Flashcards in PTE Neuro done Deck (104):
General Neurologic S&S’s
•Change in memory
•Change in muscle tone
Clinical Neuro Examination• This is used to get a
a general idea where the patient stands. It is similar to a basic examination, but the PT is looking atthe neuro integrity of the patient
• Look at Posture
• Look for synergy patterns
• Observe for gait dysfunctions
• Tone assessment
• Superficial and deep sensation assessment
• ROM restrictions and Tone
• Motor Testing
• Is the patient’s strength pure? Are they using a synergyor a substitution (secondary muscle) pattern?
• Neurological vs non neurological causes of weakness
• Special Tests
• Cranial Nerve testing
• Functional scales (Berg, Dynamic gait index, TUGS, etc)• Coordination Testing
• Bed Mobility
• Sit to stand
• Transfers from w/c to and from bed• Gait
• Balance Testing
• Static and dynamic testing•
Using disability scales
What are the different components of the sensory examination?
• Accuracy of cortical perceptions
• Able to localize and recognize
• Joint position sense
• Perception of movement in the extremities • Superficial sensory capabilities
• Superficial sensation
• (tested 1st)
• Responsible for superficial sensation
• Receive info from the external environment
• Responsible for perception of pain, temperature,light touch and pressure
Deep sensation (tested 2nd)
Responsible for deep sensation
• Receive stimuli from the muscles, tendons, liga-
ments, joints and fascia
• Responsible for position sense and awareness of joints at rest, movement awareness (Kinesthesia)and vibration
Combined cortical sensations
• (tested last)
• Combo of both deep and superficial
• Responsible for stereognosis, two point discrimina-tion
Use a sharp object that does not pierce the skin
• Should be cleaned before hand
• Ask when the pt verbally feels the stimulus
2 test tubes of different color. Cold (41-50oF) and Heat (104-113oF)
• If too cold or too hot, it may cause pain response• Pt indicates if they feel cold or heat
Light touch• Test
Use a piece of a cotton to the area to be tested
• With eyes close, pt indicates when they are beingtouched 1,
PT presses down until there is a indent into thept’s skin
• Pt tells PT when they feel that they are being
Difference betweeen propioception and kinesthesia?
Propioception is the static position and kinesthesia is the dynamic position.
Deep sensational testing are
• Proprioception• Vibration
Difference between superficial and deep swnsation?
Pressure is still part of superficial testing because the sensation is coming from the outside workd, and deep, the information is coming in from the inside world, the muscle movements and the vibration from the muscles.
• Use a tuning fork at 128 Hz
• Place the tuning fork on a bony
• Ask the pt if the tuning fork is vi-brating or not
• Test joint position
• Passively move the joint into a position with a minimal grip• Response
• Ask the pt what position is the joint is in
• Test awareness of movement
• With minimal pressure, the PT lightly grabs a pt’s joint, and they pas-sively moves the joint thru the range, back and forth.
• This is done thru a small range
• Pt is instructed to tell the PT when they feel what direction is the
joint moving in
• For larger proximal joints, it is done thru a quicker ROM
What is tone?
• Defined as the resistance of muscle to passive elonga-tion or stretch
• Hypertonia = increased
• Hypotonia = decreased
What types of hypertonia is there?
What is spasticity?
• Increase resistance to motion with an increase in
• Associated with injury to the corticofugal pathways (pyramidal tracts)
Variations of spasticity
• Clasp knife response, Initial stretch produces high resistance, followed by a sudden letting go
• Clonus, Cyclical, spasmodic alternations of ms contrac-tion and relaxation
• Babinski sign, Ext of great toe with stimulation of the lateral
sole of the foot
• Resistance to passive movement involving both agonist and antagonist muscles
• Due to lesions to the basal ganglia
• Cogwheel - rachetlike
• Leadpipe – constant rigidity
Components of Tone Assessment are?
