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PHYL2067 > Module 1: Movement & Posture > Flashcards

Module 1: Movement & Posture Flashcards

1
Q

Function of Basal Ganglia

A
  • Inhibiting muscle tone throughout body by initiating inhibitory modulation of motor pathways through thalamus
  • Selecting and maintaining purposeful motor activity via suppression of unwanted patterns of movement and coordination of slow and sustained contractions
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2
Q

2 Pathways of Basal Ganglia

A
  1. Direct: excite the motor cortex or to increase the motor activity
  2. Indirect: decreased activity of the cortical motor neurons and consequent suppression of unwanted/competing movement
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3
Q

Contents of Basal Ganglia (7 Structures)

A
  1. Caudate Nucleus = motor processing, procedural learning, associative learning and inhibitory control of action
  2. Striatum = facilitates voluntary movement
  3. Putamen = regulate movements and influence various types of learning
  4. Substantia Nigra (SN) = movement
  5. Subthalamic Nuclei (STN) = modulator of basal ganglia output
  6. Globus Pallidus Internus (GPi) = final output for both direct and indirect pathways
  7. Globus Pallidus Externus (GPe) = inhibitory control device
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4
Q

Functions of Thalamus

A
  • Reinforces voluntary motor activity initiated by the motor cortex
  • Serves as a relay station and synaptic integrating centre for sensory inputs
  • Helps direct attention to stimuli of interest
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5
Q

Functions of Cerebellum

A
  • Learns and executes instruction for movements
  • Motor skills through repetitive training
  • Ensures coordination of the force, extent and duration of muscle contraction
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6
Q

Functions of Brainstem

A
  • Links the spinal cord and higher brain regions
  • Cardiovascular centre
  • Breathing/respiratory function
  • Regulates Postural muscle reflexes
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7
Q

Contents of Brainstem

A

Midbrain, pons and medulla

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8
Q

Functions of Spinal Cord

A
  • Link between brain and peripheral nervous system

- Integration of spinal reflexes

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9
Q

Spinal Cord Afferents and Efferents

A
  • Sensory afferents (affected by environment) enter through dorsal root ganglion
  • Motor efferents (which cause an effect in the environment) leave through ventral root
  • Afferent and efferent fibres are enclosed together within a spinal nerve
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10
Q

Location of Primary Motor Cortex

A

= Anterior to central sulcus

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11
Q

Functions of Primary Motor Cortex

A
  • Controls voluntary movement produced using skeletal muscles
  • Motor cortex on each side of brain primarily controls contralateral muscles for voluntary movement
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12
Q

Homunculus Representation of Primary Motor Cortex

A

= body regions involved in movements of precision and fine control, such as face and hands, have a disproportionately large representation in the motor map

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13
Q

Location of Primary Somatosensory Cortex

A

= Posterior to central sulcus

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14
Q

Functions of Primary Somatosensory Cortex

A
  • Site for initial processing and perception of somaesthetic (surface of body) and proprioceptive (body positions) inputs
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15
Q

Homunculus Representation of Somatosensory Cortex

A

= the area of cortex allocated to each body surface is proportional to the sensitivity of that part. As such, face, hands and arms have larger representation

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16
Q

Ascending Pathways

A

Includes: Spinocerebellar, dorsal column medial lemniscus, spinothalamic

= the ascending tract refers to the neural pathways by which sensory information from the peripheral nerves is transmitted to the cerebral cortex

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17
Q

Descending Pathways

A

Includes: Pyramidal and extrapyramidal tracts

= descending pathways are groups of myelinated nerve fibres that carry motor information from the brain or brainstem to effector’s muscles, via the spinal cord. Includes pyramidal (voluntary) and extrapyramidal (involuntary) tracts

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18
Q

5 Steps of Basic Reflex Arc

A
  1. Receptor
  2. Afferent pathway
  3. Integrating centre
  4. Efferent pathway
  5. Effector
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19
Q

4 Steps of Primary Circuit of Knee Jerk Reflex

A
  1. Hammer tap stretches the tendon
  2. Sensory receptors in the leg extensor muscle are stretched
  3. Afferent sensory neuron carries signal to the spinal cord where it has a monosynaptic interaction with the efferent motor neuron
  4. This conducts an action potential to synapse on the extensor muscle fibres, causing contraction
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20
Q

3 Steps of Secondary Circuit of Knee Jerk Reflex

A
  1. Afferent sensory neuron also excites a spinal interneuron
  2. This inhibits the motor neuron to the flexor muscle
  3. This means that the flexor muscle, which opposes the extensor muscle, will relax so that the contraction of the extensor can occur unopposed, leading to leg extension
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21
Q

