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Neuroscience > Neuroscience Week 3: Lower Motor Neurons > Flashcards

Neuroscience Week 3: Lower Motor Neurons Flashcards

1
Q

Upper vs Lower Motor Neurons

A

LMN directly synapse on skeletal/visceral muscle and are the final common output from the CNS to effector organs (monosynaptic)

except General visceral motor neurons Autonomic LMNs synapse in PNS ganglia to indirectly affect muscle tone via post-ganglionic neurons (disynaptic)

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2
Q

how many pairs of spinal nerves

A

31 pairs

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3
Q

Describe the pairs of spinal nerves

A

8 Cervical

12 Thoracic

5 Lumbar

5 Sacral

1 Coccygeal

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4
Q

describe the Cervical Enlargement

A

C5-T1; Brachial plexus

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5
Q

Describe the Lumbosacral Enlargement

A

L1-S2 (lumbar plexus)

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6
Q

Spinal cord anatomy

A
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7
Q

White matter: _______ Axons

A

Myelinated Axons

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8
Q

Grey Matter: __________ Axons

A

Unmyelinated Axons

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9
Q

Cervical segments have a relatively large amount of _____________ due to the large number of __________ axons traveling from neurons throughout the spinal cord up to the brain and ________ axons traveling down from neurons residing in the brain.

A
  • White matter
  • sensory axons
  • Motor axons
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10
Q

Lower segments than the cervical have relatively less _____________ due to fewer _______________ (from the brain) that have already terminated and the lack of _________________ that lie in more anterior Spinal cord segments.

A
  • White matter
  • Upper motor neuron axons
  • sensory neuron axons
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11
Q

Grey matter consists of?

A

Unmyelinated cell bodies / dendrites

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12
Q

Grey matter in the spinal cord appearance

A

Resembles an H or a butterfly on the interior portion of the SC

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13
Q

In the spinal Cord Enlargements the _____________ are larger due to ____________________________ that control ______ and _______ function

A

In the spinal cord enlargements, the ventral horns are larger due to increased numbers of motor neurons that control arm (cervical) and leg (lumbosacral) function

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14
Q

Which segments of the spinal cord give rise to the preganglionic fibers of the sympathetic nervous system

A

Thoracic segments (T1-L2) have hips labled (“IL”) which contain the cell bodies of autonomic motor neurons that give rise to preganglionic fibers of the sympathetic nervous system

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15
Q

Major features of lower motor neurons

A

Reside in the ventral horns of the spinal cord

Use Acetylcholine

have an unmyelinated cell body, but becomes myelinated by Schwann cells

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16
Q

Neuromuscular Junctions

A
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17
Q

Motor Unit: Neurocentric Unit

A

The α-motoneuron and all the extrafusal fibers it innervates

Muscles that require fine movements have smaller motor units (e.g. lips, tongue, ocular muscles 12-20 fibers)

Larger muscles have large motor units (quadriceps, gluteus maximus > 1000 fibers)

All of the fibers that it innervates are of the same type Type I, IIa, IIb

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18
Q

Motor Neuron Pool: Musclecentric View

A
  • The pool consists of all the neurons that innervate a single muscle (all fibers of that single muscle)
  • Motor neuronal pools for larger muscles extend over more spinal segmental units than for smaller muscles
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19
Q

Purpose of redundancy of motor neuron pool

A
  • Redundancy reduces the impact of focal lesions
  • Impingement of individual segment can cause pain, hypoesthesia, paresis (weakness), but not paralysis
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20
Q

How are motor units recruited?

A
  • α-Motor neurons activate Type I fibers first and then recruit Type 2 fibers as needed; this produces the least amount of force necessary for a task
  • Proprioceptive feedback determines the need for more/less output
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21
Q

Why are _____ Fibers recruited first?

A

Type I fibers are recruited first because they are more excitable due to Ohm’s Law V=IR

they have higher R values (resistance) α-motor neurons innervating type I fibers are smaller than α-motor neurons innervating type II fibers; thus are excited first during conscious and unconscious motor output

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22
Q

How are motor neuron pools distributed?

