Neuro SC/PNS Lec 3 and 4

movement analysis definition

the systematic evaluation of human motion used to assess and understand how the body moves during various activities

examples of movement analysis

recording, quantifying, interpreting the mechanics of movement to identify inefficiencies, asymmetries, or abnormal patterns

4 ways in which we learn about movement

seeing it, feeling it, hearing it, teaching it

initial conditions - what to look for

posture, ability to interact with the environment, environmental context

preparation - what to look for

stimulus identification, response selection, response programming

initiation - what to look for

timing, direction, smoothness

execution - what to look for

amplitude, direction, speed, smoothness

termination - what to look for

timing, stability, accuracy

initial conditions - definition

individual's system and the environment conditions

preparation - definition

period of time when movement is organized in the CNS

initiation - definition

the instant segment displacement occurs

execution - definition

period of actual segment movement

termination - definition

instant when movement stops

outcome - definition

the amount of success in reaching goal of movement

control of movement

smoothness, coordination, and timing of movement

amount of movement

the amplitude of movement at each joint during the task

speed of movement

was velocity controlled appropriately with normal acceleration and deceleration during the task?

symmetry of movement

most relevant for bilateral tasks such as gait, rising from chair, bending; can also be assessed between limbs for unilateral tasks

symptoms of movement

was the movement associated with sx?

sequencing and timing

the spatial organization and temporal structure of different body segments to complete a task

smoothness

the ability to complete a task in a continual fashion without interruptions in velocity or trajectory

what three things make up coordination

smoothness, sequencing & timing

what two things make up postural control

verticality, stability

verticality

the ability to orient the body in relation to the line of gravity; vestibular

stability

the ability to control the body's center of mass in relation to the base of support

alignment

biomechanical relationship of body segments to one another as well as to the base of support, in order to achieve the task

amplitude

the extent or range of movement, either whole body or body segments, used to complete a task

symptom provocation

an observation or patient report of symptoms; movement that evokes a particular response

does learning require you to minimize OR maximize opportunities for compensatory strategies

minimize

does learning require you to minimize OR maximize training opportunities for task

maximize

what 3 things does learning require?

1. specificity

2. repetition

3. intensity

what principle does specificity belong to?

3- specificity matters

what principle does repetition belong to?

principle 1- use it or lose it; principle 2- use it and improve it; principle 4- repetition matters

what principle does intensity belong to?

5- intensity matters

retention test

ability of the learner to demonstrate a skill AFTER A LEARNING PERIOD

adaptation test

ability of a learner to modify (adapt) their movement in response to changing environmental demands

what is MSK related peripheral nerve injury?

• Neurapraxia

• axonotmesis

• neurotmesis

• Grade I

  • Overuse injuries 

  • Mild, temporary peripheral nerve injury → mild compression of the peripheral nerve 

  • Carpal and cubital tunnel syndrome

Neurapraxia

• Grades II, III, IV

  • Commonly caused by crush injuries or fractures/dislocations 

  • Moderate peripheral nerve injury where the axon is damaged but the surrounding connective tissue is intact.

  • Can cause complete motor and sensory loss below the injury site

  • Has potential for slow regeneration

axonotmesis

• Grade V

  • Most severe peripheral nerve injury

  • Common causes: laceration from knives or glass, gunshot wounds, etc. 

  • Complete transection of the nerve, including the axon, myelin sheath, and connective tissue. 

  • Results in immediate, total motor and sensory loss with no potential for spontaneous recovery

  • Surgical intervention required 

  • EMG would show no response distal to the injury

neurotmesis

what is Peripheral nerve injury response?

• result of injury or illness

• wallerian Degeneration

what is Wallerian Degeneration?

