BRAIN MECHANISMS OF MOVEMENT

The Cerebral Cortex

  • Direct electrical stimulation of primary motor cortex (precentral gyrus of the frontal cortex, just anterior to the central sulcus) elicits movement  doesn-t send messages directly to the muscles
  • Cerebral cortex is particularly important for complex actions (talking or writing)

o    Lack of cerebral control explains why it-s hard to perform actions (sneezing, coughing, laughing) voluntarily

  • The brain area controls a structure on the opposite side of the body
  • Each spot in motor cortex doesn-t control a single muscle (output of given neuron influences movements of the hand, wrist, and arm, and not just a single muscle)
  • Stimulation produced certain outcome, not a particular muscle movement
  • Motor cortex orders an outcome and leaves it to the spinal cord and other areas to find the right combination of muscles

Planning a Movement

  • Primary motor cortex important for making movement, not planning them
  • Posterior parietal cortex  one of 1st areas to become active; keeps track of position of the body relative to the world

o Damage  have trouble finding objects in space (even after describing appearance accurately), frequently bump into obstacles o Also important for planning movements (and control aim)

  • Prefrontal cortex and supplementary motor cortex  also important for planning and organizing a rapid sequence of movements

(supplementary motor cortex essential for inhibiting habits when needing to do something else)

  • Premotor cortex  most active immediately before movement; receives information about target to which the body is directing its movement (and info about body-s current position and posture)
  • Prefrontal cortex  stores sensory information relevant to a movement; also important for considering probable outcomes of possible movements o Damage: many of your movements would be illogical/disorganized (showering with clothes on, pouring water on toothpaste tube)

Mirror Neurons

  • Active both during preparation for a movement and while watching someone else perform the same/similar movement (1st reports in premotor cortex of monkeys) o Ex: mirror neurons in part of frontal cortex become active when people smile or see someone else smile, and they respond strongly in people who report identifying strongly with other people
  • Not only activated by seeing action but also by any reminder of the action

o Cells in insular cortex become active when you feel disgusted, see something disgusting, or see facial expression of disgust     Some (maybe most) mirror neurons develop their responses by learning

Conscious Decisions and Movements

  • People report that their decision to move occurred ~200ms before actual movement (it-s the decision that occurred then. People report decision later)
  • Readiness potential motor cortex produces this kind of activity before any voluntary movement (begins ~500ms before movement)
  • Brain activity responsible for the movement apparently began before the person-s conscious decision; results indicate that your conscious decision doesn-t cause your action, rather you become conscious of the decision after the process leading to action has already been under way for ~300ms
  • We are less accurate at reporting the time of a conscious decision than the time of a sensory stimulus (need to know when something happened but not when we made a decision)
  • Report of when you made decision depends on when you think movement occurred
  • Your voluntary decision is, at first, conscious; decision to do something develops gradually and builds up to a certain strength before it becomes conscious
  • Only spontaneous actions require slow deliberation

Connections from the Brain to the Spinal Cord

  • Corticospinal tracts  paths from the cerebral cortex to the spinal cord; 2 tracts, lateral and medial corticospinal tracts (nearly all movements rely on combination of both tracts, but a movement may rely on one tract more than the other)
  • Lateral corticospinal tract  set of axons from the primary motor cortex, surrounding areas, and the red nucleus (midbrain area that is primarily responsible for controlling arm muscles) o Axons extend directly from motor cortex to target neurons in spinal cord o    In bulges of medulla (pyramids), lateral tract crosses to contralateral (opposite) side of spinal cord o      Controls movement in peripheral areas (hands and feet)
  • Children with cerebral palsy, contralateral path fails to mature, and ipsilateral path remains relatively strong  result is clumsiness
  • Medial corticospinal tract  includes axons from many parts of the cerebral cortex (not just primary motor cortex and surrounding areas) o Also includes axons from midbrain tectum, reticular formation, and vestibular nucleus (brain area that receives input from vestibular system)
  • Axons of medial tract go to both sides of spinal cord (not just contralateral side); controls mainly muscles of the neck, shoulders, and trunk  walking, turning, bending, standing, sitting)
  • Both paths cross in medulla and that the touch information arrives at brain areas side by side with those areas responsible for motor control (have to know what hands doing now to control next action)
  • Damage to primary motor cortex of left hemisphere  lost of lateral tract from that hemisphere and loss of movement control on right side of body o Using medial tract can approximate intended movement