Observation portion of tone assessment
• Observe to see if a pt is fixed in to certain pos-tures
• Ie. LE fixed into ext, add, and pf
• If a limb is floppy, it will look lifeless, and the LE’s roll ou
Palpation portion of tonal assessment
• Hypotonic muscles will feel soft and flabby• Hypertonic muscles will feel taut and
harder than normal
PROM portion of tonal assessment
• Move the limb in all directs
• Detect if any resistance, in order to check for rigidity
• Then proceed with quicker speeds to check for spasticity
Hypertonic state, we do not do _________ test.
Why do we not do strength test when we notice a person in a hypertonic state?
Its just tone, an inaccurate reading.
What is the main question that we ask when we perform the motor assessment?
If there is weakness, then why is this person in this regards.
What two super major superficial things can cause muscle weakness?
Is it the neuro diagnosis, or is it other stuff.
Difference between primary and secondary weakness?
The broken ankle, it gets weak because of pain and maybe because of damaged nueral connections, but the knees and hips will get weak because of disuse due to the pain at the ankle, and this is now secondary.
PT is good for the primary neural issues or is it good for the secondary atrophy disuse and improper motor movement issues?
The secondary issues
Movement starts where?
Brain... Motor cortex.
Parietal does what?
Cerebellum does what?
Basal ganglia does...
Feedback and initiation, it is tied in with PD and hd?
When the hip flexors aref iring, what are the hip extensorsd oing?
Besides relaxing the antagonist muscles, what else will the body need to during movement?
Stabilize the body.
When doing a job, what are the compensatory muscles supposed to do?
Relax, so that thpey, which they are not used to such strenuous movement, will not tire out.
Will we want the flexor synergy to turn on when we do hip flexion?
Yes, at walking, and the other leg needs to be at its extensor synergy.
Outside of walking, do we want the flexor synergy when we hip flex?
R/O synergy = Test joint out of ...
synergy pattern, if fine, not using synergy. If cannot they are using synergy.
R/O substitution = Place secondary agonist muscle in...
lengthen position, if fine, not using substitution . If strength decreases they are using a substitution pattern.
• If patient appears to be weak, must determine cause of weakness
• Can be due to poor proximal stabilizer muscle, or due to poor motor control, or due to overactive firing of antagonist mus-cle, or due to atrophy, or to lack of afferent flow. Usually a patient will have more than one cause, so must test for all.
First, stabilize proximal bone
• If strength increases, weakness may be due to weak stabilizers, or poor motor control (not pre-firing the stabilizer mus-
• Differentiate by asking the pt to activate proximal bone by some vc or manual cues, if gets stronger poor motor control• If does not get stronger, have the pt do some active exs of stab ms, to see if that helps improve strength, if it does, that
indicates poor motor control, if not this indicates poor stabilization strength, continue to second part
If they use their motor control and it still cannot become stronger, then it indicates that there are stabilizing muscles that are at the cause of this.
Second, if stabilization does not help, rule out over firing of the antagonist muscle
• This is done by relaxing the muscle by stretching, or by placing it an over stretched position or performing a post isomet-
ric contraction relaxation
• If this helps, over firing of antagonist muscle is one possible culprit
• If does not help, the weakness may be due to the CNS/PNS lesion or due to atrophy, clinical judgment will help differen-tiate the two by observing for muscle girth, and determine how long the patient had the weakness for
• Neurological weakness fatigues quickly
SPECIAL TESTS: CRANIAL NERVE TESTS
Performed if the PT suspects any dysfunction to the cranial nervesOr if the PT suspects VBA insufficiency
If wes uspect VBA dysfunction, what do we then test?
The CN, because the brain gets fed directly from the VBA so it would show very well in the functionality of the CN.
Maybe one can argue for balance, but balance can be due to other issues as wel, CN will hone in much more directly to the VBA.
Clinical Neuro Examination: Special Tests: Coordi nati on Testi ng
How is coordination testing divided?
•. Body posture
•. Extremity movements involving large muscle groups•
Utilization of small muscle groups
How is coordination testing progressed?