• Axon degeneration occurs distal to the injury. Distal nerve segment breaks down, macrophages and schwann cells then “clean up” the debris 

• Proximal portion forms a “retraction bulb,” this is to prepare for/attempt regeneration

• Wallerian Degeneration is the immune/inflammatory response to the axon distal to the injury

  1. This is necessary for repair, but excessive inflammation can contribute to secondary damage or neuropathic pain

  2. In the PNS, this response is efficient but in the CNS it is slow and often leads to scar formation instead of regeneration

• Schwann cell function shifts to facilitate debris clearance → phagocytosis

  • Assisted by macrophages and leukocytes 

• Form “regeneration tracks” (Bungner’s bands) → strings of schwann cells that guide regrowth 

• Much greater capacity to regenerate than CNS

Reactions to peripheral injury

Schwann cell function shifts to facilitate debris clearance →

phagocytosis

• asissted by macrophages and leukocytes

Form “regeneration tracks” (Bungner’s bands) →

strings of schwana cells that guide regrowth 

• Oligodendrocytes do not phagocytose like schwann cells do

• Microglia are not as efficient as macrophages 

  • Leftover myelin debris may never be cleared

    1. Barrier to axon regeneration

• Astrocytes are activated and deposit proteins which block regrowth via scarring

  • Can leave to neuropathic pain

reactions to central injury

why does the PNS have an advantage?

• Peripheral branches regenerate 

• Cleaner environment in the PNS because schwann cells clean up debris 

• Internal state of PNS neurons

What disadvantages does the CNS have?

• Injury does not induce growth proteins 

• Growth quickly subsides 

• Sprouting rate is very slow (4 microns per hour)

• Growth cones become dystrophic

  • The ends of the proximal axon die off (unlike PNS where they bulb and regrow)

Peripheral and central changes contribute to neuropathic pain:

• brain

• spinal cord

• dorsal root ganglia

• peripheral fibers

what is brain?

• Inflammatory mediator release

• Glial cell activation (induces inflammation)

• Cortical remodeling

• Increased descending facilitation

• Decreased descending inhibition

what is spinal cord?

• Inflammatory mediator release 

• Glial cell activation

• Increased synaptic efficacy 

• Decreased inhibitory tone

what is dorsal root ganglia?

• Increased excitability 

• Altered gene expression 

• Ectopic firing (spontaneous signals from damaged region increases pain)

what is peripheral fibers?

• Increased nociceptor sensitivity 

• Ectopic firing 

• Altered signal transmission

• Fiber density changes, neuronal hyperexcitability, glia and autonomic neurons are in pain-promoting states → leads to chronic states of pain (genetic predisposition)

• Inappropriate signalling to 2nd order neurons 

• Ectopic electrical discharge, myelinated A fibers (hours), unmyelinated C fibers (weeks)

  • Drives voltage-gated Na channels 

• Inflammatory process contributes to hyperexcitability 

• Treatment targets these separately

Peripheral processes of pain

Fiber density changes, neuronal hyperexcitability, glia and autonomic neurons are in pain-promoting states →

leads to chronic states of pain (genetic predisposition)

• Central sensitization from persistent nociceptive input, occurs at 2nd order neuron (dorsal horn)

• Microglia are hyperactive 

• Misbalance between descending facilitation and inhibition

• Excitable ventral/posterior thalamus 

• Cortical plasticity contributes to painful interpretation of incoming signals 

• Leading to chronic pain

Central processes of pain

Pain from either PNI or central injury can be similar

• Acute, subacute and chronic pain

  • Time alone is not a reliable indicator of pain mechanism 

  • Persistent pain can begin early – this is important for therapists to recognize 

  • Early identification of central mechanisms is crucial for effective treatment

what are the many types of pain?

• input related pain

• processing related

• central neuropathic pain

what is under input related pain?

• peripheral neuropathic

• noccieptive

what is under processing related pain?

central nociplastic

• Pain referred in a dermatomal or cutaneous distribution

• History of nerve injury, pathology, or mechanical compromise

• Pain/symptom provocation with mechanical testing which moves, loads, or compresses neural tissue 

• Peripheral nerve damage

peripheral neuropathic

• Pain localized to area of injury or dysfunction

• Clear, proportionate mechanical or anatomical nature to aggravating and easing factors 

• Usually intermittent and sharp with movement or mechanical provocation

• Absence of:

  1. Pain with other dysesthesias 

  2. Night pain or disturbed sleep

  3. Antalgic postures or movement 

  4. Burning, shooting or electrical pain

nociceptive

what is absent with nociceptive?

