locations
Phenotype - what we see externally - 10Define epigenetics...the study of changes in organisms caused by modification of gene expression rather than alteration of the genetic code itself.
Social, psychological & environmental factors operating in early life could impact on short and long-term health outcomes e.g. diabetes, lung disease & depression
Gene expression (DNA methylation) can be modified in response to environmental cues
Changes in gene expression can be transferred across generations. - 11Define growth:Refers to a change in quantity - an increase in body size
Growth is not linear across all body segments
Body proportions vary with age
Genetics and the environment are important - 12Definitions: MATURATIONDevelopmental changes determined largely by biology as they occur in all individuals relatively independently of their differing experiences.
- 13Definitions: MOTOR BEHAVIORIs the movement expression of the human body determined by physical size, neurological and physiological functioning, information processing abilities and self-organizing properties
- 14Definitions: MOTOR DEVELOPMENTthe changes in motor behavior over the lifespan and the processes which underlie these changes
encapsulates both the product and the process of motor development - 15what are the anatomical (2) and functional divisions of the nervous system (4)?ANATOMICAL
The central nervous system (CNS) - brain + spinal cord which processes and coordinates (sensory information, motor commands, higher functions of the brain)
The peripheral nervous system (PNS) - (cranial, spinal and peripheral nerves, ganglia, sensory receptors, delivers sensory info to the CNS, carries motor commands from CNS to peripheral tissue and organs)
Functional Divisions
Afferent Division (incoming) - carries sensory information from PNS to CNS
Efferent (outgoing)- carries motor commands from CNS to PNS muscles and glands
Somatic Nervous system (SNS)- voluntary and involuntary muscle contraction (i.e reflexes)
The autonomic nervous system (ANS) - subconscious contractions of smooth and cardiac muscles + glandular secretions
ANS- can be divided into parasympathetic and sympathetic - 16Describe the structural components of neurons and how they are structurally classifiedCell body (soma)
long single axon
axon terminals
synapse
Structural classification -
Anaxonic neurons ( found in brain and sense organs)
Bipolar neurons (special sense organs i.e eye sight)
Unipolar neurons (found in sensory neurons of pns)
multipolar neurons ( CNS, skeletal muscle mtor neurons) - 17What are the functional classification of neurons?Sensory neurons
(afferent neurons of PNS, deliver info from sensory to CNS, somatic sensory neurons monitor outside conditions, visceral sensory neurons monitor the bodies interior, sensory receptors intero (inside), extero (outside) and proprioception (position and movement)
Motor Neurons
efferent neurons to PNS, deliver information from CNS to perihperal effectors, somatic motor neurons innervate skeletal muscle, viceral motor neurons innervate other effectors (i.e smooth muscle)
Interneurons
association neurons - 18Which part of a neuron is associated with nerve impulses and neurotransmitter release?Axon and axon terminal
- 19What are the various types and function of neuroglia in the CNS?Function- support function of neurons by preserving the physical and biochemical structure of neural tissue
Neuroglia of CNS
Ependymal cells (form epithelium called ependyma, line central canal of the spinal cord and brain ventricles, secrete CSF, have cilia and microvilli that circulate CSF, monitor CSF, contain stem cells for repair)
Astrocytes - (large cell bodies, maintain BBB (isolates CSF), repair damaged neural tissue, contain interstitual environment, guide neuron development)
Oligodendrocytes- wrap around axons to form myelin sheath - 20What are the neuroglia of the PNS?Microglia (smallest and least numerous, migrate through neural tissue and clean up cellular debris, waste products and pathogens.
Satellite cells - (regulate environment around the neurons - like astrocytes)
Shwann cells - form myelin sheaths around periheral neurons - 21Why are brain tumours more likely to be formed from glial cells than neurons ?Neuroglia retain, under certain conditions, the capability to divide mitotically. In fact, uncontrolled proliferation of glial cells is the most common cause of brain tumors.
- 22Explain how resting potential is created and maintained ...A charge difference is maintained across the plasma membrane of -70mv.
The plasma membrane is selectively permeable allowing movement of ions through channels. (i.e K+ and Na+)
passive channels ( always open - leak)
Active channels (open and close in response to stimuli, at resting potential most gated channels are closed)
note- the transmembrane potential is the electrical potential of the cells interior relative to its surroundings. - 23Describe how electrical signals are generated in the nervous system. Graded potential : Action potential:Graded potentials only stimulate weak signals over a short period.
can arise from stimulation of sensory receptors or via neurotransmitters (postsynaptic potential)
carry messaged along the axon- all or none principle. Propagated changes in transmembrane potential. If a stimulus reaches threshold an AP is always triggered.
(1) summation of graded potentials reaches threshold -60mv
(2) Na+ ions rush into the cytoplasm, rapid membrane depolarisation (becomes less negative), inner mebrane changes from negative to postive +30mv
(3) Inactivation of Na+ channels (close), the opening of K+ an+d repolarisation begins (returns to negative charge)
(4) k+ channels are slow to close, both high (NA+ and K+ outside cell)-
cell interior to negative restored by the NA/K+ ATPase pump
4 phases - (resting, depolarization, repolarisation, hyperpolarisation) - 24What is a refractory period?the point at which the cell membrane will not respond to any additional stimuli
Absolute refractory period (Na channels open or inactivated, no action potential possible)
Relative refractory period - membrane potential almost normal, very large stimulus can initiate an AP - 25What is a signal propagation?The mechanism to move the action potential along the axon.
Continuous propagation - Unmyelinated axons, one segment at a time, AP arrives in one direction.
Saltatory propagation (leapfrog) - myelinated axons, faster and uses less energy, myelin prevents continuous propagation, depolarization occurs at nodes)
myelin increases the speed of AP, the diameter of neuron also affects speed.
(type A- myelinated and large) = faster
Type B (myelinated smaller diameter)= medium
Type C - unmyelinated small diameter = slow - 26What are the mechanisms of communication between neurons? (2)Electric or chemical communication
Chemical synapse- (most abundant ) message transfer begins, neurotransmitter stored in synaptic vesicles, synaptic vesicles deliver content into the synaptic cleft by exocytosis, synaptic vesicles reform by endocytosis.
Post synatic neuron ( can receive signal from multple presynaptic neruons )
Electrical synapse - Located in CNS and PNS
direct physical contact at gap junctions, ions move between cells through gap junctions.
Held in position by connexons. - 27how is a stimulus transmitted across a synapseAction potential arrives at the terminal
voltage-gated ion channels open increasing intracellular ca2+
synaptic vessels fuse with membrane and neurotransmitter is released into the synaptic cleft
neurtransmitters diffuse to postsynaptic terminal - 28Understand that the postsynaptic response dictates whether the message is passed on or not.Depends on the postsynaptic potential
-inhibitory
-excitatory
Modified by a number of factors
- types of neurotransmitters
-pharmacology
-the response of the postsynaptic receptors - 29What is the difference between ESPs and ISPsExcitatory potentials - depolarize postsynaptic membrane bringing it closer to firing threshold - 60mv
Inhibitory potentials- hyperpolarises post synapic membrane moving further away from firing threshold -90 - 30what are the stages of the lifespan? (8)Prenatal ( conception to birth)
Infancy ( birth to 2 years)
early childhood (2-6 years)
middle and late childhood (6-12)
adolescence (12-20)
young adulthood (20-40)
middle adulthood (40-60)
older adulthood (60+) - 31What are the two significant stages of prenatal development?embryonic (up to 8 weeks)
foetal ( 8 weeks to birth/40wks) - 32Infancy (birth to 2 years) is a vital time for the beginnings of what?sensori motor
cognitive
communicative
social and emotional behaviours
extensive dependence of adults - 33Early childhood (2-6 years) is a time when the child builds independence and starts attending kindergarten and childcare. This is an essential time for the,,,,,Acquisition of a wide range of gross and fine motor skills through experience.
- 34What key things occur in later childhood (6-12) years.A plateau of physical growth
FMS are refined
thought processes are more concrete than adolescence
minimal gender difference in characteristics - 35Rapid changes occur in the adolescence period of the life span (12-20 years). What are they?secondary sexual characteristics (height and weight)
establishment of identity and independence
abstract thought increases - 36What are the 4 stages of Bowlby's ethological theory of attachment?Infants emotional tie to the caregiver as an evolved response that promotes survival.
