מבחן ריאשון Flashcards
Negative Sign
which reveal a disorder. This is the absence of what should be present in a normal examination
Absence of what you normally expect to see
a. Non reactive pupils, atrophy, lack of ability to move, absent reflex
b. Parkinsons lose equilibrium reaction for maintaining head, lack normal posturing
Positive Sign:
which reveal a disorder. This is a finding that should nor be normally present.
- Presence of what you do not normally expect to see
a. Clonus, babinski, dilated pupils, increase DTR reflex, spasticity, rigidity, abnormal posture,
b. TBI muscles firing and not do anything: posturing (not spasticity or rigidity but increased motor output secondary to severe head injury)
History: Try to find the Primary Focus of the Problem (8)
A. Onset: slow vs. rapid [the time frame, is it related to trauma or a slow progressive onset]
B. Duration: constant vs. intermittent [does it go away at certain times, find out what relieves pain/positional]
C. Course: static or progressive [is it slowly getting better/worse or the constant no matter what]
D. Symptoms: as stated by patient [pain, weakness, muscle spasms]
E. Results of Test: [MRI, Xray, findings of other professionals]
F. What does the patient think is the cause:
G. Past Medical History: [one may cause the other]
H. Related Family History: [genetics]
Mental Status:
assess during the history taking: evaluates association areas of the cerebral cortex, keep in mind the education level and cultural differences [you must take their SES and education level into account]
A. Orientation
B. Memory
C. Attention, Thought Processes
D. Calculation ability [count back by 7 from 100]
Language/Speech:
assess during the taking of history
A. Follows and understands: Fluent and non-fluent aphasias
B. Reads, comprehends, names objects
C. Expressive (motor) aphasia (Frontal Lobe)
D. Receptive (sensory) aphasia (Temporal Lobe)
Motor Function:
Root Distributions (know peripheral nerve and root distributions—be able to differentiate peripheral nerve involvement and a root compression)
C5
deltoid
biceps
C6
wrist extension
C7
triceps
C8
finger flexion
T1
intrinsics
L1,2,3
illiopsoas
L2,3,4
quadriceps
L4,5
anterior tibialis
L5-S1
peroneus longus and brevis
EHL
S1
gastroc
Soleus
Muscle Fasciculation:
what are they
when are they seen
causes
- Involuntary muscle twitches of random muscles
- Can be seen normally in everyone (fatigue, nervous
- Positive sign when occur with other positive or negative signs and symptoms
- Can be caused by: Nerve irritation, electrolyte imbalance (nerve will randomly discharge)
(v. s. ALS occurs in many muscles)
sometimes people have random sensory complaints of this nature which can be sensory nerve irritation or electrolyte imbalance
Deep Tendon Reflexes:
- 0 =
- 1+ =
- 2+ =
- 3+ =
- 4+ =
what makes the number lower?
what makes the number higher?
Where to test DTR? What NR? • Biceps: • Brachioradialis: • Triceps: • Quads: • Gastrocnemius:
know the root distributions and peripheral nerves:
root compression or peripheral makes the numbers lower,
CNS involvement makes the numbers go higher
- 0 = absent
- 1+ = diminished
- 2+ = Normal
- 3+ = Increased
- 4+ = Hyperactive
- Biceps: C5, C6
- Brachioradialis: C5, C6
- Triceps: C7, C8
- Quads: L2-L4
- Gastrocnemius: S1
Where to test DTR? What NR? • Biceps: • Brachioradialis: • Triceps: • Quads: • Gastrocnemius:
- Biceps: C5, C6
- Brachioradialis: C5, C6
- Triceps: C7, C8
- Quads: L2-L4
- Gastrocnemius: S1
Peripheral nerve distribution:
peripheral sensations tests peripheral nerves and does not need to be interpreted by the CNS
Cortical Sensations:
need to be interpreted in the CNS, secondary areas of cerebral cortex of parietal lobe
What are the peripheral sensations test?
peripheral sensations tests peripheral nerves and does not need to be interpreted by the CNS
a. Light touch
b. Pain and temperature
c. Proprioceptive
d. Vibrations
Test the good side first, and then test the involved side in order to be sure the person understands the testing and the response should be normal
Monofilament sensory testing is calibrated to discriminate between levels of sensation
What are the Cortical Sensation tests?