•Bilateral symmetrical tasks
•Bilateral asymmetrical tasks•Multi-limb tasks
•Finger to nose
•Shldr abd to 90, w/ elbow ext. Pt is to touch tipof their own nose
•Finger to PT’s finger
•PT sits opposite of pt. Pt touches the tip of PT’s finger. PT alternates positions
•Finger to finger
•Bilateral shoulder abd to 90, w/ elbow ext. Pthas to go back and forth between the finger tip be-
tween the PT’s left and right index finger
•Alternate nose to finger
•Pt touches their nose, and then the PT’s finger
•Pt touches the tip of the thumb, to the tip of eachfinger
! Elbow flex to 90. Pt alternatively moves in and out of pronation/supination in a rapid pace
PT perform a maximum isometric contraction, and the pt should check that motion.
Alternate heel to knee; heel to toe
In supine. Pt alternatively touches the knee and bigtoes with the heel of opposite UE
Heel on shin
In supine. The heel of one foot is slid up and down the shin of the opposite LE
Drawing a circle
Pt draws an imaginary circle in the air with upperor lower extremity
Different functional tasks
• Bed mobility
• Supine to sit
• Roll side to side
• Sit to stand
• w/c to and from bed• Gait
•Upper body trunk rotation•
Lower body trunk rotation
•Supine to sit: varies entails
•Supine to long sit > move LE’s•Roll first, Legs, UE/Trunk
•Sit to stand entails?
1.Bend forward (flexion phase)
2.Extend hips (extension phase)
3.Extend knees (extension phase)
4.Maintain standing (stability phase)
How do you go and determine what to work on?
First you must see what they csnnot do in their societal life.
Then you go and see what functional activity will limit them in that involvement.
Then see what actions are involved in performing that functional activity properly.
Then see where they are lacking and need to improve.
It can be ROM or Motor or Both.
Exacerbating Factors of MS?
Bacteria, Viral, UTI, sinus infections
• Disease of the organs = hepatitis, pancreatitis, asthma attacks• Stress (divorce, death, losing a job)
• Even minor stress (lack of sleep, dehydration)
• Exacerbations less than 24 hours
• Typically due to heat
How often should ms get a MRI?
Once a year.
Is vision an issue for MS patients?
If they are not tiring in the cool clinic, what do you do?
Have theme xercise so that you can see to them heating to bring on the symptoms, not exacerbations.
PD Four Cardinal Signs
Contractions of oppos-ing muscles
• Usually at rest, but ad-vances with disease
• “Heaviness” & “Stiff-ness”
• Usually in agonist
and antogonist mus-cle
• Starts unilateral and
• Affects ROM and
•Akinesia or Bradyki-nesia or Hypokinesia
• Bradykinesia(slow movements)
• Insufficient motor recruitment force beginning of a move-ment
• Also applies to cog-nitive processing
• Improved with ex-ternal cueing
• Loss of voluntary movement, "freezing”Triggered by com-peting stimuli (Nar-row space, obstacle,
• Hypokinesia (reduced movement size)
• >5 years
• poor postural reac-tions of COM over BOS (poor balance re-actions)
• poor feedforward reactions
• poor proprioception
Additional Symptoms Associated with PD
• Secondary Motor Problems
• Motor planning
• Difficult with dual tasks•
PD Non Motor symptoms
• 50% have paresthesias, pain, cold sensation and/or
• Dysphagia (Swallowing)
• Hypokinetic dysarthria (low volume and/or diffi-cult articulating
• Mild cognitive deficits
• executive decision making (planning, reasoning,
abstract thinking, judgement, and so forth)
• visual spatial memory
• bradyphrenia (slow thinking)
• Hypomimia (reduction in facial expressions)
• Urinary incontinence
• orthostatic hypotension
• Altered HR and BP with ex with disease progres-sion
Vertebrobasilar Artery Syndrome
Altered Pain and temp (spinotha-lamic tract)
Cranial Nerve Dysfunction
Motor Weakness (corticospinal tract)
Anterior Cerebral Artery (ACA)Syndrome