Pre-attachment - (0-6 weeks)
attachment in the making ( 6w - 6-8mnths)
clear cut attachment (6-8 months - 18 - 24 months)
Formation of a reciprocal relationship (18-24 mnths) - 37What are the impacts of attachment on later deveopment?At 4-5 yrs old securely attached babies had higher self-esteem, social skills and empathy.
at age 11 = better social skills
disorganised/disorientated attachment causes internalising problems like fear and anxiety or externalising problems such as anger and aggression - 38What are 3 factors that might effect attachment?Opportunities for attachment (disrupted formation of neural structures)
quality of caregiving (responding promptly, consistently and appropriately to infant----not routinely or resentful/rejecting ) i.e postnatal depression
infant characteristics - no direct relationship with children with the spec needs (issues with parenting skills) - 39when looking at motor development what are key concepts to remember?nature and nurture are linked
caregiving environment and appropriate stimulation are critical
periods in development but humans are resilient
age-related decline occurs but there is great heterogeneity & there are things we can do to help. - 40Define motor learning.. Why is it important?Study of the acquisition/ and or modification of movement
Is important for recovery of function and the acquisition or reacquisition of skills lost through injury - 41What are the three forms of learning and explain...Non-associative - occurs when given a single stimulus repeatedly
Habituation - decrease in responsiveness
Sensitisation - increase in responsiveness
Sensory learning - the exploration of perceptual space
Associative learning ( classical and operant conditioning)
Classical (learning to pair to stimuli)
Operant ( trial and error learning)
Procedural and declarative learning
procural - Can be performed without attention, develops slowly through repetition, leads to automaticity
Declarative learning - results in knowledge that can continuously be recalled - requires attention and reflection - 42What are the three theories of motor learning?closed loop processing - sensory feedback used for the ongoing production of movement, compared with stored memory
open loop- generalised motor program concept
search strategies to increase coordination between perception and action - 43what are 3 possible stages of motor learning?Cognitive- associative- autonomous
(relate to decreasing attentional demands and increasing automaticity)
Novice - advanced - expert
(relate to learning to control degrees of freedom - decreasing effort and increasing (efficiency/adaptability/coordination)
First stage - the second stage
The initially understanding goal, develop strategies and fix to refine movement) - 44How are MRI images produced?Radiowaves redirect alignment of H+ atoms. As H+ atoms return to their usual position they emit energy that is detected by the scanner and processed by the computer to generate images in thin slices that can be used to create a 3d image. Note- magnetic resonance field bypasses electrical current through the wire coil.
- 45What are the strengths and limitation of MRI? Clinical uses?Strengths - clear, detailed x sectional image, differentiation of soft tissues, does not use radiation, painless, non-invasive, avoids the need for biopsies and surgery, no known side effects & many different angles.
Limitations- claustrophobia, sedation, anxiety, no use with cardiac defibrillators, pacemakers, implants, allergies, loud, expensive, results longer than a CT, 20 - 90 mins.
very broad, look at soft tissue structures, diagnose lesions and tumours, bone and joint abnormalities can detect MS, neuromotor diseases, bony erosion + soft tissue disorders. - 46How are FMRI images produced?Same MRI machine. The difference in oxygenated and deoxygenated haemoglobin is detected in the MRI signal giving an indication of brain activity that is then time linked to specific functions being performed by the person being scanned. Builds up a picture of brain activation in regions relative to the task
- 47What are the advantages and limitations of FMRI Clinical uses?non-invasive, no radiation, safe, excellent spatial resolution, reasonable temporal resolution, no contrast needed, good for deep subcortical structures, high-resolution real-time info regarding brain function.
similar limitations to MRIdrugs and brain pathology may confound, requires complex numerical analysis following testing, expensive, not fully understood.
map functional areas of the brain. Monitor neurological changes in the brain (i.e Alzheimers, depression, tumours), test the success of drugs, investigate brain recovery. - 48How is EEG produced? ElectroencephalographySmall electrodes on the scalp measure, amplify and record nerve electrical signals giving an indication of brain activity in real time. These electrical signals form patterns of synchronised oscillations (movement back and forth) that have characteristic frequency ranges (brain waves)
- 49Strengths limitations and clinical implications of EEG? Electroencephalographyinexpensive, non-invasive, simple to operate, measures rhythmic activity of neurons, records spontaneous brain activity, silent, high temporal resolution
Hard to pin point where in the brain the activity is coming from, skin irritation, influenced by state of alertness, drugs, hypoglycaemia, less sensitive to smaller/ deeper lesions in the brain, prep time can be consuming.
used to monitor & diagnose neurological/ cerebral function and disorders. (Alzheimers, seizure types, sleep disorders, brain death, coma, strokes and states of altered consciousness) - 50How are CAT scan images produced? (computerised axial tomography)Provides information about brain structure. Numerous X-ray beams and a set of electronic detectors rotate around the patient measuring the amount of radiation being absorbed from the body. Data is processed by a computer to create 2D cross-sectional images and then creates a 3D image. Contrast dyes may be used to show brain vascular structures.
- 51strengths limitations clinical uses CAT Computerised axial tomographyAccurate, fast, scan large parts in seconds, can be used in critically ill patients, children and old people, the technique can be altered to reduce radiation. Views shape, size, density and texture of many different body structures. Reduces need for biopsies and surgery, painless, non-invasive and implanted medical devices can be present.
radiation higher than standard x ray, allergies, a person needs to be still so possible sedation, need to hold breath for chest imaging, the contrast material can cause nausea. minor abnormalities may be picked up and misinterpreted
Wide range of disease or disorders, rapidly identifies cancer, vascular diseases ( embolus, aneurysm, infarcts), diagnosis of spinal problems and other skeletal abnormalities
Good for chest abdomen and pelvis.
Guides biopsies and surgeries, plan radiation therapy, plan surgical reassessment, measure BMD, the precise staging of conditions. - 52How are EP (evoked potentials) images produced?Recording electrodes are placed onto the scalp. Apply a stimulus to the peripheral receptor (eyes/skin/ears) and record the electrical impulse of the brain response. Must seperate event-related activity from background activity. Early waves represent sensory processing, later waves represent the processing/subsequent psychological state.
VEP- Initiated by brief visual stimuli with electrodes placed over the occiput.
SEP- (somatosensory) - electrical stimulation is applied over the skin (over the trajectory of PN) usually in the arm or leg.
AEP- clicking sounds to the ear
MEP- made by stimulating the brain to produce neuro-electrical signals which are motor evoked potentials. - 53what are the strengths, limitations and clinical implications of EP'sCheaper than MRI with quicker results. Non-invaseive, cost-effective
VEP- initiated by brief visual pathways - good for optic nerve function/lesions
SEPS- localising sensory abnormalities, monitor peripheral nerve injuries, detect CNS lesions
AEPS- measures the integrity of auditory pathways, hearing loss, identify patients who may benefit from hearing aids, acoustic neuromas.
MEPS- Quick method for testing the integrity of motor pathways. used for intraoperative monitoring, and prognostic purposes post stroke. - 54What does the term motor control mean?Ability to regulate or direct the mechanisms essential to movement
Understanding the nature of the movement
necessary because movement underpins life - 55How does motor control relate to different levels of the CNS ; Different systems in the NS 1, Brainstem level 2, cerebellar levelThe brainstem receives information coming from the spinal cord and also sends information back down through the spinal cord to influence motor neuron activity.
Important for postural adjustments and basic gait
included vestibulospinal tracts, tectospinal tracts and reticulospinal tracts
2, the cerebellum (co-ordination) receives input from the spinal cord and (gets feedback about movements) and input from the motor cortex (i.e information on the planning of movements)
contributes to the planning of movement timing, sequencing and grading as well as modulates (i.e simple adaptation through to complex motor learning)
adjusts motor responses by comparing the intended output with the sensory signals and can update movement plans if they deviate from the intended path - 56. cortical level and basal gangliainput via the thalamus which also processes from the spinal cord, cerebellum and brainstem and also from associated areas of the cortex (S1)
Basal ganglia contribute to goal-directed behaviour and planning - (control of voluntary movement)
Premotor and motor areas (M1) recognise the need for movement, identify targets, choose a course of action and select a programme or plan
Premotor cortex - prepare for movement
Motor cortex - control execution of movement - 57how motor control relates to individuals at a behavioural level and in relation to the task we are doing and in what environment. MC at a behavioural levelmovement emerges from the interaction of 3 elements:
-Task
-environment
-individual
Each of these three elements have factors that constrain (influence or shape) movement - 58Classify tasks by attributesdiscrete (beginning & end) vs continuous
stability (bos doesn't change) vs mobility tasks
manipulation continuum (dextrous changing i.e threading a needle)
attention continuum - (cognitive aspect multitasking requires attetion)
open (task conditions change all the time) vs closed tasks (conditions don't change) - 59individual involves 3 factors that contrain/shape movementmovement and ACTION- particular activity and the control of degrees of freedom to produce that action (like walking)
movement and PERCEPTION- integration of sensory information into psychologically meaningful information
movement and COGNITION- (intent or goal) involving attention, planning and problem solving as well as the motivational and emotional aspects that underpin intention - 60And explain the environment component of motor control at a behavioural levelregulatory vs non-regulatory features
need to understand these features to prepare clients for movement (action) in varying environments - 61Define plasticity and neuroplasticityplasticity means the ability to show modification
Neuroplasticity, therefore, is the ability of the nervous system to change and modify
- can include short term changes in the strength and efficiency of synaptic connections through to ...
