Internal structure of spinal cord by z8OBCl

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									Internal Structure of
    Spinal Cord
          Laminae of Rexed
• 10 divisions based on cellular architecture
  of the spinal cord. It is numbered from
  dorsal to ventral
• Lamina I. top of dorsal horn - thin layer of small
  stellate cells & large neurons
   – receive incoming Dorsal Root fibers
   – send some axons to contralateral spinothalamic tract
• Lamina II. substantia gelatinosa - very small,
  dense cells (gelatinosa cells) with highly branched
  dendrites
   – receive afferent dorsal root axon collaterals &
     descending fibers from reticular formation
   – send unmyelinated axons to dorsolateral tract - ascend
     or descend a few segments
   – give off branches at several levels to other laminae of
     dorsal horn
   – thought to be involved especially in modulation &
     throughput of pain perception
• Lamina III. interneurons - receive dorsal root
  axons; send axon branches to other Dorsal Horn
  laminae
   – II and III (substantia gelatinosa) functions in
     regulating afferent input to the spinal cord.
• Lamina IV. tract cells - long dendrites extend into
  Lamina II, III;
   – axons cross midline to contralateral spinothalamic tract
   – projects to the lateral cervical nucleus, the posterior
     column nuclei and the thalamus (spinothalamic tract)
• Lamina I-IV all receive inputs from dorsal
  root, IV most
• V-VI. base of Dorsal Horn (indistinguishable in
  humans)
   – has long-dendrite tract cells similar to IV; and many
     various interneurons
   – afferent fibers = some dorsal root afferent; and
     especially. descending corticospinal fibers (their major
     target)
   – Tracts cells from Lamina IV, V, and VI are generally
     referred as nucleus proprius
   – Lamina 5 and 6 receives proprioceptive input AND
     sensory information relayed by lamina 4. These are the
     sites of origin of ascending projections to higher centers
• Intermediate zone:
  – VII. largest region of the spinal gray matter
     • many interneurons with collaterals within their segment and long
       axons that go out into the white matter & travel up/down to other
       segments’ gray matter
     • VII also contains a few other cell columns (not part of the Lamina
       system)
  – Nucleus dorsalis (nucleus thoracicus /Clarke’s column:)
     • in medial/base of dorsal horn/upper intermediate, T1-L3 big neurons,
       axons make up dorsal spinocerebellar tract
     • ventral spinocerebellar tract originates from lamina V, VI and VII and
       from neurons from the edge of the ventral horn in lumbar region
       (spinal border cells)
  – Intermediolateral cell column: in lateral horn of T1-L2
     • Cell bodies of preganglionic neurons of sympathetic nervous system
• Anterior / Ventral horn: (motor & interneurons)
• VIII. mostly in medial side of ventral horn ( covers
  width of ventral horn in part of thoracic segments)
   – receives terminals of descending fibers from vestibulospinal
     & reticulospinal tracts
   – sends to ipsilateral & contralateral to lamina VII & IX at their
     level & a few other close levels
   – participates in movements of muscles in the head and neck
• IX. columns of motor neurons within boundary of VII
  or VIII
   – axons make up ventral roots: alpha-motor neuron to skeletal
     muscle (gamma motor neuron to muscle spindles) four motor
     neuron columns = dorsolateral; central; ventromedial;
     ventrolateral . The axial muscles (neck, trunk) are
     represented medial and ventrally whereas limbs are
     represented in lateral and dorsal part of the spinal cord
• In Cervical cord (L IX):
  – a. Phrenic nucleus: in ventromedial column, C3-C5,
    innervates diaphragm muscle
  – b. Spinal accessory nucleus: C1-C5, lateral VH
     • axons in rootlets join to form spinal root, ascends through
       foramen magnum; joins with cranial root (XI cranial nerve) to
       form accessory nerve - exits through jugular foramen
     • spinal root innervates trapezius & sternocleidomastoid
• Nucleus of Onuf at S2 level
  – most ventral part of ventral horn
  – contribute to pudendal nerve - pelvic floor, including
    sphincters of fecal and urinary continence.
• Commissural area:
• X. immediately around central canal, smaller
  neurons than surrounding laminae
   – receives some afferents from dorsal root
   – contains decussating (crossing) fibers, glia cells
   – contains neurons that project to the opposite side of the
     cord
• Dorsal afferent fibers predominately terminate in
  the dorsal horn. Impulses concerned with pain,
  temperature, and touch reach the tract cells from
  which spinothalamic tract originates. Pain signals
  are modified mainly in Lamina II. Dorsalis
  nucleus of thoracic and upper lumbar gives off
  dorsal spinocerebellar tract.
• Dorsal horn
  – Each dorsal root branches into six to eight rootlets.
    These axons enter the dorsallateral tract (Lissauer)
    where they divide into ascending or descending
    branches terminating in their own or immediately
    adjacent segments.
• Ventral horn
  – Lamina IX has two types of motor neurons, alpha
    (numerous, large in diameter) and gamma (less
    numerous, small). Alpha innervates muscle cells and
    gamma innervates muscle spindles.
• Lateral horn
  – Sympathetic efferent neurons, located in the thoracic
    and upper lumbar segments only (T1 – L2).
•   Intermediate zone:
    –   Sacral autonomic nucleus: lateral horn S2-
        S4
        •   Cell bodies of sacral PSN preganglionic
    –   Intermediomedial cell column: just lateral to
        X (through out the length of spinal cord
        •   thought to be involved in visceral reflexes;
 Internal structure of spinal cord

