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Patho > Nervous System > Flashcards

Nervous System Flashcards

1
Q

Cell types of the Nervous System

A

Neurons AND Glial

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2
Q

Neurons

A

Excitable cells that send signals/communicate (w/ other neurons, muscles, glands)
Include:
-Dendrites
-Soma (cell body) w/nucleus
-Axon hillocle
-Axon
-Synaptic terminals/bulbs

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3
Q

Types of Neuroglia in CNS (central)

A

Supporting cells to neurons
Types:
-Oligodendrocytes: myelinate CNS neurons
-Astrocytes: blood brain barrier (BBB)
-Ependymal cells: produce cerebral spinal fluid (CSF)
-Microglia: immune role (phagocytose)

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4
Q

Types of Neuroglia in PNS (peripheral)

A

-Schwann cells: myelinate PNS neurons
-Satellite cells: myelinate cell body (ganglia) in the PNS

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5
Q

Cells of the Nervous System (NS)

A

About 100 billion neurons in the human NS
Cell body, soma, perikaryon
Dendrites
Axons
Synapse
Neurtransmitter

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6
Q

Astrocytes

A

Provide physical and nutritional support to the neurons

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7
Q

Ependymal cells

A

From the epithelial lining of the ventricles of the brain and the central canal of the spinal cord

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8
Q

Schwann cells (PNS) and Oligodendrocytes (CNS)

A

Myelination

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9
Q

Microglia

A

Immunological cells, phagocytosis

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10
Q

Myelination of Axons

A

Axons can be over 4 feet long
Support cells:
~Schwann cells (PNS) - Myelination of single axon section
~Oligodendrocytes (CNS) - Myelination of multiple axons

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11
Q

Gray Matter

A

Accumulations of neuron cell bodies
~CNS - nucleus
~PNS - ganglion

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12
Q

White Matter

A

Accumulations of nerve axons
~CNS - fasciculus, brachium, peduncle, column, lemniscus
~PNS - nerve, nerve root, nerve trunk, nerve cord, ramus

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13
Q

Central Nervous System (CNS)

A

~Cerebral hemispheres: Basal ganglia and Diencephalon (thalamus)
~Cerebellum
~Brainstem: Midbrain, Pons, Medulla
~Spinal cord
~CNS is surrounded by meninges
-Connective tissue layers: Pia mater, arachnoid mater, dura matter

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14
Q

Traumatic Brain Injury (TBI)

A

~Damage that impairs brain function, resulting from external physical force
~Diminished or altered state of consciousness
~Impairment of cognition and physical function are common and may be temporary or permanent
~Changes may be seen in behavior and emotional control
~Majority: mild category - Concussion
~Moderate to severe

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15
Q

TBI Incidence and Risk Factors

A

~Mild: Result of falls (47.9%), being struck by or against an object (17%), and motor vehicle crashes (13.2%)

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16
Q

Concussion

A

~A subset of mild traumatic brain injury (mTBI) that is generally self-limited and at the less-severe end of the brain injury spectrum but still involves a complex pathophysiological process

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17
Q

Clinical Manifestations of Moderate to Severe TBI

A

~Disorders of consciousness (Coma, Vegetative state (Wakeful unrespons.), respiratory abnormalities)
~Cognitive and Behavioral Impairments (memory)
~Pain (headaches)
~Cranial Nerve damage (loss of senses)
~Motor Deficits (motor control, sensory loss, and abnormal balance reactions)
~Heterotopic Ossification (abnormal bone growth in the periarticular tissue)
~Medical Complications (paroxysmal sympathetic hyperactivity (PSH))

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18
Q

Clinical Manifestations of Mild TBI or Concussion

A

~Concussion due to falls, motor vehicle crashes, being hit in the head with or against an object, violence, and as a result of recreational and sport injury
~No loss of consciousness, rather with an alteration in mental status, such as feeling disoriented or confused

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19
Q

Vascular Changes

A

~Internal or extremity injuries caused by trauma can cause excessive bleeding and decreased blood pressure, which if persistent can cause hypoperfusion to the brain, accentuating secondary injury
~Vascular damage can lead to ischemia and infarction within the cortical gray matter

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20
Q

Hypoxia

A

Hypotension occurring between injury and resuscitation occurs in one-third of severe TBI victims.
~Caused by blockages = decreased blood in the brain, by decreased oxygen in the blood due to concomitant pulmonary insult, or by internal bleeding or extremity injuries that cause excessive blood loss
~Double mortality rate and a significant increase in morbidity

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21
Q

Parenchymal Changes

A

~Shear and tensile forces disrupt the axolemma
~The distal axon segment can detach and trigger Wallerian degeneration; triggering reactive axonal swelling, forming retraction balls that are full of axon material
~Primary injury triggers a metabolic cascade that causes secondary injury through excitotoxicity and free radical formation
~Secondary cell death by necrosis of the cellular membrane results from edema. Apoptosis, or programmed cell death from within the cell through changes in the DNA, can result in cell loss that occurs days, weeks, or months after injury