need to be interpreted in the CNS, secondary areas of cerebral cortex of parietal lobe
a. Two Point Discrimination
b. Stereognosis (shape held)
c. Graphesthesia (drawn)
d. Bilateral Simultaneous
e. Localization
Test the good side first, and then test the involved side in order to be sure the person understands the testing and the response should be normal
Monofilament sensory testing is calibrated to discriminate between levels of sensation
Abnormal Adult Tone and Reflexes:
Clasp knife: spasticity: corticospinal tracts
- Resistance and then resistance melts away
- Such as when opening up a pocket knife, or stretching silly putty
Lead pipe: rigidity: Basal Ganglia (ie Parkinson’s)
- Constant resistance throughout the range
- Such as a lead piece
Clonus: Corticospinal
- Can be sustained (continuous beats as long as maintain stretch after the quick movement) or un-sustained (3 beats)
- Both abnormal but different severities
Babinski: (CNS) Corticospinal tracts
Grasp Reflex: Frontal Lobe
1. Stimulation in the palm of hand cause closure of hand
Clasp knife:
spasticity: corticospinal tracts
1. Resistance and then resistance melts away
2. Such as when opening up a pocket knife, or stretching silly putty
Lead pipe rigidity:
Basal Ganglia (ie Parkinson’s)
- Constant resistance throughout the range
- Such as a lead piece
Clonus:
Corticospinal
- Can be sustained (continuous beats as long as maintain stretch after the quick movement) or un-sustained (3 beats)
- Both abnormal but different severities
Babinski:
(CNS) Corticospinal tracts
Grasp Reflex:
Frontal Lobe
1. Stimulation in the palm of hand cause closure of hand
Interpretation of Results and Clinical Implications:
A. Symmetrical distribution is WNL’s
B. Hypoactive Response:
C. Hyperactive Response:
D. Key:
A. Symmetrical distribution is WNL’s
B. Hypoactive Response: decreased responses (peripheral)
C. Hyperactive Response: exaggerated responses (CNS, but immediate stage we see flaccid in spinal shock for SCI when cannot reach threshold)
D. Key: finding a pattern of abnormalities fitting one or more distributions, then fitting this in with the subjective information
• SEE FLOW CHART: pick one thing and follow through the flow chart and see if it makes sense o Myopathy (muscular dystrophy ie Duchene’s, Steroid cause muscle weakness)→
Weakness→ Motor Complaint (Sensory would be normal)
o Peripheral Nerve or Branch → Anatomic Distribution → Sensory Complaint
o LMN or Peripheral Nerve → Weakness → Motor Complaint
Gait
- Scissoring
- Peripheral in severe weakness
- Ataxic gait
- Parkinsons
- Scissoring goes with CNS, high tone of adductors
- Peripheral in severe weakness (not high tone, not narrow base of support—do sensory testing and look at impairments in tibial sural, peroneal/superficial tibial nerve, test sensation, for absent reflexes, no babinski, 0 DTR. Absence of CNS findings)
- Ataxic gait is about placement: if it is cerebellar: reflexes intact, muscle testing intact, sensory intact, all peripheral intact. Do Frankel’s, placing foot on target to practice better control
- Parkinsons: face, hand tremor,
Recovery of Function:
A. Effect of Age:
B. Type of Lesion:
C. Prior Experience:
A. Effect of Age: infants and children recover very well to some CNS injuries. Brain plasticity is very real but varies with type of injury.
B. Type of Lesion: small lesions have a better chance of recovery as long as the functional area is not totally lost. Slowly developing lesions allow for a better recovery. (location and size) (a slow growing lesion will allow more ability for brain to slowly accommodate to the changing size and pressure)
C. Prior Experience: greatly enhances recovery. Enhanced environment facilitates better recovery. (someone who had a more challenge to their brain before will recover better. Prior high level learning)
Motor System and Motor Control:
Sherrington Reflex Model
Is sensation needed for movement?
