Neuro Flashcards
UMN lesion s/s
Spasticity Increased DTR Babinski Clonus Hyperreflexia Atrophy Associated rxns Synergistic mvmnts
Medial tracts
Medial corticospinal Tectospinal Medial reticulospinal Medial vestibulospinal Lateral vestibulospinal
Lateral tracts
Lateral corticospinal
Lateral reticulospinal
Rubrospinal
Medial corticospinal tract
Controls neck, shoulder, and trunk mm
Tectospinal tract
Reflexive head movement toward sound/visual object
Medial reticulospinal tract
Postural mm, limb extensors, APAs
Medial vestibulospinal tract
Neck and upper back extensors
Lateral vestibulospinal tract
Ipsilaterally facilitates LMN extensors, inhibits flexors
Only tracts that innervate LEs
Medial reticulospinal
Lateral vestibulospinal
Lateral corticospinal tract
Contralateral fractionation of the hand
Rubrospinal tract
Contralateral upper limb flexors
Lateral reticulospinal
Facilitates flexors and inhibits extensors
Lesion to frontal lobe
Contralateral weakness Inattention Personality changes Brocas aphasia Emotional liability
Lesion to parietal lobe
Contralateral sensory deficits Impaired language comprehension Visuospatial prob (poor body awareness)
Lesion to temporal lobe
Learning deficits Wenickes aphasia Aggressive bx Difficulty recognizing emotions Hearing loss
Lesion to occipital lobe
Homonymous hemianopsia
Extra ocular dysfunction
Reading/writing impairments
Blindness
LMN lesion s.s
flaccidity dec DTR hyporeflexia atrophy fasciculations weakness
PMA
Involved in visually guided movement
Contains mirror neurons that are activated during observation of others performing a task
Shows that demonstration of task is important! - helps prime the PMA
SMA
Activated during execution of learned tasks and bimanual tasks
Sequential movements
CBM
Error detection and correction center
Compares actual movement to intended movement and helps make corrections
3 parts - spino, vestibulo, cerebro
Involves PMA more than SMA
Loop =
M1 - PMA - Prefrontal - pons - CBM - thalamas - M1 - PMA - Prefrontal (and feedback to vestibular/RF for posture)
Main output of CBM
Inhibitory via purkinje fibers - Resets
Romberg Test
CBM ataxia will NOT be able to maintain balance with either EC or EO!
Romberg - sensory ataxia - usually only unable to balance with EC
CBM lesion
Ataxia - jerky, inaccurate movements
Dysdiadochokinesia (RAMs), Dysmetria, Action tremor
IPSILATERAL SIDE OF BODY
BG
Involved in selection of intended movement
Direct is excitatory (gas - glutamate and DA) - facilitate mvmnt
Indirect is inhibitory (brake - GABA) - inhibit movement
Globus pallidus is a natural inhibitor
FINISH
Function of BG
Monitoring and optimizing the pattern of mm activity so goal is reached efficiently
Selection/optimization/fine tune movement
Does not determine basic parameters of the movement though (that is the PMA)
Hypokinetic disorders (PD)
The lack of DA - cannot inhibit the globus pallidus
Direct is not facilitated
Indirect is not inhibited
Hyperkinetic disorders (Huntingtons)
Lack of inhibition by globus pallidus
Just going off direct pathway
Lose the indirect (inhib) pathway
BG are activated during what movement
Coordination and skilled movements
So when you tx someone with brain injruy who has poor coord, don’t just work on gait - need to activate the BG
Add reward based action , dual tasking
Motor input nuclei of BG
Putamen
Sensory input of BG
Caudate
Substantia nigra =
Produces DA
Semicircular canals
Angular acceleration
SC canals = 3 rings with receptors that sense motion of endolymph
Each ring opens at end to utricle - that expands into ampulla - ampulla has crista in it - has hair cells imbedded in cupula
Semicircular canals - each canal in pair produces
reciprocal signals - inc in one canal lead to dec from its partner
So rotate R - depolarize R and hyperpolarize L
Otolithic Organs
Saccule and Uttricle
Sense liner acceleration of head and head position relative to gravity
Saccule - vertical
Uttricle - horizontal
Saccule and Utricle contain
Macula inside with hair cells in a gel topped by otoconia
Two major roles of vestibular system in motor control
Gaze stabilization
Postural adjustments
Vision - R visual field is processed in the
L visual cortex!