A

Motor neuron pools are not randomly distributed but instead are ordered as such:

αMNs innervating proximal muscles are medially located

αMNs innervating distal muscles are laterally located

This image also shows the descending pathways (red and blue outlines in white matter)

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23
Q

The myotatic (Stretch reflex)

A

Renshaw cell also sends a signal to inhibitory interneuron to inhibit antagonistic muscle

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24
Q

Golgi Tendon Organ reflex (clasp-knife)

A
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25
Q

Myotomes and clinically-relevant reflexes

spinal origins and reflex loops

A
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26
Q

LMN Lesions usually cause _________ deficits

A

Ipsilateral

(there are a few exceptions in the CNS)

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27
Q

More medial spinal lesions in the ventral horns affect what?

A

More proximal or medial muscles as more lateral lesions affect more distal or lateral muscles

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28
Q

Spinal Cord placement in the vertebrae

A
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29
Q

Spinal cord root compression usually occurs here

A

Against the superior articulatory process or pedicle

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30
Q

How are cervical spinal nerve roots named?

A
  • Nerve roots are named according to the lower spinal segment that the nerve root runs between for example the nerve at the C5-C6 level is called the C6 nerve root
  • The cervical nerve roots are named this way because as the root exits the spine it passes over the C6 pedicle
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31
Q

How are lumbar nerve roots named?

A
  • Lumbar nerve roots are named according to the UPPER segment that the nerve runs between
  • For example, the nerve at the L4-L5 level is called the L4 nerve root
  • The lumbar nerve roots are named this way because as it exits the spine is passes Under the L4 pedicle
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32
Q

How are Spinal nerve roots named at the C7-T1 transition?

A
  • Naming change occurs is at the C7-T1 level.
  • Here, the C8 nerve exits UNDER the C7 Vertebra and Over the T1 vertebra
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33
Q

Disc Herniations General Rule

A

The nerve affected usually corresponds to the lower of the two segments of the intervertebral disc herniated

Posterolateral are the most common disc herniations (lack of vertebral ligament support)

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34
Q

Most common Disc Herniations

A
  • L4-L5 95%
  • C5-C6 or C6-C7 second most common
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35
Q

Disc Herniations Clinical Presentations

A

Pain, numbness/tingling, sometimes weakness in dermomyotome innervated by compressed nerve (e.g. for L4-L5 herniation: in lower back, buttocks, thigh, and may radiate to foot; sciatica is most common)

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36
Q

Disc Herniations Diagnosis

A
  • Physical examination (e.g. straight leg raise)
  • CT/MRI (T2 w/o contrast)
  • X-rays to rule out other causes (e.g. fractures)
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37
Q

In Disc herniation, what causes the symptoms to be principally sensory with more minor motor components?

A

because muscle innervation is redundant across spinal cord segments

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38
Q

Why is the most common disc herniation posterolateral

A

the anterior longitudinal ligament and posterior longitudinal ligament resist disc herniation but there is no ligament laterally

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39
Q

Lower Motor Neuron Syndrome Symptoms

A
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40
Q

Paresis definition

A

Weakness (partial paralysis)

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41
Q

-Plegia suffix definition

A

No movement

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42
Q

Paralysis definition

A

No movement

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43
Q

Palsy Definition

A

imprecise term for weakness or no movement

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44
Q

Hemi- prefix definition

A

one side of the body

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45
Q

Para- prefix definition

A

Both legs

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46
Q

Mono- prefix definition

A

one limb

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47
Q

Di- prefix definition

A

both sides of body equally affected

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48
Q

Quadri- or tetra- prefix definition

A

All four limbs

49
Q

Poliomyelitis Etiology

A
  • Polio virus (fecal-oral transmission)
  • Virus replicated in oropharynx and small intestine; spreads to the blood stream; then to CNS
  • Destroys cells of the anterior horn of the spinal cord
50
Q

Last case of wild polio in the U.S.? other countries?

