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Neuroscience II > Quiz 1 > Flashcards

Quiz 1 Flashcards

1
Q

Cell bodies of nerves entering the dorsal root are located in the __, whereas the cell bodies of motor neurons entering the ventral root are embedded in the ___.

A

Cell bodies of nerves entering the dorsal root are located in the DORSAL ROOT GANGLION, whereas the cell bodies of motor neurons entering the ventral root are embedded in the GREY MATTER.

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2
Q

The spinal nerve forms in the ___. It consists of [dorsal root/ ventral root/ both roots] and then splits into the __ and __.

A

The spinal nerve forms in the INTERVERTEBRAL FORAMEN. Spinal nerve consists of the COMBINED dorsal and ventral roots before it splits into the DORSAL PRIMARY RAMUS and VENTRAL PRIMARY RAMUS.

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3
Q

The dorsal primary ramus innervates ___ and the ventral primary rami go to ___

A

The dorsal primary ramus innervates TRUE BACK MUSCLES AND SKIN OF BACK and the ventral primary rami go to THE PLEXI (brachial, lumbar, sacral), INTERCOSTAL NN

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4
Q

There are 3 axon types in peripheral nn: somatic __, somatic __, and visceral [motor/sensory]. Describe what each innervates.

A

SOMATIC MOTOR
- to skeletal muscle

SOMATIC SENSORY
- sends info back to CNS from skin, muscle, bone, and joints

VISCERAL MOTOR
- sympathetic innervation to smooth muscle of blood vessels, sweat glands, etc.

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5
Q

The two main types of peripheral nn are __ and __.

A

Fibroblasts

Schwann Cells

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6
Q

Fibroblasts are found in all types of ___ tissue. They generate __. The outer margin or edge of a nerve is a wrap made up of __ and __ called the __.

A

Fibroblasts are found in connective tissue
They generate COLLAGEN fibers
The outer margin or edge of a nerve is a wrap made up of COLLAGEN and FIBROBLASTS called the EPINEURIUM.

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7
Q

Schwann cells surround and support [myelinated axons/ unmyelinated axons/ all peripheral axons]. They produce ___ in segments that wrap around larger axons. One Schwann cell produces ___ (#) myelin segment(s).

A

Schwann cells surround and support ALL PERIPHERAL AXONS WHETHER OR NOT THEY’RE MYELINATED. They produce MYELIN SHEATH in segments that wrap around larger axons. One Schwann cell produces ONE myelin segment.

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8
Q

Each peripheral nerve consists of nerve fibers of [the same/a variety of] diameter(s). Are all of the fibers myelinated or unmyelinated in the same nerve? Are all fibers motor or sensory?

A

Each peripherals nerve consists of fibers with a VARIETY OF DIAMETERS, SOME are myelinated but some are not, SOME are motor, some are sensory!

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9
Q

Axons (nerve fibers) can be classified based on __ or __.

A

Classify by…

CONDUCTION VELOCITY

FIBER DIAMETER

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10
Q

Describe the premise and classification behind conduction velocity classification of nerve fibers

A

Not all impulses arrive at the same time after a nerve is stimulated because of different conduction velocities of various FIBERS. We see THREE main peaks representing 3 major groups of fibers:

(1) A (heavily myelinated sensory and motor fibers)
- A alpha (alpha MN)
- A beta
- A gamma (gamma MN to muscle spindle)
- A delta (fast pain fibers)

(2) B (thinly myelinated, slower, preganglionic autonomic fibers)
(3) C (unmyelinated)

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11
Q

Describe the nerve fiber classification based on fiber diameter

A

*Mostly used to reference sensory fibers, e.g. from muscle spindle (Ia & II). Most sensory receptors are assoc. with Type II fibers (touch)

4 groups:

  • I (most heavily myelinated; Ia is assoc. with muscle spindle, Ib is assoc. with GTO)
  • II (assoc. with muscle spindle)
  • III (myelinated)
  • IV (unmyelinated)
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12
Q

The [number/letter] classification system is primarily used to describe myelinated efferents (e.g. ___ and ___ motor neurons). The [number/letter] system is used to describe myelinated afferents (e.g. ____)

A

The LETTER classification system is primarily used to describe myelinated efferents (e.g. A-alpha and A-gamma MNs). The NUMBER system is used to describe myelinated afferents (e.g. Ia from primary muscle spindle afferents, Ib from GTO, II from muscle spindle and from some receptors of skin & joints)

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13
Q

The fastest conducting axons send signals as fast as __-__m/s. The slowest travel at __-__ m/s.

A

The fastest conducting axons send signals as fast as 70-120 m/s. The slowest travel at 0.5-2 m/s.

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14
Q

We can also classify axons by function. Large myelinated axons transmit sensation of __, __, and __. These are [sensory/motor] (___ specific type?) neurons

Small, unmyelinated and finely myelinated axons transmit __, __, and ___ as part of the ___ nervous system.

A

We can also classify axons by function. Large myelinated axons transmit sensation of PROPRIOCEPTION, JOINT POSITION, and VIBRATION. These are motor (ALPHA & GAMMA) neurons

Small, unmyelinated and finely myelinated axons transmit PAIN, TEMPERATURE, and POORLY LOCALIZED TOUCH as part of the AUTONOMIC nervous system.

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15
Q

Name the nerve wrapping layers from superficial to deep.

A

Epineurium
Perineurium
Endoneurium

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16
Q

The __ is the outer connective tissue that surrounds each peripheral nerve. It consists mostly of __ and __. It is [think/thick] at the nerve trunk and [thickens/thins] as it branches toward its termination. It is continuous with the __ at the level of the spinal nerve. Its role is to protect the __ from [compressive/tensile] forces.

A

The EPINEURIUM is the outer connective tissue that surrounds each peripheral nerve. It consists mostly of COLLAGEN FIBERS and FIBROBLASTS. It is THICK at the nerve trunk (30-70% cross sectional area!) and THINS as it branches toward its termination. It is continuous with the DURA MATER at the level of the spinal nerve. Its role is to protect the FASCICULI from COMPRESSIVE forces.

