hypothesis Flashcards
What is Spasticity?
Spasticity is an involuntary, velocity-dependent increase in muscle tone and is a component of upper motor neuron (UMN) syndrome. It occurs in 60–84% of people with MS (Hugos & Cameron, 2020).
What is normal muscle tone?
Normal muscle tone is a constant state of mild muscle tension, maintaining the readiness of a muscle to contract. Normal postural tone allows the body to maintain an upright position against gravity, while also permitting selective movement to attain functional skills.
What is the pathophysiology of spasticity?
Neural component: Due to an UMN lesion, there is an interruption of the dorsal reticulospinal tract, medial reticulospinal tract, and vestibulospinal tract. This causes an imbalance between excitatory and inhibitory influences on the anterior horn cell, leading to uncontrolled overactivity of certain muscle groups and exaggerated stretch responses. There’s a lack of inhibition and an inability to switch off firing due to damage to central processors.
Non-neural component: Stiffness and contracture occur due to biomechanical changes from the UMN lesion, including fixed shortening of muscles and contracture of periarticular structures, as well as an increase in collagen in contractile muscles.
Why is spasticity assessed and what is expected to be seen?
Assessment is important to understand the effects of spasticity on movement and function. Common patterns of muscle synergies include:
Lower limb extensor synergy:
- Hip: Flexion (F), Internal Rotation (IR), Adduction (ADD)
- Knee: Extension (E)
- Ankle: Plantarflexion (PF), Inversion (I)
Upper limb flexor synergy:
- Shoulder: Internal Rotation (IR), Adduction (ADD)
- Elbow: Flexion (F)
- Forearm: Supination (Sup)
- Wrist: Flexion (F)
- Fingers & Thumb: Flexion (F), Adduction (ADD)
What is the relationship between decreased strength and stroke?
- Greater weakness is typically found at shorter muscle lengths (inner range) after a stroke (Ada et al., 2003).
- Muscle weakness is often greater distally than proximally (Andrews & Bohannon, 2000).
What is muscle strength?
Muscle strength is the highest amount of tension or force that a muscle or muscle group can voluntarily exert in a single maximal effort.
What causes pre-CNS pathology weakness?
Pre-CNS pathology weakness can be caused by factors such as ageing, sedentary lifestyles, and other conditions like osteoarthritis (OA), rheumatoid arthritis (RA), and diabetes.
What are the pathophysiological hypotheses of weakness after stroke?
Primary neural weakness: After a stroke, reduced upper motor neuron recruitment, decreased cortical output, and less input to the spinal motor-neuron pool reduce motor unit recruitment.
Non-neural secondary adaptive weakness: If some time has passed since the stroke, immobility leads to disuse atrophy and stiffness, reducing muscle fiber density, cross-sectional area, number of motor units, and increasing resistance to contraction in agonist muscles.
Pre-CNS pathology weakness:Contributing factors include ageing, sedentary lifestyle, and conditions like OA, RA, and diabetes.
What are somatosensory deficits and how common are they after a stroke? and how does it form normal movement
- Somatosensory deficits are common after a stroke, with more than 60% of patients presenting with sensory impairments (Schabrun & Hillier, 2009).
- Normal movement relies on accurate somatosensory afferent information being received by the central nervous system to guide and control motor function.
pathophysiology of sensory loss
Deep pressure: The ascending pathway for deep pressure is the medial/anterior spinothalamic tract, which crosses over at the spinal cord.
Light touch: The ascending pathway for light touch is the dorsal column-medial lemniscus pathway, which crosses over at the medulla oblongata.
pathophysiology of length
- Non- neural components of tone – when muscles are immobilized in the shortened position there is an increase in the proportion of collagen to contractile muscle
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- stiffness and contracture due to secondary adaptive biomechanical changes because of UMN lesion – fixed shortening of the muscle and contracture of the periarticular structures, increased collagen in muscles
length common contracture sites
Upper limb
- loss of finger and wrist extension
- Loss of thumb extension, abduction and opposition
Lower limb
- Loss of ankle dorsiflexion and eversion
- Loss of hip abduction
coordination pathophysiology
- Lesion or damage to cerebellum which is an area of the brain in which plays a role in movement control – timing, coordination & integration of movements
- Cerebellar dysfunction leads to ataxia
Dysmetria coordination
inaccurate (undershoot or overshoot) amplitude of movement of intended limb at end-position
Dyssynergia coordination
decomposition of movement, loss of smooth performance of multi-joint movements and lack of coordination between agonist and antagonist
Dysdiadochokinesis
Inability to perform rapidly alternating movements of force or rhythm
Tremor- coordination
movement oscillations due to lack of coordination between agonist and antagonist
- Intention tremor – exaggerated with movement
- Resting tremor – seen at rest, reduces with movement
