Test 1 Flashcards
Symptoms
Subjective findings
Signs
Objective findings
Positive symptoms
Release of abnormal behaviors
Spasticity
Negative symptoms
Loss of normal behaviors
Motor cortex deficits
Motor weakness
Abnormal synergies
Coactivation
Abnormal muscle tone
Neural aspects of strength
Number of motor units recruited
Type of motor units recruited
Discharge frequency
Weakness
Inability to generate normal levels of force
Major impairment in those with UMN lesions
Paresis
Mild or partial loss of muscle captivity
From lesion in descending motor pathways
Interferes with central excitatory drive to the motor units
Paralysis or paresis
Decreased voluntary motor unit recruitment
Inability to recruit skeletal motor units to generate torque or movement
Reduced descending drive is associated with…
Failure to recruit high threshold motor units
Reduced ability to increase motor unit discharge to increase voluntary forces
More distally than proximally
Reduced excitatory input to the spinal motor neurons…
Reduces maximal voluntary power
Lesions to corticospinal centers
Can lead to loss of ability to recruit a limited number of muscles controlling movement
Inability to control individual joints
Mass movements called abnormal synergies
Abnormal synergies
Stereotypical patterns of movement that cannot be changed or adapted to changes in task or environmental demands
Reflect lack of fractionation
Muscles so strongly linked, movement outside of fixed pattern not possible
Fractionation
Ability to move single joint without simultaneously generating movements in other joint
Co activation
Common characteristic of unskilled early stages of learning
Not necessarily a result of impairment of function but rather a primitive form of coordinating
Spasticity
A motor disorder characterized by a velocity dependent increase in tonic stretch reflexes with exaggerated tendon jerks resulting from hyper excitability of the stretch reflex
- abnormalities within segmental stretch reflex
Lesion in the descending motor systems result in…
Increase in alpha motor neuron excitability with a resulting increase in muscle tone and exaggerated tendon jerks
- I.e hypertonicity
Spasticity is a combination of
A decrease in stretch reflex threshold
Reflex hyper excitability
Enhanced stretch reflex can occur because…
The alpha motor neuron pool at the segmental levels is hyper excitable
The amount of excitatory afferent input is increased
Or both
Hyper excitability of alpha motor neuron pool can be due to
A loss of descending inhibitory input
Post synaptic denervation hyper sensitivity
Shortening of the motor neuron dendrites
Collateral sprouting of dorsal root afferents
Behavioral indications of spasticity can include:
Change in the resting position of a limb
Presence of characteristic movement patterns
Pendulum or drop test for what?
Spasticity
Hypotonicity
Impairments associated with cerebellar pathology
Hypotonia
Coordination
Intention tremor
Impaired error correction affecting motor learning
Lesions of the vermis and fastigial nuclei
Disturbances in axial and postural control, balance, speech deficits
Medial- axial
Lateral- distal
Damage to intermediate cerebellum or imposed nuclei
Action tremor in limbs
Lateral cerebellar lesions
Delay in initiating movement
Impaired control of multi joint movements
Hallmark sign of cerebellar pathology
Coordination problems
Coordination problems
Movement trajectories uneven and lack a bell shaped profile
- because of the loss of coordinated coupling between synergistic muscles and joints
Paralysis
Total or severe loss of muscle activity
Coordination problems could present as
Delayed reaction time
Errors in range and direction of movement
Inability to sustain regular rhythmic movements
Decomposition- moving one joint at a time bc cannot time or scale multi joint movements
Inability to terminate movement and change direction
- stop agonist and generate force in antagonist
- rebound phenomena
Dysmetria
Problems judging the distance or range of a movement
Scale forces appropriately for a task performance
Intention tremor
Occurs during performance of a voluntary movement