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17
Q

The ___ lies deep to the epineurium and surrounds the __. It is composed of __ and__. The cells of this layer are connected by __ which effectively close off each ___ from those around it. It creates a microenvironment and adds [compressive/tensile] strength to nerve so it can resist stretch. Its role is to maintain ___ pressure and it accounts for the __ and __ of the nerve.

A

The PERINEURIUM lies deep to the epineurium and surrounds the FASCICLES (bundles). It is composed of CONNECTIVE TISSUE CELLS and COLLAGEN FIBERS. The cells of this layer are connected by TIGHT JUNCTIONS which effectively close off each FASCICLE from those around it. It creates a microenvironment and adds TENSILE strength to nerve so it can resist stretch. Its role is to maintain INTRAFASCICULAR FLUID PRESSURE and it accounts for the ELASTICITY and TENSILE STRENGTH of the nerve.

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18
Q

The ___ is the deepest layer of neural wrappings. It consists of ___ that extends in from the ___ to surround individual nerve [fascicles/ fibers].

A

The ENDONEURIUM is the deepest layer of neural wrappings. It consists of LOOSE CONNECTIVE TISSUE that extends in from the PERINEURIUM to surround individual nerve FIBERS (individual axons)

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19
Q

The epi-, peri-, and endoneurium receive their blood supply from ___. What is the effect on nerves in the context of peripheral vascular dz?

A

The epi-, peri-, and endoneurium receive their blood supply from ARTERIOLES. These vessels are also susceptible to PVD; as PVD gets worse, the nerve health will decline too!

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20
Q

Name three mechanisms of peripheral neuropathies

A

Neurapraxia
Axonotmesis
Neurotmesis

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21
Q

___ is a transient, localized conduction block with NO signs of denervation due to local damage to neural membrane. Full recovery occurs in __ to ___ (time line). Likely due to a mild ___ injury.

A

NEURAPRAXIA is a transient, localized conduction block with NO signs of denervation due to local damage to neural membrane. Full recovery occurs in DAYS or WEEKS. Likely due to a mild COMPRESSION injury (e.g. leg falls asleep –> ischemia along length of nerve. Restore blood supply and you’re okay!)

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22
Q

___ describes a neural injury in which there is axon disruption but the endoneurial sheath remains intact. ___ takes place and regrowth occurs. The length of recovery depends on the __ needed for regrowth. Likely due to a [stretch/compression] injury, in which the [axon/myelin sheath] broke before the [axon/myelin sheath].

A

AXONOTMESIS describes a neural injury in which there is axon disruption but the endoneurial sheath remains intact. WALLERIAN DEGENERATION takes place and regrowth occurs. The length of recovery depends on the DISTANCE needed for regrowth. Likely due to a STRETCH injury, in which the AXON broke before the MYELIN SHEATH (& connective tissue)

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23
Q

___ describes a neural injury in which there is a complete transection of the nerve with disruption of axon and endoneurial tube. ___ takes place and regrowth occurs. Could be caused by ____ injuries.

A

NEUROTMESIS describes a neural injury in which there is a complete transection of the nerve with disruption of axon and endoneurial tube. WALLERIAN DEGENERATION takes place and regrowth occurs. Could be caused by CUT, CRUSH, or SEVERE STRETCH injuries.

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24
Q

3 general types of traumatic nerve injuries include…

A

Laceration
Crush (compression)
Stretch

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25
Q

Compressive nerve injuries can be further classified as:

(1) __ (e.g. ___),
(2) ____ (which can be __ or ___, e.g. ___)
(3) ____ (which can occur with longstanding of which type? or constant ___)

A

Compressive nerve injuries can be further classified as:

(1) ACUTE (e.g. arm falls asleep when you lay on it),
(2) INTERMITTENT (which can be POSTURAL or OCCUPATIONAL, e.g. Carpal Tunnel, Guyon’s canal syndrome)
(3) CHRONIC (which can occur with longstanding INTERMITTENT (e.g. carpel tunnel) or constant COMPRESSION)

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26
Q

Iatrogenic compressive nerve injuries are a type of [acute/ intermittent/ chronic] nerve injury caused by ___.

A

Iatrogenic compressive nerve injuries are a type of CHRONIC nerve injury caused by TREATMENT (e.g. cast too tight, setting fracture).
- Can happen due to postural, biomechanical, or callus formation (in bone healing)

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27
Q

Describe symptoms of ACUTE, SHORT TERM, or INTERMITTENT compressive peripheral neuropathies.

  • Neuropraxia or neurotmesis?
  • Changes in NCV?
  • Sensory or motor changes?
  • Pain?
  • Symptoms develop rapidly or progressively?
  • Symptoms are short lived or long term?
  • Sx are reversible or permanent?
A

Describe symptoms of acute, short term, or intermittent compressive peripheral neuropathies.

  • Neurapraxia
  • Reduced NCV over compressed segment
  • Sensory involved before motor
  • Paresthesia especially at night
  • Pain and temperature changes do NOT occur
  • Symptoms develop rapidly (though it depends)
  • Symptoms are short lived and reversible
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28
Q

Describe symptoms of CHRONIC compressive peripheral neuropathies.

  • Neuropraxia or neurotmesis?
  • Changes in NCV?
  • Sensory or motor changes?
  • Pain?
  • Symptoms develop rapidly or progressively?
  • Symptoms are short lived or long term?
  • Sx are reversible or permanent?
A

Describe symptoms of CHRONIC compressive peripheral neuropathies.

  • May develop into neurotmesis
  • NCV further reduced or abolished with a reduction or loss of touch and/or pressure
  • Motor denervation changes with atrophy
  • Pain, hyperesthesia, allodynia
  • Symptoms and deficits are progressive
  • External decompression may not alleviate sx, so they may be permanent
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29
Q

Non-traumatic causes of neuropathies include… (4, give examples)

A

(1) Disease related - Guillian Barre, thyroid function
(2) Metabolic - alcoholism, diabetes, aging
(3) Toxins
(4) Genetics - Charcot Marie Tooth

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30
Q

____ describes the fragmentation of axon and myelin distal to a nerve injury that begins hours after injury. By __-__ hours post cut, the axon is discontinuous and the axon swells. This means that action potentials [can/ can no longer] propagate along the length of the distal segment.