The Cerebellum

  • Contains more neurons than the rest of the brain combined and enormous number of synapses
  • One effect of cerebellar damage  trouble with rapid movements that require aim, timing, and alternations of movements (tapping rhythm, clapping hands, speaking, writing, etc.); they are normal, however, at continuous motor level (drawing circles)
  • Saccades depend on impulses from cerebellum and frontal cortex to cranial nerves (with damage  difficulty programming the angle and distance of eye movements)
  • Finger-to-nose test  Move function depends on cerebellar cortex (surface of cerebellum), which sends messages to the deep nuclei

(clusters of cell bodies) in the interior of the cerebellum; hold function depends on nuclei alone o     Damage to cerebellar cortex, person has trouble with initial rapid movement; if cerebellar nuclei damaged, person may have difficult with the hold segment (symptoms of cerebellar damage resemble alcohol intoxication)

Roles in Functions Other than Movement

  • Cerebellum responded to sensory stimuli even in the absence of movement
  • Masao Ito  proposed key role of cerebellum is to establish new motor programs that enable one to execute a sequence of actions as a whole
  • Cerebellum is important mainly for tasks that require timing; also appears critical for certain aspects of attention; people with cerebellar damage need longer to shift their attention

Cellular Organization

  • Cerebellum receives input from spinal cord, from each of the sensory systems by way of cranial nerve nuclei, and from the cerebral cortex  information eventually reaches cerebellar cortex
  • Purkinje cells are flat (2D) cells in sequential planes, parallel to one another
  • Parallel fibers are axons parallel to one another and perpendicular to planes of Purkinje cells; AP-s in parallel fibers excite one Purkinje cell after another  each Purkinje cell transmits inhibitory message to cells in nuclei of the cerebellum and the vestibular nuclei in the brainstem (send information to midbrain and thalamus) o If parallel fibers stimulate only first few Purkinje cells, result is brief message to target cells; if they stimulate more Purkinje cells, message lasts longer; output of Purkinje cells controls timing of movement (onset and offset)

The Basal Ganglia

  • Applies to a group of large subcortical structures in the forebrain  caudate nucleus, putamen, and the globus pallidus
  • Input comes to caudate nucleus and putamen, mostly from cerebral cortex; output from caudate nucleus and putamen goes to globus pallidus and from there mainly to the thalamus  relays it to the cerebral cortex (especially motor areas and prefrontal cortex)

o Most of the output from globus pallidus to thalamus releases GABA (inhibitory transmitter) and neurons in area show much spontaneous activity  globus pallidus constantly inhibiting thalamus o  Input from caudate nucleus and putamen tells globus pallidus which movements to stop inhibiting o   Damage to globus pallidus (Huntington-s Disease), result is decreased inhibition and therefore involuntary, jerky movements

  • Choosing its own starting time, the basal ganglia highly active; critical for initiating an action but not when the action is directly guided by a stimulus

Brain Areas and Motor Learning

  • Neurons in the motor cortex adjust their responses as a person/animal learns a motor skill; motor cortex increases its signal-to-noise ratio
  • Basal ganglia critical for learning new habits; damage to area are impaired at learning motor skills and at converting new movements into smooth, “autonomic” responses

Inhibition of Movements

  • Antisaccade task  looking at opposite direction of movement
  • Performing this task requires sustained activity in parts of prefrontal cortex and basal ganglia before seeing wiggling finger
  • As the brain prepares itself, it sets itself to be ready to inhibit the unwanted action and substitute a different one
  • Ability to perform antisaccade task matures slowly because the prefrontal cortex is one of the slowest brain areas to reach maturity

MOVEMENT DISORDERS

Parkinson’s Disease

  • Symptoms  rigidity, muscle tremors, slow movements, difficult initiating physical/mental activity; slow on cognitive tasks (imagining events/actions)
  • Loss of olfaction is early symptom or even 1st symptom
  • Basal ganglia have cells specialized for learning to start/stop voluntary sequence of motions  cells are impaired in Parkinson-s, and result is difficulty with spontaneous movements in absence of stimuli to guide their actions

Causes

  • Immediate cause is gradual progressive death of neurons (especially in substantia nigra  sends dopamine-releasing axons to caudate nucleus and putamen); people with disease lose axons and therefore dopamine
  • Direct pathway of connections from substantia nigra to cerebral cortex:
    • Axons from substantia nigra release dopamine that excites caudate nucleus and putamen  caudate nucleus and putamen inhibit globus pallidus (in turn inhibits parts of thalamus)
    • People with Parkinson-s, decreased output from substantia nigra means less excitation of caudate nucleus and putamen