longer-term structural changes in organisation and numbers of connections among neurons - 62Neuroplasticity can occur at many levels... What are those levels?genetic
within cells (intracellular activity, NT production, biochemical)
between cells (effectiveness, synaptogenesis)
systems and whole brain level (changes in networks, remapping, reorganisation) - 63At a cellular level, what are 3 changes associated with neuroplasticity?regenerative synaptogenesis (injured axons sprout to reinnervate target)
reactive synaptogenesis (collateral sprouting of undamaged neighbours to reinnervate target)
unmasking of silent synapses (previously unused) - 64what changes occur at a network or system level?functional re-organisation - changes in cortical maps
cortical areas routinely adjust the way they process information and retain the ability to develop new functions, particularly in response to sensory input and motor demands
competition between neuronal groups for domination of neurons borders
Competition is use dependant occurs in healthy adults in response to activity, behaviour and skill acquisition. - 65What are the 10 principles of neuroplasticity?use it or lose it -
(Failure to use neural networks or functions can lead to degradation of those functions.
Impoverished environments offer poor stimulation== poor neuroplasticity
use it to improve it
(training or usage can maintain and protect networks and connections. Need opportunities to move sense, perceive and act. drives plasticity)
specificity
the nature of the training dictates the nature of the plasticity. You cant practice the same old thing that you already know (compensation) there has to be newness or skill reacquisition
repetition matters
(To induce plasticity you need sufficent repetitions to make the changes more lasting)
intensity
(need sufficient intensity to make changes last- allows training to adapt and progress according to the persons changing skill level) i.e level of newness, point of challenge
timing matters
different forms of plasticity occur at different times. you need early training for later training to build on - 66Cont'dsalience matters
HAS TO HAVE MEANING- it must be functionally relevant and significant to the person as motivation and engagement increase the likelihood of neural adaptation.
age matters
Synaptic potentiation and reorganisation may diminish with age. However, older people may be more engaged.
transference
interference
One training to induce plasticity may enhance the aquisition of similar skills. However, other experiences may interfere with the aquisition of other behaviours. - 67Understand the different senses involved in movement (motor control) - feedback and feedforwardKinaesthesia (movement sensation) is the sense of movement that uses many receptors such as ..
Located in muscles (GTO - tension & spindles length) - also propriorecptors
Joint receptors (proprioceptors)
cutaneous receptors (skin pressure and friction)
Vision (shifting images, colour, space, size, shape position)
vestibular (movement of the head) - 68Outline a feedforward loop (anticipatory)I.e incoming ball
-sensor detects distant event (i.e eye)
-input processing (filtering amplification)
-feedforward controller (with memory) - remember how to catch a certain type of ball and anticipate
-controller filtering amplification
-actuator (i.e muscle)
-sensor
-input processing
-controler (filtering amplification)
- actuator - muscle - 69outline a feedback loop (updating movement and making it better)Ball is caught
sensor (i.e muscle spindle)
input processing (filtering amplification)
controller- filtering amplification
actuator (muscle) - 70In terms of sensation and movement, proprioception is a key component. Can you explain neuromuscular spindles? body position in time and space?neuromuscular spindles are sensory receptors that detect muscle stretch. they contribute to the myotatic (stretch) very short reflex between agonist and antagonist
*Can be tonic or more dynamic
*Can detect not only length but also velocity (rate of length change) - we can anticipate length change because it detects velocity which changes much quicker than the length and therefore we can predict where the limb will end up
the brain can modify prorioreceptor sensitivity according to data from from the gamma MN's. (each spindle has priming muscles)
This modulation of sensitivity enables adaptation (relative to task and environment) also enable us to anticipate movement.
Joint proprioreceptors (mechanoreceptors i.e capsule and ligaments) are thought to fire at end range. - 71can you explain cutaneous receptors?TOUCH
Tactile sensitivity - receptors in the skin that sense contact with the external world
Meissener and pacinian corpusles detect pressure, others detect variation in pressure or are more sensitive to long duration pressure.
Receptors attached to hairs are sensitive to fricition and stroking via bending of the hairs
thermo receptors - heat/ cold
nociceptors - transmit painful stimuli
those that detect rate and change of (pressure, velocity are capable of anticipation )
sensitivity to tactile information is modulated by context and attention/intention (meaning we can inhibit some senses i.e clothes you wear- we can block that stimulus)
they can detect force but not whether its internally or externally generated - 72explain the somatosensory cortex (SSC or S1) in relation to proprioception and touch Also Secondary SSC or SII1proprioreception and touch information contralaterally in somatotopic distribution is integrated here
similar to S1 bit is bilaterally activated putting the whole picture together and has a higher level of processing and integrating function for afferent information - 73What does a Golgi tendon organ do ?measures change in muscle tension
unclear how this occurs and if in combination with other motor commands and information about velocity and muscle stretch
We do know that we can imagine the force and this influceneces the motor system - 74can you explain the vestibular sensesproprioreceptors can only detect relative movement
the vestibular senses can recognise absolute (whole) movement is space using the forces of inertia.
Semicircular canals detect angular acceleration but can't distinguish between gravity and an acceleration of the same magnitude due to a movement (requires visual input to clarify which)
SSC can detect rotary movement and accel/decel and can anticipate. (e.g if you all they tell you to put your hand's out) - 75In the vestibular system, we have semicircular canals and otoliths. What are there functions and how do they work?Endolymph and hairs - As head accelerates/decelerates, inertia forces cause a lagging motion in the endolymph - therefore are sensitive to angular acceleration or reverse
can detect acceleration of a few tenths of a degree per second per second
Otoliths are also and accelerometer and detects linear translations and direction of gravity (tilting head).
utricle (horizontal) and saccule (verticle) are two cavities with a mass of crystals floating in the endolymph above the hairs arising from the macula. As crystals move back and forward trigger hair cells to discharge firing relative to the magnitude of linear acceleration.
without gravity can still interpret acceleration but not the angle of tilt. - 76the vestibular system and gaze stabilizationvestibular ocular reflex stabilises images of the world on the retina. Connects vestibular system with ocular system ( i.e as head moves to the right eyes move to the left)
- 77VISIONCortical (central) and subcortical (peripheral) vision is unconscious and conscious.
can be illusory
usually results in postural adjustments
intensity can be related to the size of the field in motion, its velocity, the number of detectable elements, their distance and the duration of flow - 78What are the sensory capabilities of a newborn?sensory systems are present before birth and many are highly developed
Types of receptors -
intero/enteroreceptors: sense stimuli from within like BP, thirst and includes proprioreceptors which detect tension in muscle and tendons.
Exteroreceptors: sensory stimuli from environment (i.e light and sound) - 79what are the senses poorly developed at birth? and ones that are well developed?Poorley developed
Vision
tactile (light touch, pressure, temp and pain)
proprioreception
well developed
Hearing
smell (olfactory)
Taste (gustatory)
vestibular
tactile (light touch, pressure, temp and pain) - 80The least developed sensory system in infancy is a vision where there is only some colour at birth. When does visual pursuit occur along with depth perception and acuity???visual pursuit - by 1-2 weeks
depth perception - by 2-3 months
depth perception is the ability to see things in three dimensions (including length, width and depth), and to judge how far away an object is.
acuity-ability to discriminate detail by 6-7 months - 81At what age does a baby make eye contact coupled with limb movements to engage adult ? Holds a rattle and brings it to the visual field? Increase in the density of synapses in visual corrtex rapid to what age?3 months
4-6 months
8 months - 82how does the vestibular system develop in a child?Somewhat developed at birth, mature in teens
SSC in inner ear detects movement (linear and angular acceleration)
important for the development of postural control - 83How does the proprioceptive system develop in a child?Touch and pain well developed but sensors in joints and muscles are poorly developed at birth.
Important for the development of postural control - 84How does the hearing system develop in a child?at birth able to discriminate a wide range of sounds (i.e a baby prefers to listen to a mothers voice instead of a strangers0
The auditory nerve is well myelinated
the auditory cortex is less well developed - 85How does the smell and taste system develop in a child?able to discriminate smlells and and taste at birth
sweet, sour, bitter, salter etc. - 86How does age affect sensation ?general decline in sensation with age.
