Movement Flashcards

1
Q

• Why do we have a brain?

A

to Control behaviors

• Ultimately, behaviors are movements

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2
Q
  • All movement depend upon muscle contraction

* 3 categories of muscles:

A
  • Smooth muscles (digestive system and other organs)
  • Skeletal muscles (movement of body in relation to the environment)
  • Cardiac muscles (heart muscles – properties of both skeletal and smooth muscles)
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3
Q

Muscle Fibers

A
  • Muscles are composed of many individual fibers
  • Each muscle fiber receives information from only 1 axon
  • 1 axon may innervate many muscle fibers
  • A neuromuscular junction is a synapse between a motor neuron axon and a muscle fiber
  • Acetylcholine (always) causes/excites the muscle to contract (deficit in acelthycholine impairs movement)
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4
Q

neuromuscular junction

A

a synapse between a motor neuron axon and a muscle fiber

• Acetylcholine (always) causes/excites the muscle to contract (deficit in acelthycholine impairs movement)

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5
Q

Antagonistic Muscles

A

• Movement requires the alternating contraction of opposing sets of muscles called antagonistic muscles
• Acetylcholine always excites skeletal muscles to contract
• 2 Types:
• Flexor – bend or flex a joint
• Extensor – straightens and extends
example of antagonostic muscles in arm: when you want to bend elbow, bicep contracts (flexor) + tricep (extensor – tricep should relax) – when we want to extend the arm, the tricep should contract, bicep should relax.

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6
Q

Fast and Slow Muscles

A
  • Skeletal muscles fibers can be fast or slow:
  • Fast-twitch: fibers produce fast contractions but fatigue rapidly (e.g. jumping)
  • Slow-twitch: fibers produce less vigorous contraction without fatigue (e.g. walking)

Slow-twitch fibers do not fatigue because they are
aerobic—they use oxygen during their movements. You can
think of them as “pay as you go.” Prolonged use of fast-twitch
fibers results in fatigue because the process is anaerobic—
using reactions that do not require oxygen at the time but
need oxygen for recovery. Using them builds up an oxygen
debt.

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7
Q

Fast-twitch muscles/fibers

A

fibers produce fast contractions but fatigue rapidly (e.g. jumping)

Prolonged use of fast-twitch
fibers results in fatigue because the process is anaerobic— using reactions that do not require oxygen at the time but need oxygen for recovery. Using them builds up an oxygen debt.

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8
Q

Slow-twitch muscles/fibers

A

fibers produce less vigorous contraction without fatigue (e.g. walking)

Slow-twitch fibers do not fatigue because they are
aerobic—they use oxygen during their movements. You can think of them as “pay as you go.”

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9
Q

Proprioceptors

A

• Proprioceptors: receptors that detect the position or movement of a part of the body

Muscle proprioceptors detect the stretch and tension of a muscle and send messages that enable the spinal cord to adjust its signals. When a muscle is stretched, the spinal cord sends a signal to contract it reflexively. This stretch reflex is caused by a stretch; it does not produce one.
• 2 Kinds
• Muscle spindles: (proprioceptors parallel to the muscle itself) - respond to a stretch and cause a contraction of the muscle (if muscle stretched too far) – stretch-reflex occur when muscle proprioceptors senses stretch, sends signal to spinal cord to contract.
• Located in the muscle
• The Golgi tendon organ: responds to increases in muscle tension (the “pull” on the tendon)
• Located in the tendons (connects muscle to bone) – connects skeletal muscle to bone. – responds to increase in muscle tension (that occurs during contraction).
• Sends info about tension + Acts as a “brake” against excessively vigorous contraction by sending an impulse to the spinal cord where motor neurons are inhibited

The proprioceptors not only control important reflexes but also provide the brain with information. When what happens differ from what you expected, it sends info to brain

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10
Q

• Muscle spindles

A

proprioceptors parallel to the muscle itself) - respond to a stretch and cause a contraction of the muscle (if muscle stretched too far) – stretch-reflex occur when muscle proprioceptors senses stretch, sends signal to spinal cord to contract.
• Located in the muscle
= CREATES a contraction

