1 more specifically cell bodies are in: (Kingsley 242-243)
    A. primary motor cortex (area 4)
    B. premotor & supplementary motor areas (area 6)
    C. parietal lobe (areas 3,1,2,5,7,39,40)

  2. The axons leave the cortex and travel through white matter
      (Kingsley p. 244)
    A. some of these fibers synapse in brainstem nuclei (corticobulbar division)

  3. The rest (corticospinal tract) descend in the pons & make their way thru
       the medullary pyramids

  4. At the level of the caudal medulla most of the fibers decussate forming the
      lateral  corticospinal tract (LCT)

  5. the rest of the fibers descend through the ipsilateral spinal cord forming
      ventral corticospinal tract (VCT).

  6. corticospinal fibers terminate in laminae IV-IX

II. rubrospinal tract (RST):  A major pathway from the brainstem
   (Kingsley p. 246)
  1. red nucleus receives input from the cerebral cortex and cerebellum
 
  2. originates in the red N. (midbrain) & cross immediately after leaving

  3. Axons from the RST terminate mostly on interneurons in laminae IV-IX
      of the spinal cord

  4.  this controls movements of forelimbs and hindlimbs
 
 

III. reticulospinal tract: originates in the reticular formation of the medulla,
      & pons  (Kingsley p. 248)
  1. most synapse on interneurons in laminae VII & VIII

  2. some of these fibers control movements that do not require conscious
       effort (maintaining posture)

  3. other fibers influence the ANS
 
 

IV. vestibulospinal tract: cell bodies in the vestibular nuclei of the medulla
  1. there are 2 parts both receive afferents from vestibular system (p.249
      Kingsley).  They both innervate more proximal muscles.

    A. lateral vestibulospinal tract
      a. originates in lateral vestibular nucleus
      b. axons terminate in laminae VII-IX

    B. medial vestibulospinal tract
      a. originates in the medial vestibular nucleus
      b. This tract does not travel below the upper cervical level
      c. axons terminate in laminae VII-IX
 
 

2. called primary for several reasons:

3. afferents from
  A. other cortical motor areas & somatosensory  cortex
  B. posterior part of the ventral lateral thalamus

4. efferents:
  A. corticospinal & corticobulbar tracts

5. damage to this area results in
  A. if only area 4 is damaged you see
    a. voluntary paresis of the corresponding part of the body
    b. apraxia: inability to perform a learned motor skill (but no paralysis)
 

II. supplementary motor cortex:
1. located in Brodman’s area 6 primarily (much on medial side)
 
2. afferents:
  A. from other cortical areas
  B. ventral anterior (VA) & anterior part of the ventral lateral (VLa) thalamus

3. efferents:
  A. to the corticospinal & corticobulbar tracts
  B. to the primary motor cortex

4. damage to this area (e.g., stroke) can result in
  A. loss of most voluntary movements & loss of speech
    a. the person may have no motivation to move or speak (akinetic mutism)
  B. apraxia:
 

III. premotor cortex:
1. located in Brodman’s area 6 & a the lower part of  area 8

2. afferents from VA & VLa nuclei of the thalamus

3. efferents:
  A. to the corticospinal & corticobulbar tracts
  B. to the primary motor cortex

4. damage to this area can result in
  A. apraxia: impaired performance of learned movements

5. frontal eye fields: in the lower part of Brodman’s area 8 (often included)
  A. it controls voluntary movements of the eyes
 
 

IV. posterior parietal area:
1. some cells that form the corticospinal & corticobulbar tract are here

2. with damage here (especially in the nondominant hemisphere) you see
    neglect
 
 

I. the brain has a dampening (inhibiting) effect on spinal cord reflexes.  Thus
   when motor signals from the brain are disrupted you see:

  1. hyperactive MSR reflexes (jerky spastic movements)

  2. clonus: rapid series of muscle contraction & relaxation (oscillations)
 

II. a distinction is made between the effects of damage to motor neurons &
   damage involving descending motor pathways (Kingsley p. 266)

  1. lesions of lower motor neurons (LMN): i.e., motor neurons in cord

  2. upper motor neuron (UMN) lesion: occurs after damage to the motor
     tracts (i.e., cerebral cortex, brain stem, spinal cord).
 

III. more upper motor neuron damage information

1. spinal cord transection
  A. tetraplegic (quadriplegic): if the upper cervical cord is transected

  B. paraplegic: if damage is between the cervical & lumbar enlargements

  C. hemiplegic: if partial transection is in the upper cervical cord

  D. monoplegia: after hemisection of the thoracic cord
    a. Brown-Sequard syndrom (p. 269 Kingsley)

  E. spinal shock: occurs immediately after spinal injury (lasts 1-6 weeks)
 

2. brainstem lesions often result in crossed paralysis (Kingsley p. 271)
  A. ipsilateral LMN paralysis of at least some muscles of the head

  B. UMN signs on the side of the body contralateral to the lesion
    a. Also sensory loss on the contralateral side.

3. internal capsule damage (usually caused by a stoke)

4. cerebral cortex damage (usually caused by stroke)
  A. the impairment would depend on the area that is destroyed
 
 

II. There are 2 types

  1. cerebral hemorrhage: bleeding into the brain when a cerebral blood
      vessel ruptures

    A. aneurysm: a balloon-like swelling in the wall of a blood vessel.

  2. cerebral ischemia: blood supply is disrupted to a part of the brain

    A. thrombosis: blockage of the blood flow at the site of its formation
       a. arteriosclerosis: is a common cause, blood vessel walls become narrow
       b. transient ischemic attack (TIA): neurological deficits occur but clear
           within 24 hours
        ?this can herald an actual thrombotic stoke

    B. embolism: plug formed in larger blood vessel & carried to a smaller one
 

III. causes of stokes:
  1. high blood pressure:
   A. this is thought to damage blood vessel walls & cause atherosclerotic
        plaques

 2. hyperlipidemia, tobacco use & diabetes mellitus all accelerate
     atherosclerosis
 

IV. excitatory amino acids (glutamate) may cause stroke related brain damage
    A. oxygen deprived neurons release excessive glutamate
      a. this overstimulates neighboring postsynaptic cells
      b. overstimulation causes large amounts of Na+ & Ca++ to enter the
          postsynaptic cell
      c. possible treatment:
        ->a glutamate receptor blocker
        ->magnesium blocks Ca++ from entering cell

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