- reduced number of receptors in periphery
- sloing of conduction velocities
-slowing of perceptual/cognition skills
MAJOR CONTRIBUTOR TO FALLS RISK - 87Boudreu et al. Discuss 3 ways to optimise rehabilitation success in people with musculoskeletal problems using the ideas of neuroplasticity and motor learning. Choose 3 that you can connect with.Quality Vs. Quantity - focusing on technique and quality of learning & skill acquisition rather than quantity
Encourage cognitive effort: Goal orientated and have meaning to the patient. You want them to be interested in rehab to encourage adherence to program and increase the success rate in areas of deficit
Motor Skill training - Can protect against cortical neuroplastic changes associated with pain. A patient with pain may be reluctant to participate in rehabilitation due to the threat of pain and psychological factros. - 88Why is it important for physiotherapists to understand the concept of negative neuroplasticityBecause patients can experience compensatory behaviours (exposed to the same old thing), cortical smudging, chronic pain can increase the risk of hypersensitivity, reorganisation of synapses
Negative neuroplasticity can occur clinically by not supplying an enriched environment and reducing sensory motor stimulation. - 89For postivie adaptations to occur what must happen?ensure the patient stays challenged
increase neurons firing
learning from mistakes and incorporating levels of newness to tasks. - 90What is perception?Making sense of the senses.
What you perceive is constantly shaped by experience, learning, context, environment and tasks.
Much more than simply sensing a stimulus from the outside world.
perceptions shape our experience and experience shape our perceptions
What you expect based on experience - 91What is postural control?Postural control involves controlling the bodies position in space for stability and orientation.
Postural orientation - ability to maintain the relationship between body segments and between the body and task environments
Postural stability: ability to control COM in relationship to the BOS - 92desribe: balance : COM: COP: COM and COP:ability to maintain equilibrium at rest or in motion. Also the ability to maintain COM within the BOS
COM- is the point at the centre of the total body mass
COP: is the centre of distribution of total force applied to the supporting surface
Relationship between COM and COP provides better insight into stability thean either COP or COM alone - 93what are the motor mechanisms to postural control?alignment (all segments must be aligned to form overall COM)
muscle tone
postural tone
muscle synergies (Ant/post)
- ankle, hip, stepping, suspensory strategy
muscle synergies mediolateral
- hip/ trunk> knee/ankle
controlling forward and backward sway
feedback control
feedforward (anticipatory control) - 94Explain multidirectional stability.Continuum of response patterns that control stability in the 360-degree continuum of possible perturbation directions
Ability to balance in all directions - 95What is adapting motor strategies referring to?subjects without neural pathology can shift relatively quickly from one postural movement to another
repeated exposure to a given postural task causes refinement of response to optimize efficiency
postural stability is controlled by the brainstem and cerebellum - 96What are the sensory mechanisms regarding postural control ?Visual - position and motion of head with reference to nearby objects
somatosensory - position and motion of body , with reference to supporting surfaces, includes proprioreception and light touch.
vestibular - position and movement of the head with gravity and inertial forces
All three contribute in centrally integrated ways. ( intermodal, selected and weighted) - 97Somatosensory inputs from the backwards rotation of pelvis trigger postural response synergies in sittingtrue
- 98Infants follow a sequence of motor milestones, but how they achieve skills is quite individual and infants developmental trajectories follow individual pathways. at what age should a baby be ablt to lye in Supine Head in the midline, chin tuck, hands-on chest (symmetry)?2 1/2 - 4 months
- 99Supine Hands to knees (abdominals activated, symmetry) & pull to sit with chin tuck?3- 1/2 - 5 months
- 100Prone Reaching with forearm support?5-7 months
- 101Sitting without hand support Rolling supine to prone (without rotation) Reciprocal crawling (on tummy)6-8 months
5 1/2 - 9 months
7 1/2 to 9 months - 102* Pulls to stand at furniture * 4 point kneel to sit * Controlled lowering from standing * Reciprocal creeping (hands and knees)8- 9 1/2 months
8-10 months
9 - 11 1/2 months
8 1/2- 13 months - 103* Cruising along furniture * Stands alone * Walks * Squats9- 13
10 ½ - 13
11 ½ - 14
12- 15 - 104What should the key achievements be by 4 months?strong head - able to hold head against gravity
midline orientation ( able to keep head in midline, bring hands together, feet together and hands to knees
eye hand coordination - able to track an object with eyes 180 deg, holds objects but not yet reaching and grasping - 105What are the key achievements by 6 months?Strong arms and trunk - grasps feet and puts in mouth, lifts head to anticipate pull to sit, props on extended arms, props in sitting, takes weight in supported standing
weight shift - able to shift weight laterally in prone
eye-hand coordination - reaches and grasps a toy, transfers from one hand to the other, brings to mouth. - 106what are the key achievements by 9 months?sitting - able to sit and play hands free and change BOS
Rolling- rolls from supine to prone and back
crawling- props on hands and knees (commando crawl)
lateral weight shift and rotation
eye-hand coordination - holds and object in each hand, bangs together and takes turns. - 107key acheievements by 9 - 15 monthssitting - able to move in and out of sitting position
crawling- crawls on hands and knees
pulls to stand
cruises - walking along furniture
stands alone and walks
squats
eye hand coordination - uses fine pincer grasp. - 108Understand the way postural control develops in infants and throughout childhood.At birth infants have little ability to control movement against gravity withing a few months they have developed...
head control 3-5m
progress to trunk control 6-8 m
by end of first year- usually develop standing without support - 109developing postural responsesdevelopmentally infants learn to make postural adjustments in response to gravity and to being moved by another= reactive
Also, develop anticipatory strategies as their stability in posture increases
Adaptive last to develop in any particular orientation or posture - 110can you explain reactive responses and anticipatory responses (postural adjustments)reactive - response of the whole body to maintain or restore balance when a force is applied or surface moved
trunk and limbs move in opposing the direction of the force
Anticiaptory - prepare the body for movement or in anticipation of being perturbed. - 111when an infant is able to sit independantly will begin to develop postural control in response to perfection at what age do they develop forward saving responses: sideways: backwards:6 months
8 months
10-12 months
NOTE- once a child can stand they develop stepping strategies
i.e of protective test is parachute response. - 112refinement of postural control 12 months to 7 - 10 years. Body morphology influences PC development.... WHY?children are shorter than adults
body segments are proportioned differently
com in children is approx t12
postural sway is faster in children than adults
static balance is more difficult to achieve in children than in adults - 113How does postural control change in terms of postural sway and reactive responses?Control of spontaneous sway in a quiet state :
The amplitude of sway decreases with age
sway in young children has a variable rate
reach adult levels of spontaneous sway with eyes open at 9-12 years
eyes closed at 12-15 years
reactive responses: compared with adults children have a greater amplitude of sway and take longer to respond (increased latency) and sway for longer - 114changes in postural control factsfindings that responses in 4-6 years of age are slower than those in 15 months - 3 years and 7-10 years.
- 4-6 years may reflect a period of critical dimension changes
- the system in a state of stability
- most likely to be as a result of changes to the nervous system - 115Development of sensory adaptation PC is categorised as the ability to interpret sensory information and apply it to postural actions. KEY FACTSNeed sensory input from vestibular, vision and proprioception
when input reduced then children sway more and may fall
visual cues are the primary input for balance until the age of 3
somatosensory input then predominates but not efficiently until after 6 years of age. - 116Aging and postural control: FALLS are the most common indicators of reducing PC. How and why?often defined as a situation where the person has fallen tp the ground or is found lying on the ground
or as unintended contact with nearby surfaces
may be when the COM moves outside the BOS - 117What are fall risk factors in terms of postural control?usually multiple and can include extrinsic environmental factors as well as intrinsic (physiological, musculoskeletal and psychosocial factors)
greater in women as age, being depressed, or anxious or social isolation
presence of stairs, rugs, slippery surfaces, poor lighting
Reduced PA, reduced strength, arthritis of knees, stroke, impairment of gait, hypotension and certain medications - 118What are some age-related changes in the PC systems?musculoskeletal-
muscle strength
less loss in endurance
max isometric force reduced
more rapid fatigue
slower to generate tension
ranges of motion and loss of flexibility - can lead to stooped posture, forward head, kyphosis, shift in COG down posteriorly
REduced range of motion as a result of degeneration and pain
concentric affected more than eccentric
control systems:
very old and very young may have more difficulty keeping sway minimal
use of strategies may become altered onset latencies delayed.
alterations in the recruitment of strategies (i.e proximal Hip before ankle)
may be different responses because of impairments in other systems.
limitations in adapting
tactile sensation often decreases with age
loss of visual field and reductions in acuity
a decrease in vestibular function - 119Describe the steps and concepts involved in assessing postural control in a generic way... static anticipatory reactive adaptiveAim to perform tasks in a hierarchy of difficulty
identify how much help they need to be safe, quality (how well do they execute postural control) & quantity.
postural control is the bodies way of keeping it safe
PC ASSESSMENT
1. "static" pc - ability to safely maintain posture such as sitting (then standing). Observe alignment and weight distribution.
can be progressed to more difficult by changing BOS (i.e tandem or standing on one leg)
2. 'anticipatory'
(e.g maintaining postural control during known movements such as sitting (then standing) and leaning in all directions, reaching and lifting.
