UMN vs LMN

UMN Defintion

Brain matter to grey matter of SC

LNM Defintion

Grey matter of SC to m

Structures Involved in UMN Lesions

- CNS

- Brain stem

- SC (esp Corticospinal tract aka primary influence of voluntary movements)

Ortho Examples UMN Lesions (3)

- Cervical myelopathy

- Lumbar stenosis

- Slipped disc leading to SCI

Spasticity

Abnormal response to a quick stretch movement

- Velocity dependent

Hypertonia

Increased resting m tone

Clonus

>3 beats or sustaining

Babinski

Toes upward flaring

Hoffman's

Formation of "ok" sign after pain elicited to nail bed of middle finger

Lhermitte's Sign

Electric feeling down SC during maximal cervical flexion

Structures Involved in LMN Lesions (4)

PNS

- CNs

- Anterior horn cells

- Ventral root

- Inn to skeletal m via peripheral nn

Flaccidity

Absence of voluntary movement in a limb

Hypotonia

Decreased resting m tone

Hyporeflexia

<2 reflex grading scale

Anterior horn cell damage dx ex

Spinal muscular atrophy

Brachial plexus injury is an example of a ___?

Peripheral n injury (LMN)

2 Types of Brachial Plexus Injuries

- Erb's palsy

- Klumpke's palsy

Bell's Palsy is an example of ___?

CN injury (LMN)

Neuroplasticity

The ability of the nervous system to change in response to intrinsic or extrinsic stimuli

How does change in neuroplasticity occur via? (2)

- Neuronal regeneration/collateral sprouting

- Functional reorganization

3 Types of Neuroplasticity

- Developmental neuroplasticity

- Learning associated plasticity

- Experience dependent plasticity

Glial Cells

Supportive cells of the nervous system

Oligodendrocytes

Create myelin in the CNS

Schwann Cells

Create myelin in the PNS

Developmental Neuroplasticity

During second trimester of gestation to early post-natal

Neurogenesis

Development of neurons during formation of neural tube

Gliogenesis

Development of glial cells

Connectivity

The connections between different axons and synaptic targets

Pruning

Elimination of unnecessary axon collaterals in combo with programmed neuronal cell death

Reorganization

Modification of structures and connections

Long Term Potentiation

Converts synapses that are normally silent to active synapses

- As these synapses are activated more often these pathways become "stronger" creating long lasting changes

Initial Learning

Large and diffuse active regions of increased synaptic activity in the brain occur

Task Repetition

Decreased number of active regions in the brain as a task becomes learned

Learned Task "Skill"

Small and distinct areas of increased synaptic activity in the brain

Long Term Depression

Converts active synapses into silent synapses

Adult Neurogenesis

- Neurogenesis significantly declines after early post-natal period

- Gliogenesis continues thruogh adulthood

Learning Associated Neuroplasticity Mechanisms

- Habituation vs sensitization

- Implicit vs explicit learning

Habituation

A decreased response in synaptic activity between sensory neurons and interneurons after a repeated, benign stimulus

Presynaptic Depression

Short term decrease in release of excitatory NTs

Rest

= decreased effects of habituation

Prolonged Repetition

= more permanent decrease in synaptic connections

Sensitization

An increased response in synaptic activity between sensory neurons and interneurons after a repeated, painful stimulus

Implicit Learning

Nondeclarative learning

- Ability to learn without conscious awareness

Explicit Learning

Declarative memory

- Retention of personal experiences and facts

Experience Dependent Neuroplasticity

Cellular processes after a CNS or PNS injury/lesion

Neurogenic Shock

Occurs very soon after injury and is the CNS first response

Neurogenic Shock: Results in ___?

- Flaccidity

- Areflexia

- Hypotension

Resolution of Neurogenic Shock

Occurs over a few weeks following injury

Resolution of Neurogenic Shock: Results in ___?

Spontaneous recovery

- Synaptogenesis

- Angiogenesis

- Expansion/reorganization of motor maps

Injury to Distal Axon Segment

Wallerian (anterograde) Degeneration

- Axon dies

Injury to Proximal Axon Segment

Retrograde Degeneration

- No projections = may completely degenerate

- Some projections = axon may survive

Denervation Hypersensitivity

New receptor sites develop on the post-synaptic membrane

- Makes synapses more sensitive

Synaptic Hypereffectiveness

Larger amounts of NT are distributed through a decreased number of presynaptic branches

- Makes synapses more sensitive

Collateral Neural Sprouting

Undamaged axon bridges to connect to distal segement

Regenerative Neural Sprouting

Damaged axon recovers and reconnects to distal segment

Can Schwann cells regrow in the PNS?

Yes

Can Oligodendrocytes regrow in the CNS?

No

Adaptive Plasticity

Promotes recovery post-injury

Maladaptive Plasticity

"Learned non-use"

- Long term inhibition = pruning and cell death

- Develop compensatory strategies that may inhibit recovery