Sherrington—Reflex Model (he was a neurophysiologist, grandfather, thought movement to be sensory driven, not always the case but it is an effective tool to help the patient)
- Sensory stimuli drive movements. Motor output predetermined by a specific type of sensory input.
- However: Sensation not required for movement
- Deafferented monkeys function almost normally
a. The study where importance of sensation was looked at, deafferented monkey on one side and with that loss of sensation the monkey didn’t use that side, but in bilateral deafferentation the monkey still used both sides
Hierarchical Model:
Movement organized from LOWEST levels in the spinal cord to INTERMEDIATE levels to HIGHER
levels in the cortex control is TOP-DOWN.
- Movement from higher up in CNS
- reflex from bottom, control from top from motor cortex, lets get muscles moving an activate primary motor cortex
- when someone has injury in CNS, lower systems take over because loss of higher inhibitory control (one model says spasticity and clonus when lose inhibition over spinal reflex and reflexes become more exaggerated)
Motor programs drive movement. Reflexes dominate with CNS injuries.
Prevent primitive reflex patterns
Types of reflexes elicited help identify general location of injury
Sophisticated movements at spinal cord level
Motor development is more sensory feedback oriented, not just hierarchical
Motor Programming Theories:
engrams
handwriting
apraxia
other factors that influence movement
A. Motor engrams exist and become wired with practice [new movement done slowly and purposefully with trial and error and hardwire a movement pattern to do automatically]
B. Handwriting on paper is similar to writing on a whiteboard [environment changes, task carryover, ie sit to stand and vary height of the chair]
C. Apraxia is loss of ability to execute a movement [lose the ability to tap into the engram and need to relearn]
D. Many other factors influence movement (environment, position, gravity)
Systems Model-Bernstein:
A. Are movements are not peripherally or centrally driven?
B. How is finer coordination achieved?
Systems Model-Bernstein: (he came up with degrees of freedom)
A. Movements are not peripherally or centrally driven but an INTEGERATION on many systems in the CNS, PNS, the musculoskeletal system, and the environment
B. Movement involves few or many degrees of freedom. Finer coordination exists as more degrees of freedom are achieved.
(complex movements multiple degrees of freedom, incorporating environment/person etc for how they perform an activity)
What is the Motor Homunculus?
- what areas hive highest areas in the motor humunculus. Can it vary?
- what has the lowest threshold for activation? what is activated first?
- what requires more stimulation, primary motor cortec or pre-motor cortex or supplemental motor cortex requires?
- Areas for highest dexterity have highest area in the motor homunculus, vary based upon individuals use. the same applies in the sensory
- The primary motor cortex has lowest threshold for activation
- –with use and practice that is the area that gets activated first because it has the lowest threshold
Betz Cells
1 to 1 correspondence between cells and individual AHC’s
- stimulation of pre-motor cortex or supplemental motor cortex requires more stimulation and produces more complex movements
Corticospinal Tract:
- where does stroke commonly occur, what
- what determines extremity affected
- what is recovery based on
Corticobulbar and Corticospinal Tracts:
Stroke commonly internal capsule where Corticospinal Tract fibers go through, if lesion in the INTERNAL CAPSULE
extremity will be affected dependent on WHERE and AMOUNT, there is REDUNDANCY in the motor system, some is outside the internal capsule,
recovery is based on this redundancy and where the stroke was
B. 40-50% of corticospinal tract fibers originate in the primary motor cortex. The majority come from the premotor, supplementary motor areas and the parietal lobe
***Corticospinal Tract: Produce discrete movements and modify indirect motor centers in the Brain Stem
___% of corticospinal tract fibers originate in the primary motor cortex
B. 40-50% of corticospinal tract fibers originate in the primary motor cortex. The majority come from the premotor, supplementary motor areas and the parietal lobe
Corticospinal Tract:
what it does
***Corticospinal Tract: Produce discrete movements and modify indirect motor centers in the Brain Stem
Lesions of the Corticospinal Tracts
what it causes
????