- OBSERVE strategies - motor - (trunk, ankle, hip, stepping etc. ) & sensory (eyes open, eyes closed, head tipped, poor surface etc)
Reactive - test postural conrol in various positions to sudden unexpected nudges or pertebations in different directions - observe strategies - motor and sensory.
Adaptive- Test PC in different environments (usually done later as a progression) e..g corridor, outside, home in community etc. - 120What are some functional tests for PC?Berg Balance scale - 56 point scale, excellent reliability and valid
TUG- timed up and go test- pnt stands up from chair, walks 3 m, turns around and resturns to the chai. Normal is less than 10 sec. - valid pred of falls &quick screen
Functional reach test - examines limits of stability. reliable and valid- norms adjusted for age/gender/height - 121write a summary on atypical postural control...sequencing problems (reversal of orderly recruitment)
delayed activation of postural responses
problems scaling the amplitude of responses (too much or too little)
adaptation problems
alignment issues
change in muscle structure and function, strength
loss of anticipatory control
loss of one sense - 122In terms of managing postural control disorders can you explain intervention at the impairment level? Strategy level-Correct impairments that can be changed (i.e crouch gait, foot orthoses)
- prevent the development of secondary impairment by teaching new postural control
- Strategy level (recover)
- the goal is to help pts recover or develop sensory or motor strategies
alignment- (mirror, flashlight, use of the wall, force plate)
movement stratgies - inlcudie ankle hip and stepping
- anticipatory- sway with flashlights, standing on scales, reaching, lifting tasks
reactive - wobble boards, perturbations
Adaptive strategies- change environment
Strategy level (retrain)
- limit or remove visual input to train vest/somato.
-Change surface of the support
- sensory attention training
- combination of the above to increase difficulty. - 123what does an intervention at a functional level involve?practice tasks requiring postural control in specific ways and in specific environments with a controlled degree of difficulty.
work at level of error safely - 124What are the requirements of human gait? 3 essential :Gait is a complex behaviour
Progression: Ensures body moves through space, as well as start/stop
stability/postural control: Maintain appropriate posture and dynamic stability of moving body
adaptation: to meet the goals and demands of the environment
all achieved with energy efficiency and minimising stress on the body, high level of shock absorbtion. - 125Explain the human gait cycleTwo main phases (stance and swing)
**stance***- force generation must be adaptable to deal with different conditions, speeds, accel & decelerations
- commences when foot strikes the ground and completes when the same foot leaves (60%)
further divided in 5 subphases
swing- advances swinging leg cleanly and reposition to prepare for stance according to environment
further divided into 3 sub phases
accounts for 40% of the cycle (commences as foot leaves the ground and comletes when the same foot strikes - 126what are the 5 sub-phases in stance phase?IC- initial contact
LL- loading response
M-st - mid stance
T -St- terminal stance
ps- pre swing - 127What are the three phases of swing phase?I-sw - initial swing
M-sw - mid swing
T-sw - terminal swing - 128What are the temporal and distance factors of gait?Velocity - metres per second (norm for yound adults is 1.46ms/)
Step length - distance from one foot strike to the next (contralateral) (norm 76.3)
step frequency - (cadence) - number of steps per unit of time (norm 1.9 steps per second)
stride length - distance from strike to next strike of the same foot
step width- distance path of left foot to path of right foot. - 129When we increase velcity by increasing step length and rate (cadence) until length is limit is reached and rate continues to increase. Stance time decreases more than swing. In running what is the ratio as a percent of stance and swing?60% swing
40% stance - 130preferred walking speeds are related to minimize energy expenditure. WHY?lower or higher speeds are less efficient
- 131Explain the kinematics of gaitKinematics- movement of joints and segments of the body through space
the motion of pelvis, hip, knee and foot in frontal, sagittal and transverse planes- a combination of linkages provides elegant efficient coordination
contributes to smooth sinusoidal motion of COM- can then achieve transfer of mechanical energy.
muscles instance act to support/stabilise and propel forward
muscles in swing act to initiate and brake the pendular motion
propulsive force to keep the body in motion
(concentric PF - push off)
assist from knee flexors
COM anterior to supporting foot
activation of extensor muscles during stance. - 132Explain the kinetics of gait.proposed that hip muscles contribute more to PC in gait than in quiet stance due to an increased influence of HAT acting on hips
Joint movement pattern are less variable in swing than instance
in swing early flexor movement in the hip initiates swing.
muscle action and gravity then late extensor moment to slow down flexion motion at end of swing and prepare for heel strike
Shock absorption from :
Hips - lat shift and flexion
knee - flexion
ankle - pronation
Momentum - swing of hip and knee extension
NOTE; efficient gate has little muscle activity - uses momentum - 133what are the control mechanisms of human gait?pattern generators- soinal PG can produce sterotypical locomotor patterns
Descending influences: modulation from the brainstem, cerebellum & from cortex in particular in use of visual input
- spinal preparation
decerebrate preparation
decorticate preparation
higher level influences add increasing ability to adapt gait to environment and task, including feedforward mechanisms
- cerebellum - spinocerebellar tracts (dorsal and ventral)
all sensory systems involved in feedback and gait modulation----- visual, somatosensory, and vestibular both reactively and proactively. requires precise stabilisation of head (telereceptors) - telereceptors?
also non neuronal contributions - biomechanical and environmental factors - 134Sensory feedback and adaptation of gait referring to a, REACTIVE CONTROL b, PROACTIVE CONTROL*reactive control
- somatosensory system (cadence)
-vision (speed, alignment to gravity)
vestibular- (stabilizes head, gaze)
Anticipatory and proactive control
Vision - avoidance, accomodation - 135Gait measurement - how is it done?Laboratory - highly technologically based for EMG, kinematic and kinetic data including space trackers- 2d and 3d. Electro goniometers, force places, o2 consumption (gait efficiency).
clinically - observation
use simple measures of basic temporal and distance measures
footprints, timewalks, lined walks, videotaping, distance measures, obtacles, environmental challenge - 136what is the sequence of developing mobility? Supine to prone prone progression transitions and mobility kneels and pulls to stand upright mobility stands alone walks alone squats to playR
Rolling supine to prone without rotation (5 1/2 - 9 months) - shoulder and pelvis in line lateral head righting
Progresses to rolling with rotation between hips and shoulders ( 6 1/2 - 9 months)
Prone Progression :
Pivoting and reciprocal crawling ( progresses forward using arms and legs- tummy on ground) (71/2 - 9 months)
Transitions and mobility
sitting to 4 point kneel, reciprocal crawling tummy off the ground
Kneels and pulls to stand
first needs tupport to pul up but then is able to dissociate hips
upright mobililty (9-11)
controlled lowering from standing
cruieses furniture
holding with 2 hands to one
stands alone (10-13m)
Walks alone (11 1/2 - 14 mnths)
Squats to play ( 12 15mnths)
walk - 137What are the differences in early gait compared with matured gait? Early Walker: 2 yo: 3-7mature gait by 7 - a child can have the gait pattern but not the PC and will therefore cruise.