Most marked at the end when the person attempts to brake the movement
Impaired error correction affecting motor learning
Cerebellum provides internal feedback reporting intended movement and external feedback that report actual movement
Creates a feed forward signal to reduce subsequent errors
Lesions affecting error reporting contribute to motor learning deficits
Dysmetria and intention tremor result from
Disruption of feed forward mechanisms
BG pathology include
Hypokinetic
Hyperkinetic
Dystonia
Dyscoordination
Parkinson’s disease
Flexed posture and impaired gait and balance
From degeneration of dopamine
Akinesia, bradykinesia, rigidity, resting tremor
Akinesia
Reduced ability to initiate spontaneous movement
Bradykinesia
Slow and reduced amplitude voluntary movements
Rigidity
Increased muscle tone regardless of velocity
Hyperactivity in fusimotor system
Predominantly in flexors of the trunk
In motor impairments as well
Resting tremor
Tremor occurring in a body part that is not voluntarily activated and is supported against gravity
Amplitude increases during mental stress or movement of another body part (gait)
Action tremor
Produced by voluntary contraction of a muscle
- postural: voluntarily maintaining position against gravity
- kinetic: during a voluntary movement
Akinesia and bradykinesia coordination problems seen in…
Handwriting because of a reduced capacity for coordinating wrist and finger movements
Frontotemporal dementia
Inappropriate behaviors
Language problems
Difficulty with thinking and concentration
Movement problems
Hyperkinetic disorders
Excessive and involuntary movements and decreased muscle tone
Chorea
Athetoid
Chorea
Involuntary rapid irregular jerky movements
Athetoid
Slow involuntary writhing and twisting movements usually involving UE>LE
May also involve neck, face, and tongue
Dystonia
Sustained muscle contraction Twisting and repetitive movements of abnormal posture Diverse; can be slow or quick Cocontraction of agonist and antagonist Focal, hemi, multi focal Idiopathic, symptomatic
Lesion of medial lemniscus
Loss of discriminative touch
- light touch, kinesthetic sense
Lesion of lateral spinothalamic
Pain
Temperature
Course touch
Kinesthetic discrimination
Lesion of somatosensory cortex/ DC
Loss of discriminative sensations; proprioception, 2 point discrimination, stereognosis, and localization of touch
Contralateral to side of lesion
Visual deficits following unilateral damage to cerebral cortex
Homonymous hemianopsia
Vestibular deficits
Gaze stabilization
Blurred vision due to disruption of vestibuloocular reflex
Posture and balance
Vertigo and dizziness
Body imaging disorders associated with parietal and temporal lobe lesions
Parietal lobe damage present with deficiencies related to body image and perception of spatial relations
Body scheme
Awareness of body parts and their relationship to one another and the environment
Difficulty dressing and unsafe transfers
Somatagnosia
Lack of awareness of the body structure and relationship of body parts to one another
Unilateral spatial neglect
Inability to perceive and integrate stimuli one one side of the body
Temporoparietal junction and posterior parietal cortex
Looks like lack of attention to the left side
Perceptual impairments
Body image
Spatial relation disorders
Apraxia
Anosognosia
Denial of presence or severity of ones paralysis
Unsafe functional activities
Perceptual deficit
Spatial relation disorders
Difficulty perceiving oneself in relation to other objects or other objects in relation to oneself
Topographic
Figure ground
Position in space
Topographic disorientation
Inability to remember the relationship of one place to another
Figure ground perception
Inability to distinguish foreground from background
Apraxia
Inability to carry out purposeful movement in the presence of intact sensation, movement, coordination
Usually in left sided brain damage
5 types of apraxia
Verbal Buccofacial Limb Constructional Dressing
Limb apraxia 2 types
Ideomotor: cannot carry out command
Ideational: purposeful movement not possible automatically or on command
Perception