A. Loss of distal extremity strength and dexterity [do not appear flaccid]
B. Babinski Signs
C. Loss of control over Brain Stem Control Centers [loss of high inhibition]
- Increased Tone—does he want this or spasticity??? [spasticity is velocity dependent increased stretch reflex because not able to inhibit that from the higher centers, and tone is when one muscle is firing and another firing co-activation, cannot selectively recruit prime mover, happens after stroke]
- Hyperreflexia
- Clasp-knife phenomenon [increased response to stretch]
Lesion Primary motor cortex:
- weakness or paralysis.
2. Hypotonia (decreased tone) and chronic change in tone.
Lesion Sensory Cortex:
- loss of sensation,
- loss of perception,
- loss of proprioception,
- problems with motor control. 5. Loss of dexterity.
(in deficits with sensory may not be aware of sensation, may be impaired, may not be able to interpret sensation)
Lesion Premotor Cortex:
- weakness from disuse,
- difficulty with planning motor tasks,
- apraxia.
Anticipating motor needs based upon sensory information. [not pure flaccidity]
Lesion Supplemental Motor Region:
- weakness from disuse,
- difficulty with complex motor tasks.
- difficulty with programming and planning movements.
- Motor apraxia.
Lesion Basal Ganglia:
absence of movement, weakness from disuse, abnormal movements (chorea, tremor), or abnormal tone (rigidity) [not the primary motor system, ie Parkinson’s]
Lesion Cerebellum
- incoordination
- weakness from disuse
- balance problems
- changes in tone
Spinal Cord Injury:
- UMN signs below the injury
- LMN signs at the level of injury
- Therefore: LMNL signs locate the level of the SCI
- Above level of injury things will be normal, below level present with upper motor neuron signs because loss connection between higher motor area and the muscles so everything occurs on a spinal reflex level. At level of injury may have flaccid weakness if anterior horn cell problem (cell body of motor neuron [like in ALS and polio). Weakness or paralysis.
- Sensation will be intact since this is a motor problem and dorsal root ganglia is fine sensory system is fine.
Lesion Alpha Motor Neuron:
(My famous AHC): weakness or atrophy
Lesion Muscle
weakness or flaccid: directly affected (muscular dystrophy, myopathy…). The nerve going to it is intact.
Afferent Sensory Input:
- loss of sensory awareness
- uncoordinated movement
- balance problems
Receptors:
A. distribution is according to function. Consist of free nerve endings or highly specialized receptors.
B. Ex Meissner’s Corpuscles (respond to rapidly moving touch, low vibration) decrease in density in the hand from 40-50/mm^2 to 10/mm^2 by age 50. Decrease responsiveness not necessarily due to peripheral neuropathy.
also density of receptors on the back is less than on the hand
Dorsal Columns:
largest, rapid conducting
- High degree of spatial orientation, Cortical Sensations
- Lesion results in decreased proprioception, tactile discrimination, balance and coordination deficits, and general function of extremity is decreased. Graphesthesia.
Anterior and Lateral System:
pinothalamic. Slow conducting, low spatial orientation. Pain, temperature, crude touch.
1. Redundancy between these two systems is probably responsible for functional recovery after SCI. (dorsal and anterolateral)
Sensory Homunculus-
primary and secondary areas (close to 1:1 relationship with density of receptors, importance of sensory info, to area of the sensory cortex of brain—more in face and hands compared to leg or back—loss of interpretation in cortical tests)
A. Spomato-topic orientation in postcentral gyrus
B. The size of each body part representation is proportional to the number of receptors
C. Lesion produces inability to localize different sensations
D. Cannot judge critical degrees of pressure on the body. Unable to judge weights, shapes, texture. [be aware of this for safety]
Deficits with Lesions in the Somatosensory Area I:
A. Unable to localize sensations in the different body parts
B. Cannot judge critical degrees of pressure
C. Unable to judge exactly the weights of objects being held (not judge the change, difference)
D. Unable to judge shapes—Asterognosis
E. Unable to judge textures
F. Poor localization of pain and temperature (may think it is more proximal)
Peripheral Nerve Lesion:
loss of all sensations in the nerve distribution
Peripheral Polyneuropathy:
loss of all sensations in distributions. Distal stocking and glove loss. “Stocking and Glove Distribution” LE gets involved before UE, lower before upper –nerves along it more susceptible to injury (longer nerves)
Sensory Root Lesion:
sensory abnormalities in distribution (ex. Root compression in herniated/bulging disc)
Posterior Column Lesion:
loss of position sense, vibration sense, stereognosis and 2 point discrimination
Complete Spinal Cord Lesion:
loss of all sensation below the level (Aisa)
Thalamic Lesion:
loss or decrease all sensations and pain, on entire body on opposite side of lesion (in thalamic stroke where thalamus effected which is relay station for sensation, a stroke there will cause thalamic pain due to lesion in thalamus which is very hard to treat)
Sensory Cortex Lesion:
loss of discriminative sensations on entire body on opposite side of lesion
what is the motor unit made up of
The motor unit: made up of
- anterior horn cell which is located in the spinal cord. **Therefore anterior horn cell body is LMN (UMN is anything proximal to the anterior horn cell). Severe involvement will not cause spasticity. .
