Week 3-4 (Motor Control) Flashcards
<p>Why is motor control important to study?</p>
<p>The ultimate function of the nervous system is to control behaviour (move muscles).</p>
<p>Examples that the brain is essential for behaviour? (3)</p>
<p>1.) Locked in Syndrome</p>
<ul> <li>Paralyised, butawake &cognitively intact</li> <li>Caused by brainstem stroke</li></ul>
<p>2.) Sea Squirt</p>
<ul> <li>Larvae: Brain in head and big tail for swimming</li> <li>Adult: Eat its own brain after attaching to a rock</li> <li>Suggests brain is useless once the need to move is lost</li></ul>
<p>3.) Blindsight</p>
<ul> <li>Ability of cortically <strong>blind</strong> people to respond to visual stimuli that they don’t consciously see.</li> <li>unable to consciously process</li></ul>
<p>What are the 3 kinds of muscle cells/fibres</p>
<p><u>Voluntary</u></p>
<ul> <li>Skeletal (Straited)</li></ul>
<p><u>Involuntary</u></p>
<ul> <li>Smooth: Gut and Lungs</li> <li>Cardiac: Heart</li></ul>
<p>Kinds of skeletal muscles?</p>
<p>What kind of movements do they make?</p>
<ul> <li>Agonist/Antagonist (Flexor/Extensor)</li> <li>They can only make one movement (i.e. contract)</li></ul>
<p>What are the types of muscle contractions (2) and what is its underlying mechanisms (1)</p>
<p>Isometric contraciton: Length of muscle stays the same</p>
<ul> <li>e.g. Trying to lift table</li></ul>
<p>Isotonic contraction: Tone of muscle stays the same</p>
<ul> <li>e.g. Picking up a ball</li></ul>
<p><strong>Sliding Filament Theory </strong>is the underlying mechanism</p>
<p>What is the anatomy of skeletal muscle? Fine vs Gross motor control?</p>
<ul> <li>Many muscle fibres in each muscle</li> <li>Each muscle fibre isinnervated by only one motor neuron, but one motor neuron innervates many muscle fibres <ul> <li>Fine motor control: Few muscle fibres in onemotor unit</li> <li>Gross motor control: Many muscle fibres in one motorunit</li> </ul> </li></ul>
<p>What is the anatomy of the muscle fibre?</p>
<p><u>Myofibrils</u></p>
<p>Main work force that causethe muscle contraction. They contain thick filaments (<u>myocin</u>) and thin filamenets (<u>actin</u>)</p>
<p><u>T-Tubules</u></p>
<p>Folded cell membranes outside the muscle fibre</p>
<p><u>Sarcoplasmic Reticulum</u></p>
<p>Modified endoplasmic reticulum and is<strong> full of calcium.</strong></p>
<p>What are differences between synaptic trasmission and muscle contraction (3)</p>
<p>In muscle contraction,</p>
<ul> <li>AP always causes muscle twitch (no threshold)</li> <li>AP propogrates in all directions</li> <li>Only Acetylcholine is released</li></ul>
<p>How is force modulated in muscles?</p>
<p>Force is modulated by:</p>
<ul> <li>Number of motor neurons activated</li> <li>Rate of firing of motor neuron</li></ul>
<p><em>An AP ALWAYS result in muscle twitch</em></p>
<p>What is the sliding filament theory?</p>
<ul> <li>Motor neuron from the spinal cord synapses on a muscle fibre at the neuromuscular junction (<strong>NMJ</strong>), releasing <strong>acetylcholine</strong>(Axon-to-Membrane)</li> <li>Acetylcholine <strong>depolarises membrane</strong> by opening sodium-gated channels, creating AP</li> <li>AP propagatesin all directions and including <strong>going down the t-tubules</strong> <ul> <li><strong>Sarcoplasmic reticulum releases calcium</strong></li> <li>cause<strong>Myocin (Thick) and Actin (Thin) filaments in myofibrils to slide</strong> over each other, causing <strong>contradction</strong></li> </ul> </li> <li>WhenAP is gone,calcium is gradually taken up by the sarcoplasmic reticulum <ul> <li>Muscle relaxes and goes back to its resting position (the filaments goes back to its resting position)</li> </ul> </li></ul>
<p>What are the 2 kinds of reflexes?</p>
<p><u>Muscle Spindles/ Intrafusal Fibres</u></p>
<ul> <li>Located in muscle</li> <li>Detect muscle length</li></ul>
<p><u>Golgi Tendon Organs</u></p>
<ul> <li>Located in tendons</li> <li>Detect muscle stretch (or rather, tension and force because of the stretch)</li></ul>
<p>What is the difference between extrafusal and intrafusal muscle fibres</p>
<p><u>Extrafusal Muscle Fibres</u></p>
<ul> <li>Voluntary movement</li> <li>Innervated by alpha motor neuron</li></ul>
<p><u>Intrafusal Muscle Fibres</u></p>
<ul> <li>Involuntary movement</li> <li>Innervated by gamma motor neuron</li></ul>
<p>How does the intrafusal fibres/muscle spindles work?</p>