Integration of sensory impressions into psychologically meaningful information
Deficits in cognitive and perceptual systems
Affect patients ability to move effectively and efficiently throughout their environment
Impairment in association cortices- gershman
Right hand dominant with lesions in left angular gyrus
- confusion between right and left
- difficulty naming fingers
- difficulty writing although sensory and motor are intact
Primary motor cortex lesions
Weakness or paralysis
Change in tone
Sensory cortex lesion
Loss of sensation, perception, proprioception
Problems with motor control
Premotor cortex lesions
Weakness from disuse
Difficulty with planning motor tasks,purposeful movement, apraxia
Supplemental motor region lesion
Weakness
Difficulty with complex motor tasks
BG lesion
Absence of movement
Weakness
Abnormal movement
Abnormal tone
Cerebellar lesion
Incoordination
Weakness
Balance
Corticospinal tract lesion
Weakness
Alpha motor neuron lesion
Weakness
Atrophy
Afferent sensory input impairment
Loss of sensory awareness
Uncoordinated movements
Balance
Frontal lobe
Personality Behavior Emotions Judgement Planning Problem solving Intelligence Speaking Writing Self awareness
Parietal lobe
Interpretation of language Sensation of touch, pain, and temperature Vision Hearing Memory and visual/ spatial perception
Temporal
Understanding language (Wernickes) Memory Hearing Sequencing Organizing
Cortical layer
Outer gray matter
Location of cell bodies (neurons,glia)
Subcortical
White matter ( includes internal capsule)
-Highways that connect cell bodies
Deep nuclei: gray matter
-BG, thalamus, hypothalamus
Meninges outside to in
Epidural -dura mater Subdural -arachnoid mater Subarachnoid - pia mater
Epidural space
Arterial blood
Torn meningeal artery- bleed out
Subdural space
Venous blood
Torn bridging vein
Subarachnoid space
Usually contains CSF
Arterial blood : aneurysm rupture
Path of CSF
Lateral ventricles Foramen of Monroe Third ventricle Cerebral aqueduct 4th ventricle Subarachnoid space Arachnoid villi project from SAS into sinuses
Anterior circulation of the brain
2 carotid arteries
Posterior circulation of the brain
2 vertebral arteries
Lateral corticospinal tract
Volitional movement
The UMN
DC/ML
Larger fiber Proprioception/ kinesthesia Discriminative touch Vibration Dull
Spinothalamic tract
Small fiber Pain Temp Crude touch Itch Tickle Sharp
Pain and temp are lateral
Crude touch and pressure are anterior
Primary efferent track in spinal cord
Lateral corticospinal
Cells in CNS that give rise to efferent track
Pyramidal
Pain, touch, volitional movement is controlled be…
Contralateral side
Thalamus infarcts usually affect
Pain and touch
Impairments in right lateral cerebellum
Difficulty in verb generation
Learning & performing complex nonmotor tasks
warning signs of stroke
Face
Arms
Speech
Time
modifiable stroke risk factors
blood pressure education smoking diabetes weight gain cholesterol inactivity sleep apnea
non modifiable stroke risk factors
TIA gender: females Age Race Family history
Types of stroke
Ischemic: 87% - embolic - thrombotic - lacunar Hemorrhagic: 13% TIA
Ischemic Stroke
Result of thrombus, embolus, or conditions that produce low systemic perfusion pressures
Lack of cerebral blood flow deprives the brain of oxygen and leads to injury and death of tissues
Embolic stroke
most common type of ischemic stroke
Blood clot that forms in another location and moves to the brain
Cardiac origin most common; 80% of cardiac emboli occlude the MCA
Vascular origin: starts as plaque formation and moves forward. Most commonly the aorta or vessels of the aorta
May be paradoxical
- congenital such as patent foramen oval, DVT
Thrombotic stroke
- forms in arteries directly feeding the brain
- typically related to abnormalities w/in the vessel wall such as atherosclerosis, arteritis, dissections, and external compression of the vessels- Due to risk factors
- Common precursor is htn
- may also be caused by hematologic disorders and/or hypercholersterolemia
- large vessel thrombosis that occurs in extra cranial vessels such as the carotid and vertebral arteries can lead to severe strokes.