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11
Q

• The Golgi tendon organ

A

responds to increases in muscle tension (the “pull” on the tendon)
• Located in the tendons (connects muscle to bone) – connects skeletal muscle to bone. – responds to increase in muscle tension (that occurs during contraction).
• Sends info about tension + Acts as a “brake” against excessively vigorous contraction by sending an impulse to the spinal cord where motor neurons are inhibited
= INHIBITS a contraction

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12
Q

Reflexes

A
  • Reflexes are involuntary, consistent, and automatic responses to stimuli
  • Monosynaptic reflex (compared to more complex reflexes (multisynaptic connections))
  • Reflex requiring one synapse between sensory input and movement
  • Example: knee-jerk reflex

Tap on patellar tendon right below knee cap = causes leg to kick out and stretch quadriceps.

The stretch triggers receptors known as muscle spindles to fire – the sensory signal from spindles travels along axons to spinal cord (at dorsal root ganglion) (it is an excitatory signal) – send it to motor neuron which sends a signal back out – activation of alpha motor neuron is what causes quadriceps to move/contract.
Also, sensory neuron, in addition to sending out signal, the sensory neuron also stimulates an interneuron, so the interneuron receives EXCITATORY input, but sends out INIHIBTORY output, that inhibits the activity of a motor neuron controlling the opposing muscle (the hamstring)

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13
Q

Voluntary and Involuntary Movements

A
  • Most movements are a combination of voluntary and involuntary; reflexive and nonreflexive
  • Movements vary with respect to feedback
  • Some are ballistic and cannot be changed once initiated
  • Others are guided by feedback (to allow for precision) – e.g. when threading a needle, you can readjust.
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14
Q

Sequences of Behaviors

A
  • Many behaviors consist of rapid sequences of individual movements
  • Central pattern generators are neural mechanisms in the spinal cord or elsewhere that generate rhythmic patterns of motor output (in absence of sensory feedback)
  • Example: wing flapping in birds or “wet dog shake”
  • A motor program refers to a fixed sequence of movements that is either learned or built into the nervous system
  • Once begun, the sequence is fixed from beginning to end
  • Example: yawning
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15
Q

Central pattern generators

A

neural mechanisms in the spinal cord or elsewhere that generate rhythmic patterns of motor output (in absence of sensory feedback)
• Example: wing flapping in birds or “wet dog shake”

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16
Q

motor program

A

a fixed sequence of movements that is either learned or built into the nervous system
• Once begun, the sequence is fixed from beginning to end
• Example: yawning

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17
Q

• Brain-computer interface (BCI)

A

• Uses the brain’s signals (electrical like eeg, or other biological signal) to direct computer-controlled devices (e.g. neuroprosthetics – field focusing on developing computer-assisted devices to replace lost limbs – so robotic limbs can be controlled by brain signals)

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18
Q

Major Components of the Motor System

A
  • Cerebrum (forebrain): conscious control of movement
  • Brainstem: direct movements
  • Spinal cord: direct movements
  • Other regions of the motor system:
  • Subcortical basal ganglia help produce the appropriate amount of force for grasping.
  • The cerebellum helps regulate the timing and accuracy of movement.
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19
Q

Role of The Cerebral Cortex

A
  • Role: initiating a motor sequence
  • Much of motor learning is about learning to carry sequences out, and what sequence follows another one, so to create smooth movements.
  • Frontal lobes – 3 particular areas
  • Prefrontal cortex: plans complex behavior (+seems to be involved in “goal-directed”/ considerate behavior)
  • Premotor cortex: produces the appropriate complex movement sequences
  • Primary motor cortex (precentral gyrus – axons connect to brainstem and spinal cord, generating impulses that control the muscles): specifies how each movement is to be carried out – what we mostly consider when studying movement.
  • Additional from book: supplementary motor cortex

The cerebral cortex is particularly important for complex
actions such as talking or writing. It has much less control
over coughing, sneezing, gagging, laughing, or crying (Rinn,
1984). Perhaps the lack of cerebral control explains why it is
hard to perform those actions voluntarily. The primary motor
cortex is also active when you imagine movements, remember
movements, or understand verbs related to movements