A

WALLERIAN DEGENERATION describes the fragmentation of axon and myelin distal to a nerve injury that begins hours after injury. By 48-96 hours post cut, the axon is discontinuous and the axon swells. This means that action potentials CANNOT propagate along the length of the distal segment.

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31
Q

In Wallerian Degeneration, distal segment receptors are ___. Myelin degeneration is advanced by __-__ hours post injury. This occurs because __ cells are activated. What’s the relationship between Schwann cells and mast cells? Schwann cells activate within __ of injury, undergo [mitosis/ meiosis] and help __ cells get rid of degenerated distal nerve segment and myelin (aka the process = ___). The site of the injury is cleared within ___ - ___ (timeframe), leaving behind only the ___ and ___. In more mild to moderate injuries, the Schwann cells form __ to guide the growth of ___ from regenerating axons. In more severe injuries, when the endoneurium is disrupted, so are ___, resulting in __.

A

In Wallerian Degeneration, distal segment receptors are DEGENERATED. Myelin degeneration is advanced by 36-48 hours post injury. This occurs because MAST CELLS are activated. SCHWANN CELLS CONVERT INTO MAST CELLS AND CAN ALSO PHAGOCYTIZE. Schwann cells activate within 24 HOURS of injury, undergo MITOSIS and help MAST cells get rid of degenerated distal nerve segment and myelin (aka the process = PHAGOCYTOSIS). The site of the injury is cleared within 1 WEEK - SEVERAL MONTHS POST INJURY, leaving behind only the ENDONEURIAL SHEATH and SCHWANN CELLS. In more mild to moderate injuries, the Schwann cells form STACKS to guide the growth of GROWTH CONES from regenerating axons. In more severe injuries, when the endoneurium is disrupted, so are CAPILLARIES, resulting in HEMORRHAGE. (–> inflammation –> dense fibrous scar)

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32
Q

After a nerve injury, within 6 hours, the nucleus of the cell body (proximal segment) becomes ___ and the ___ breaks down. This process is called ___. ___ cells proliferate and phagocytize the proximal segment, but this may be minimal in [mild/ moderate/ severe] injuries. Injury can trigger ___, resulting in the cell death of __-__% of dorsal root ganglion cells. This is more likely if the injury is more [proximal/ distal].

A

After a nerve injury, within 6 hours, the nucleus of the cell body (proximal segment) becomes ECCENTRIC (drifts off to the side) and the NISSL SUBSTANCE (aka rough ER or chromatin) breaks down. This process is called CHROMATOLYSIS. SCHWANN CELLS proliferate and phagocytize the proximal segment, but this may be minimal in MILD injuries. Injury can trigger APOPTOSIS, resulting in the cell death of 20-50% of dorsal root ganglion cells. This is more likely if the injury is more PROXIMAL.

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33
Q

Functional recovery following nerve injury is more likely in [neurapraxia / axonotomesis / neurotmesis] where the endoneurial tube is intact. Without the tube, the sprouting axons have little guidance. Regrowth can begin as soon as __ post injury up to ___ (time frame) depending on the severity. The axon sprouts many ___ hoping that one will find the tube and grow to innervate the proper areas.

A

Functional recovery following nerve injury is more likely in NEURAPRAXIA & AXONOTMESIS where the endoneurial tube is intact. Without the tube, the sprouting axons have little guidance. Regrowth can begin as soon as 24 HOURS post injury up to MONTHS LATER depending on the severity.The axon sprouts many COLLATERALS hoping that one will find the tube and grow to innervate the proper areas.

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34
Q

A typical rate of nerve regrowth is ___ (distance) per ___ (time period), though this varies depending in injury severity and cell body health.

A

A typical rate of nerve regrowth is 1 mm (distance) per DAY (approx 25mm in an inch), though this varies depending in injury severity and cell body health.

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35
Q

Regenerated nerves initially have:

  • [larger/ smaller] axons
  • [larger/ smaller] diameter
  • [more/ less] axons (why?)
  • [thicker/ thinner] myelin
  • [more/ fewer] myelin segments
  • [faster/slower] conduction velocity
A

Regenerated nerves initially have:

  • SMALLER axons
  • SMALLER diameter
  • MORE axons (why? b/c COLLATERAL SPROUTING!)
  • THINNER myelin (initially, but eventually recovers)
  • MORE myelin segments (and therefore, MORE NODES of RANVIER)
  • SLOWER conduction velocity (more stops at each node of ranvier!)
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36
Q

Severe muscle atrophy takes place with nerve denervation - can lose __% reduction in cross sectional area in 2 months if not innervated!

A

Severe muscle atrophy takes place with nerve denervation - can lose 70% reduction in cross sectional area in 2 months if not innervated!

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37
Q

With denervation, we see intramuscular ___ that occurs with proliferation of connective tissue. A fibrosed muscle does not secrete ___, so reinnervation becomes [more/less] likely. Reinnervation of muscle can result in ___ motor units which form when collaterals of [a single/ multiple] alpha motor neuron(s) innervate a large number of all the same type of muscle fiber. This reorganization of the motor unit takes __ (how much time?) post injury.

A

With denervation, we see intramuscular FIBROSIS that occurs with proliferation of connective tissue (CT thickening). A fibrosed muscle does not secrete NERVE GROWTH FACTOR, so reinnervation becomes LESS likely. Reinnervation of muscle can result in GIANT motor units which form when collaterals of A SINGLE alpha motor neuron innervate a large number of all the same type of muscle fiber. This reorganization of the motor unit takes 1 YEAR - 18 MONTHS post injury.

38
Q

Summary of denervation effect on muscle:

(1) severe __ of muscle
(2) Intramuscular ___
(3) Reinnervation of muscle can result in __ motor units
(4) Muscle reinnervation may be ___

A

Summary of denervation effect on muscle:

(1) severe ATROPHY of muscle
(2) Intramuscular FIBROSIS
(3) Reinnervation of muscle can result in GIANT motor units
(4) Muscle reinnervation may be INCOMPLETE or INFEFFICIENT

39
Q

Muscle reinnervation may be incomplete or inefficient. Axons originally of one fiber type innervate [the same/other] fiber types. Are all muscle fibers reinnervated?