• A. White matter - stains black or dark blue
  with Weigert's stain
  – is composed of axons that form tracts or
    funiculi
  – ascending or descending - travel rostrally or
    caudally
  – divided into 3 areas: dorsal, ventral & lateral
    funiculi
            Dorsal Funiculus
• between dorsal gray horns
• axons from dorsal root ganglia (DRG) ascend
  ipsilaterally;
• carry sensory discrimination for tactile,
  proprioception, movement, vibration, synapse in
  Nuclei gracile and nuclei cuneate in medulla then
  cross over to the contralateral side.
• Different pathway for discriminative touch and
  proprioception
                   Receptors
• Sensory receptors:
  – exteroceptors: response to pain, temperature,
    touch, pressure on skin
     • like free nerve endings, Merkel endings, Pacinian
       corpuscles
  – proprioceptors: in muscles, tendons, joints,
    provide information for awareness of position
    and movement
     • like neuromuscular spindles, Golgi tendon organs
       (neurotendinous spindles)
         Discriminative touch
• Receptors are tactile receptors (Meissner’s
  corpuscles), sent to dorsal root ganglia
   – fasciculus gracilis - medial - lower extremity,
     somatotopic origins (lower = more medial)
   – fasciculus cuneatus - lateral - appears above mid-
     thoracic level (information from the upper extremity)
   – Both funiculi terminate to gracile and cuneate nucleus,
     respectively at medulla level. Then by internal arcuate
     fibers cross over to the contralateral side, project to
     ventral posterior nucleus of thalamus by medial
     lemniscus, then to the ipsilateral primary somesthetic
     cortex (be aware the medial lemniscus turns 90, then
     lower body information is on the lateral side now) .
    Three levels of perception
• primary afferents neurons (pathway)
  at dorsal root ganglia (spinal cord
  level)
• At the medulla, the primary afferents
  finally synapse. The neurons
  receiving the synapse are now
  called the secondary afferents
  neurons.
• At thalamus, a third and final neuron
  will go to cerebral cortex, the final
             Proprioception
• Receptors are neuromuscular spindles,
  neurotendeninous spindles,
• Upper limb:
  – Same as above mentioned mechanism
              Proprioception
• Lower limb:
  – dorsal funiculus goes only up to mid-thoracic level,
    terminates into nucleus dorsalis
  – axons from nucleus dorsalis ascend ipsilaterally as
    dorsal spinocerebellar tract. At medullar level, before
    entering cerebellum by inferior cerebellar peduncle,
    gives off collaterals entering nucleus Z (rostral to
    gracile nucleus), which are concerned with conscious
    proprioception from the lower limb.
  – Cells from nucleus Z then give rise to internal arcuate
    fibers that cross the midline and join the medial
    lemniscus, then enter the ventral posterior nucleus of
    thalamus, then primary somatosensory cortex
    ipsilaterally.
             Proprioception
• - also carry descending fibers:
• a. from nucleus gracile, and nucleus cuneate -
  modulation of sensations from higher centers
• b. from dorsal root ganglia afferents - help
  coordinate / integrate sensory info from nearby
  levels
• c. spinal gray - thought to coordinate upper &
  lower limbs in reflexes
           Lateral funiculus

