Lower Motor Neurons: Poliomyelitis Flashcards
brifly describe the architecture of the spinal cord
- grey-white orientation opposite of cerebral cortex
- white matter = outside: axons
- grey matter = inside: a mix - parikaryons, dendrites, synapses, axons, ect.
describe a “typical” mutlipolar neuron
- perikaryon (cell body)
- dendites: input side
- axon: output side
label picture & explain important features
- outside = white matter, divided into R and L halves by:
- ventral median fissure
- deeper (aka fissure): makes broader split between halves
- dorsal median sulcus
- ventral median fissure
- inside = grey matter surrounding central canal
- gray matter:
- dorsal horn: extends to spinal cord surface (d for distance)
- ventral horn: wider, does NOT extend to spinal cord surface - contain LMNS*
- lateral horn - contain LMNs*
- central canal: continuation of the 4th ventricle
- gray matter:
where are lower motor neurons (LMNS) found?
- ventral horns (gray matter)
- lateral horns (gray matter)
- cranial nerves - except I, II & VIII
LMNs in the ventral horn
- are divdided in what groups?
- will take what path out of the spinal cord?
- path: ventral roolets -> ventral roots -> spinal nerve -> ventral ramus -> muscle
- can be categorized in two ways based on:
- types of muscle fibers innervated:
-
alpha: extrafusal
- these extrafusal fibers form motor end plates
- carry excitatory impules only (cholinergic)
- receive inputs from interneurons (m/c), UMNs, dorsal root ganglion neuron
- beta: intrafusal & extrafusal (b for both)
- gamma: intrafusal fibers of spindle apparatus
-
alpha: extrafusal
- location of muscle fibers innervated - ie., somatropoic map:
- distal parts (extremities): lateral ventral horn
- flexors: dorsal ventral horn
- extensors: ventral ventral horn
- proximal parts (trunk): medial ventral horn
- types of muscle fibers innervated:
describe the innervation mediated by alpha motor neurons
(alpha motor neurons = LMNs in ventral horn)
- receive input from either
- UMNs (brain)
- interneurons (m/c)
- dorsal root ganglion neurons (sensory)
- deliver: excitatory (cholinergic) innervation only
- innervate: extrafusal fibers that form a motor end plate
alpha motor neurons most commonly receive input from….?
(LMNs in the ventral horn)
interneurons
what is a motor unit?
the total muscle fibers innervated by a single alpha motor neuron
what is muscle recrtuiement?
activating additional motor units
the smaller the motor unit the…?
more refined the movement
damage to LMNs
- results in what pathology?
- explain the mechanism
- flaccid paralysis: hypo - reflexia, tonia in a somatotropic map
- LMNs cannot receive:
-
hypotonia b/c:
- no input from UMNs (brain), thus nocontraction via conscious thought
- UMNs & LMNS required
-
hyporeflexia b/c:
- no contraction following sensory feedback
- LMNs required
- what renders the paralysis “flaccid”
-
hypotonia b/c:
somatgotropic map in ventral horn
- lateral: distal body parts (appendages)
- dorsal: flexors
- ventral: extensors
- medial: proximal body parts (trunk + proximal appendages)
what infection can lead to acute flaccid paralyis?
= hyporeflexia, hypotonia
polio infection
what part of the pathology behind flaccid paralysis renders the paralysis flaccid?
- the disrupted communication sensation from the motor unit and the LMNs
- stimulation of muscle does not yield reflex
- = hyporeflexia component of definition
summarize the clinical and histological presentation poliomyeltitis
- clinical: acute flaccid paralysis due to LMN destruction
- hypotonia: muscles appear flacid
- hyporeflexia: no DTR or Bakinsi reflexes
- however, SENSATION INFACT
- histologically:
-
muscle: denervation neurogenic atrophy
- shrinked fibers
- filled with adipose tissue
-
spinal cord: neuronophagia
- microglial nodules (microglial cells surrounding necrotic tissue), d/t microglial cells -> transform into macrophages -> ingest damaged tissue
-
muscle: denervation neurogenic atrophy
identify & explain
decreased neurogenic atrophy: shrinked fibers size + adipose in perimysial muscle
manifestation of poliomyeltiis
identify & explain
neuronphagia - microglial nodules in spinal cord
manifestation of poliomyelitis
identify & explain
neuronphagia - microglial nodules in spinal cord
manifestation of poliomyelitis
what key relay centers are found in the dorsal horn?
list them & explain their arrangement:
- from most superficial - i.e., from most distal part of horn, to most deep - ie., most proximal part of horn
- dorsolateral tract
- substantia gelatinosa
- nucleus propius
- dorsal nucleus of clark
which dorsal horn center (s) feed into the spinothalamic tract?
- dorsolateral tract
- substantia gelatinosa
- nucleus proprius
which dorsal horn centers feed into the spinocerebellar pathway?
dorsal nucleus (of clarke)
which dorsal horn centers serve as synapses?
list the key information transmitted at each synapse.
- substantia gelatinosa: pain + temp + light touch
- pain = important: can be modulated via this tract*
- nucleus proprius: mechanical info + temp
- dorsal nucleus: propriorecption
which dorsal horn centers are secondary neurons?
what does this mean?