(less inhibition of globus pallidus) o Globus pallidus (free from inhibition) increases its (inhibitory) output to thalamus  result is decreased activity in thalamus and therefore also parts of cerebral cortex o     Loss of dopamine activity in substantia nigra leads to less stimulation of motor cortex and slower onset of movements

  • If number of surviving substantia nigra neurons declines below 20-30% of normal, Parkinsonian symptoms being
  • Equal concordance for both kinds of twins (MZ/DZ) implies low heritability
  • Young adults developed symptoms of Parkinson-s after using drug similar to heroin  substance responsible for symptoms was MPTP

(chemical that body converts to MPP +  accumulates in and then destroys neurons that release dopamine)

  • People who smoke cigarettes or drink coffee have less chance of developing Parkinson-s disease
  • Parkinson-s disease probably results from mixture of causes  what they have in common is damage to mitochondria

L-Dopa Treatment

  • If Parkinson-s results from dopamine deficiency  dopamine pill ineffective because dopamine doesn-t cross blood-brain barrier
  • L-Dopa  precursor to dopamine; crosses blood-brain barrier; reaches brain and neurons convert it to dopamine

Other Therapies

  • High-frequency electrical stimulation especially effective for blocking tremors and enhancing movement  also leads to depressing mood by inhibiting serotonin release
  • Inject chemical (6-ODHA, modify dopamine) to brains of rats to damage substantia nigra of 1 hemisphere  producing Parkinson-s symptoms on opposite side of body, then remove substantia nigra, replace with normal one; most rats recovered normal movements
  • For humans, blood-brain barrier protects brain from foreign substances, give drugs to supress rejection of transplanted tissue.
    • Only immature cells from a fetus can make connections, still need to learn behaviour dependent on cells (animal practices using transplanted cells)
  • Can transplant tissue from patient-s own adrenal gland, not composed of neurons but still produces and releases dopamine (not much benefit)
  • Can transplant brain tissue from aborted fetuses; neurons can survive for years and synapse with the patient-s own cells (need many fetuses to do this)
  • Grow cells in tissue culture, genetically alter so they produce L-dopa, transfer to brain; useful if cells grown in tissue culture of stem cells(immature cells capable of differentiating into many cells)
  • Limitations: surgeons limit to patients with advanced symptoms; research shows transplants work best if damaged area small and surrounding cells healthy
  • Transplanted tissue often fails to survive, or differentiated into cells other than dopamine  show behavioural recovery; transplanted tissue may stimulate axon/dendrite growth in brain

Huntington’s Disease

  • Severe neurological disorder that strikes about 1 person in 10,000 in the U.S
  • Motor symptoms being with arm jerks and facial twitches; tremors spread to other parts of body and develop into writhing
  • Ability to learn and improve new movements is especially limited
  • Disorder is associated with gradual, extensive brain damage (especially in caudate nucleus, putamen, and globus pallidus; also cerebral cortex)
  • Also suffer psychological disorders (depression, sleep disorders, memory impairment, anxiety, alcoholism)
  • Deficits in memory and reasoning precede motor symptoms (usually misdiagnosed as having Schizophrenia)

Heredity and Presymptomatic Testing

  • Results from dominant gene on chromosome #4  implies that it produces gain of some undesirable function
  • Critical area of the gene includes sequence of bases C-A-G (repeated 11-24 times in most people)  people with 39 or more repetitions are likely to get the disease (unless they die of other causes earlier)
  • Variant forms of genes controlling glutamate receptors don-t produce Huntington-s disease by themselves, but they influence age of onset of symptoms
  • People with later onset, role of genetics is weaker/less certain
  • Identification of the gene for Huntington-s led to discovery of protein that it codes (huntingtin)
    • Occurs throughout the human body (its mutant form produces no known harm outside the brain); within the brain, it occurs inside neurons, not on membranes
    • Impairs neurons by increasing neurotransmitter release (sometimes causing overstimulation of target cells); later, protein forms clusters that impair neuron-s mitochondria; also impairs transport of chemicals down the axon o
  • Biologically, the necessary condition for life is a coordinated set of chemical reactions
  • Every chemical reaction in a living body takes place in a water solution at a rate that depends on the identity and concentration of molecules in the water and the temperature of the solution