• Ascending:
• 1. dorsal spinocerebellar tract:
  – begins from above L3
  – axons from ipsilateral Nucleus dorsalis
    (Clarke’s column cells) to ipsilateral cerebellar
    cortex via inferior cerebellar peduncl
  – Participates the pathway for lower limb
    proprioception (see above)
             Lateral funiculus
• 2. ventral spinocerebellar tract:
   – mostly from contralateral spinal border cells of ventral
     horn at edge of lumbar sacral ventral horn
   – largely crossed fibers ascend up to midbrain level turns
     into superior cerebellar peduncle
   – fibers cross again in cerebellum before entering to
     cerebellar cortex
   – therefore, deliver sensory info from same side of body
   – Both spinocerebellar (ventral and dorsal) carry same
     side of the information into cerebellum. Although,
     dorsal tract entering the cerebellum via the inferior
     cerebellar peduncle and ventral by the superior
     cerebellar peduncle.
            Lateral funiculus
• lateral spinothalamic tract: carry pain,
  temperature, light touch sensations
• Receptors are nociceptor (nerve endings) for pain,
  Merkel etc for light touch, unknown receptors for
  temperature. Fibers enter the dorsal lateral tract.
  Axons from dorsal horn (nucleus proprius) IV, V-
  VI cross the midline in ventral white commissure,
  then travels ipsilaterally in the ventral part of
  lateral funiculus end in the ventral posterior
  nucleus of the thalamus.
             Spinothalamic
• upper limb is represented more medial
  (close to the gray matter); lower is lateral,
  superficially (somatotopically arranged)
• From medulla level up , spinothalamic
  fibers constitute most of the spinal
  lemniscus, which also includes fibers from
  spinotectal tract
           Lateral funiculus
• Other tracks in lateral funiculus
  – spinotectal tract: same source as spinalthalamic
    tract; cross, then up to superior colliculus,
    midbrain reticular formation
  – spinoreticular tract:
     • probably pain perception for internal organs
     • originates from laminae IV-VIII crossed midline to
       pontine reticular formation (crossed)
     • from ipsilateral side, terminates to medullary
       reticular formation (uncrossed)
            Lateral funiculus
• Descending: (modify ascending activities)
• lateral corticospinal tract:
  – Originate from frontal and parietal lobes, pass
    through internal capsule, basis pedunculi, midbrain,
    pons
  – Cross as medullar level to enter (become) lateral
    funiculus.
     • a. fibers from frontal lobe: end in ventral horn &
       intermediate zone of gray matter
     • b. fibers from parietal lobe : end in dorsal horn
       gray matter
   Lateral Corticospinal Tract
• Functionally, these tracts (lateral and
  anterior) have a strong influence on voluntary
  motor activity. Some of the fibers of the lateral
  corticospinal tract terminate directly on the
  motor neurons (anterior horn cells) of the
  spinal cord, particularly those involved in fine
  motor control of the fingers and hand. Most
  others act via the interneurons of the anterior
  horn, which then influence the motor neurons.
  Lateral Corticospinal Tract
• Damage to the corticospinal tract results
  in changes in modulation of the deep
  tendon reflexes to cause hyperreflexia
  and spasticity at segments below the
  level of corticospinal damage. The three
  clinical characteristics of hyperreflexia
  are amplitude of reflex, speed of action
  and spread of reflex.
          Other descending tracts
• Rubrospinal tract
   – from contralateral Red Neucleus - only extends to C2 in
     humans
• Medullary reticulospinal tract:
   –   from nucleus reticular formation
   –   control motor neurons
   –   mostly ipsilateral, but some fibers cross in medulla
   –   control of un/ subconscious motor activity
       (corticospinal tracts control skilled/conscious
       movement)
           Ventral funiculus
• Descending:
• 1. ventral corticospinal tract = uncrossed portion
  of corticospinal tract
• These then cross in the anterior commissure of the
  cord at the level where fibers synapse with the
  anterior horn cell
   Anterior Spinothalamic Tract
• Light (crude) touch and pressure
  – Info to dorsal spinal ganglion, synapse with
    substantia gelatinosa group (Lambda II, III)
  – Second order cross to the opposite side and
    ascend as anterior spinothalamic tract, new
    fibers are added to the medial aspect of the
    track as it goes up (lower lateral, upper medial)
  – At medula level, joins with lateral
    spinothalamic tract and spinotectal tract to form
    spinal lemniscus
   Anterior Spinothalamic Tract
• The spinal lemniscus continues to ascend to
  the ventral posterolateral nucleus of
  thalamus (third order neuron)
• Axons from third order neuron, then project
  to post central gyrus
Other tracks in anterior funiculus
• (lateral) vestibulospinal tract: uncrossed fibers
  from lateral vestibular nucleus of medulla
   – terminates at Lamina VIII, & medial VII
   – mediates equilibrium reflexes
• descending medial longitudinal faciculus: (also
  called medial vestibulospinal tract)
   – from medial vestibular nucleus of medulla
   – mediates equilibrium-oriented head movements -
     primarily in upper cervical levels
         Spinal cord damage
• 1. This initial period of "hypotonia" after
  upper motor neuron injury is called “Spinal
  Shock” and reflects the decreased activity
  of spinal circuits suddenly deprived of input
  from the motor cortex and brainstem
         Spinal cord damage
• After several days, however, the spinal cord
  circuits regain much of their function for
  reasons that are not fully understood.
  Thereafter, a consistent pattern of motor
  signs and symptoms emerges, including:
     Upper motor neuron damage

