Transcript Upper Motor Neuron

UPPER MOTOR NEURON
SYNDROME
Aims
• Expand the participants’ understanding of
upper motor neuron syndrome.
• Introduce the application of the concepts of
movement as used in the assessment and
treatment of adults in the analysis posture
and movement.
Motor Neuron
• Upper motor neuron
- cell body lives in a CNS processing center
- synapses on the lower motor neuron
- activity in upper motor neuron may facilitate or inhibit
lower motor neuron
•
-
Lower motor neuron
cell body lives in a nucleus of the brain stem or spinal cord
triggers a contraction in innervated muscle:
destruction of or damage to lower motor neuron
eliminates voluntary and reflex control over innervated
motor unit
Upper Motor Neuron
Upper motor neurons are neurons that originate in higher
regions of the brain, such as the motor cortex, and synapse
on the lower motor neurons to convey descending
commands for movement (Mayer 2003)
Lower Motor Neuron Lesions
Impaired reflex actions
-causes flaccidity
• atrophy
-can grow back
• 1 mm a day
Amyotrophic Lateral Sclerosis
Lou Gehric, July 4, 1939
UMN Syndrome
Damage to the descending motor
pathways anywhere along this trajectory
gives rise to a set of symptoms
Upper motor neuron
syndrome
• Following a brain injury an individual will often have a
complex presentation impacting not only on the
neuromuscular system but also on the musculoskeletal,
sensory-perceptural and cognitive system (Cohon 1999)
• The upper motor neuron syndrome encompasses all the
dyscontrol characteristics associated with a lesion affecting
some or all of the descending motor pathway (Barnes 2001)
• Motor dysfunction after UMN lesion is classified into positive
and negative signs. (Canning et al. 2004)
Negative & Positive Signs
Hughlings jackson
(1835~1911)
UMN Syndrome
• Negative signs are those represent a loss of
Pre-existing function.
• Positive signs relate to secondary changes
(Canning et al. 2004)
• This classification does not encompass cognitive or
Perceptual dysfunction or psychological reaction.
UMN Syndromes
Negative signs
Positive signs
Weakness
Clonus
Fatigue
Associated reactions
Sensory loss
Acute hypotonia
Non-neural changes in
muscle
Spasticity
Loss of dexterity
Hyperreflexia
Weakness
- Constitutes a major cause of the patient’s disability.
- Reduced neural excitation may cause weakness.
- Muscular weakness may cause secondary weakness of neural
transmission.
- Reduce muscle activation may cause atrophy and change in
the muscle fiber population.
Weakness
Muscle atrophy could be due to
• Disuse
• Loss of central trophic effects
• Neurogenic atrophy
Number of motor units reduced post stroke
(Hura et al 2000)
Muscle length associated with weakness at certain ranges
Central Loss of Force Production
Loss of central command generate and sustain force.
No loss of contractile capacity: not the same as
peripheral weakness, myopathy or general weakness
(Sahrmann 2002)
Compensatory movement patterns
Sensation
Action
↑
Cognition
↑
Perception
↑
Sensation
Sensory Deficits
Deficits in awareness, processing and interpretation and
kinesthetic memory
Fewer attempts at spontaneous movements
Altered sense of “weight” of a limb
Altered sense of timing and speed
Contributes to development of pain
Loss of Dexterity
- Ability to solve any motor task precisely, quickly, and
deftly.
- To coordinate muscle activity to meet environmental
demands.
Fatigue
- Many stroke patient suffer from fatigue.
- Reduced force production causes an increase in the effort
required to move.
- Weakness may be another reason for fatigue.
Associated Reaction
- Is the abnormal muscle activation during moving, be called
dyssynergic pattern of movement.
- Indicate weak postural control mechanism and loss of the
normal balance strategies.
- Occur in response to perturbation either intrinsic or
extrinsic generation
- Can change the muscle type from phasic to tonic.
- Promote learned non-use.
Definition of spasticity
•
As…motor disorder characterised by a velocity
dependent increase in the tonic stretch
reflex(muscle tone) with exaggerated tendon jerks,
resulting from hyperexcitability of the stretch reflex,
as one component of the upper motor neuron
syndrome (Lance 1980)
• What is frequently forgotten is that the Lance
definition refers to only one component of the
UMN syndrome (Ivanhoe & Reistetter 2004)
Spasticity
Before the 1970’, spasticity was seen as the major
contributors to disability.
Excessive antagonist activity could not have caused the
observed movement abnormality
(Dietz et al. 1981, Sahrmann & Norton 1977).
Spasticity
• Exaggerated stretch reflexes may not be the major
cause of established spasticity.
• Factors which are thought to contribute to the
increased mechanical resistance to movement
include reduced tendon compliance and
physiological and histochemical change in muscle
fiber (Dietz 1992)
Spasticity
• “Spasticity is a sensori-motor phenomenon related
to the integration of the nervous system motor
response to sensory input”
• “It is related to hypersensitivity of the reflex arc as
a result of the loss of descending inhibition”
(Ivanhoe & reistetter 2004)
Spasticity
- Research definition is increment of muscle tone
due to hyperexcitability of stretch reflex.
- Clinicians definition is much broader, includes the
entire UMN syndrome.
- Misconception
• Hyperactive stretch reflex are cause of excess muscle stiffness
and associated movement
• But hyperstiffness is often the result of nonreflexive factor :
myoplasticity and/or muscle overactivity.
Alpha-gamma coactivation
New Definition
“Disordered sensory-motor control resulting from
an UMN lesion presenting as intermittent or
sustained involuntary activation of muscles,”
SPASM 2005
Mechanism of Hypertonia
CNS lesion
Reflex hyperexcitability
Altered muscle function
(eg prolonged shortening)
Non-CNS factors
(eg immobilization)
Hypertonia
Altered passive mechanical
Properties(contracture)
The Neurological Deficits
Primary Impairments
- Neurological weakness
- Muscle activation deficit
- Change in tone
Secondary Impairments
- Altered alignment
- Change in muscle length
and position
- edema
- pain
Composite Impairment
- Clinical hypertonicity
(spastic movement disorder)
- Altered postural control
- Loss of selective movement
Chemical
Communication
Neural Problem
Non-Neural Problem
Mechanical Impairment
IMPAIRMENT
Secondary impairment
Primary impairment
Composite impairment
Movement deficits
Atypical movement
Compensation
Primary Impairment
•
•
•
•
Changes in muscle strength
Changes in muscle / postural tone
Changes in muscle activation
Sensory changes
Secondary Impairment
• Orthopedic changes in alignment and
mobility
- Changes in alignment
- Changes in joint mobility
• Changes in muscle and soft tissue
length
Composite Impairment
(Movement dysfunction)
• Movement deficits
• Atypical movement
• Compensation
References
• Shumway-Cook & Woollacott: Motor control. 2007
• Janet M.Howel: Neuro-Development Treatment Approach. 2002
• Eric C. Kandel: Principle of neural science. 1999.
• Geoffrey Kidd MSc :Understanding Neuromuscular Plasticity.1992.
• Dr. Nigel Lawes , Ms Mary lynch-Ellerington: Changing the
Nervous System “ From Cell to patient”. 2007.
• Bente E. Bassoe Gjelsvik : The Bobath Concept in Adult
Neurology
• Mary lynch-Ellerington : Bobath course note. 2006,2007,2010
• Mary lynch-Ellerington, Sue Raine : Bobath Concept. 2009