<ul> <li>Signal from brain telling muscle to contract <ul> <li>AP generated in alpha and gamma motor neurons</li> <li>Extrafusal fibres contract and intrafusal fibres contract a bit (not as much)</li> </ul> </li> <li>Whenintrafusal fibrescontract <ul> <li>Afferent fibre detects small <em>change in length</em> and sends information back to the alpha motor neuron in spinal cord (via. monosynaptic connection)</li> </ul> </li></ul>
<p>What is the gorgi tendon reflex. What is the function and give an example.</p>
<p><u>Golgi Tendon Reflex</u></p>
<ul> <li>Bundle of nerves located in tendons, at the ends of the muscle</li> <li>Prevent muscle damage and a polysynaptic reflex <ul> <li>e.g. Increasing tension in muscle to hold more weight. Golgi tendon organ sends information tospinal cord and an inhibitory interneuron sends an inhibitory signal to alpha motor neuron so that the muscle relaxes a little</li> </ul> </li></ul>
<p>How is M1 distributed?</p>
<ul> <li>Each area of M1 correspond to a particular region of the body (Somatotropic Distribution)</li> <li>Majority of nerves projecting to our spinal cord for body movements starts here</li></ul>
<p>What are the nerves that take information from M1 to muscles (i.e., what are the descending motor tracts)?</p>
<p></p>
<p><u>Descending Motor Tracts</u></p>
<ul> <li>Lateral tracts: <ul> <li>Control <strong>peripheral</strong> muscles for fine, precise, discreet movements</li> </ul> </li> <li>Ventromedial (Medial) tracts <ul> <li>Control <strong>core</strong> muscles for postural movements and bilateral movements</li> </ul> </li></ul>
<p>Elaborate on descending motor tracts (lateral)</p>
<p>Lateral Tracts:</p>
<ul> <li>Independent limbs movements</li> <li>Axons from M1 and red nucleus (midbain area involved in arm movements) project to spinal cord and cranial nerves</li> <li>Axons cross over to contralateral sides in bulges of medulla (pyramids)</li> <li>Axons also project to cranial nerves directly</li></ul>
<p>Elaborate on descending motor tracts (ventromedial)</p>
<p><u>Ventromedial Tracts</u>:</p>
<ul> <li>Coordinated movements</li> <li>Axons from many parts of cerebral cortex (not just M1).</li> <li>Axons go to BOTH sides of spinal cord (unlike lateral, don't cross-over in medella)</li></ul>
<p>Explain the brain processess in planning and producing a movement</p>
<ul> <li>PPC (7-10s) <ul> <li>Location of item in space</li> </ul> </li> <li>PFC (2-3s) <ul> <li>Action Plan; Inhibition</li> <li>Damage results in illogical disorganised movement</li> </ul> </li> <li>SMC and PMC (???) <ul> <li>SMC: Sequences (e.g., key-in-lock); Inhibiting habitual motions</li> <li>PMC: Complex; Receives arbitrary ("when I clap jump" and non-arbitrary ("where my arm is") information</li> </ul> </li> <li>M1 (0.5s) <ul> <li>Sends via. descending tracts</li> </ul> </li> <li>Desision Conscious (0.2s)</li> <li>Sensory stimuli (0.03-0.05)</li> <li>Movement (0s)</li></ul>
<p>What is the basal ganglia (including input, outputs)</p>
<ul> <li>Large group of structures in the forebrain that forms<strong> </strong>loops<strong> </strong>with motor regions. <ul> <li>Input <ul> <li>M1, Somatosensory</li> </ul> </li> <li>Output <ul> <li>M1, SMC, PMC, Brainstem</li> </ul> </li> </ul> </li></ul>
<p>What are the pathways of basal ganglia? (2) What is the function of the basal ganglia? (3)</p>
<p><u>Pathways</u></p>
<ul> <li>Direct: excitatory effect on movement</li> <li>Indirect: inhibitory effect on movement</li></ul>
<p><u>Function</u></p>
<ul> <li>Regulate the vigour of movement (Force modulation)</li> <li>“Self initiated” movements</li> <li>Movement inhibition (e.g., "Don't touch this")</li></ul>
<p>What brain structures are important when inhibiting a movement</p>
<p>PFC and Basal Ganglia</p>
<p>(That's why before age 5, poor inhibition due to slow maturation of PFC)</p>
<p>What is the function of cerebellum?</p>
<p><u>Cerebellum</u></p>
<ul> <li>Originally thought for balance and coordination</li> <li>Important for rapid, <strong>repetitive</strong> movements where <strong>aim</strong> is important (e.g., basketball; start-stop initiated movement)</li> <li>Continous movements (e.g., cycling) unaffected by cerebelluar damage</li></ul>
<p>What does the lateral zone of the cerebellum do? (2)</p>
<p><u>Lateral Zone</u></p>
<ul> <li>Receives information about movement plan (e.g,, location of limbs)and send to M1 for modification</li> <li>Damage results in decomposition ofmovements<strong></strong></li></ul>
Summarize motor control
Movements are initiated in cerebral cortex, but assisted and modified by cerebellum and basal ganglia
What does motor imagery activate? And what happens when imagining a demanding task and and exhaustion task?