Lacunar strokr
small vessel strokes. ischemia in one distal or small artery
typically assoc with chronic HTN and diabetic microvascular disease
size of infarct from 2mm- 3cm in size
about 25% of all ischemic strokes.
different types of lacunar strokes
pure motor pure sensory sensorimotor ataxic hemiparesis clumsy hand syndrome dysarthria-just speech issues
hemorrhagic stroke
approx. 13%
cellular destruction caused by ischemia secondary to pressure/bursting
- mechanical injury caused by edema and the pressure of blood collection
75% of hemorrhagic strokes caused by a bleeding blood vessel occur in people who have htn
Common causes of hemorrhagic stroke
hypertensive bleed
ICH in the presence of an AVM or tumor, ruptured aneurysm- SAH, TBI
stroke from an aneurysm is called…
subarachnoid hemorrhage
ACA
medial aspect of frontal and parietal lobes
sub cortical structures such as the BG
MCA
entire lateral aspect of the cerebral hemisphere (frontal, temporal, parietal)
PCA
occipital lobe medial/ inferior temporal lobe upper brain stem midbrain thalamus
Differentiation of stroke types
- hemorrhagic strokes do not follow an artery distribution, sx may not follow typical pattern
- vomiting, severe headache, and/or impaired consciousness are sx that may differentiate hemorrhagic from ischemic
- important to determine hemorrhagic from ischemic for medical management
TIA
symptoms include focal deficits of an ischemic stroke and typically follow a vascular distribution
- resolve in 24 hours. may not be completely normal, but resolve
Reversible; no infarction of cerebral tissue
35% of people with TIAs have a stroke w/in 5 years
work up essential to determine the cause and prevent future stroke
hemorrhagic conversion
- ischemic infarct may convert into hemorrhagic lesion
- thrombi can migrate, lyse, and reperfuse into an ischemic area leading to small hemorrhages
- damaged capillaries and small blood vessels no longer maintain their integrity
- more common in large infarcts such as occluded MCA
Tissue plasminogen activator
Assists with bleeding for ischemic stroke
Thrombolysis; powerful clot buster
clinical diagnosis of ischemic stroke
no recent trauma, surgery, or bleeding (may cause bleeding elsewhere)
No rapidly improving symptoms (TIA)
BP <185/110
treatable w/in 3 hrs of onset
CT w/out ICH or major early infarct signs (will not reverse it)
normal blu and platelets (PT/PTT)
Homunculus
discovered in 3rd century AD
map of the primary sensory cortex
shows areas of the cortex that respond to somatosensory stimulation
shows area of the brain that controls motor and sensory input from different portions of the body
left sided stroke presentation
right sided weakness right sided sensory deficits speech and language deficits - non fluent (brocas) -fluent (wernickes) -global aphasia slow, cautious behavioral style difficulty planning and sequencing movements - apraxia more common (ideomotor, ideational) disorganized problem solving very aware of impairments anxious about poor performance difficulty with processing delays difficulty expressing positive emotion difficulty processing verbal cues and commands memory deficits: typically related to language
right sided stroke presentation
left sided weakness
left sided sensory deficits
spatial perceptual deficits
- left sided unilateral neglect
- agnosia
Difficulty sustaining movement
quick, impulsive behavioral style
difficulty grasping overall pattern, problem solving, synthesizing info
unaware of impairments; poor judgement
rigidity of thought; no abstract reasoning
difficulty processing visual cues
difficulty with perception of emotion and expressing negative emotion
memory deficits: typically related to spatial- perceptual information
clinical signs of brain stem stroke
changes in: breathing movement sensation eye movement heart rate blood pressure
clinical signs of cerebellar stroke
abnormal reflexes of the head and torso impaired coordination ataxic movement/ gait balance issues dizziness vomiting
ACA syndrome
occlusion of the ACA
- cognition, personality, reasoning, decision making, talking
ACA syndrome clinical signs
contralateral hemiparesis involving mainly LE
contralateral hemisensory loss involving mainly LE
urinary incontinence
slowness, delay, motor inaction
MCA syndrome clinical signs
contralateral hemisensory loss/ hemiparesis (mainly UE and face)
motor speech impairment (Brocas or non fluent aphasia with slow speech)
Receptive speech impairment (wernicke’s or fluent aphasia)
global aphasia
perceptual deficits and limb kinetic apraxia
ataxia of contralateral limbs
PCA syndrome clinical signs
occlusion of the PCA, peripheral territory
contralateral homonymous hemianopsia
visual agnosia
memory deficits
To test: come in from side and find where they see you