A

Muscle reinnervation may be incomplete or inefficient. Axons originally of one fiber type innervate ALL THE SAME TYPE MUSCLE FIBER. NOT ALL muscle fibers are reinnervated

40
Q

Reestablishment of sensation to the original pattern can still happen __-__ months post injury. The receptors will wait for up to __ (how long?) in a __ state to be reinnervated. Effective reinnervation depends on axons regenerating down the correct ___ to make contact with the original receptor.

A

Reestablishment of sensation to the original pattern can still happen 6-12 months post injury. The receptors will wait for up to ONE YEAR in a DORMANT state to be reinnervated. Effective reinnervation depends on axons regenerating down the correct ENDONEURIAL TUBE to make contact with the original receptor.

41
Q

Demyelinization can be caused by certain __. How does this affect AP conduction? If the cause of demyelinization is an inflammatory process (e.g. __), the damage may be permanent.

A

Demyelinization can be caused by certain CONDITIONS OR DISEASES. AP CONDUCTION CAN BE SLOWED OR BLOCKED. If the cause of demyelinization is an inflammatory process (e.g. GUILLIAN BARRE SYNDROME), the damage may be permanent.

42
Q

Guillian Barre Syndrome, aka ___ ___, occurs in [older/young] adults through early middle age. It usually appears following ___ and [is/is not] chronic. ___ (what cell types?) are sensitized to the peripheral nerve and attack it as if it were a(n) ___. We see [localized/ patchy & diffuse] segmental demyelinization of peripheral nerves. It may progress over __ days, stay stable for __ weeks, and then take ___ (how long?) to recover. __% do not fully recover.

A

Guillian Barre Syndrome, aka POSTINFECTIOUS POLYNEURITIS, occurs in YOUNG ADULTS through early middle age. It usually appears following INFECTIOUS ILLNESS and IS NOT CHRONIC. LYMPHOCYTES are sensitized to the peripheral nerve and attack it as if it were a(n) ANTIGEN. We see PATCHY & DIFFUSE segmental demyelinization of peripheral nerves. It may progress over 10 days, stay stable for 2 weeks, and then take 6 MONTHS - 2 YEARS to recover. 10% do not fully recover.

43
Q

Symptoms of Guillian-Barre Syndrome include

  • [ascending/descending] weakness over hours to days
  • Changes in reflexes?
  • [high/ low] CSF Protein
  • Involvement with other systems?
  • May have mild [motor/sensory] loss, disproportionate [motor/sensory] loss
  • Inflammatory segmental ___
A

Symptoms of Guillian-Barre Syndrome include

  • ASCENDING weakness over hours to days
  • AREFLEXIA
  • ELEVATED CSF Protein
  • Possible CRANIAL NERVE and RESPIRATORY involvement
  • May have mild SENSORY loss, disproportionate MOTOR loss
  • Inflammatory segmental DEMYELINIZATION
44
Q

Early indicators of possible incomplete recovery in Guillian-Barre Syndrome include:

  • More than __ weeks from max weekness to initial improvement
  • Reduced [motor/sensory] nerve ___ velocity
  • EMG evidence of ___
  • Need for ___ support
A

Early indicators of possible incomplete recovery in Guillian-Barre Syndrome include:

  • More than 3 weeks from max weekness to initial improvement
  • Reduced MOTOR nerve CONDUCTION velocity
  • EMG evidence of DENERVATION
  • Need for RESPIRATORY support
45
Q

Treatment for Guillian-Barre syndrome includes ___ or ___ treatment. The latter occurs via several mechanisms and interrupts the abnormal immune response for the inflammation.

A

Treatment for Guillian-Barre syndrome includes PLASMAPHERESIS or INTRAVENOUS IMMUNOGLOBULIN TREATMENT treatment. The latter occurs via several mechanisms and interrupts the abnormal immune response for the inflammation.

46
Q

____ is another disease that may appear initially as Guillian Barre. It is [chronic/not chronic], [static/ progressive] autoimmune-mediated inflammation of the peripheral ___. It follows a __/___ course. [Sensory/motor/ both equally] involved. Leads to severe disability over a period of __ (time frame). Treatments include __, __, and __.

A

CHRONIC INFLAMMATORY DEMYELINATING POLYNEUROPATHY (CIDP) is another disease that may appear initially as Guillian Barre. It is CHRONIC, PROGRESSIVE autoimmune-mediated inflammation of the peripheral MEYLIN. It follows a RELAPSING/ REMITTING course. SENSORY & MOTOR ARE EQUALLY involved. Leads to severe disability over a period of YEARS (time frame). Treatments include STEROIDS (short term use), PLASMAPHERESIS, and IV IGg (for episode/relapse).

47
Q

___ is an autoimmune disease characterized by the appearance and relapse of neurological deficits in multiple areas of the [peripheral/central] nervous system with primary damage to [myelinated/ unmyelinated] axons. It is produced by a(n) [infectious/ environmental] agent in a ___ susceptible individual resulting in an alteration of immune mechanisms in the [PNS/CNS].

A

Multiple Sclerosis is an autoimmune disease characterized by the appearance and relapse of neurological deficits in multiple areas of the CENTRAL nervous system with primary damage to MYELINATED axons. It is produced by a(n) ENVIRONMENTAL agent (exposure to a certain antigen by a certain age) in a GENETICALLY-SUSCEPTIBLE individual resulting in an alteration of immune mechanisms in the CNS

48
Q

MS occurs 2x as frequently in [men/women] and is diagnosed mainly in [older/young] adults. It is more prevalent in [north/south] temperature latitudes. There are __ (#) types of MS, but the most common is [acute/chronic] ___-___.

A

MS occurs 2x as frequently in WOMEN than men and is diagnosed mainly in YOUNG adults (avg. age in US = 24). It is more prevalent in NORTH temperature latitudes. There are 4 (#) types of MS, but the most common is CHRONIC RELAPSING-REMITTING

49
Q

Symptoms of MS include:

  • Sensory: __, __, and __
  • Motor: decreased __, ___
  • Visual: ___
  • Bladder ___
  • Brain: signs in __ and ___
  • ___
A

Symptoms of MS include:

  • Sensory: DYSESTHESIA, PARESTHESIA, ANASTHESIA
  • Motor: decreased CONTROL, SPASTICITY
  • Visual: OPTIC NEURITIS
  • Bladder DYSFUNCTION
  • Brain: signs in CEREBELLUM and BRAINSTEM
  • DEMENTIA

*Lesions result from the inflammatory process in MS. Lesions scar and cause permanent damage.