Motor imagery
- Imagining a movement activates many of the brain regions involved in the early stage of motor control.
- SMC
- PPC
- Basal Ganglia
- Cerebellum
- If imagining demanding task, cardiovascular and respiration increase and the muscles used have increased activity.
- If imagine performing a task to exhaustion then the muscles involve fatigue more quickly.
Apraxia: Symptoms (2)
Apraxia
Symptoms:
- "Without Action" but not paralysed
- Inability to imitate or perform actions to vocal instructions
Apraxia: Types
- Limbs: Kicking, etc.
- Oral (Speech/Muscle): Facial muscles and vocalization
- Constructional agraphia (rare): Imitating a picture/ Legos
- Apraxic agraphia (rare): Can spell word (understand) but cannot write
Apraxia: Causes and Treatment
Causes
- Parietal Lobe Lesions
- Limb: Left frontal and parietal
- Constructional: Right parietal
Treatment
- Physical/occupational/speech therapy
Ataxia: Symptoms
Symptoms
- "Without coordination"
- Poor coordination, speech change, unsteady walking, difficulty swallowing
Ataxia: Causes
Causes
- Cerebellar damage
- Alcohol abuse
- Stroke & Tumour
- Multiple Sclerosis
- Hereditary forms
- Virus
Ataxia: Treatment/Management
Ataxia: Treatment
- Treat underlying cause (e.g. alcohol consumption)
- Virus may reverse spontaneously
Ataxia: Management
- Physical/Speech/Occupational therapy
- Devices to aid mobility when untreatable
PD: Symptoms
PD: Symptoms
- Muscle tremor, slow movement, rigidity
- "Freezing gait"
- Cognitive difficultiies, memory loss, depression
- Loss of oflaction (early)
PD: Causes
PD: Cause
- Neuronal death in substantia nigra which have dopamine releasing axons to basal ganglia
- Genetics and environmental contributions
PD: What are the 2 pathways of dysfunction? What does it mean for the pathways when there is no DA
1.) Direct
- Overall excitatory
2.) Indirect
- Overall inhibitory
No DA > Both pathways are inhibitied > Everything is dampaned (Inhibitory)
What is freezing gait. Which disease is it related to and how does one avoid it?
Freezing gait in PD:
Involuntary inability to move at unpredictable times
Avoiding
- Marching: Stepping rhythmically
- Stepping over an imaginary line
One can cycle but cannot walk
PD: Treatment
PD: Treatment
- Behavioural (Exercise)
- Dopamine Agonists and Mao-B inhibitors (inhibit dopaine breakdown)
- Deep Brain Stimulation (Advanced disease)
Polio: Prevalance and Symptoms
Polio: Viral disease.
Asymptomatic in 90-95%; Symptomatic in 5-10%
Symptoms
- Symptomatic: Flu-like, full recovery
- Non-Paralytic (1%): Headache, pain, full recovery
- Paralytic (0.5%): Muscle paralysis, weakness, not all recover
- Post-polio syndrome (25-50% of all): Weakeness years after
Polio: Causes. What is paralyptic polio
Polio
- Viral infection spread through faeces-mouth.
- Paralytic Polio
- Virus attacks the spinal alpha motor neurons.
Polio: Treatment
Treatment:
- None
- Focus on prevention via vaccination (Booster vaccination recommended if travelling to active areas (Afghanistan, Pakistan, Nigeria))
Myasthenia Gravis: Symptoms and Causes
Symptoms
- Muscle weakness and fatigue, usually starting with head muscles (often eyelids).
Cause
- Bodies own immune system creates antibodies that bind to Acetylcholine receptor.
Myasthenia Gravis: Treatment
Treatment
- Immunosuppressant’s that slow antibody production.
- Acetycholinesterase inhibitors to increase the time that Ach is present in the neuromuscular junction.
Anarchic hand (Alien hand syndrome). Definition and Cause
Definition
- Rare disorder of involuntary, yet purposeful, hand movements.
Causes
- Anterior cerebral artery strokes, midline tumors, and neurodegenerative illnesses.
What are the variants of Anarchic hand and what are the brain parts implicated?