5 Steps of Withdrawal Reflex

A
  1. Stepping on/touching something (i.e. a tack) stimulates sensory receptor (dendrites of pain sensitive neuron)
  2. Sensory neuron excited
  3. Within integrating centre (spinal cord), sensory neuron activates interneurons in several spinal cord segments
  4. Motor neurons excited
  5. Effectors (flexor muscles) contract and withdraw the limb
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22
Q

5 Steps of Crossed Extensor Reflex

A
  1. Stepping on/touching something (i.e. a tack) stimulates sensory receptor (dendrites of pain-sensitive neuron) in RIGHT FOOT
  2. Sensory neurons excited
  3. Within integrating centre (spinal cord), sensory neuron activates several interneurons
  4. Motor neurons excited
  5. (minor) flexor muscles contract and withdraw RIGHT LEG (via withdrawal reflex)
    (major) effectors (extensor muscles) contract and extend LEFT LEG
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23
Q

Structure of Muscle Spindles

A
  • Intrafusal fibres lie within a connective tissue capsule parallel to extrafusal muscle fibres (ordinary muscle fibres)
  • Intrafusal fibres differ from extrafusal fibres by not having contractile elements in the central portion
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24
Q

Afferent Muscle Spindles

A
  • Afferent (sensory) endings
  • Primary (annulospiral) are wrapped around central portion of intrafusal fibres; these detect changes in muscle length and speed of muscle stretch
  • Secondary (flowerspray) endings clustered at end-segments of intrafusal fibres, these detect only changes in muscle length
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25
Q

Efferent Muscle Spindles

A
  • Efferent motor neurons supply the intrafusal spindle (gamma motor neuron) and extrafusal fibres (alpha motor neuron)
  • With sensory and motor innervation along the muscle spinale, we have micro-monitoring of our muscle length
26
Q

Mechanisms of Parkinson’s disease

A
  • Due to selective loss of dopaminergic neurons in the substantia migration pars compacta of the brain
  • The substantia nigra is the major origin of dopaminergic innervation of the striatum, mainly responsible for posture regulation and muscle tone
  • Post mortem brains of PD patients may have only 10% of normal dopamine levels
  • Hypokinetic disorders = less movement
  • Degeneration of the striatum, effecting both the direct and indirect pathways
  • Reduced activity of direct pathway = inability to initiated wanted movements
  • Increased activity of indirect pathway = increased suppression of unwanted movements
  • Results in bradykinesia (slowness of movement) and akinesia (absence of movement)
27
Q

Symptoms of Parkinson’s disease

A
  • Most common: idiopathic “paralysis agitates” (shaking palsy)
  • Bradykinesia and akinesia
  • “TRAP”
    Tremor at rest
    Rigidity of limbs
    Akinesia
    Postural problems (leading to loss of balance)
28
Q

Causes of Parkinson’s disease

A
  • Age: the most important risk factor
  • Family history of PD
  • Male gender
  • Possibly environment (pesticide)
  • Trauma
  • Repetitive Head Injury
29
Q

Normal vs. Parkinson’s Brain

A

Normal:
DAergic neurons from substantia nigra normally inhibit the GABAergic output from the striatum, while cholinergic neurons are excitatory

PD:
In PD, the loss of DA neurons leads to overactivity of the acetylcholine component, with activation of GABA release and muscle rigidity

30
Q

Pharmacological Interventions for Parkinson’s disease

A
  • Dopamine - Boosting drugs (e.g. Levodopa)
    = these drugs increase dopamine activity and restore the natural balance with acetylcholine
  • Anticholinergic drugs (e.g. Muscarinic acetylcholine receptor blockers)
    = these drugs reduce the effects of acetylcholine and restore the balance of dopamine by blocking the brain receptors for acetylcholine
31
Q

Other Interventions for Parkinson’s disease

A

= Deep Brain Stimulation (DBS)

  • 20% patients undergo with 65-85% success rate
  • DBS stimulates sub thalamic nucleus and globus pallidus internus (areas that influence motor control)
  • Suppresses some of the disabling symptoms of PD
32
Q

Mechanism of Disease of Huntington’s Disease

A
  • 75% reduction in activity of glutamic acid decarboxylase, an enzyme responsible for synthesis of GABA
  • It is thought that with GABA concentration declining in the brain, dopaminergic circuits are allowed to operate without the usual “brake” > this means there is excessive movement > it is unexpected, involuntary movements
33
Q