Nasal retina processes infor from
Lateral visual fields
Nasal retina info - cross or no?
Yes! Cross at optic chiasm and goes to contralateral primary visual cortex
Lateral R/L fields
Temporal retina info - cross or no?
No!
Go ipsilateral
Medial R/L fields
L optic nerve processes info of the
L eye!
The left optic tract processes info of the
L temporal retina
R nasal retina
Makes up the R visual field!
The right optic tract processes info of the
R temporal retina
L nasal retina
Makes up the L visual field
Lesion at chiasm =
Both peripherals out
Tunnel vision
Lesion at optic nerve =
Ipsilateral vision loss (cross hasn’t happened yet)
Lesion at optic tract =
Contralateral homonymous hemianopsia
If L tract cut - lose R visual field in both eyes
So cut L optic tract = lesion to L visual cortex = lose R visual field
VOR
Stabilize visual images during head movements
Eyes move in opp direction of head movement
Exercises specific for VOR = vestibular adaptation exercises
Role of vision in motor control
Allows for feedforward (anticipatory control)
Primary visual cortex - streams
Dorsal = the where Ventral = the what
After being processed by the visual cortex, visual information flows where
Dorsally to the posterior parietal lobe
Central to the temporal lobe
Dorsal and ventral streams!!!
Tau is what
Time to contract info
Involves object getting larger on retina as it approaches the individual
Makes you aware things are getting closer to you
Optical flow is what
Stoplight effect
Visual info that is streaming past you as you move through an environment that gives you a sense of how you environment/you are moving
Sleep stages
1 = transition btw sleep and awake
2 = firest sleep stage, dec arousal, temp, RR
3, 4 = slow wave sleep, deepest stage
STAGE 2 = MOST MOTOR LEARNING!
1 to 4 = NREM
4 to 1 = NREM
REM
Continues like this - but depth of NREM decreases and duration spent in REM increases throughout the night
Hippocampus
Memory storage and consolidation!
HM epilepsy case study - showed hippocampus specific for laying down new memory - Took out hippcampus, part of temporal, and amyG
He had normal LTM (could remember before accident) Working memory (seconds, minutes)
Couldn’t do transfer from STM to LTM though
PROCEDURAL MEMORY was there though - his hand would “remember” drawing the star - but his brain would not
Hippocampus injury - leads to loss of
memory in recent events
Can still remember how to ride a bike and tie shoe laces - these are procedural memories
Declarative memory =
Conscious/explicit
Facts, events
Declarative is split into: 1 episodic (events, experiences) - special to you 2 semantic (facts, concepts) - more common knowledge
Procedural memory
Unconcious/implicit
Skills, tasks
Motor learning falls here!
STM is defined how
Working memory
Less than 1 min
Prefrontal lobe!
LTM - Declarative = things you
can TELL others
LTM - procedural = things you ____
KNOW that you can SHOW by DOING
Skill learning - ride bike
Priming - more likely to use recently heard word
Conditioning - salivate when see food
Visuospatial working memory
Specific part of the prefrontal cortex that is dedicated to it!
heavily connected to parietal and visual input - takes that info to premotor areas to plan appropriate motor response
LTM - 4 operations
Encoding - new info is attended to and linked with existing info
Storage = neural mechanisms by which memory is retained overtime
Consolidation = makes temporarily stored info more stable
Retrieval = when stored info is recalled
Motor learning =
set of processes associated with experience or practice leading to relatively permanent change in ability to perform skilled action
Change in capability to perform a skill inferred from permanent improvement in performance as a result of practice
(infer learning based on performance)
Requirements for motor learning
Improvement Consistency Stability (dec variability) Persistence Adaptability
Motor behavior =
Motor control
Motor learning
Motor development
Stages of motor learning - Vereijken
Initial/Cognitive stage
Intermediate/Associative stage
Advanced/Automatic stage
Stages of motor learning - Vereijken - Initiative/Cognitive
CBM signaling motor error
Prefrontal/DLPFC/ACC - involved in concious/cognitive recognition of error
BG inc activity in caudate with early learning (caudate connects with DLPFC) - this is how BG learns which action to select
Stages of motor learning - Vereijken - Intermediate/Associative
Less PFC/DLPFC with more practice
CBM stays active but is less active than initial stage