- nerve root
- plexus
- axon
- NMJ
- Muscle it innervates
Is anterior horn cell body UMN or LMN?
**it is part of the motor unit, anterior horn cell body is LMN
(UMN is anything proximal to the anterior horn cell).
Severe involvement will not cause spasticity. .
Peripheral Neuropathies and Neuromuscular Transmission Deficits
where can they occur?
a. Peripheral Nerve:
b. The motor unit: (anterior horn cell, nerve root, plexus, axon, NMJ, Muscle it innervates)
c. Schwann Cells:
d. The NMJ:
Schwann Cells:
what is Wallerian Degeneration
Axon-Schwann Cell becoming a myelinated nerve fiber:
Wallerian Degeneration is breakdown of myelin sheath composed of multiple layers of Schwann Cells
—Myelin sheath around the axon
—Multiple layers of connected sheath that insulates the nerve and helps the AP travel down the nerve
—The AP travels along the node of ranvier (less than 1mm)
The NMJ:
what is it
what is collateral nerve sprouting
the end of the motor axon, where myelin sheath ends, last segment not myelinated
–Collateral nerve sprouting when nerve axon sends out new branches to innervate adjacent muscle fibers that became de-innervated
Peripheral rediculopathy affects the _____, plexopathy affects the ____
Peripheral rediculopathy affects the nerve root, plexopathy in the plexus
Symptoms of Peripheral Neuropathy:
- Motor: (Weakness, DTR absent, Atrophy, Fibrillations, Fasiculations)
- Sensory: (numbness, decreased sensation: hypoesthesia, Pins and needles, tingling-paresthesia (large fiber involvement), Burning: dysesthesia (small fiber involvement) [unmyelinated small fibers], Increased Sensitivity: hyperesthesia [sign of nerve coming back], Severe Deficits )
c. Sympathetic: if localized within a limb, then usually neuropathic (Altered sweating, blood flow, temperature (change in autonomic system), Trophic changes—texture, color, smoothness, Hair loss, edema, hyperesthesia (hair loss can also be vascular), Cardiac, GI, GU symptoms )
Motor Sx
Peripheral Neuropathy
- Weakness,
- DTR absent (could still be in normal range or decreased)
- Atrophy (muscle atrophy can be mild, moderate, severe)
- Fibrillations: muscle fibers: diagnostic EMG will show it, the muscle is discharging randomly by itself without any voluntary effort. Mainly when the muscle gets irritated.
- Fasiculations: entire motor units randomly discharge, often associated with peripheral neuropathy but can be totally normal
Sensory Sx
Peripheral Neuropathy
- numbness, decreased sensation: hypoesthesia
- Pins and needles, tingling-paresthesia (large fiber involvement)
- —when it re-awakens get the tingling
- —Tinel’s Sign: a way to detect irritated nerves by tapping over the nerve to elicit pins and needles – see when nerve is re-awaken, nerve regeneration when this occurs - Burning: dysesthesia (small fiber involvement) [unmyelinated small fibers]
- Increased Sensitivity: hyperesthesia [sign of nerve coming back]
- Severe Deficits: decreased joint position sense and sensory ataxia
- —Ataxic gait can be related to sensory impairment—test sensation. If it is UE and LE more likely to be cerebellar, especially post stroke, but can have a sensory ataxia. Sensory neuropathy affects proprioception.