wide base
no reciprocal arm swing (high guard)
IC with toes or flat foot
circumduction
extension of knee after IC
2yo
width of base diminises
smoother movements
reciprocal arm swing starts
initial contact with heel
increase step lenfth and velocity
3-7 yo
3- higher cadence , shorter stride length
7- spatial (length and width) and temporal (velocity and cadence) poarameters reach adult values - 138Age related changes to foot position 12 - 18/ 2yrs 2y - 2.5 yrs 2.5 - 3.5 yrs 4- 6 yrs adultsout toe
straighten
intoe
straigten
8deg out toe - 139Age-related changes to step width (spatial) The base gradually narrows due to bony changes combined with with increasing postural control abilities to maintain the centre of gravity over increasingly smaller bos. What is the % of pelvic width at ages 1 3 470%
45%
close to adult values - 140Age related changes to timing 1 7 adult Female adult male0.64 m/s
1.14 m/s
1.30 m/s
1.46m/s - 141What are the physical and biomechanical factors affecting early mobility?physical growth
very rapid growth in the first 12 months
slows from 5 years
ossification:
enchondral: growth in length of epiphyseal plates and membranous growth with is increase in circumference
major percentage of growth comes from shoulder, wrist and knee
types of growth plates-inc: long bone epiphyses (femur), apoptosis (iliac crest), ring epiphysis (tarsal and carpal)
Body proportions :
head to trunk ratio changes from 1:4 (newborn) to 1:7.5 as maturity
infants limbs short compared with trunk - 142The relationship of lower limb segments is also affected by growth. How so? 18m 2 1/2 - 3 1/2 6-7 yvarus (bow legs)
knock knees (valgus)
straight - 143What are the potential effects of ageing on gait and mobilityDecrease speed
stride length
step length
decreased proactive and anticipatory response
a decrease in balance
, lower limb strength
, sensory input (i.e eyes), cognition and attention
decreased progression, stability and adaptability
altered gait patterns
altered velocity
decreased shock absorption
strain on joints and soft tissue
increased energy expenditure
a tendency to fall, trip, collapse & lose balance
to help with abnormal a gait aid or orthoses may be prescribed
can range from elite performers to dependant need for assistance needs to be careful assessment to match the needs of the patient- not one size fits all - 144what are some examples of specific influences of impairments on gait patternsWeak DF: Foot drop
results in foot slap, high step
Cant eccentrically contract gastoc and concentrically contract tib ant.
Weak hip abductors:
results in a contralateral drop of pelvis
i.e glute med - trunk lean, pelvic drop Trendelenburg gait)
spasticity of P- flexors:
results in limited DF at IC - toe contacts first also unable to build tension in push off , decreased velocity
contracture of hip flexors
decrease hip extension, prevent thigh moving forward, increases lumbar lordosis, forward trunk lean, crouch gait
pain
decreased velocity, antalgic gait, short stance on painful limb, decreased force of push off
loss of propriorecepton
stamp feet (hear), ataxic
anxiety and fear
overuse of arms, stay near furniture, lower COG, increase bos, rigid trunk no arm swing, decrease velocity, lacks rythym
cardiopulmonary
reduces speed and endurance, increased fatigue, may see postural adaptations like limited arm swing and trunk rotation and flexed posture - 145What are some specific examples of effect of pathology on gait pattern ?Ataxic gait
Wise bos,in coordinated Limb movement, may beer toward side of lesion, reduced protective stepping , may self limit movements - rigid trunk, decreased arm swing, decreased step and stride length , decreased velocity
Parkinson’s gait - akinesia
Poor gait initiation, generally slow, small shuffling steps, narrow bos, lacks heels strike, flexed posture, rigid trunk , decreased arm swing, may freeze at turns doorways etc.
hemiplegic gait - stroke
Asymmetry , gait pattern one side weakness (hemiparesis) , inability to generate force for push off, decreased velocity, had elbow wrist flexed, toe strike
Cerebral palsy - anoxic episode (deprived 02 to baby brain ) - variable and complex!
Ataxic gait, spastic diplegic gait (maintain hip and knee flexion and hip adduction
. - 146What are the influences of aids and equipment on gait ? Walking aids Prosthesis and orthosesWalking aids
Many reasons ( pain, fatigue, weakness, reduce load on joints, injured part , balance ,safety etc)
Prosthesis for partial foot , below or above knee amputation, hip disarticulation (NO SENSORY FEEDBACK INSENSATE APPARATUS)
AFo assist DF
Knee ankle foot orthosis
Swedish knee cage - prevent knee hyperextension
Calipers - long leg braces
Shoe inserts/modification - 147Can you describe the assessment t of gait in the clinic?SAFETY- can they mobilise independently with or without assistance (must check postural control first)
Establish baseline data and the type of gait abnormality they display
identify factors contributing to functional and gait limitations
monitor progression of change due to intervention / disease processes
quantigfy end clinical result
certain assessment techniques include :
kinematics at individual joint levels
walking on a level surface
within lines
sit to stand and walk
alter speed, directions, turning
change BOS (heel-toe)
manage doorways, obstacles, stairs, curbs, ramps, uneven surface
walk and talk, carry loads
run, jump ball games, cross roads etc. - 148management of gait in the clinic Intervention at impairment level : Intervention at a strategy level:correct impairments that can be changed and prevent secondary changes.
(i.e - range and tone (passive stretches +/- WB, eccentric lengthening, casting, splinting, botox, surgery etc. )
specific strengthening techniques (i.e hip abductors, extensors, ankle DF and PF)
Fitness and endurance
proximal control and balance - (standing, kneeling, half kneeling, supine, side lye, sit on ball etc)
Strategy:
Develop strategies that are effective and efficient in meeting essential requirements of progression, stability and function adaptation.
we often work with stages of gait pattern as part practice. (i,e swng , foot placement, load onto one leg, knee control, arm swint etc.)
Functional level:
Part/ whole practice of gait (task and environment specific)
teaching strategies - cueing
alter attentional demands (conversation, look up look down side ways) - 149why are arms important for everyday function?Vital for nearly all ADLS
coupled with stability/orientation and mobility functions - if we are not stable our hand skills will be less - 150what are the four basic components of arm function?location of the target (=visual regard)
reaching (transportation of the arm/hand in space plus pc)
grasp- grip formation and release
hand manipulation skills (not covered in this lecture) - 151how is movement controlled in upper limbs?feedforward vs feedback
Feedback control
-input from the sensory systems
reference signal
Feedforward (anticipatory) control
previous experience used to predict consequences of sensory input
(anticipates what's going to happen)
occurs before sensors are stimulated. - 152locating a target involves what?eye, hand and trunk coordination
location typically involves eyes moving to get to target in central field, may require head position adjustment or if further in the periphery head, eye and trunk motion
need to train all three components - appear to occur sequentially but are triggered synchronously - 153Can you desribe the kinematics of a, reaching b, graspingFirst- reach and grasp are controlled by different parts of the brain
Kinematics depends on the task, for example, pointing uses all segments of the UL whereas grasping the hand acts independently of other arm segments
Reaching - if reaching for a grasp function, produce a bell-shaped velocity curve and longer duration.
Reaching for pointing or hitting the target is shorter and smaller final deceleration period
When retraining we need to consider - reach and grasp, reach grasp and throw, reach grasp and manipulate
Grasp kinematics
four handshapes: - poke, pinch, clench and palm
Classification of grasping patterns:
precision:
forces directed between thumb and finger
pincer, pulp to pulp, key and lumbrical
POWER:
fingers and thumb directed toward the palm to transmit force to a held object
include:
hook, spherical, cylindrical
-able to anticipate and react to varying weights
-once contact is made grip forces and load force increases
-one load force has overcome the weight of the object, the lifting motion can commence
when lift is completed decrease load and grip force. - 154when does maximum hand opening occur?75- 80 % of the transport phase
reach and grasp must be trained separately and together - 155What is the sequence of events in control of UL function?-sesnory inputs - i.e where you are in space
-visual input (2 parallel pathways 1 for perception and object recognition (temp cortex) 1 localisation and action systems (parietal)
-higher centres make a plan for the input relative to the goal, the goal becomes refined
-the plan sent to motor cortex and muscle groups are selected
-the updated plan sent from cerebellum tomotor cortex and brainstem
- from there visa descending pathways to spinal cord .
any unexpected parameters in the target object are detected by spindles and spinal reflex pathways
sensory consequences are evaluated and updated by the cerebellum - 156Quick facts about UL secsequence sensory and motorVISUAL CONTRIBUTION
visual feedback not used much for grasp but is for reaching
visual processing is harder if target/ action is in the contralateral field (crossing midline)
reaching and manipulation is slower in contralateral field
SOMATOSENSORY CONTRIBUTION
can compensate for lack of somatosensory input using vision
somatosensory seems to be most important for learning new reach and grasp plans
small muscles in hand rich in muscle spindles
cutaneous receptors on the palmar surface of the hand
Anticipatory control of reaching:
proactive use of visual and somatosensory inputs work collaboratively together - also used reactively for error correction during the performance.
MOTOR SYSTEMS:
separate descending pathways for reach and grasp formation:
reach with the use of proximal muscles may be predominantly (midbrain and brainstem pathways red nucleus and reticular nuclei)
grasp for fine motor control uses pyramidal pathways
distinct neurons for precision grip.
requires muscle tone and strength. - 157The emergence of prehension( reach grasp and release )reaching- moving hand from initial location to target
grasping: shaping hand around an object
(functionally interrelated but emerge at different times in the first year)
the stage before successful reach and grasp:
10 WEEKS GESTATION- the movement of hand to mouth
FROM BIRTH- hand to mouth movement continues - intentional
Pre reaching guided by proprioreception rather than vision.
achieve head control. coactivation of shoulder develops, hands open more and together within the visual field, achieve stability in sitting and move from bilateral to unilateral reach.