A

1991 in U.S. due to vaccination

still endemic in Afganistan, Pakistan, Nigeria

51
Q

Poliomyelitis Symptoms

A
  • LMN signs (weakness, hypotonia, flaccid paralysis, hyporeflexia, atrophy)
  • typically asymmetric; distal predominance; skeletal deformities can develop; not progressive (EXCEPT for Post-Polio Syndrome)
  • Symptoms appear 1-10 days; maximal in under a week
  • Infection: (Malaise, headache, fever, nausea (can be asymptomatic)
52
Q

Poliomyelitis Diagnostic Tests and Findings

A
  • CSF has increased WBCs (10-200/mm3), increased protein (40-50mg/dl), No change in CSF glucose
  • ↓ NCV (nerve conduction velocity)
  • PCR + for polio viral DNA (stool)
53
Q

Poliomyelitis Overview

A
54
Q

Guillian-Barré Syndrome Description

A

Immune-mediated neuropathy (idiopathic)

most common in post-polio era

55
Q

Guillian-Barré Syndrome Pathogenesis

A
  • Most common antecedent is Campylobacter jejuni, others include CMV, Epstein-Barr Virus, HIV, Zika
  • Secondary demyelination possibly due to mimicry of viral antigens with myelin proteins (cross-reactivity of antibodies)
56
Q

Guillian-Barré Syndrome Clinical Presentation

A
  • LMN Signs: (Weakness, hypotonia, flaccid paralysis, hyporeflexia, atrophy)
  • First symptoms: Pain numbness, paresthesia, limb weakness,
  • Rapidly progressing: ascending bilateral and symmetric weakness
  • Typically reaches maximum in 2-4 weeks
  • Respiratory muscles affected in 25% of patients (ventilation required)
57
Q

Guillian-Barré Syndrome Diagnostic Tests and Findings

A
  • CSF has ↑ protein (>45mg/dl); WBC count usually remains ↓ (<10/mm3)
  • NCV ↓ (nerve conduction velocity)
58
Q

Guillian-Barré Syndrome Treatment

A
  • Plasmapheresis to remove damaging antibodies from plasma
  • IVIg (to block damaging antibodies that may contribute to Guillian-Barré Syndrome)
59
Q

Guillian-Barré Syndrome Overview

A
60
Q

Spinal Muscular Atrophy (SMA) Types

4 listed

A
  • SMA Type I (Acute Werdnig-Hoffman) “Floppy baby”
  • SMA Type II (Chronic Werdnig-Hoffman)
  • SMA Type III (Kugelberg-Welander)
  • SMA Type IV
61
Q

Spinal Muscular Atrophy Type I Etiology

A
  • Congenital degeneration of anterior horns
  • Autosomal recessive inheritance of mutations of the Survival of Motor Neuron 1 (SMN1) gene: 60% of all SMA
  • The most common genetic cause of infant death
  • Two copies of SMN2 are little compensation for SMN1 mutation)
62
Q

Spinal Muscular Atrophy Type I Clinical Presentation

A
  • LMN Signs: (Weakness, hypotonia, flaccid paralysis, hyporeflexia)
  • Proximal muscles affected first (including lungs)
  • Weak cry, respiratory distress
  • Tongue fasciculations
  • Difficulty sucking, swallowing (latching on)
63
Q

Spinal Muscular Atrophy Type I Prognosis

A
  • Presents <6 Months
  • Respiratory failure within weeks to 2 years
  • The median age for death for Spinal Muscular Atrophy Type I is 7 months
64
Q

Spinal Muscular Atrophy Type I Overview

A
65
Q

Spinal Muscular Atrophy Type II (Chronic Werdnig-Hoffman) Brief Overview

A
  • Presents 6-12 months of age
  • typically has 3 copies of SMN2 (greater compensation for SMN1 mutations)
  • Distal predominance (weakness worse in lower extremities)
  • Can sit but not walk
  • Life expectancy: 5th decade
66
Q