Symptoms of Huntington’s Disease

A
  • Uncontrolled writhing of the muscles in the face, trunk and neck > Chorea
  • Also progressive dementia
34
Q

Causes of Huntington’s Disease

A

= Huntingtin Protein

  • “CAG” trinucleotide repeats add glutamine residues to the protein
  • Normal “CAG” sequence repeats 11-30 times, in HD repeats 36-125 times
  • Excess glutamates cause Huntingtin protein to misfold and not function for cellular transport as normal
  • Heredity: autosomal dominant
35
Q

Normal vs. Huntington’s Disease Brain

A

Normal:
DAergic neurons from substantia nigra usually inhibit GABAergic output from the striatum, while cholinergic neurons are excitatory

HD:
In HD, GABAergic neurons degenerate. Inhibitory regulation is lost, with net excitation as the result, leading to uncontrolled motor activity

36
Q

Pharacological Interventions for Huntington’s Disease

A

Tetrabenazine
= Employs two mechanisms of action to reduce the amount of dopamine in the brain. Decrease in dopamine activity reduces the effects of chorea in HD patients

Mechanism 1:

  • Proteins called vesicular mono-amine transporters (VMATs) normally put the neurotransmitter dopamine into vesicles
  • Tetrabenazine binds to VMATs, preventing the transporters from allowing dopamine particles into vesicles

Mechanism 2:

  • Dopamine binds to the receptors, causing the signal to be sent down the receiving nerve cell
  • Tetrabenazine competes with dopamine by binding to receptors on the surface of the receiving nerve cell, blocking dopamine from binding and passing on electrical signals
37
Q

Other Interventions for Huntington’s Disease

A
  • Experimental transplant of fetal brain tissue/stem has been attempted (is promising)
  • DBS, disrupting activity patterns causing chorea
  • Genetic counselling and in vitro conception
38
Q

Mechanisms of Disease of Multiple Sclerosis

A
  • Autoimmune disease in which the immune system attacks and degrades the myelin sheaths which usually insulate and protect nerves of the brain, spinal cord and optic nerves
  • MS may also have plaque development in the CNS, which may physically obstruct signalling between the brain and spinal cord
39
Q

Symptoms of Multiple Sclerosis

A
  • Numbness and tingling, cognitive dysfunction, depression, fatigue, muscle spasms, weakness, difficulty walking, dizziness, vision problems, pain, bladder and bowel dysfunction
40
Q

Cause of Multiple Sclerosis

A

Mainly unknown

  • Gender (women 2:1)
  • Race (white)
  • Possible genetic link
  • Herpes possibly risk factor for MS
41
Q

4 Types of Multiple Sclerosis

A
  1. Clinically Isolated Syndrome (CIS)
  2. Relapsing Remitting MS (RRMS)
  3. Secondary Progressive MS (SPMS)
  4. Primary Progressive MS (PPMS)
42
Q

Clinically Isolated Syndrome (CIS)

A
  • First episode with symptoms caused by inflammation and demyelination in the CNS (must last 24 hours)
  • Every MS patient experiences CIS; however, some people never progress past CIS
  • If CIS diagnosis and lesions on brain seen via MRI, there is a high likelihood of second episode in future and MS diagnosis
  • If no lesion present, MS likelihood is lower
  • Treatment includes “disease modifying therapy” which may delay onset of MS
43
Q

Relapsing Remitting MS (RRMS)

A
  • Most common disease course
  • Relapse of new or increasing neurological symptoms
  • These relapses have a period of time with partial or complete recovery (remission)
  • During remission, all symptoms may disappear or some may continue and become permanent
  • RRMS may be worsening (an increase in disability following a relapse) or not worsening
  • 85% of MS patients have this diagnosis
  • RRMS can be active (with relapsed or new MRI activity) or not active
44
Q

Secondary Progressive MS (SPMS)

A
  • SPMS starts as RRMS, but patient transitions into secondary progressive phase, in which there is progressive worsening of function
  • Can be characterised as either active (relapses and/or new MRI activity) or not active, as well as with progression (disability accumulation over time without relapses or new MRI activity) or without progression
45
Q

Primary Progressive MS (PPMS)

A
  • PPMS has worsening accumulation of disability from the onset of symptoms, without relapses or remissions
  • Can also be active or not active, with or without progression
  • Approx. 15% of patients diagnosed with PPMS
46
Q