Frontal variant:
- Groping movements
- SMC, prefrontal cortex, corpus callosum
Posterior variant:
- Levitating hand, withdrawal.
- PPC, thalamic, occipital lobe damage.
Tourette Syndrome: Symptoms and What are the simple and complex variants
Tics: Rapid, repetitive, “involuntary” muscle movements and vocalisations
- Commonly associated with OCD and ADHD
Simple
- Motor: eye blink, head jerk, nose twitch, shrugging.
- Vocal: grunts, sniffs, throat clearing, barking noise
Complex
- Motor: jumping, twirling, pulling at clothes
- Vocal: words or phrases, coprolalia, echoalia, palilalia
Tourette Syndrome: Causes
Cause:
Unclear pathophysiology but
- Abnormal activity in the cortico-basal ganglia loops.
- Genetic involvement assumed
Tourette Syndrome: Treatment
Treatment
- Mild: Nothing
- Comorbid conditions (ADHD, OCD, anxiety)
- Problematic: Antipsychotics (haloperidol, pimozide) deep brain stimulation.
What are psychogenic movement disorders
- Abnormal movements not attributable to an organic neurologic disorder.
- Considered to be psychologically mediated (conversion disorder)
- Many patients lack clear psychological distress and don’t believe there is a psychological cause of abnormality.
- CBT can be useful.
What is target muscle reinnervation?
Targeted muscle reinnervation
- Nerves for missing muscles are reattached to existing muscles to prevent neuroma
- Nerves activate new muscles when attempting 'old' function
- Electrical activity generated in re-innervated muscle (from old nerves forming new NMJ with existing muscles) can be mapped out and used by the prosthetic and to make 'natural' movement
What is quadriplegia?
What did prosthetics demonstrate?
Quadriplegia: No signal going through to spinal cord and to muscles
Prosthetic
- Microelectrode planted over M1 and connected to computer
- Electrodes can be stimulated by computer and computer can control/receive information
- Can move muscle
- Showed that motor cortex is still able to function over a decade after loss of descending motor outputs
Aflalo (2015): Other than M1, where else could electrodes be implanted to enable movement control?
What is the issue?
Anywhere in the pathway but PPC (Think) + M1 (Move)
Issue
No feedback – there is no sensation arising back from the arm etc (eggshell)
How does somatosensory feedback work
- Different forms of stimuli will activate different receptors, but
- Strech/pressure/chemical on receptors open Na+ channels in axons, causing AP
- AP sends to brain via. spinal nerves which have different characteristics for different receptors
- Dermatome: Area of body each spinal nerve innervates
How does sensory information reach the brain?
- Receptors > Spinal cord > Somatosensory cortex (behind M1)
How is somatosensory cortex organised?
How is it different from M1?
Somatotropic organization
- All the information about sensation from the face come in right next to the region of the motor cortex that corresponds to the face.
Difference
- You feel tooth pain but you can’t move your teeth
- You have lots of sensory information from the genitals but not much control over it.
Other than somatosensory cortex, where is information sent to?
What happens if there is damage to one region
Somatosensory information is also sent to insula, which is also involved in emotions
- Feather = Nice
- Hard harshake = Unpleasant
Damage to one region can cause separation of emotional content versus sensation
When sensory nerves are damaged, what can be useful and why?
What are some criticisms
Sensory feedback with prostheses:
- Microarrays placed over somatosensory cortex
- Mimics natural biology
- Adaption/Learning (e.g picking up egg)
Critics
- Some scientists argue that sensory feedback not essential with visual feedback and practice
What is the efference copy?
What is the advantage?
Efference Copy (corollary discharge)
A copy of the motor command sent to sensory regions (instead of muscles).
Advantage
- Enables planned movement to be compared with actual movement
- Enables sense of self-generated movement
Explain why when we copy someone's force, it gets stronger?
How does it relate to tickle
Efference Copy
- We pay more attention to externally generated information than internally generated sensations (because we cannot anticipate)
- So if you push someone else you think that you’re not doing it as hard as it feels to them
Because we know the tickle is coming (efference copy), it doesn't work
What are the 2 kinds of tickles? And what does it activate
Tickle
- Light feather touch "itch type"
- light touch + Itch
- Somatosensory and ACC (pleasure)
- Deeper laughter provoking type
- Pain + Deep Pressure
- Anterior SMC
Self-tickle with delay. What are the results?
- If there is a delay between thinking and action, one can self-tickle
- 100ms: More ticklish
- 200ms: About the same as when someone else does it
Explain the link between tickle and schizophrenia
SZ may result from faulty efference copies of speech and movement
- SZ don't reognise speech/movement as self-geneated, attirbuting it to external sources.
Tickle
- SZ without hallucinations = Same as controls
- SZ with hallucinations = Equally ticklish regardless of delay