Spinal Muscular Atrophy Type III (Kugelberg-Welander) Brief Overview

A
  • Presents 2-15 years of age
  • between 4-8 copies of SMN2
  • Proximal weakness greater than distal
  • can walk as children
  • Typically confined to a wheelchair as adults
  • Life expectancy: normal
  • some cases need respiratory support
67
Q

Cauda Equina Syndrome (CES) Description

A

Spinal root or cord compression of CES (L2 and below)

68
Q

Cauda Equina Syndrome (CES) Etiology

4 listed

A
  • Central disc herniation/trauma (sudden onset)
  • ependymoma/metastisis (somewhat common, gradual onset)
  • Staphylococcus/tuberculosis
  • epidural hematoma
69
Q

Cauda Equina Syndrome (CES) Clinical Presentation

A

Motor:

  • LMN Symptoms at and below the level of the lesion
  • Rectal tone reduced
  • Bladder/bowel incontinence (anal reflex absent) or inability to evacuate completely
  • erectile/clitoral dysfunction
  • lower limb weakness (paraplegia)
  • Patellar and Achilles reflexes absent

Sensory:

  • Low back pain
  • Saddle anesthesia (perianal, genital)
  • Sciatica-type pain
70
Q

Cauda Equina Syndrome (CES) Diagnostic Tests and Findings

A
  • Diagnosis usually confirmed by an MRI or CT scan
  • CES is usually treated as a medical emergency as deficits may become permanent if left untreated
71
Q

Amyotrophic Lateral Sclerosis (ALS) Etiology

A
  • 95% sporadic / 5% hereditary
  • Sporadic usually observed in 5th decade of life
  • genetic can be in 20s or 30s
  • Superoxide dismutase (SOD-1) leading to free radical toxicity

or

  • Reduced glutamate transport leading to glutamate toxicity
72
Q

Amyotrophic Lateral Sclerosis (ALS) Clinical Presentation

A
  • Primarily LMN signs
  • Progressive weakness over time
  • Early signs may be: UMN (asymmetric hyperreflexia/Babinski)
  • Late signs may be: becoming more symmetric hypotonia, flaccid paralysis, hyporeflexia, atrophy
  • Typically spares oculomotor function, sensory, bowel/bladder function
73
Q

Amyotrophic Lateral Sclerosis (ALS)​ Treatment

A

Riluzole: Glutamate antagonist (inhibits presynaptic release)

Glutamate toxicity is thought to be causative for degeneration

74
Q

Bulbar Amyotrophic Lateral Sclerosis (BALS)

A
  • Degeneration of lower brain stem cranial motor nuclei occurs early
  • Abnormalities of swallowing/speaking (CN IX, X involvement)
  • Can also have CN XII involvement (weakening of the tongue)
75
Q

Cranial Nerves Mnemonic

A
76
Q

Nerves functions, effectors/glands, lesion symptoms table

A
77
Q

CN III Lesion: Oculomotor clinical presentation

7 listed

A
  • Ipsilateral ophthalmoplegia
  • Ptosis (levator palpebrae)
  • Mydriasis (blown pupil) from sphincter pupillae
  • Eye turned down and out (extraocular muscles)
  • Diplopia
  • Dry Eye
  • Anisocoria
78
Q

CN III Lesion: Oculomotor Etiology

3 listed

A
  • Aneurysm of vessels in Circle of Willis (Pcomm)
  • Uncal herniation (secondary to tumor, subdural hematoma)
  • Meningitis (Syphilitic/tuberculosis) also likely due to inflammation/edema
79
Q

CN III Lesion: Oculomotor Partial Palsy

A

pupil sparing: Microvascular disease (diabetes/hypertension)

80
Q

CN III Lesion: Oculomotor Palsy Overview

A
81
Q

CN IV Lesion: Trochlear Palsy Clinical Presentation

5 listed

A
  • diplopia
  • strabismus (contralateral to nucleus)
  • Diagnosis may take years due to developmental compensation (head tilt)
  • Acute onset blurriness or diplopia most noticeable when reading/walking down stairs
  • Contralateral head tilt (ocular torticollis)
82
Q