50
Q

MS generally presents as [bilateral/ one-sided] involvement, and progresses to ___. Why?

A

MS generally presents as HEMIPARESIS and is ONE-SIDED. It progresses to BILATERAL involvement. This is because signs follow lesion development..eventually they are bilateral

51
Q

___ is a recording of spontaneous and voluntary motor unit activity to determine the integrity of muscle and nerve

A

ELECTROMYOGRAPHY (EMG)

52
Q

___ is a measurement of the speed of transmission of a motor or sensory impulse along a nerve

A

NERVE CONDUCTION VELOCITY (NCV)

53
Q

EMG instrumentation requires a __ and ___, as well as a computer for sound and motor unit activity. ___ are placed in the muscle.

A

EMG instrumentation requires a AMPLIFIER and OSCILLOSCOPE, as well as a computer for sound and motor unit activity. RECORDING ELECTRODES are placed in the muscle

54
Q

Recall that a motor unit consists of the ___ neuron axons and all of its branches, the ___, and all of the ___ it innervates. A muscle contraction is detected by EMG electrodes by transmitting ___ to a ___ and recording it as ___ (aka the difference in ___ between 2 points).

A

Recall that a motor unit consists of the ALPHA MOTOR NEURON axons and all of its branches, the MOTOR END PLATE, and all of the MUSCLE FIBERS it innervates. A muscle contraction is detected by EMG electrodes by transmitting ELECTRICAL SIGNALS to a RECORDER and recording it as VOLTAGE (aka the difference in POTENTIAL between 2 points).

*The MUs closest to the stimulating electrode will be stimulated earlier vs those that are farther will be stimulated later

55
Q

All of the fibers in a motor unit contract [simultaneously/ asynchronously]. Why?

A

All of the fibers in a motor unit do NOT contract simultaneously. This is because the alpha MN has different-length collaterals that come off…the shorter fibers get to the muscle sooner.

56
Q

A motor unit action potential represents the activity of ____. Typically, single MUPs are ___phasic (how many phases?), differentiated by each time the potential crosses ___. Upward reflections are [negative/ positive], and downward is [positive/ negative]. The amplitude (think, graphically) is the sum of ____ contracting at the same time and is __-___ (amplitude range & units?). The first upward deflection is the ____, after which ___ join to produce the wave form. The entire duration is _-__ [seconds/ milliseconds], and the typical firing rate (frequency) is __-__x/second.

A

A motor unit action potential represents the activity of the MUSCLE FIBERS OF A SINGLE MOTOR UNIT. Typically, single MUPs are BI- or TRI-PHASIC differentiated by each time the potential crosses BASELINE. Upward reflections are NEGATIVE, and downward is POSITIVE The amplitude (think, graphically) is the sum of MUSCLE FIBERS contracting at the same time and is 300uV (small MU) to 5mV (large MU). The first upward deflection is the ACTIVITY OF THE MUSCLE FIBER CLOSEST TO THE ELECTRODE, after which OTHER FIBERS join to produce the wave form. The entire duration is 3-16 MILLISECONDS, and the typical firing rate (frequency) is 5-15X/SECOND (for as long as MU is contracting)

57
Q

What factors influence the size, shape, and duration of the MUAP?

A
  • Distance between electrodes
  • Location of electrodes
  • Size of electrodes
  • Size of motor unit and dispersion of fibers
  • Depth of motor unit and distance from electrodes
  • Asynchrony of contraction of muscle fibers in MU.

Big MU with lots of muscle fibers = bigger amplitude

58
Q

During a normal EMG, we see the following activity:

(1) ____ Activity - results from disruption of the ___. The duration of this phase is up to __ milliseconds.
(2) ____ - this should occur in normal muscle at rest

(3) Activity from [multiple/single] motor units with [max/minimal] effort.
Amp: \_\_\_
Duration: \_\_\_
# Phases?
Sound: \_\_\_
Frequency: \_\_\_

(4) Increased effort (moderate) results in [incr/decr] amplitude and the pattern starts to fill in as more, [larger/smaller] [fibers/motor units] are being recruited. The firing frequency [incr/decr]. ___ happens as some units fire simultaneously.
(5) ____ Pattern. This fills out with [min/mod/max] effort. The amplitude is [larger/smaller] than what is seen in a single MU because the MUs ___.

A

During a normal EMG, we see the following activity:

(1) INSERTIONAL Activity - results from disruption of the MUSCLE MEMBRANE. The duration of this phase is up to 300 milliseconds.
(2) ELECTRICAL SILENCE AT REST - this should occur in normal muscle at rest

(3) Activity from SINGLE motor units with MINIMAL effort.
Amp: 300uV - 5mV
Duration: 3-16 milliseconds
BI- or TRI-PHASIC
Sound: THUMPING
Frequency: 5-15X/SEC

(4) Increased effort (moderate) results in INCR AMPLITUDE and the pattern starts to fill in as more, LARGER MOTOR UNITS are being recruited. The firing frequency INCREASES. SOME SUMMATION happens as some units fire simultaneously.
(5) INTERFERENCE Pattern. This fills out with MAX effort. The amplitude is LARGER than what is seen in a single MU because the MUs SUMMATE.

59
Q

You need a [minimal/ moderate/ maximal] contraction to see a MU AP in normal muscle. On an EMG, no contraction (i.e. at rest) yields ___, and max contraction yields ___.

A

You need a MINIMAL contraction to see a (biphasic or triphasic) MU AP in normal muscle. On an EMG, no contraction (i.e. at rest) yields SILENCE AT REST, and max contraction yields FULL INTERFERENCE PATTERN.

60
Q

You might perform EMG on a person with a neuropathy in order to record activity from the [muscle/nerve] which tells you something about the health of the [muscle/nerve].