From birth to 12 months babies learn from the environment by visual exploration, tactile experiences and mouthing. - 158can you describe the relationship between play and development of FMS?4-6 months - actively explore objects to create sounds and visual effects
6-12 months - explore a variety of manipulative skills
experiment to get different responses
cause and effect established
imitate actions
begin to use one object in relation to another - 159At what ages are reaches and grasps achieved?reaching 3- 4 months (proprioreception greater than vision (jerky)
at 2 months infants bring (grasp) an object to mouth and explore and at 4-5 months bring it into the visual field
GRASPS
Neonate - fisted hand (grasp reflex which decreases by 3-4 months )
palmar grasp all fingers flexed around the object 4-6 months
radial palmar - combined with supination, inspection and mouthing 6-7 months
radial digital grasps with fingers 7-9 months
scissor grasp 9-10 months
10-11 inferior pincer
11-12 fine pincer - 160can you explain release in terms of infant ages?Release involves extensor movement patterns so has slightly different developmental trajectory from grasp
neonate - touch dorsum of hand and fingers open reflexively
5-6 months - transition to purposeful release
6-7 months - transfers object from hand to hand - lets objects go whilst on a supported surface
9-10 months casting - drops objects from highchair
12 months - graded relsease, starts stacking etc. - 161at 7 months the child uses bilateral hand use (manipulation and engages in .....visual inspection
hand to hand transfer
progress to holding a toy in each hand
note at 9 months one hand holds an object while others explore it
12 months two hand begin to have coordinated asymmetric roles- drawing - 162examples of play activities by type of play. functional/sensorimotor play constructive make belief (pretend/ symbolic and socio dramatic) games with rulesfunctional/ sensorimotor play:
simple repetitive movements, with or without objects. i.e shaking, mouthing objects (0-2 years)
constructive: conructing and creating: block building, drawing, puzzles (12months on)
make believe/ symbolic play :
acting out everyday and imaginative roles (i.e mums and dads) 2-6 years
Games with rules:
Following rules in plat. Board games, cards, sports etc 5- 8yrs + - 163How does a child play in relation to other children? Solitary ( repetitive and functional) parallel (symbolic and early socio-dramatic) associative ( similar to parallel but child more interested in being with other children- activity i s not as important) cooperative - socio-dramatic and progressing to rule based play1. birth - 2/3 years
2. 2-6 years
3.5- 5
5- 8 - 164Outline the sequence of play development Sensorimotor constructive symbolic socio dramatic rule defined playSensorimotor - earliest form of play child gets pleasure from sound, texture, colour, shape and shakes bangs and mouths
( 0-2 years)
Constructive play - goal orientated, requires PC and fine motor skills - puzzles, building, drawing etc. (12m and on)
Symbolic: once object constancy has been established the child begins to think representationally (i.e use one box to represent another
symbolic 2 years)
Socio-dramatic: children play out the role they have experienced through stories , adults around them or through tv.
(4-6 years)
rule defined play - requires a highly socialised child, need to keep their actions within the conext of the rules
( 5 - 8+) - 165To gain an overview of the key points of pathology in the nervous system at the cellular levelEach cellular element may undergo physical changes in response to disease states
The pathological alteration can lead to physiological changes AND/or
physical changes
Key concepts in relation to neurons:
Cell death ( Necrosis or apoptosis (programmed cell death))
Wallerian degeneration (PNS quicker in few weeks regeneration possible.... in CNS slower few months and no regeneration)
NEUROFIBRILLARY DEGENERATION – plaque formation
INCLUSION BODIES – abnormal deposits in neurons
Oligodendroglia:
Demyelinating diseases - 166In clinical pathology you need to localise site of disease processes. Important terminology i need to know are Site: focal, multifocal, diffuse time course: acute , subacute or chronic evolution: transient, improving, progressive or stationary.focal - one site
multifocal - multiple sites
diffuse- widespread multifocal
acute - recent
sub acute - rather recent
chronic - long term
transient - short lasting (not permanent)
progressive - worsening, growth and spread
stationary - just there. - 167The seven main types of neuropathology1. Degenerative
2. Neoplastic
3. Vascular - infarction or haemorrhage
4. Inflammatory
5. Immunological Disease
6. Toxic Metabolic Disease
7. Traumatic
(also consider Congenital) - 168list examples of transient disorders on neuronal functionIncreased excitability :
Focal seizures
Tonic spasm
Muscle cramp
Paraesthesia
Paroxysmal pain
Decreased excitability:
TIA
Migraine
transient mononeuropathy
General disorders (excitable )
generalised seizure
tetany
Decreased excitability (general)
Syncope
concussion
catalepsy
periodic paralysis - 169What are the systems level neuropathologyCSF system( hydrocephalus, raised ICP - pushes brainstem down, meningitis, meningeal irritation)
sensory and motor systems (various)
consciousness system- (narcolepsy, delirium, confusion, coma, concussion, seizure, syncope)
vascular system - ischaemia, infarction, ICH, aneurysm , embolus, TIA, syncope - 170What are the clinical features in terms of movement disorders reflect damage to the cns?ataxia
dystonia
chorea (jerky involuntary movements)
ballismus
tremor
bradykinesia - 171What are the motor and sensory impairments as a result of damage to the CNS?Motor Impairments:
Weakness
Muscle tone
Spasticity
Flaccidity
Rigidity
Sensory Impairments:
Altered cutaneous sensation
Altered proprioception
Pain - 172What are the Clinical Features of Damage to CNS?Cognitive Impairments
Behavioural Changes
Auditory Disturbances
Autonomic Issues
Communication / swallowing issues
Dysarthria
Aphasia
Dysphagia - 173Stroke Why not CVA? Clinical syndrome of vascular origin Non-progressive Ischaemic or Haemorrhagic The best treatment is prevention – manage risk factors Clinical signs depend on which artery is involved How does it present?Sudden weakness/numbness of the face, arm or leg – especially on one side of the body
Sudden confusion, trouble speaking or understanding
Sudden trouble seeing in one or both eyes
Sudden trouble with walking, dizziness, loss of balance or coordination
Sudden headache with no known cause
Middle cerebral artery:
Face & UL > LL involved
Posterior cerebral artery:
Memory loss, Thalamic syndrome, Cortical blindness
Anterior cerebral artery:
LL > UL
Behavioural changes - 174Traumatic Brain Injury Prevalence - Males > Females Mortality is high among those who are hospitalised Causes Direct blows to the head Deceleration and rotational force Coup-Countercoup lesions Diffuse Axonal Injury What are the clinical features of TBI?Post-traumatic epilepsy
Post-traumatic hydrocephalus
Autonomic disorders
Cranial nerve involvement
Orthopaedic issues
Continence
Sexual dysfunction
Sensory issues - 175Parkinson’s Disease Second most common neurodegenerative disease after AD Risk Factors Age Genetic Environment Gender Selective degeneration of dopaminergic neurons of the substantia nigra Symptoms generally appear when 60% of neurons are lost in the SN What are the cardinal signs of PD? (4) and other clinical features?Cardinal signs
Tremor
Rigidity
Akinesia/Bradykinesia
Postural instability
Other:
Loss of dexterity
Falls
Shuffling / Festinating Gait
Frozen shoulder
Quiet voice, mumbling
Dribbling salivaDisturbed sleep
Swallowing in later stages
Bladder disturbance
Constipation
Postural hypotension
Cognitive impairment
Psychosis/hallucinations
Depression - 176Multiple Sclerosis Progressive, demyelinating disease of the central nervous system Autoimmune Can occur anywhere in the CNS What are the clinical presentations?Vision
Sensory issues
Motor function - Ataxia
Swallowing issues
Bladder/bowel
Pain
Fatigue
Cognition - 177Motor Neurone Disease The progressive degeneration of neurones Types Amyotrophic Lateral Sclerosis Progressive Muscular Atrophy Progressive Bulbar Palsy Primary Lateral Sclerosis clinical features?Weakness
Muscle wasting
Fasciculation
Spasticity
Breathing difficulties
Insomnia
Fronto-temporal dementia
Emotional lability - 178Guillain-Barre Syndrome Most common cause for acute generalised weakness Demyelinating Auto-immune disease Generally reported after a respiratory / GI clinical features?Symmetrical, ascending, progressive
Begins distally
Paresthesia or Hypesthesia
Can affect diaphragm
Pain
Oro-motor involvement – swallowing and speaking
Bulbar palsy - 179Dementia Dementia describes a collection of symptoms that are caused by disorders affecting the brain. It is not one specific disease. Dementia affects thinking, behaviour and the ability to perform everyday tasks. Brain function is affected enough to interfere with the person’s normal social or working life. what are the types of dementia?Alzheimer's Disease – most common 50-70% case
Vascular Dementia – the second most common