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20
Q

Prefrontal cortex

A

plans complex behavior (+seems to be involved in “goal-directed”/ considerate behavior)

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21
Q

Premotor cortex:

A

produces the appropriate complex movement sequences

22
Q

Primary motor cortex

A
  • Responsible for control of specific areas of the opposite side of the body
  • Active when people intend a movement
  • “orders” an outcome

“Homonculus” mapping

(precentral gyrus – axons connect to brainstem and spinal cord, generating impulses that control the muscles): specifies how each movement is to be carried out – what we mostly consider when studying movement

23
Q

supplementary motor cortex

A

The prefrontal cortex and the supplementary motor
cortex are also important for planning and organizing a rapid sequence of movements. If you have a habitual action, such as turning left when you get to a certain corner, the supplementary motor cortex is essential for inhibiting that habit when you need to do something else. The supplementary motor cortex also becomes active after an error in movement, developing ways to inhibit the incorrect movement the next time.

24
Q

Planning a Movement

A
  • Posterior parietal cortex:
  • Role: keeps track of the position of the body relative to the world
  • Damage to this area causes difficulty in coordinating visual stimuli with movement
  • Important for planning movement
25
Q

Inhibition of Movements

A
  • Antisaccade task: inhibits a saccade (a voluntary eye movement from one target to another) – e.g. stare at finger, wiggle the other (you want to make a saccade to moving finger, but in antisaccade task you have to inhibit that urge) – if you inhibit it well = parts of PFC + basal ganglia activity BEFORE seeing stimulus.
  • Performing this task well requires sustained activity in parts of the prefrontal cortex and basal ganglia before seeing the moving stimulus
  • Ability to perform this task matures through adolescence (children younger than 7 have lots of challenge with this task + ADHD impaired too, suggesting these individuals may have some disorder affecting PFC or basal ganglia structures from inhibiting unwanted action) + deteriorates at old age because PFC is highly vulnerable to damage.
26
Q

Mirror Neurons

A
  • Active during in preparation of a movement and while watching someone perform the same movement
  • important for understanding, identifying, and imitating
  • social behaviors
  • Unknown whether they cause or result from social behavior
  • Develop properties by learning
  • Really exciting because they provide possible mechanism for social cognition (e.g. understanding/imitating others) – but unknown if they CAUSE social behavior, or is result of behavior.

there is some evidence of mirror neurons being innate (newborns showing face reactions when seeing that face reaction (above what we would expect at chance level)

Several types of evidence suggest that mirror neurons develop their properties by learning. In both monkey and human infants, many mirror neurons do not respond to observations of others’ movements until after the infants have practiced making those movements themselves

27
Q

Connections from the Brain to the Spinal Cord

A
  • Messages from the brain are sent to the medulla and spinal cord to control the muscles
  • Corticospinal tracts are paths from the cerebral cortex to the spinal cord - they are white matter tracts (myelinated axons)!
  • Both tracts contribute in some way to nearly all movements, but certain movements rely on one tract more than the other
  • Two such tracts:
  • Lateral corticospinal tract
  • Medial corticospinal tract
28
Q

Lateral corticospinal tract

A

• A set of axons from the primary motor cortex, surrounding areas, and red nucleus go to the spinal cord
• These areas are important for Control of movement in peripheral areas (hands and feet)
• Red nucleus: a midbrain area with output mainly to the arm muscles
Axons of the lateral tract extend directly from the motor cortex to their target neurons in the spinal cord.

• Axons extend from one side of the brain to the opposite side of the spinal cord, and control opposite side of the body
• Crossover happens at “pyramids of medulla” – also called “pyramidal tract” – cross over to affect movement on contralateral side.
= handles LATERAL body

29
Q

Medial Corticospinal Tract

A

• A set of axons from many parts of the cortex (not just primary motor area and surrounding areas)
• Incl. Reticular formation, midbrain tectum, and vestibular nucleus
• Vestibular nucleus is a brain area that receives information from the vestibular system (used in balance, combining movement with balance)
• The medial tract controls the muscles of the neck, shoulders, and trunk
• Axons of the medial tract go to both sides of the spinal cord, not just to the contralateral side. (10% ipsilateral, 90 % contralateral)
• moves muscles of midline / trunk of body.
• Responsible for bilateral movements like walking, turning, bending, standing up, and sitting down
=handles MEDIAL body