A

You might perform EMG on a person with a neuropathy in order to record activity from the MUSCLE which tells you something about the health of the NERVE.

61
Q

During ABNORMAL EMG (neuropathies), we see the following activity:

(1) [Shortened/prolonged] Insertional Activity - the ___ is unstable, so needle insertion yields excessive exchange of ___ across the membrane.
(2) ____ (aka ___) and [positive/negative] ___ waves at rest -these are [larger/smaller] than single MUAPs. These represents the depolarization of [single muscle fibers/ whole motor units].
(3) With minimal contraction in a partially denervated muscle, you see activity from [multiple/single] motor units, though there will be [smaller/fewer] MUAPs vs. normal.
(4) With moderate to max contraction, the interference pattern [is more condensed/ is incomplete]. Therefore, the pattern will show up with [gaps/ dense areas]. The [frequency/ amplitude/ duration] may be abnormal because ___.
(5) A fully denervated muscle has [a dense/ NO] interference pattern because ___.

A

(1) PROLONGED Insertional Activity - the MUSCLE MEMBRANE is unstable, so needle insertion yields excessive exchange of IONS across the membrane. (abnormal and denervated muscle is hypersensitve to ion shifts –> incr insertional activity)

(2) SPONTANEOUS POTENTIALS (aka FIBRILLATION POTENTIALS) and POSITIVE SHARP WAVES at rest - these are SMALLER than single MUAPs. These represents the depolarization of SINGLE MUSCLE FIBERS
* this is due to spontaneous exchange of ions across the membrane (it’s leaky!)

(3) With minimal contraction in a partially denervated muscle, you see activity from SINGLE motor units, though there will be FEWER MUAPs vs. normal.
(4) With moderate to max contraction, the interference pattern IS INCOMPLETE Therefore, the pattern will show up with GAPS. The AMPLITUDE may be abnormal because YOU’RE MISSING SOME MUs SO THEY DON’T SUMMATE & THERE AREN’T ENOUGH MUs CONTRACTING TO FILL IT IN COMPLETELY.
(5) A fully denervated muscle has NO interference pattern because THERE IS NO CONTRACTION.

62
Q

Fibrillation potentials occur in [normal/ abnormal] muscle and are ranked as __, __, and __. A partially denervated muscle will have [more/fewer] and a completely denervated muscle will have [more/fewer] of these.

A

Fibrillation potentials occur in ABNORMAL muscle and are ranked as +1, +2, or +3. A partially denervated muscle will have FEWER and a completely denervated muscle will have MORE of these.

63
Q

Positive sharp waves are [upward/downward] reflections, and fibrillation potentials are [upward/downward] reflections.

A

Positive sharp waves are DOWNWARD reflections, and fibrillation potentials are UPWARD reflections.

64
Q

Fasiculations are wave forms that represent contraction of a group of [muscle fibers/ motor units]. These [can be/ are not] present in normal individuals, occurring in about ___% of observed potentials. They can occur in normal muscle when it is ___, but more fasiculations can be a sign of pathology in dz states such as ___.

A

Fasiculations are wave forms that represent contraction of a group of MUSCLE FIBERS These CAN BE present in normal individuals, occurring in about

65
Q

What could cause a partially denervated muscle?

A

What could cause a partially denervated muscle?

  • Stab wounds
  • Carpel tunnel
  • Crush injury
  • Diabetes
66
Q

Summary of Denervation:

(1) [incr/decr] insertional activity due to unstable __
(2) ___ and __ are seen at rest due to unstable ___ (and spontaneous ___).
(3) Minimal contraction: ___ may be absent in complete denervation, or less [intense/ frequent] in partial denervation.
(4) Mod-Max Contraction: ___ may be absent in complete denervation, reduced in partial denervation.

A

Summary of Denervation:

(1) INCREASED insertional activity due to unstable MUSCLE MEMBRANE
(2) POSITIVE SHARP WAVES and FIBRILLATION POTENTIALS are seen at rest due to unstable MUSCLE MEMBRANE (and spontaneous CONDUCTANCE).
(3) Minimal contraction: MUAPs may be absent in complete denervation, or less FREQUENT in partial denervation.
(4) Mod-Max Contraction: INTERFERENCE PATTERN may be absent in complete denervation, reduced in partial denervation.

67
Q

In a myopathy, the primary disease is in the [nerve/ muscle]. Clinical presentations vary.

A

In a myopathy, the primary disease is in the MUSCLE. Clinical presentations vary.

68
Q

Myotonic dystrophies are a group of muscle diseases characterized by muscle __ and [shortened/prolonged] muscle contractions. [High/ Low] frequency discharges are generated from the [muscle/nerve] and occur at the ___ or with movement. You may also see/hear the characteristic “____” on an EMG, indicative of myotonia.

A

Myotonic dystrophies are a group of muscle diseases characterized by muscle WASTING and PROLONGED muscle contractions. HIGH frequency discharges are generated from the MUSCLE and occur at the NEEDLE INSERTION or with movement. You may also see/hear the characteristic “DIVE BOMBER” on an EMG, indicative of myotonia.

69
Q

Summary of Reinnervation:

(1) Insertional activity is [increased/ decreased/ returns to normal over time].
(2) Early recovery: begin to see nacent units characterized by MUAPs that are [long/short] duration, [high/low] amplitude, [monophasic/biphasic/ polyphasic] because [many/few] muscle fibers reinnervated MU, [synchronized/ not synchronized], terminals conducting at [same/different] velocities
(3) MUAP [decreases in/ gains] amplitude and duration as time goes on
(4) If normal recovery does not happen, ___ motor units may form if some MUs do not effectively regrow. This is a [short/long] term development (__-__ months)
(5) The interference pattern fills in and gains [freq/duration/amplitude] as more MU come back on line.

A

Summary of Reinnervation:

(1) Insertional activity RETURNS TO NORMAL OVER TIME
(2) Early recovery: begin to see nacent units characterized by MUAPs that are are SHORT duration, LOW amplitude, POLYPHASIC because FEW muscle fibers reinnervated MU, NOT SYNCHRONIZED, terminals conducting at DIFFERENT velocities
(3) MUAP GAINS amplitude and duration as time goes on
(4) If normal recovery does not happen, GIANT motor units may form if some MUs do not effectively regrow. This is a LONG term development (12-18 months)
(5) The interference pattern fills in and gains AMPLITUDE as more MU come back on line.