thalamic pain syndrome
occlusion of the central territory of PCA
thalamic pain syndrome clinical signs
involuntary movements: stroke doesn’t cause pain, the result of it does
contralateral hemiplegia
paresis of vertical eye movement
Medial medullary syndrome
Dejerine syndrome
occlusion of the vertebral artery, medullary branch
medial medullary syndrome signs
ipsilateral:
- paralysis with atrophy of 1/2 of tongue with deviation to paralyzed side
Contralateral:
- paralysis of UE and LE
- impaired tactile and proprioceptive sense
Lateral Medullary syndrome
wallenburg’s syndrome
occlusion of PICA or vertebral artery
Lateral Medullary syndrome signs
ipsilateral:
- decreased pain and temperature sensation to the face
- cerebellar ataxia
- vertigo/ nausea
- nystagmus
- dysphagia
contralateral:
- impaired pain and thermal sense over 50% of the body
Complete basilar artery syndrome
locked in syndrome signs: - hemiparesis to quadriplegia - bilateral cranial nerve palsy - consciousness and sensation are spared - patient cannot more or speak but remains alert and oriented
medial inferior pontine syndrome
foville’s syndrome
occlusion of paramedic branch of basilar artery
medial inferior pontine syndrome signs
ipsilateral:
- paralysis of conjugate gaze to side of lesion
- nystagmus
- ataxic gait
- double vision with lateral gaze
Contralateral:
- paresis of face, UE, and LE
- impaired tactile and proprioceptive sense over 50% of the body
lateral inferior pontine syndrome
occlusion of the AICA
lateral inferior pontine syndrome signs
ipsilateral:
- horizontal and vertical nystagmus, vertigo, nausea, and vomiting
- facial paralysis
- deafness/ tinnitus
- ataxia
- impaired sensation over face
Contralateral:
- impaired pain and thermal sense over 1/2 the body
PT precautions with stroke
- acute pt usually on bed rest for first 24-48hrs. check activity order
- may be taking anticoagulant and considered a fall risk
- monitor vitals carefully; be aware of MAP ranges
- ischemic: 130-140
- hemorrhagic <110
- MAP= (2DBP+SBP)/3
- If pt presenting with new stroke like symptoms, place flat and call an MD
Evaluation tips for stroke
- determine ability to communicate. consider expressive, receptive, and global aphasia; watch documentation
- hemorrhagic strokes may present similar to TBI
- if patient moving in synergistic pattern- pronation, flexion of the elbow
- important to demonstrate standing and ambulation for rehab acceptance; may also attempt w/c mobility
- watch for change in symptoms- evolving stroke
factors that determine motor recovery
- CNS damage promotes shift to intact neural subsystems rather than spared components within lesioned area
- reorganization dependent upon learning styles, timeliness of tx, age and envt of brain, active engagement, unmasking latent pathways
treatment techniques for stroke
- want to decrease pain first
- if neglect, orient them to body position, want to acclimate them and make them aware of their envt
- stand on side of neglect to increase awareness
- if decreased tone in shoulders, provide elbow support to prevent shoulder subluxation
- to facilitate move outside of synergy patterns, position pt in positions to isolate targeted muscle group
- reduce spasticity: PROM and stretching with slow gradual movements
circuit training and stroke
greater gains in gait velocity over the course of inpatient rehab compared to the standard care
ESTIM and stroke
found FES to perineal nerve had higher success avoiding obstacles than AFO
lower muscle strength benefit the most
negative effects of constraint induced movement therapy and stroke
may alter CoG temporarily limiting postural control
limits functional training: transitions in infants/ toddlers
increased patient irritability secondary to restraint
positive effects of constraint induced movement therapy
allows for emphasis on postural control and stability
long term improvement in functional mobility from using B UE for functional tasks
opportunity to focus on other primary impairments (endurance, balance)
PT sessions and CIMT
with restraint on, focus on postural control
perform functional mobility tasks with emphasis on affected UE use
focus on other impairments: balance, endurance
Acute care PT implications
Do not break test pt to determine strength
assess sensation and corresponding dermatomes
pt family education essential
decreased arousal may be due to medications
pain management essential
note what they are connected to
RBC
delivers oxygen to tissues, absorption of cellular metabolic byproducts, maintains acid base balance
normal: 3.6to 5.0x10^6
anemia
decreased RBC increased fatigue watch for signs of hypoxia chest pain dizziness SOB muscle cramping
polycythemia
compensatory increase in RBC
may occur due to reduction in plasma volume