- this means they are synaptic centers. therefore
- substantia gelatinosa
- nucleus proprius
- dorsal nucleus
dorsalolateral tract
- relative location on dorsal horn
- carries what sensations?
- synaptic center - y/n
- contributes to what pathway?
- recieves information for dorsal root ganglion*
- location: most superficial / distal relay center - forms “cap over dorsal horn”
- carries:
- discrete pain
- temperature
- synapse center - NO
- contributes to - spinothalamic pathway
substantial gelatinosa
- relative location on dorsal horn
- carries what sensations?
- synaptic center - y/n
- contributes to what pathway?
- location: most distal relay (synaptic) center - dorsalateral most distal overall
- carries:
- pain (can modulate)
- temperature
- light touch
- synapse center - YES
- contributes to - spinothalamic pathway
nucleus proprius
- relative location on dorsal horn
- carries what sensations?
- synaptic center - y/n
- contributes to what pathway?
- location: middle relay (synaptic) center
- carries:
- mechanical touch
- temperature
- synapse center - YES
- contributes to - spinothalamic pathway
dorsal nucleus (of clarke)
- relative location on dorsal horn
- carries what sensations?
- synaptic center - y/n
- contributes to what pathway?
- location: most proximal relay (synaptic) center
- carries: proprioreception from golgi tendon organs & spindle apparatus
- synapse center - YES
- contributes to - spinothalamic pathway
which dorsal center carries mechanical information?
nucleus proprius
which dorsal center can regulate pain perception?
substantia gelatinosa
which dorsal center carries propioreception?
dorsal nucleus (of clarke)
where does the spinothalamic pathway decussate?
ventral white commissure
what is the commissural region?
into what components is it divided?
- is the region immediately surrounding the central canal:
- dorsal grey commissure
- ventral grey commissure
- white commissure
- also ventral (only seen on ventral spinal cord)
- carries fibers from:
- ventral corticospinal tract
- spinothalamic tract
what is the white commisure and why is it important?
- portion of the commissure region to ventral to ventral grey commissure
- carries fibers for anterior cortisospinal & spinothalamic pathways
- site of dessucation for spinothalamic
what key features / changes of a spinal cord cross section can help identify the vertebral level of the cut?
- overall: white matter increases inferiorly
- region specific:
-
ventral horn lateral expansion: d/t high LMNs -> motor tissue
- C5-T1 (upper limbs)
- L2-S3 (lower limbs)
-
presence of a lateral horn (aka intermediolateral nuclei)
- T1- L2
- S2-S4
- presence of cuneate nuclei: until T6
- narrow ventral & dorsal horns: thoracic
-
ventral horn lateral expansion: d/t high LMNs -> motor tissue
how does the gray:white matter ratio generally change moving down the spinal cord?
increases (more gray, less white going down)
in what spinal cord will cross-section show lateral expansion of the ventral horn?
explain.
lateral expansion of ventral horn d/t high # of LMNs innervating appendeges (flexors dorsal, extensors, ventral), and will thus be seen in segments responsible for limb innervation.
- C5-T1 (upper limb)
- L2-S3 (lower limb)
in what spinal cord segments will cross sections show the presence of a lateral horn?
- T1-L2
- S2-S4
in what spinal cord sections will cross sections show narrow ventral & dorsal horns?
thoracic - this is b/c the thoracic musculature (intercostals, ect) doesn’t require much motor innervation / give much sensation feedback
in what spinal segments will a cross section show the cuneate fasciculis?
everything above T6
identify corresponding vertebral region & how you know
cervical
- medium gray: white ratio
- lateral expansion of ventral horn: C5-T1 (upper limbs)
- presence of cuneate tracts lateral to gracile (up to T6)
identify corresponding vertebral region & explain how you know
- low gray: white matter ratio
- very narrow ventral & dorsal horns (all thoracic)
- presence of lateral horn: T1-L2, S2-S4
- presence of cuneate tract lateral to gracile tract: up to T6
identify corresponding vertebral and explain how you know
- high gray:white ratio
- lateral expansion of ventral horn: S2-L3 (lower limb)
- presence of lateral horn: T1-L2, S2-S4
what is recurrent inhibition?
how is recurrent inhibition mediated:
- definition: inhibitory synapses onto an alpha motor neuron (ventral LMN)
- carried out by an inhibitory neuron - commonly, inhibitory interneurons
what are reeshaw cells?
what role do they play?
are inhibitory interneurons that mediate recurrent inhibition by syanpses onto alpha motor neurons in the ventral horn
what will disruption of rucurrent inhibition lead to?
how can this happen?
- continuous activation of LMNs: rigid paralysis + hyperreflexia
- can be caused by strychine poisoning - inhibits renshaw cell
post-polio syndrome (SSP)
- definition?
- cause?
- presentation?
- risk factors?
- definition: resurgence of polio sx ~35 after acute paralytic poliomyelitis
- cause: collateral growth of axons (following injury to PMNs) temporarily recovers innervation to affected motor unit but then excessive reinervation -> stress -> eventual atrophy
- presentation:
- fatigue - m/c
- muscle weakness: affected muscles > not previous affected
- muscle / joint pain
- higher risk associations:
- young age of initial infection
- severe initial infection
- greater physical activity in intervening years