Pharmacological Interventions for Multiple Sclerosis

A
  1. Interferon beta 1a or 1b
    - Proteins which are copies of human interferon protein (1a) or similar in structure (1b). These suppress the immune system, used to reduce risk of disability progression with fewer relapses and reduction in number and size of active lesions in brain
    - Weekly injection
  2. Glatiramer Acetate
    - A small fragment of protein that resembles myelin protein. This decreases relapse frequency
    - Daily injection
  3. Ocrelizumab
    - Reduces the activated immune response and protects myelin. Targets B-cells which can cause inflammation and activate the autoimmune response. Also delays onset of PPMS
47
Q

Mechanisms of Disease for Motor Neuron Disease

A

Disruptions in the signals between the:
- Lower motor neurons and the muscle: The muscles do not work properly; the muscles gradually weaken and may begin wasting away and develop uncontrollable twitching

  • Upper motor neurons and the lower motor neurons: The limb muscles develop stiffness (called spasticity), movements become slow and effortful and tendon reflexes such as knee and ankles jerks become overactive
  • Over time, the ability to control voluntary movement can be lost
48
Q

Symptoms of Motor Neuron Disease

A
  • Muscle wasting, weakness and respiratory failure leading to death within 2-5 years
49
Q

Causes of Motor Neuron Disease

A

Unclear

  • 5-10% of cases have genetic links, ~90% are sporadic
  • One gene mutation linked to MND is SOD1. This serves to protect cells from Reactive Oxygen Species (ROS) that can damage if not neutralised
  • Cell damage is induced by ROS (a.k.a. free radicals)
  • If neurons are unable to repair damage caused by ROS, cell death is started (via DNA breaks and mutations). If these are motor neurons, this can contribute to MND
50
Q

Muscle Atrophy and Wasting

A

Disuse Atrophy: which can be reversed with activity and nutrition

Neurogenic Atrophy: in which there is damage to the nerve innervating the muscle, not readily reversed

51
Q

Pharmacological Interventions for Motor Neuron Disease

A
  1. Riluzole: protects neurons from excitotoxicity and may prolong motor neuron survival
    - Riluzole may block voltage gated sodium channels, reducing glutamate release from motor neurons. Glutamate is excitatory and reducing this may be neuroprotective
    - Riluzole postpones the time that a patient may need a tracheotomy by up to 3 months
  2. Antioxidant Edaravone: less deterioration in functional rating and quality of life when started early
  3. Baclofen: a GABAb agonist which inhibits spasticity. For treatment of symptoms
52
Q

Other Interventions for Motor Neuron Disease

A
  1. Respiratory Care: not just for end stage of life, crucial for maintaining good respiratory function
  2. Assisted eating and feeding tube to assist with eating due to muscle weakness in arms
53
Q

Mechanisms of Disease of Muscular Dystrophy

A
  • MD is a group of disorders which involve progressive loss of muscle and loss of strength
  • Caused by genetic mutations which interfere with the production of muscle proteins required to build and maintain muscle tissue
54
Q

Symptoms of Muscular Dystrophy

A
  • Pain and stiffness in muscles, mobility issues, walking on toes, waddling gait, frequent falls, learning disabilities and delayed speech
55
Q

Causes of Muscular Dystrophy

A
  • More than 1000 possible mutations on the X-chromosomes
  • These mutations impact on the ability of the body to produce the cytoskeletal protein dystrophin, a protein essential for building and repairing muscle
56
Q

Diagnosis of Muscular Dystrophy

A
  • Elevated levels of Creatine Kinase (CK) can suggest MS
  • Genetic testing
  • Heart monitoring
57
Q

Pharmacological Interventions for Muscular Dystrophy

A
  1. Corticosteriods
    = can help increase muscle strength and slow progression, their long-term use can weaken bone and increase weight gain
  2. Heart Meds (beta blockers)
    = if the MD impacts the heart, beta blockers may be useful
58
Q

Other Interventions for Muscular Dystrophy

A
  1. General exercises: ROM, stretching
  2. Breathing assistance
  3. Mobility adis
  4. Braces: keep muscles and tendon stretched and help slow their shortening
59
Q

Mechanisms of Disease of Cerebral Palsy

A
  • CP is caused by brain injury or brain malfunction that occurs before, during or immediately after birth while the infants brain is under development
60
Q

Symptoms of Cerebral Palsy

A
  • Low muscle tone (floppy)
  • Muscle spasms/feeling stiff
  • Poor muscle control, reflexes and posture
  • Delayed development
  • Feeding/swallowing difficulties
61
Q

Treatment Options for Cerebral Palsy

A
  • Physical therapy
  • OT
  • Speech therapy
  • Assistive tech
  • Medications (Baclofen which inhibits spasticity)
  • Surgery

PHYL2067 (5 decks)

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