70
Q

As a nerve recovers and is reinnervated, you will continue to see [incr/decr] insertional activity, ___, and ___ until all [motor units/ muscle fibers] are reinnervated.

A

As a nerve recovers and is reinnervated, you will continue to see INCREASED insertional activity, POSITIVE SHARP WAVES, and FIBRILLATION POTENTIALS until all MUSCLE FIBERS are reinnervated.

71
Q

Positive sharp waves and fibrillation potentials will ONLY go away after a nerve injury if the nerve is ____ or the muscle fibers have ___.

A

Positive sharp waves and fibrillation potentials will ONLY go away after a nerve injury if the nerve is COMPLETELY REINERVATED or MUSCLE FIBERS HAVE FIBROSED.

72
Q

As muscle fibers begin to reinnervate, you begin to see ___ units. These are very [large/small] amplitude, [long/short] duration, [mono/bi/poly] phasic potentials.

Why are they [large/small]?
Why are they [mono/bi/ polyphasic]?

A

As muscle fibers begin to reinnervate, you begin to see NASCENT units. These are very SMALL amplitude, SHORT duration, POLYphasic potentials.

SMALL because we don’t have a lot of muscle fibers yet in this MU (they summate to give you a big amplitude!)

POLYPHASIC because there’s a lot of ASYNCHRONY (because nascent collaterals from regrowing nerve have more myelin segments, slower conduction) because signals are arriving at different times and aren’t summating as much.

73
Q

If a muscle fiber is never reinnervated, you may see ____ from [proximal/distal] terminal ends of preserved adjacent axons in an effort to pick up denervated muscle fibers. These collateral innervated muscle fibers can produce [mono/bi/poly] phasic long duration MUAP at __-__ weeks, which is [sooner than /later than/same time as] nascent units would appear. Sometimes, either surviving axons with collaterals or regenerated axons pick up MORE than the normal number of [muscle fibers/motor units], forming ____. This reorganization takes at least __-__, but may take years to reach final size.

A

If a muscle fiber is never reinnervated, you may see COLLATERAL SPROUTING from DISTAL terminal ends of preserved adjacent axons in an effort to pick up denervated muscle fibers. These collateral innervated muscle fibers can produce POLYPHASIC, long duration MUAP at 6-8 weeks, which is SOONER THAN nascent units would appear. Sometimes, either surviving axons with collaterals or regenerated axons pick up MORE than the normal number of MUSCLE FIBERS, forming GIANT MOTOR UNITS (4-5x size of normal MU!). This reorganization takes at least 12-18 MONTHS, but may take years to reach final size.

74
Q

[EMG/ NCV] involves voluntary muscle contraction, whereas [EMG/ NCV] requires stimulation of the nerve and is not a voluntary contraction.

A

EMG involves voluntary muscle contraction, whereas NCV requires stimulation of the nerve and is not a voluntary contraction.

75
Q

To test nerve conduction velocity, what equipment do you need beyond what is required for EMG?

A

A stimulator & surface recording electrodes!

Total list:

  • Amplifier
  • Oscilloscope
  • Computer (sound, MU activity)
  • Recording electrodes (superficial!)
  • Stimulator
76
Q

An orthodromic conduction goes in the [opposite/expected] direction:

Motor nerves go from [distal/prox] to [distal/prox], and sensory nerves go from [distal/prox] to [distal/prox].

A

An orthodromic conduction goes in the [opposite/expected] direction:

Motor nerves go from PROXIMAL to DISTAL and sensory nerves go from DISTAL to PROXIMAL

77
Q

To measure the NCV of a motor response, the nerve is [orthodromically/ antidromically] activated, and for the sensory response it is [orthodromically/ antidromically] activated. The stimulation is intense enough so that [all/most/a few/none] of the MUs of the muscle contract.

A

To measure the NCV of a motor response, the nerve is ORTHODROMICALLY activated, and for the sensory response it is ANTIDROMICALLY activated. The stimulation is intense enough so that ALL of the MUs of the muscle contract.

78
Q

For each NCV stimulation, there is a ___ that identifies when the stimulus was applied to the nerve. The subsequent muscle contraction is recorded by [intramuscular needle/ surface electrodes] and produces a ___.

A

For each NCV stimulation, there is a STIMULUS ARTIFACT that identifies when the stimulus was applied to the nerve. The subsequent muscle contraction is recorded by SURFACE ELECTRODES and produces a M WAVE.

79
Q

___ is the time from the stimulus artifact to the very beginning of the M wave deflection, when the [fastest/slowest] axons arrive and start muscle contraction. An M wave is a ___ wave form; to stimulate a maximum contraction, you need ___ by stimulating all of the MUs in that muscle.

A

CONDUCTION TIME is the time from the stimulus artifact to the very beginning of the M wave deflection, when the FASTEST axons arrive and start muscle contraction. An M wave is a COMPOSITE wave form; to stimulate a maximum contraction, you need SUMMATION by stimulating all of the MUs in that muscle.

80
Q

To calculate NCV, you stimulate at 2 different sites: a __ and __ site. [One/ each] generates an M wave. The [proximal/ distal] M wave should occur sooner than the [proximal/ distal].

A

To calculate NCV, you stimulate at 2 different sites: a PROXIMAL and DISTAL site. EACH ONE generates an M wave. The DISTAL M wave should occur sooner than the PROXIMAL.

81
Q

___ is the time from stimulation at the more proximal site to its M wave.

___ is the time from stimulation artifact associated with the distal site to the beginning of the M wave deflection.

A

PROXIMAL LATENCY is the time from stimulation at the more proximal site to its M wave.

DISTAL LATENCY is the time from stimulation artifact associated with the distal site to the beginning of the M wave deflection.

*Recall that the distal M wave should occur sooner than the proximal one, so the Distal latency should be LESS THAN the proximal latency

82
Q

To calculate conduction velocity, take the difference between the __ and __ to get the conduction time of the segment of the nerve between the 2 stimulation sites. This [includes/eliminates] the most distal part of the nerve. Conduction velocity can be compared to standardized values. Why do you want to do that?