CN IV Lesion: Trochlear Palsy Etiology

A

Congenital

  • absent in 73% of cases isolated CNIV palsy
  • Cranial Dysinnervation syndrome possibly due to trauma during birth

Acquired

Head Trauma (44% of CNIV Palsy had a head trauma) (it is only nerve to exit on dorsal surface and has long intracranial course (vulnerable to contusion/avulsion)

83
Q

CN IV Lesion: Trochlear Palsy Overview

A
84
Q

CN VI Lesion: Abducens Palsy Description

A

Esotropia (medial deviation; ipsilesional eye)

Most commonly affected oculomotor nerve

85
Q

CN VI Lesion: Abducens Palsy Clinical Presentation

A

Diplopia

Blurry Vision

86
Q

CN VI Lesion: Abducens Palsy Etiology

A
  • Small-vessel disease (diabetes, hypertension, ischemia) (AICA or basilar artery)
  • Trauma (most common oculomotor nerve affected
  • Brainstem glioma in children; compression against the clivus due to increased intracranial pressure
87
Q

CN VI Lesion: Abducens Palsy Overview

A
88
Q

CN V Lesion: Trigeminal Palsy Mnemonic

A
  • 3 muscles close jaw: Maesseter, TeMporalis, Medial Pterygoid (M’s Munch)
  • 1 open: Lateral pterygoid (Lateral Lowers)
89
Q

CN V Lesion: Trigeminal Palsy Clinical Presentation

A
  • Loss of corneal reflex (V1 sensory loss)
  • Jaw deviation due to unopposed action of intact pterygoid
  • Jaw jerk reflex impaired (loss of proprioception - V3 division)
  • An isolated motor function is rare and would likely be due to viral infection or neoplasm
  • More common presentation is Facial Neuralgia (severe pain) - repeated short, lightning-like bursts (V2-V3) unilateral, not accompanied by sensory loss
90
Q

CN V Lesion: Trigeminal Palsy isolated motor dysfunction

A

An isolated motor dysfunction is rare and would likely be due to viral infection or neoplasm

91
Q

Most commonly affected CN in children

A

CN IV trochlear

92
Q

CN V Lesion: Trigeminal Palsy Etiology

A
  • Arterial compression (superior cerebellar/AICA 69%)
  • aneurysm or malformation
93
Q

CN V Lesion: Trigeminal Palsy Overview

A
94
Q

CN VII Lesion: Facial Palsy Description and epidemiology

A

Facial Nerve Palsy

Bell’s palsy

incidence 20/100,000

95
Q

CN VII Lesion: Facial Palsy Clinical Presentation

A
  • Dry eye, crocodile tears (lacrimal fluid doesn’t drain to nasolacrimal duct)
  • Facial asymmetry: Drooping of ipsilateral face (smoothing of nasolabial fold, forehead)
  • Inability to smile, close eye, raise eyebrow
  • Loss of corneal reflex (efferent limb)
96
Q

CN VII Lesion: Facial Palsy Etiology

A
  • Isolated: Infection/inflammation (viral HSV Reactivation, chicken pox virus/shingles, Lyme disease)
  • Skull fracture
97
Q

CN VII Lesion: Facial Palsy in combination with CNVIII

A

Acoustic Schwannomas/cerebellopontine angle (CPA) tumors

98
Q

CN VII Lesion: Facial Palsy Overview

A
99
Q

CN IX, X Lesions Clinical Presentation

A
  • Dysphagia (swallowing; esp. liquid) / Dysarthria (hoarse/whispering)
  • Palatal sag ipsilateral; Uvula deviates away
  • Gag reflex absent particularly in IX lesion (afferent limb) but also in X (efferent limb)
100
Q