results in increased blood viscosity which may decrease peripheral flow
hematocrit
measurement of the percentage of whole blood occupied by cells
women: 37-47%
men: 41-53%
no exercise <25%
hemoglobin
iron containing protein with strong affinity for oxygen
single RBC carries 4 Hb molecules
men: 13-18
women: 12-16
therapy contraindicated when < 5 leads to heart failure
platelets
essential in clotting blood
normal: 150,000-300,000
no exercise when <120,000
thrombocytopenia
platelets <140,000
increased risk of bleeding
avoid activities that may cause bruising or loss of balance
prothrombin time
time required for clot to form
normal is 11-13.5 seconds (oral meds, coumadin may effect)
Partial thromboplastin time
blood separated into plasma and cells
looks at intrinsic cascade
normal is 30-45 sec (IV meds/ heparin)
international normalized ratio
unitless measure used to correct for differences in prothrombin time by various institutions
2-3 may be therapeutic
alert
state of being aware, attentive, and mentally functional
agitated
pt is excessively restless
demonstrates increased physical and/or mental activity
delirium
state of disorientation accompanied by irritability, agitation, suspicious, and/or fear
pt may also misperceive stimuli
dementia
state of altered mental processes that usually does not change arousability
somnolent
prolonged drowsiness
resembles a sleepy trance
obtundant
dulled response to stimuli
patient typically confused and requires constant stimulation for all activities
stupor
patient aroused only by intense stimuli
motor response and reflex reaction typically preserved
coma
unconsciousness without spontaneous eye opening and with minimal or no response to external stimuli
modified ashworth scale
0-no increase
1- slight catch, release at end of motion
1+ resistance after catch
2 increase tone throughout
3 difficult to move throughout but can get through
4 rigid
3 sensory inputs to balance
visual
vestibular
somatosensory/ proprioception
reflex theory
reflexes are building blocks of motor control
work in sequence to create movement
reflex theory limitations
they require an external stimulus to be generated
does not explain spontaneous or volitional movement
hierarchical theory
top down approach to control of movement
higher, middle, lower levels of control
higher control middle, middle control lower without variation
hierarchical theory limitations
cannot explain withdrawal reflex
in a top down, the motor could only be initiated by the higher cortical center not by a reflexive lower level pain response
motor programming theory
motor programs (CPGs) drive movement without the need for sensory input
motor programming limitations
same motor program can produce different results depending on the external forces at work
systems theory
look at whole body as a mechanical system and integrate all the forces acting on the body to control or influence movement
DF
all of the varied DF in any given movement need to be coordinated in order for a smooth motion
use synergistic patterns to control
systems theory limitations
does not account for the environmental influences on movement
dynamic action theory
movement emerges as a result of the elements in the environment as needed
- not a result of specific commands from the CNS or premeditated motor programs
Control parameters can change and create a change in the system and a new motor behavior
increasing velocity of gait will transition one into a jog and then a run
dynamic action theory limitations
relegates the CNS to a relatively unimportant role
ecological theory
we detect information from our environment relevant to action and use that information to control movement
perception more important than basic sensation
nervous system is perception action system not a sensory motor
- person chooses higher chair in room
ecological limitations
less emphasis on organization and function of the nervous system
closed loop theory
sensory feedback aids in learning the skill to perform it better on the subsequent trials
- perceptual trace: knowledge of the correct movement, detects error in movement and corrects
- Memory trace: selection and initiation of movement
schema theory
novel movement is completed
ML enhanced by practicing specific motor tasks under different conditions
- Recall schema: same movement with difference force using memory to choose correct response
- recognition schema: evaluates the response
fitts and posner 3 stage
cognitive: what to do and determines what to do to complete it
Associative: how to do, determines strategy
Autonomous: how to succeed
systems 3 stage model
novice: simplify movement to decreases DF
advanced: release some DF, allowing more joints to be involved
Expert: releases all DF needed for task