A

To calculate conduction velocity, take the difference between the PROXIMAL LATENCY and DISTAL LATENCY to get the conduction time of the segment of the nerve between the 2 stimulation sites. This ELIMINATES the most distal part of the nerve. CONDUCTION VELOCITY can be compared to standardized values.
*There are also some standardized distal latencies which are used when you can’t use 2 stimulation sites, e.g. in carpel tunnel

Why do you want to do that?
You don’t want to involve the actual synapse at the muscle. You’re looking for the conduction time down the length of the nerve, but you don’t want to calculate in the motor endplate time. The goal of the exam is JUST to find nerve conduction velocity (whereas synaptic transmission is slower).

83
Q

If you suspect nerve compression, you would test NCV [proximal to/ distal to/ across] that point.

A

If you suspect nerve compression, you would test NCV ACROSS that point.

84
Q

The M wave is a composite of [the early/ some of the/ the late/ all of the] axons in the nerve and their contracting [Motor Units/ Muscle fibers]. Bigger MUs are [faster/slower] and come in [early/ late] in the M wave, and all of the fibers summate in a [jagged/ smooth] curve.

A

The M wave is a composite of ALL OF THE axons in the nerve and their contracting MUSCLE FIBERS. Bigger MUs are FASTER and come in EARLY in the M wave, followed by slower & smaller MUs, and all of the fibers summate in a SMOOTH curve.

85
Q

The M wave may lose its smooth curve in the case of certain conditions - we call this change ___. Dips in the curve represent that some ___ are not innervated. This might be seen [early/late] in recovery during which some __ are reinnervated but some aren’t.

A

The M wave may lose its smooth curve in the case of certain conditions - we call this change DISPERSION. Dips in the curve represent that some MUSCLE FIBERS are not innervated. This might be seen EARLY in recovery during which some MUs are reinnervated but some aren’t.

86
Q

With nerve regeneration, nerve conduction velocity is [faster/ slower] because ____. This improves with time, generally __-__ (units?)

A

With nerve regeneration, nerve conduction velocity is SLOWER because MORE MYELIN SEGMENTS (=more Nodes of Ranvier, more stops on train). This improves with time, generally 1-2 YEARS

87
Q

With full degeneration or lesion, NCVs may be [high/ low/ zero].

With pure myelin disease WITHOUT axonal involvement, you could have [incr/ decr/ zero] NCV with [what changes?] on EMG, though a lot of times these go together and you have signs of both.

During reinnervation, NCV is [faster/slower] than normal.

M wave may appear ___ in chronic neuropathy (e.g. __, __) or partial reinnervation.

A

With full degeneration or lesion, NCVs may be ZERO.

With pure myelin disease WITHOUT axonal involvement, you could have DECREASED NCV with NO SIGNS OF DENERVATION on EMG, though a lot of times these go together and you have signs of both.

During reinnervation, NCV is SLOWER than normal.

M wave may appear DISPERSED in chronic neuropathy (e.g. DIABETES, CARPEL TUNNEL) or partial reinnervation.

88
Q

The [H Reflex/ F Response] follows the same pathway as the monosynaptic stretch reflex (aka ___). The amplitude of this response can be measured, but it is only used for the __ nerve root to test the ___ muscle. It tests the integrity of the [dorsal root/ ventral root/ both dorsal & ventral roots].

A

The H REFLEX follows the same pathway as the monosynaptic stretch reflex (aka DTR). The amplitude of this response can be measured, but it is only used for the S1 nerve root to test the SOLEUS muscle. It tests the integrity of the BOTH THE DORSAL & VENTRAL ROOTS

89
Q

In the H reflex, we see the ___ from the short latency stimulation of the muscle because you’re getting [orthodromic/ antidromic] stimulation of some motor fibers.

Next, we see the __ which reflects the function of the reflex loop (travels to spinal cord, synapses, and returns back down).

A

In the H reflex, we see the M WAVE from the short latency stimulation of the muscle because you’re getting ORTHODROMIC stimulation of some motor fibers.

Next, we see the H WAVE which reflects the function of the reflex loop (travels to spinal cord, synapses, and returns back down).

90
Q

The F response is a [submaximal/ maximal/ supramaximal] response. It uses only the ___ neuron which is [orthodromically/ antidromically] activated. Basically, the stimulation causes __-gated channels on the [sensory/motor] neuron to fire [ortho/anti]dromically, reach the cell body at the axon hillock, and then reopen the channels on the axon to generate an [ortho/anti]dromic AP down the axon. It can be elicited anywhere on the nerve, and tests the [dorsal root/ ventral root/ both dorsal & ventral roots] of the spinal cord.

A

The F response is a SUPRAMAXIMAL response. It uses only the ALPHA MOTOR NEURON which is ANTIDROMICALLY activated. Basically, the stimulation causes VOLTAGE-gated channels on the ALPHA MOTOR neuron to fire ANTIdromically, reach the ALPHA MN cell body at the axon hillock, and then reopen the channels on the axon to generate an ORTHOdromic AP down the axon. It can be elicited anywhere on the nerve, and tests ONLY THE VENTRAL ROOT of the spinal cord.

91
Q

If the H reflex is ABNORMAL, and the F reflex is NORMAL, what’s wrong?

A

Dorsal root dysfunction (F root uses only the ventral root, so if that’s fine and the H reflex is messed up [which uses both roots], then we can identify the problem in the dorsal root!)

92
Q

Identify EMG vs NCV:
___ evaluates passive qualities of nerve and muscle
___ also examines voluntary contraction on single MU level
___ is only motor system exam
___ always involves stimulated response
___ produces a composite potential
___ can examine sensory separate from motor
___ can examine different segments of the nerve

A

EMG evaluates passive qualities of nerve and muscle
EMG also examines voluntary contraction on single MU level
EMG is only motor system exam
NCV always involves stimulated response
NCV produces a composite potential (M wave!)
NCV can examine sensory separate from motor
NCV can examine different segments of the nerve

Neuroscience II (3 decks)

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