Parkinson's Disease
Dementia with Lewy Body
Fronto-Temporal Lobar Degeneration – 50% familial
Huntington’s Disease – Inherited - 30 -50 yrs of age
Alcohol related dementia ( Korsakoff’s syndrome)
Creutzfeldt-Jacob disease (1 in 1,000,000 per year) - 180Alzheimer's Disease Brain cells shrink, abnormal cells build up as ‘tangles’ in the brain cells and ‘plagues’ outside the brain cells Results in impaired memory, thinking , behaviour. Affects short term memory first. Normal functioning and ability is slowly lost.Vascular Dementia
– dementia associated with circulation – may present similarly to Alzheimer's and may have a combination
Multi-Infarct – strokes, TIAs – most commonly vascular dementia
Binswanger's disease (subcortical vascular dementia) – High BP, thickening arterial walls and decreased blood flow - 181Dementia with Lewy Body Caused by degeneration and death of nerve cells in the brain Spherical structures called Lewy bodies, which develop in the nerve cells Tend to have hallucinations Parkinsonism Often rapid presentation, with fluctuations even within an hour;)
- 182Clinical Features of DementiaInsidious but progressive (slow)
Remote memory, language, visuospatial skills will show gradual deterioration
Motor skills (including walking) affected at later stage
6 – 15 year course - 183Physiotherapy Evaluation IN NEUROPATHOLOGY invovles what:Movement Analysis is key
Knowledge of pathology and clinical patterns
Hypothesise why your patient is moving a particular way
Patient-centred / goal-directed
Assess for impairments
Use objective measures – outcome measures - 184Physiotherapy Treatment neuropathology ?No one treatment approach has been shown to be superior over the other
Task-specific / goal directed
Observe the principles of neuroplasticity
Be evidence-informed
Patient centred - 185To understand the impairments that arise in the motor system as a result of various neurological pathologiesMuscle weakness- paresis & paralysis;
Weakness is the inability to generate normal levels of force, mildly/partially (paresis) or completely (paralysis)
Can result from disruption to descending motor pathways
If prolonged can lead to peripheral changes in muscle (secondary) - selective atrophy of Type II (fast) and Type I (slow) fibres
Abnormalities of muscle tone:
TONE - muscle’s resistance to passive stretch; related to activity and readiness to produce tension
Spasticity - hypertonicity
A motor disorder characterised by a velocity-dependent increase in muscle tone with exaggerated tendon jerks.
hyperactive stretch reflexes
abnormal posturing of the body part/s
excessive coactivation of antagonist's muscles
associated movements
clonus
stereotyped movement synergies
Rigidity:
Also characterised by resistance to passive stretch BUT IS NOT VELOCITY DEPENDENT
result of hyperactivity in fusiform system, disinhibition of cerebral structures normally inhibited by Basal Ganglia,
more often seen in flexor groups
two types:
Lead pipe - constant resistance throughout ROM
Cogwheel - - 186hypotonicity ?Hypotonia
Flaccidity - complete loss of muscle tone
Hypotonicity - reduction in “stiffness”, lengthened
Found in variety of disorders particularly spino-cerebellar lesions, or developmental syndromes (e.g. Downs). Also in “floppy babies” - low toned - 187To have an understanding of the techniques physiotherapists may employ to assess the impairment.Observation of resting position, active movement to note deviations from normal mm balance
apply passive ROM to muscle, feel resistance (lack of) with respect to different velocities
subjective rating scales (e.g. Ashworth, Tardieu)
Pendulum test
Stretch Reflexes (tendon reflexes), Babinski, clonus
instrumented measures (e.g. isokinetic XS equipment, electrogoniometer, computerised video equipment)
Always assess in context of functional movement and remembering weakness, local changes etc. - 188co- ordination is another form of motor impairments other than weakness, paralysis, hypertonicity and hypotonicity?Coordination
Involves sequencing, timing and grading of activation of multiple muscle groups (synergies)
commonly after lesions in motor cortex, basal ganglia and cerebellum
Activation and sequencing problems
Abnormal synergies
- stereotypical patterns, lack of fractionation (differentiation)
Coactivation - of agonist and antagonist
Impaired inter-joint coordination - resulting in abnormal movement trajectories or decomposition
3.2 Timing Problems
Problems initiating movement, slowed reaction time - inadequate (or decreased rate of) force generation, insufficient ROM, reduced motivation, abnormal postural control, Slowed movement time
Problems terminating (or changing) movement
Problems scaling or grading e.g. dysmetria - under or over shooting in reaching or pointing tasks - 189Assessment of coordination issues include?Finger to nose; finger opposition; pronation/supination, rebound test; tapping (RAM); pointing; heel to shin; placing and holding; drawing a circle.
Tested EO and EC ( latter for sensory ataxia) - 190Involuntary movements - DYSTONIA 2 Associated movements 3 Tremor Choreiform and Athetoid movementsAbnormal movements - various forms from slow athetoid to fast myoclonic
Idiopathic or symptomatic (DYSTONIA)
2 Unintentional movement of one limb during voluntary movement of another
3 tremor
Rhythmical involuntary oscillatory movements of body part/s
Resting T - occurs at rest
Action T - occurs during voluntary activity
4. Choreiform movements (chorea) - involuntary, rapid, irregular, jerky (BG lesions)
Athetoid (athetosis) - slow, involuntary, writhing, twisting (UL>LL), also in tongue, neck, face. - 191What doest the assessment for involuntary movements comprise of?Assessment of involuntary movements:
systematic observation - describe in which body parts, nature of movements, conditions when movement occurs
(or ↑or decrease) - 192describe the effect of neurological impairment on the somatosensory systemSomatosensory
somatic sensory information ascends to the cortex via the dorsal column-medial lemniscal system and anterolateral system
Lesions in ML = loss of discriminative touch (light touch and kinaesthetic sense - proprioception)
Lesions in LST - effect pain, thermal change, detection, course touch and kinaesthetic discrimination
Lesions in the somatosensory cortex - contralateral = LOSS OF DISCRIMINATIVE SENSES, PROPRIORECEPTION, STEROGNOSIS (OBJECT RECOGNITION) AND LOCALISATION -can't tell when and where someone touches you - 193How do physiotherapists assess somatosensory system>light touch (pressure)
thermoreception
proprioreception
sterognosis (recognition)
#Consider hireachy
- detection ( can they feel it?)
- Discrimination
Quantification - if the R side is 10/10 what is the L side
Recognition - object recognition , can they recognise weight and shape
not the locale and distribution of loss - 194What are the visual deficits caused by neurological pathology and how are they tested?visual acuity (clarity of vision) - may test directly with chart, ask if wear glasses, check notes, pre morbid.
depth perception (three dimensions, coupled with the ability to gauge how far away an object is) - use two identical objects held at different distances
Visual fields - (area in which objects can be seen in the side (peripheral)- depends on the location of the lesion within the visual system may include hemianopia, quadrantanopia. Test via confrontation and detection of stimulus on visual field and patients gaze centrally
oculomotor paresis - test control of eye- near and far focus, tracking left, right , up and down . NOTE - if the eye can focus they will have double vision
diplopia (double vision)- from subjective report may be vertical or horizontal second image - 195What are the vestibular deficits caused by neuropathology?if the lesion is peripheral the eye will beat toward the affected side
pathology within the vestibular system can produce impairment of:
gaze stabilization - blurring or oscillating vision
posture and balance
vertigo and dizzyness
tests are covered in 3rd year - 196How can neurological pathology effect perception? How would we test it?*Body image and Body Schema*
Can affect the awareness of body parts in relation to another body or the environment.
Disorders include somatognosia (failure to recognise body parts) , right and left discrimination, unilateral neglect (don't recognise one side of the body), anosognosia - no insight into their disability (had a stroke but think they had a fall)
*spatial relations*
Position in space, spatial relations to other objects, topographical orientation, , figure-ground (recognise specific face)
apraxia and dyspraxia
- Inability to carry out purposeful movmement it out.
ideomotor- movement can be performed automatically but not to command- OR ideation cannot be performed at all
Gestural tests - 197What effect does neuropathology have on cognition?arousal and level of consciousness allows a person to respond to stimuli in the environment.
Hospital - assessed by GCS, in post-acute settings by RLAS.
Orientation:
understanding people, place, time and situation.
Assessed by questioning who they are, who others are, where they are, what time it is, day, date etc. - 198—
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