30
Q

Brainstem Role in Movement

A

• Brainstem: organizes many adaptive movements
• Maintaining posture, standing upright, coordinating movements of the limbs, swimming and walking, grooming the fur, and making nests
controls lot of involuntary behaviors

31
Q

• Cerebral palsy

A
  • Voluntary movements difficult to make, whereas conscious behavior controlled by the cortex may remain intact
  • Caused by brainstem trauma
  • Often occurs during pregnancy or childbirth – can occur from lack of oxygen to brain, or trauma (trauma in brainstem) – conscious behaviors (by higher cortical functions) remain intact.
32
Q

• Locked-in syndrome

A
  • Condition in which a patient is aware and awake but cannot move or communicate verbally because of complete paralysis of nearly all voluntary muscles except the eyes (sometimes FULL paralysis, ocular paralysis more rare though)
  • Due to brainstem damage (signals from cortex cannot get through to spinal cord)
33
Q

Spinal Cord - why is it important + reflexes

A
  • Spinal cord important for movement to occur - example:
  • Christopher Reeve’s spinal cord was severed near its upper end (C1–C2 level). (topmost portion) – from horseback riding accident. = became quadroplegic.
  • Left his brain intact and functioning; his remaining spinal cord intact and functioning, too; but his brain and spinal cord were no longer connected.
  • He was completely paralyzed and unable even to breathe without assistance
  • In humans and other animals with a severed spinal cord, spinal reflexes still function even though the spinal cord is cut off from communication with the brain.
  • Paralyzed limbs may display spontaneous movements or spasms.
  • The brain can no longer guide the timing of these automatic movements
34
Q

Paralysis

A

Inability for voluntary movement in part of the body

cause: Damage to motor neurons or their axons in the spinal cord

35
Q

Paraplegia

A

Loss of sensation and voluntary muscle control in the
legs (Despite the lack of sensations from the genitals,
stimulation of the genitals can produce orgasm.)

cause: A cut through the spinal cord in the thoracic region or
lower

36
Q

Quadriplegia

or tetraplegia

A

Loss of sensation and voluntary muscle control in both
arms and legs

cause: Cut through the spinal cord in the cervical (neck) region
(or cortical damage)

37
Q

Hemiplegia

A

Loss of sensation and voluntary muscle control in the arm and leg of either the right or left side

cause: Cut halfway through the spinal cord or damage to one
hemisphere of the cerebral cortex

38
Q

Tabes dorsalis

A

Impaired sensations and muscle control in the legs and
pelvic region, including bowel and bladder control

cause: Damage to the dorsal roots of the spinal cord from the late
stage of syphilis

39
Q

Poliomyelitis

A

paralysis

cause: A virus that damages motor neurons in the spinal cord

40
Q

Amyotrophic lateral sclerosis

A

Gradual weakness and paralysis, starting with the arms
and spreading to the legs

cause: Unknown. Traced to genetic mutations in some cases, and to exposure to toxins in other cases

41
Q

The Cerebellum

A
  • A structure in the brain often associated with balance and coordination
  • More neurons in the cerebellum than in all other brain areas combined
  • Damage to the cerebellum causes trouble with rapid movements requiring aim/timing
  • Examples: clapping hands, speaking, writing
  • Allows for execution of a sequence
  • Responds to sensory information, especially violations of sensory info
  • Important for certain aspects of attention
  • “controls” timing – when cerebellar damage impairs movement, the reason may be that the damage impaired the perception of timed stimuli related to the movement. – damaged people = generally bad at timing tasks.
42
Q

How the Cerebellum Improves Movement Control

A
  • Cortex sends motor instructions to the spinal cord.
  • Copy of same instructions sent to the cerebellum.
  • Sensory receptors code actual movement and report to the cerebellum.
  • Cerebellum has information about both versions of the movement—what you intended to do and what you actually did—and can calculate the error and tell the cortex how to correct the movement.
  • By comparing actual and intended movement, the error message is sent to the cortex and increases accuracy in subsequent movements. Otherwise, clumsiness! Cerebellum one of first things affected by alcohol  finger to nose test for drunk driving.
43
Q