Sympathetic Sx:
Peripheral Neuropathy
if localized within a limb, then usually neuropathic
- Altered sweating, blood flow, temperature (change in autonomic system)
- Trophic changes—texture, color, smoothness
- Hair loss, edema, hyperesthesia (hair loss can also be vascular)
- Cardiac, GI, GU symptoms
In peripheral neuropathy get ______sx before _____ sx because those nerves are more sensitive
In peripheral neuropathy get sensory before motor because those nerves are more sensitive
Reflex Sympathetic Dystrophy: CRPS Type I (Complex Regional Pain Syndrome I)
etiology
treatment
ETIOLOGY: light splint or cast, localized trauma or surgery, improper use of a sling, not elevating a limb to reduce edema, failure to use the limb after minor episode
- A small involvement or injury
- Redness, edema, swelling, pain—disuse—cycle of more painful
TREATMENT for CRPS Type I:
1. use the limb!—try to reverse the overly protective response, desensitize with stimulation that is continuous but low intensity at first , get them to be able to deal with light sensations and not interpret it as pain and slowly increase it over time (they have hypersensitivity or pain on non-painful stimuli), use and get muscles working, try to reverse the whole sequence
- Reduce edema: get rid of swelling, we do not want stasis of edema and we don’t want the condition to worsen
- Progressive, intense, multidisciplinary therapy
Neurogenic Neuropathy:
(Neurological)
1. Skin dry: peripheral nerve denervation of sweat glands
- Localized Trophic Changes (shiny skin)
- Edema can cause nerve compression
- —-General swelling puts pressure on all structures including nerves and they are susceptible to nerve compression, ie if wearing a cast and swelling occurs
Vascular Neuropathy:
- If majority of the limb presents with hair loss, shiny skin, cold
- Blue skin-venous insufficiency
- Pale skin—arterial insufficiency
***We can use a doppler to check pulse
Neurapraxia:
what is it
what causes it
when recover
mechanism
how to treat
local conduction block
- Usually mechanical compression:
- –Mild compression, usually intermittent compression.
- –Not systemic
- –Common nerve compression: herniated disc, carpal tunnel syndrome
2.. Mechanism:
—First:
compression cause vein collapses–>
poor vascularity to area of nerve= hypoxia nerve—>
nerve less functional sensory complaints first
—Second:
the capillary walls breakdown and fluid leaks in—>more pressure (increase pressure like mini compartmental syndrome)
—Third: Intraneural fibrosis, secondary fibroblast proliferation and resultant NEUROPRAXIA –more breakdown of the nerve itself
3.. Recovery starts in less than 1 minute. After release:
As a PT try to recognize this, we want to get rid of the cause of the compression.
***Removal of compression, nerve re-waken within a minute
Mechanism: Neurapraxia:
—First:
due to the compression the vein collapses,
poor vascularity to that area of the nerve due to localized mechanical compression causes hypoxia to the nerve
which will lead to the nerve becoming less functional, sensory nerve first affected, sensory complaints
—Second:
the capillary walls breakdown and fluid leaks in,
get more pressure on the nerve like a mini compartmental syndrome, increased pressure like mini compartment syndrome
—Third:
Intraneural fibrosis, secondary fibroblast proliferation and resultant neuropraxia –more breakdown of the nerve itself
Axonotomesis:
damage to axon with Wallerian Degeneration
- Demyelination with axonal degeneration
- > 6 hours of continuous compression—this is due to the compression lasting continuously more than 6 hours or it could also be due to compression of higher intensity of less duration
- true anatomical changes to the nerve as each single nerve axon goes through wallerian degeneration due to prolonged compression and prolonged anoxia
- sensory more here too
- axons may take weeks or months to heal if remove the compression source
Axonotomesis:
damage to axon with Wallerian Degeneration
Demyelination + axonal degeneration
- CAUSE:
>6 hours of continuous compression
or compression of higher intensity of less duration
- wallerian degeneration due to prolonged compression and prolonged anoxia :
anatomical changes to the nerve
sensory more here too
- axons may take WEEKS or MONTHS to heal if remove the compression source