CN IX, X Lesions etiology

A
  • Recurrent laryngeal nerve paralysis
  • Iatrogenic (thyroidectomy due to a tumor; carotid endarterectomy due to stenosis), Aortic Aneurysm (X only)
  • Glomus tumor of jugular foramen
  • Tumors of the cerebellopontine angle (CPA)
  • Schwannomas/meningiomas usually also include CNVII/VIII or IX
101
Q

CN IX, X Lesions Overview

A
102
Q

CN XI Lesions Spinal Accessory Palsy Clinical Presentation

A
  • Atrophy, fasciculations and partial paralysis of sternocleidomastoid and trapezius
  • Weak/absent shoulder shrug and turning head away from lesioned side
103
Q

CN XI Lesions Spinal Accessory Palsy Etiology

A
  • Iatrogenic (due to medical procedures): radial neck surgery for cervical lymph node biopsy
  • Laryngeal carcinoma with lymph node metastasis (Squamous cell carcinoma)
104
Q

CN XI Lesions Spinal Accessory Palsy Overview

A
105
Q

CN XII Lesions Hypoglossal Clinical Presentation

A

Tongue deviates toward the side of lesion due to unopposed action of intact genioglossus “lick your wounds”

106
Q

CN XII Lesions Hypoglossal Etiology

A
  • Isolated palsy is very rare
  • more common is progressive bulbar palsy (combined with CN X dysfunction)
  • Tuberculosis
  • Neoplasms
107
Q

CN XII Lesions Hypoglossal Overview

A
108
Q

CN Lesions symptoms and causes

A
109
Q

Cavernous Sinus

A
110
Q

Cavernous Sinus Syndrome Etiology

A

Vascular

  • Carotid artery hemorrhage (cavernous fistula) or aneurysmal compression
  • Pituitary adenoma (other neoplasias)
  • Thrombosis related infections (herpes zoster) (facial vein drains into CS via ophthalmic vein (lesions to face can cause CS infection)
  • Retroorbital eye pain nasal discharge, may have CS infection
111
Q

Cavernous Sinus Syndrome Clinical Presentation

A
  • Variable ophthalmoplegia (CNIII, IV, VI)
  • CN VI is most susceptible to injury
  • decreased corneal sensation/reflex (CNV1)
  • Horner Syndrome (ptosis, anhidrosis, miosis)
  • occasional decreased maxillary sensation
  • Non-nervous proptosis (protrusion of eye)
112
Q

Cavernous Sinus Syndrome Overview O TOM CAT Mnemonic

A
113
Q

Sympathetic and parasympathetic divisions of the autonomic nervous system

A
114
Q

Horner Syndrome (Sympathetic) Etiology

A

1st order: hypothalamic sympathetic fibers synapse in the ciliospinal center (C8-T1) 13% of total

Lesions can occur in the spinal cord above T1 (e.g. cervical transection, late-stage syringomyelia) or hypothalamus and brainstem (multisymptom)

2nd order: Preganglionic fibers ascend through stellate ganglion/carotid sheath and synapse in superior cervical ganglion 44% of total (lesion of stellate ganglion (e.g. pancoast pulmonary tumor, NF tumor)

3rd order: post ganglionic neurons travel with internal carotid into cavernous sinus, then V1 into the orbit. 43% of total (lesion of superior cervical ganglion, cavernous sinus, carotid dissection)

115
Q

Horner Syndrome (Sympathetic) Clinical Presentation

A
  • Ipsilateral
  • sympathetic symptoms related to face
  • Ptosis
  • Anhidrosis
  • Miosis
  • (PAM)
116
Q

Horner Syndrome (Sympathetic) Overview

A
117
Q

Sympathetic pathway for pupil dilation

A
118
Q

Most commonly affected oculomotor nerve

A

Abducens nerve

119
Q

Copies of SMN2 in various types of SMA

A

SMA 1 - 2 copies little compensation for SMN1 loss

SMA 2 - 3 copies some compensation for SMN1 loss

SMA 3 - 4-8 copies more compensation for SMN1 loss

Neuroscience (96 decks)

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