Organization f cerebellum and its cells

A

The cerebellum receives input from the spinal cord, from
the sensory systems by way of the cranial nerve nuclei,
and from the cerebral cortex. That information eventually reaches the cerebellar cortex, the surface of the cerebellum

●● The neurons are arranged in a precise geometrical pattern,
with multiple repetitions of the same units.
●● The Purkinje (pur-KIN-jee) cells are flat (twodimensional)
cells in sequential planes, parallel to one
another.
●● The parallel fibers are axons parallel to one another and
perpendicular to the planes of the Purkinje cells.
●● Action potentials in parallel fibers excite one Purkinje
cell after another. Each Purkinje cell then
transmits an inhibitory message to cells in the
nuclei of the cerebellum (clusters of cell bodies in the
interior of the cerebellum) and the vestibular nuclei in
the brainstem, which in turn send information to themidbrain and the thalamus.
●● Depending on which and how many parallel fibers are
active, they might stimulate only the first few Purkinje
cells or a long series of them. Because the parallel fibers’
messages reach Purkinje cells one after another, the
greater the number of excited Purkinje cells, the greater
their collective duration of response

44
Q

The Basal Ganglia

A

• The basal ganglia is a large group of large subcortical structures in the forebrain
• Responsible for initiating an action not guided by a stimulus
• Comprises the following structures – surrounds thalamus
• Caudate nucleus
• Putamen
• Globus pallidus
(caudate and putamen = striatum)
• Function: modulate cortical motor system activities (inhibits thalamus)- used in wide range of functions (also e.g. emotion I think)

The direct pathway from the striatum inhibits the globus
pallidus, which inhibits part of the thalamus. By inhibiting an inhibitor, the net effect is excitation

Probably the direct pathway enhances the selected movement, whereas
the indirect pathway inhibits inappropriate competing movements.

  • Cerebral cortex –> caudate nucleus and putamen —> globus pallidus
  • Globus pallidus –> thalamus –> motor areas and the prefrontal cortex
  • Basal ganglia select a movement to make by ceasing to inhibit it
  • Tourette Syndrome
  • Involuntary tics and complex movements
  • Abnormality of basal ganglia
  • The basal ganglia are particularly important for spontaneous, self-initiated behaviors. (compared to stimulus-initiated actions)
  • In general, self-initiated behaviors have a slower onset than those in response to a stimulus
45
Q

Brain Areas and Motor Learning

A
  • The learning of new skills requires multiple brain areas involved in the control of movement
  • Basal ganglia are critical for learning motor skills, organizing sequences of movement, “automatic” behaviors, and new habits
  • Example: driving a car
  • The pattern of activity of the neurons in the motor cortex becomes more consistent (and the neurons fire more when the movement becomes faster) as a new skill is learned
46
Q

Conscious Decisions and Movement

A
  • The conscious decision to move, and the movement itself, occur at two different times
  • A readiness potential: activity in the motor cortex that occurs before we make the conscious decision and before voluntary movement
  • Decision to move (conscious) Begins on average 200 ms before the movement
  • But readiness potential occurs 500 ms before movement.
  • Implies we become conscious of the decision to move, AFTER the decision to move has occurred.

An experiment by Soon et al. demonstrated brain activity occurs 7-10 seconds before “voluntary decision”
= you see the importance of the distinction between stimulus-triggered movements and self-initiated movements (stimulus = fast, voluntary = slow)

47
Q

Parkinson’s Disease - symptoms

A

Movement Symptoms:
• muscle tremors (shaking movements – often exhibited as trembling in extremities)
• rigidity (stiffness of arms or legs, contributes to decrease in “range” of motion)
• slow movements (also very shuffled gait)
• difficulty initiating physical and mental activity
• decrease in ability to initiate spontaneous movement in absence of stimuli

Symptoms also include depression, memory and reasoning (and lnugauge and attention) deficits, loss of olfaction, and other cognitive deficits (+ lack of motivation and pleasure)