Contralateral HP and sensorymainly LE
Problems with imitation, apraxia
Middle Cerebral Artery (MCA)Syndrome
Contralateral HP and sensory
Aphasia: Broca’s (non-fluent), Wer-nicke’s (fluent) aphasia
Loss of gaze to the opposite side
Ataxia of contralat limb
Internal Carotid Artery Syndrome
MCA and ACA symptoms
Posterior Cerebral Artery Syndrome
Topographical disorientation (in-ability to orient to surroundings)
Prosopagnosia (difficulty naming people on sight)
Visual agnosia (cannot recognize objects)
hemiplegia (Cerebral penducle of midbrain contains corticospinal tracts)
Brunnstrom’s Stages of Recovery for CVA
Stage 1: Flaccidity, no mvt
Stage 2: Minimal voluntary mvt, associ-ated reactions; spasticity begins to develop
Stage 3: Voluntary control of mvt syner-gies; spasticity peaks in severity
Stage 4: Mastery of some mvt combo outside of the synergies; spasticity begins to decline
Stage 5: Difficult mvt combo are learned; synergies lose their dominance
Stage 6: Spasticity disappears, isolated joint mvt & coordination achieved
Neurological level of injury is defined as
the most cau-dal level of the spinal cord that exhibits intact sensory and motor functioning bilaterally
How do you figure out the most caudal intact region?
By determining the ability for the patient to •
Feel light touch
• Feel pinprick
Minimal level intact to walk?
The transition point from where they can be more independant?
Who gets balance tests?
Anyone with dizziness or a history of falls.
What comes in and what goes out euring balance?
Afferent comes in, and efferent goes out.
If the patient is falling forward what will they need to do at their ankle?
If the patient is falling backward what will they need to do with their ankle?
What is nystagmus?
Type of involuntary movement of the eyes
• A diagnostic indicator used in identifying central or peripheral vestibular lesions
• Composes of a slow and fast phase
• The direction is named by the direction of fast
phase of the eye movement (due to recovery from the slow side which has the dysfunction)
Test the posterior SCC
• Pt positioned in long sitting on a mat
• The head and neck extend over the upper edge of the surface
• The examiner holds the head of the sitting client between both hands, then rapidly moves the client backward and down with the head turned to the side and the neck extended 30 to 45 degrees below the horizontal
Held for 20 to 30 seconds
• PT looks for sx’s of vertigo and observes for nystagmus
Vestibular occular reflex (VOR)
• Test examines the interaction of the visual and ves-tibular systems for eye and head orientation
• The ability to hold the eyes fixed on a target while
the head is moving (gaze stabilization)
• The ability to synchronize eye and head move-
ments in the same or opposite directions rely on
• Performed in a horizontal, vertical and diagonal di-rections
• Observe the eyes for velocity, smoothness and nystagmus
Head thrust test
• VOR is examined by using slow and rapid head rota-tion in a horizontal direction. SN = 76% SP =96%
• Pt fixates on PT’s nose, while PT rotates head slowly at first
• If a pt has vestibular loss, the head movement will
causes the eyes to move off target (no VOR), and the patient will make a saccade to refixate on the target
• Saccade is fast eye movement
• PT will to be able to maintain gaze when the head is rotates quickly toward the side of the lesion
• Then redone with pt looking at something 6 feet
VOR vs. HEAD THRUST
The head thrust tests the VOR
Functional reach test
Pt stand near a wall that has a yard stick on it
• Pt is asked to stand in 90 shldr flexion, and
with a fist, is asked to reach as far forward
with out falling
Normal 10 inches
Tested in MS, CVA, PD, TBI, and LBP popula-tion
>6 inches, predictor of recurrent falls
(Brauer et al 2000)
Variations – Backward, Left, Right