• The Babinski
  sign
  – Seen in spinal
    cord injury and
    infants with
    incomplete
    upper motor
    neuron control
    Upper motor neuron damage
• Spasticity. Spasticity is increased muscle tone,
  hyperactive stretch reflexes, and clonus (an
  oscillatory motor response to muscle stretching).
  Extensive upper motor neuron lesions may also be
  accompanied by rigidity of the extensor muscles
  of the leg and the flexor muscles of the arm (called
  decerebrate rigidity; see below). Spasticity is
  probably caused by the removal of inhibitory
  influences exerted by the cortex on the postural
  centers of the vestibular nuclei and reticular
  formation.
    Upper motor neuron damage
• Hyporeflexia of superficial reflexes. Further signs
  are the decreased vigor (and increased threshold)
  of superficial reflexes such as the corneal reflex,
  superficial abdominal reflex (tensing of abdominal
  muscles in response to stroking the overlying
  skin), and the cremasteric reflex in males
  (elevation of the scrotum in response to stroking
  the inner aspect of the thigh). The mechanism of
  this diminishment of superficial reflexes is not
  well understood.
   Upper motor neuron damage
• A loss of the ability to perform fine
  movements. If the lesion involves the
  descending pathways that control the lower
  motor neurons to the upper limbs, the
  ability to execute fine movements (such as
  independent movements of the fingers) is
  lost.
   Lower motor neuron damage
• The cell bodies of the lower neurons are located in
  the ventral horn of the spinal cord gray matter and
  in the motor nuclei of the cranial nerves in the
  brainstem.
• Symptoms include paralysis (flaccid), loss of or
  paresis (weakness) of the affected muscles, loss of
  reflexes (areflexia) due to interruption of the
  efferent (motor) limb of the sensory motor reflex
  arcs
Assessment of Spinal Cord Damage

• Dermatome
Assessment of Spinal Cord Damage

• Spinal reflexes:
  –   Biceps reflex: C5 to C6
  –   Triceps reflex: C6 to C8
  –   Quadriceps reflex (Knee jerk reflex), L2 – L4
  –   Gastrocnemius reflex (ankle reflex), S1 to S2
                 Biceps reflex

• The biceps reflex is
  elicited by placing
  your thumb on the
  biceps tendon
• Biceps reflex: C5 to C6
               Triceps reflex
• The triceps reflex is
  measured by striking
  the triceps tendon
  directly with the
  hammer while holding
  the patient's arm with
  your other hand
• Triceps reflex: C6 to
  C8
              Knee Jerk Reflex

• With the lower leg
  hanging freely off the
  edge of the bench, the
  knee jerk is tested by
  striking the quadriceps
  tendon directly with
  the reflex hammer
• Quadriceps reflex
  (Knee jerk reflex), L2
  – L4
                    Ankle Reflex
• The ankle reflex is
  elicited by holding the
  relaxed foot with one
  hand and striking the
  Achilles tendon with
  the hammer and noting
  plantar flexion
• Gastrocnemius reflex
  (ankle reflex), S1 to S2
      Lou Gehrig's disease
• Amyotrophic lateral sclerosis (ALS),
  sometimes called Lou Gehrig's disease,
  is a rapidly progressive, invariably fatal
  neurological disease that attacks the
  nerve cells (neurons) responsible for
  controlling voluntary muscles. Both
  upper and lower motor neurons are
  damaged.
      Lou Gehrig's disease
• Symptoms of upper motor neuron
  damage include stiffness (spasticity),
  muscle twitching (fasciculations), and
  muscle shaking (clonus). Symptoms of
  lower motor neuron damage include
  muscle weakness and muscle shrinking
  (atrophy).

								
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