BG - shifts from caudate/DLPFC loop to putamen/SMA loop
Stages of motor learning - Vereijken - Advanced/Autonomous
Overall brain change from multiple brain areas to high activity of a focused smaller set
BG - inc skeletal motor SMA/putamen loop
Allows for voluntary movement sequences to be run off automatically - like sit to stand
NDT - key points
Symmetry Posture Weight shift (after get equal WB in midline)
CIMT
Restrain uninvolved to force pt to use involved
Constrained 90% of awake time for 2 wks
Locomotor training improves ___
Average for norm
GAIT SPEED
1.2 m/s
Muscle spindles
Monitor change in length
If mm lengthened a lot - will cause contraction at some point to prevent from getting too long
Like stretch reflex
GTOs
Monitor mm tension
When cx too much will eventually lead to relax
Autogenic inhibition
Spasticity
VELOCITY DEP
with inc in velocity = inc in resistance
Corticospinal damage or UMN
CLASP KNIFE
Rigidity
Lead pipe - rigid in both directions
Cog wheel - series of catching and jerks with passive stretch
Due to BG damage, loss of direct pathway
DTR normal, no clonus
Drugs for spasticity
Baclofen - mimic GABA Dantrolene - prevent Ca release Tizanidine - inhibits alpha motor neurons Phenol - inject to block nerves Botox - prevents release Ach Rhizotomy - cut spinal nn root
LE flex synergy
hip.knee flex
abd.er
DF/INV
Associated reactions - Homolateral Synkinesis
Resisted elbow flex causes ipsilateral hip flexion
Associative reactions - Raimiste’s Phenomenon
Resist good side abd or add and get that same movement (abd or add) on the affected side
Associative reactions - Soques finger phenomenon
Shoulder flexion facilitates finger extension
Brunstrom stages of CVA recovery
1 - flaccid 2 - spasticity starts, weak synergy 3 - spasticity severe, some volitional mv 4 - dec spasticity, some isolated mvmnt 5 - more complete isolated mvmnt 6 - normal tone
Modified ashworth scale
Measures spasticity on scale 0-4
0 = no inc in mm tone
1 = slight inc catch/release or min resistance at end of ROM
1+ = throughout remainder of ROM (less than half)
2 = more marked inc in mm tone throughout most ROM
3 = inc in mm tone, PROM hard to do
4 = affected parts rigid in flex or ext
Tardieu scale
Measures angle of clasp knife
Pendulum
Measures rigidity
3 components of postural control system
Sensory detection (visual, vestibular, somatosensory) - vis dominates
Integration
Execution of msk responses
Ankle strategy
If perturbation causes displacement forward =
If perturbation causes displacement back =
Distal to prx activation (gastroc - hams - paraspinals)
Small perturb with firm surface
If perturbation causes displacement forward = gastroc, hams, ps
If perturbation causes displacement back = DFs, hip flex, abs
Hip strategy
Proximal to distal activation
Pulls COM in direction of recovery
Larger, faster perturbations on smaller or compliant surface
Falling forwards, recover with = ab and hip flex cx
Falling backwards, recover with = hams and ps
Stepping strategies
Rapid step in direction of displacing force
Can be changed!!
APAs
Anticipatory postural control!
Medial reticulospinal!
Activation of mm to stabilize body prior to voluntary movement
APAs are context dependent - this is why important to NOT always supply with ad or hand on gait belt when working balance
Static balance tests
Romberg SLS Perturbations Functional reach CTSIB
Dynamic balance tests
FSST Ambulation Reaching Berg TUG Mini Best ABC
Locomotion - strength?
Walking does NOT require a lot of strength (2+) - what you need is mm to fire/burst and the timing of the bursts is most important
Essential requirements for gait
Progression - CPGs, BG
Postural control - CBM
Adaptation - V1
Locomotor region of brain
midbrain locomotor region (MLR)
peduncle pontine nucleus (PPN)
Both initiate locomotion and control speed
Can bypass BG and get to these with visual and auditory cueing (using the SMA)
A 50 yr old pt with recent stroke impacting hippocampus would have all these deficits EXCEPT what:
Difficulty learning new facts
Difficulty describing a recent event
Difficulty learning a new vocab word
Difficulty recalling a childhood memory
Deficits in all listed! EXCEPT recalling a childhood memory
They can do this because long term memory is stored all over the brain
A pt has a confired diagnosis of unilateral vestibular hypofunction - the chief complaint of the patient is dizziness and blurred vision with head movements
What type of exercise would be MOST appropriate to target the patient’s chief complaint?
Vestibular Adaptation!!!