48
Q

Movement Disorders

A

• Brain disorders, such as Parkinson’s disease and Huntington’s disease not only affect movement, but also impair mood, memory, and cognition

49
Q

Causes of Parkinson’s Disease

A
  • Caused by gradual and progressive death of neurons, especially in the substantia nigra
  • Substantia nigra usually sends dopamine-releasing axons to the caudate nucleus and putamen
  • With the loss of this input, the striatum decreases its inhibition of the globus pallidus, which therefore increases its inhibitory input to the thalamus
  • Loss of dopamine leads to less stimulation of the motor cortex and slower onset of movements

Loss could be due to…
• Genetics (particularly early onset parkinson’s seems to have genetic link – michael j fox in 30’s) – genetic factors really only a small factor in later onset. (28 potential genes identified – none of them have large effects on their own, but may accumulate)
• Drugs (i.e. MPTP) and Toxins (e.g. much exposure to insecticides, herbicides, and fungicides)
• Trauma (e.g. TBI)
• Lifestyle factors (e.g. cigarette smoking and coffee drinking – with DECREASED chance)
• Damaged mictochondria seem to be the most common thing in these factors to developing PD.
• Conclusion = most cases are likely a result of a combination of factors.

50
Q

Treatments of Parkinson’s

A

As the disease results from a dopamine deficiency, a logical goal is to restore the missing dopamine
• The drug L-dopa is the primary treatment for Parkinson’s and is a precursor to dopamine that easily crosses the blood-brain barrier - L-dopa reaches the brain, where neurons convert it to dopamine.
• But often ineffective for people in later stage – doesn’t prohibit further loss of neurons – and may have other side effects.
• Other “disappointments”:
It increases dopamine release in all
axons, including those that had deteriorated and those that
were still functioning normally. It produces spurts of high release
alternating with lower release. Even if it adequately replaces
lost dopamine, it does not replace other transmitters
that are also depleted
• Other Treatments
• Drugs that directly stimulate dopamine receptors
• Drugs the block the metabolic breakdown of dopamine
• Both of these may decrease symptoms but don’t halt the disease.
• Implanting electrodes to stimulate areas deep in the brain (Deep brain stimulation)
• Experimental: Stem cells (still much in the research phase) – stemm cells to produce large quantities of l-dopa
• Brain transplants: transplanted tissue released neurotrophins that stimulated axon and dendrite growth in the recipient’s own brain. Work with mice has shown promising results for a neurotrophin to repair Parkinson-like damage – surgery needed, as neurotrophins doesn’t cross blood brain barrier.

51
Q

Huntington’s Disease

A
  • A neurological disorder characterized by various motors symptoms (has movement, cognitive and emotion components/symptoms) – considered hereditary?
  • Affects 1 in 7,000 in Canada
  • Usually onset occurs between age 30-50 (earlier than parkinson’s)
  • Associated with gradual and extensive brain damage especially in the basal ganglia but also in the cerebral cortex

Symptoms
Motor symptoms usually begin with arm jerks and facial twitches. Then tremors spread to other parts of the body and develop into writhing. Gradually, the tremors interfere more and more with walking, speech, and other voluntary movements. People lose the ability to develop motor skills

  • Physical symptoms: (also arm jerks and facial twitches) weight loss, involuntary movements (chorea), diminished coordination, difficulty walking, talking and swallowing
  • Cognitive symptoms: difficulty with focus, planning, recall of information and making decisions; impaired insight
  • Emotional symptoms: depression, apathy, irritability, anxiety, obsessive behaviour
  • Presymptomatic tests can identify with high accuracy who will develop the disease
  • Huntington’s controlled by an autosomal dominant gene on chromosome #4 (the gene is longer than it should be) – child of huntington parent and healthy parent has 50% risk of huntington
  • The higher the number of consecutive repeats of the combination C-A-G, the more certain and earlier the person is to develop the disease
  • But there is still variation (especially in age of onset for those with fewer CAG repetitions = Evidently other factors besides genes also influence the age of onset, such as stressful experiences, drug or alcohol abuse, and perhaps diet and exercise)

As a rule, heritability is greater for early-onset disorders than for those with later onset.