• Pain with other dysesthesias 

• Night pain or disturbed sleep

• Antalgic postures or movement 

• Burning, shooting or electrical pain

• Disproportionate, non-mechanical unpredictable pain pattern in response to multiple or non-specific aggravating/easing factors

• Pain disproportionate to the nature and extent of injury or pathology 

• Diffuse/non-anatomic areas of pain/tenderness on palpation

• Strong association with maladaptive psychosocial factors 

• Altered pain processing (central sensitization) without clear damage resulting in widespread, persistent pain 

central nociplastic

• Arises from CNS injury/illness (SCI, stroke, MS)

  • Results from direct damage to the brain or spinal cord causing burning or shooting pain in specific nerve distributions

• Can have spasticity → assess contributor to pain

  • Central injury = gain of nerve function = spasticity 

  • Can treat spasticity to reduce the pain

• Spinothalamic tract MUST be impaired in the painful area

  • Not getting normal sensation in the periphery 

  • If they have normal sensation it is NOT central neuropathic pain

central neuropathic pain

• sensitization

• central neuropathic pain

• neurologic patient can have either

  • Ex: shoulder pain in complete SCI (overuse); knee pain on unaffected side in stroke 

• To be central neuropathic pain, pain MUST be impaired in the area of involvement 

  • The spinothalamic tract MUST be abnormal (pain and temperature sensation), if normal, it is not central neuropathic pain

Differentiating central sensitization from central neuropathic pain

peripheral nerve injury- loss of function:

• could be from entrapment, but not always 

  1. Numbness

  2. Weakness/paresis

  3. Weak or absent reflexes

peripheral nerve injury- gain of function:

• Pain

• Itch

• Paresthesia (“pins and needles”)

• Hypersensitivity (allodynia/hyperalgesia)

what are Typical impairments from CNS injury ?

• Positive and negative signs - depends on disease/injury

• Primary effects

• secondary effects

• Paresis

• Muscle tone

  • Increased with CNS damage, decreased with PNS damage

• Loss of selective muscle activation, abnormal synergy - depends on disease/injury

  • Incomplete activation of synergies. Ex: Patient trying to reach may be able to extend elbow but cannot elevate shoulder. Or lacking activations that lead to gait deviations.

• Sensory systems - depends on disease/injury 

• Spatial deficits 

• Non-spatial deficits (arousal, attention, memory)

primary effects of CNS injury

• things we can measure (primary effects lead to secondary effects)

  1. Decreased strength 

  2. Decreased ROM 

  3. Skeletal bone

secondary effects of CNS injury

what is used to diagnose Peripheral neuropathy

• nerve conduction study

• needle EMG

• medical treatment

• Lifestyle changes → nutrition, decreased alcohol consumption, illicit drug use, exercise, blood sugar.

• Autoimmune/inflammation → intravenous immunoglobulin (IVIg), steroids.

  • Immunosuppressive drugs: prednisone, cyclosporin, azathioprine

  • Plasmapheresis 

• Decrease glutamate

  • Gabapentin - blocks Ca+ channels

  • Lidocaine patch - blocks Na+ channels 

• Increase serotonin 

  • Duloxetine hydrochloride - DM

  • Nortriptyline

• Nerve block - bundle of nerves 

• Surgery (carpal tunnel)

medical treatment

what is Lifestyle changes →

nutrition, decreased alcohol consumption, illicit drug use, exercise, blood sugar.

what is Autoimmune/inflammation →

•  intravenous immunoglobulin (IVIg), steroids.

  1. Immunosuppressive drugs: prednisone, cyclosporin, azathioprine

  2. Plasmapheresis 

what is under decrease glutamate?

• Gabapentin - blocks Ca+ channels

• Lidocaine patch - blocks Na+ channels

what is under increase serotonin?

• Duloxetine hydrochloride - DM

• Nortriptyline

what is nerve block?

bundle of nerves

what surgery can a patient receive ?

carpal tunnel surgery