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22
Q

Compressive Damage

A

~Intracranial hypertension and mass bleeding inside the skull can produce herniation, causing shifts from the normal brain symmetry
~The most common herniation is transtentorial and downward, at the lateral tentorial membrane separating the cerebral hemispheres from the posterior fossa
~Cause compression of the brainstem, the pituitary, or other delicate brain structures = paralysis or death
~changes in pulse and respiratory rates and regularity, temperature elevations, blood pressure changes, excessive sweating, salivation, tearing, and sebum secretion

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23
Q

Peripheral Nervous System (PNS)

A

~31 pairs of spinal nerves
~12 pairs of cranial nerves
~Peripheral nerves consist of:
-Nerve fibers (axons)
-Schwann cells
-Connective tissue layers
-Blood vessels
-Additional nerve fibers in the connective tissue layers

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24
Q

PNS Divisions

A

~Somatic and visceral sensory (afferent) fibers: bring information from the periphery to the CNS
~Motor (efferent) fibers:
-Somatic: innervate voluntary /skeletal muscle
-Automatic: innervate smooth muscle, cardiac muscle, glands
-Sympathetic and Parasympathetic
~Thus a peripheral nerve can contain a variety of fibers: sensory, somatic motor, autonomic motor

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25
Q

Myelinated Peripheral Nerve Fiber

A

~Nerve cell axon
~Myelin sheath wrapping around the axon as extension of a Schwann cell
~Basement membrane
~Endoneurium: connective tissue sheath
-Surrounds a single myelinated nerve or a group of nonmyelinated nerves
-Endoneurial tubule

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26
Q

Connective Tissue Layers

A

~The epi-peri- and endoneurium are composed of collagen and a few elastin fibers in an irregular lattice pattern
-Fibers are oriented in all directions
~About 25-80% of a peripheral nerve is connective tissue
-Nerves w/ more connective tissue/fascicles are more resistant to pressure (sciatic n)
-Nerves w/less need to be able to glide more to avoid damaging forces (ulnar n)

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27
Q

Connective Tissue Layers - Mesoneurium

A

~Helps nerve trunks to slide next to adjacent tissue
-This can be inhibited by scarring or injury or in the presence of inflammation

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28
Q

Connective Tissue Layers - Perineurium

A

~Specialized and forms a blood-nerve barrier
-Allows for the regulation of movement of molecules form the blood capillaries to the nerve axons, isolating the nerve axon contents from the rest of the body fluids - creating a unique environment for the nerve axon

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29
Q

What is present in epineurium and a smaller amount in the endoneurium that serves as a source of a vigorous inflammatory response with injury?

A

Mast cells

30
Q

Biomechanics of Peripheral Nerves

A

~Readily function during stretching, sliding, compression
~NS forms a tissue continuum throughout the body

31
Q

What movements forms the tissue continuum?

A

~Movement in one location can cause neural tension elsewhere
~Movement of the fingers impacts the median nerve fibers in the upper arm and shoulder
~Neck flexion alters knee mobility in the slumped sitting position
~Ankle DF impacts lumbosacral nerve roots

32
Q

Impact of Compression

A

~Compression of a nerve can induce symptoms such as numbness, pain, and muscle weakness
~Can cause disturbances in intraneural blood flow, axonal transport, and nerve function

33
Q

30mm HG of local compression

A

~Causes impairment of blood flow in the compressed area
~Longstanding (4-6 hours) or intermittent at low pressure levels induces intraneural edema which can induce fibrotic scar formation
~Causes alterations in axonal transport leading to depletion of proteins/nutrients distal to the compression

34
Q

Magnitude and the duration of the application of compression are correlated with what?

A

With the severity of the induced neural lesion

35
Q

Nerve Injury - Peripheral nerve vulnerabilities
Tunnels

A

~Nerve can rub against the walls of the tunnel; edema from the nerve or other tissues (blood vessels, lymphatic vessels, tendons) passing through the tunnels during inflammation

36
Q

Nerve Injury - Peripheral nerve vulnerabilities
Branches

A

~Where a nerve branches, it is more difficult for the nerve to move away from applied forces

37
Q

Nerve Injury - Peripheral nerve vulnerabilities
Hard interfaces

A

~Where a nerve lies on a bone for passes through fascia, it is more readily compressed

38
Q

Nerve Injury - Peripheral nerve vulnerabilities
Proximity to surfaces

A

~More vulnerable to external compression

39
Q

Nerve Injury - Peripheral nerve vulnerabilities
Where nerves are Fixed to interfacing structures

A

~Adherent section of nerve cannot move and slide next to adjacent tissues during movement

40
Q

Categories of Nerve Injury
When addressing injury one must consider each of the following:

A

~Conduction block (physiology within the intact axon)
~Axonal damage
~Schwann cell damage
~Connective tissue layers damage

41
Q

Seddon and Sunderland Categories Respectively

A

~Neurapraxia - Grade I
-injured myelin
~Axonotmesis - Grade II
-injured myelin, axon
~Neurotmesis - Grade III
-injured myelin, axon, endoneurium
~Neurotmesis - Grade IV
-injured myelin, axon, endoneurium, perineurium
~Neurotmesis - Grade V
-injured myelin, axon, endoneurium, perineurium, epineurium

42
Q

Neurapraxia / Sunderland I

A

~Local conduction block, axon continuous, innervated tissue patent

43
Q

Axonotmesis / Sunderland II

A

~Loss axonal continuity, some degeneration of distal axons (severe entrapment or traction injury)

44
Q

Neurotmesis

A

~Loss of continuity by severance or scar

45
Q

Neurotmesis / Sunderland III

A

~Loss of axonal and endoneurial continuity, perineurium intact

46
Q

Neurotmesis / Sunderland IV

A

Loss of perineurium with epineurium intact

47
Q

Neurotmesis / Sunderland V

A

Complete nerve severance

48
Q

Response to axonal transection

A

~Wallerian degeneration

49
Q

Wallerian degeneration - Over a week or two the severed axon segment and its myelin are removed by macrophages

A

~Anterograde degeneration of the axon
~May include the release of inflammatory substances such as cytokines
~Chromatolysis - swelling in the cell body, nuclear shift, up regulation of growth related activity and down regulation of synapse related activities

50
Q

Peripheral Nerve Repair - Potential for recovery

A
  1. If damage is restricted to only the myelin sheath, full recovery is expected
    -Compression causing local ischemia; Guillain-Barre syndrome
  2. If damage affects the myelin and the axon but the connective tissue layers are intact, a slower but full recovery is expected
    -Prolonged compression
  3. If damage affects the myelin, axon, and the connective tissues, full functional recovery is not likely
    -Penetrating injury (stab or gunshot wound), nerve avulsion, severe prolonged compression
51
Q

What happens shortly after peripheral nerve injury?

A

Schwann cells proliferate waiting for the new axon

52
Q

When does axon regeneration begins?

A

Begins within hours in severance injury and within a week of crush injuries

53
Q

What is happening as the axon sprouts emerge from the proximal side of the injury and try to make contact with Schwann cells on the distal side of the injury?

A

~Upon contact a growth cone is formed (filopodia) and anchors to the basement membrane and enters the endoneurial tube
~The axon sprout then continues to grow down the tube at a rate of about 1 mm/day or 1 inch/month
~Sprouts can enter the wrong enduneurial tube and will grow toward an incorrect target resulting in altered function
~If sprouts encounter scar tissue or debris, a NEUROMA forms and the nerve axon does not return to its target

54
Q

T/F It is thought that peripheral nerve repair process is similar to other tissues -inflammation, proliferation, remodeling; resulting in scar formation

A

True; Since the connective tissue sheaths of nerves have an extensive blood supply and are well innervated = effective repair routinely occurs

55
Q

What consequences does the scar formation have on nerves?

A

Can be problematic for axon regeneration, as endoneurial tube blockage can occur (with crush injuries or severe traumatic injuries

56
Q

T/F It is possible to immobilize the NS.

A

False; it is essentially not possible since the NS has so many interconnections and branches, any bodily movements will result in mobilization of portions of the NS

57
Q

Is mobilization of nerves and their surrounding structures important for effective rehabilitation?

A

Yes, as nerves are normally very mobile structures during functional task performance.
Mobilization is encouraged, though experimental support is absent

58
Q

Why is mobilization important for repair of the connective tissue sheaths?

A

To minimize adhesion formation between connective tissue layers of the nerve and the surrounding structures

59
Q

Guillain-Barre Syndrome

A

Demyelinating disease that attacks the peripheral nerve
-autoimmune attack of the myelin of peripheral nerve axons; results in a slowing of the response time bc conduction is disrupted

60
Q

Onset of Guillain-Barre Syndrome

A

Often occurs after experiencing a viral upper respiratory or gastrointestinal infection
Rapidly evolving motor paresis/paralysis, sensory, and autonomic deficits
Attack starts distally and progresses proximally, and recovery occurs in reverse
Involvement of the nerves of the respiratory system results in need for mechanical ventilation - seen in 30% of cases
Recovery can take months to years

61
Q

Poliomyelitis

A

Viral destruction of the alpha motor neuron cell body in the spinal cord
-results in permanent paralysis of muscles of the arms and legs; may also attack the diaphragm
-now rare in US due to effective immunization program since the mid 1950s

62
Q

Postpolio syndrome

A

20-30 years after original disease see gradual increase in muscle weakness
-reflects pruning of branches within motor units due to diminished metabolic capacity with in the PNS (part of the aging process)

63
Q

Diabetes mellitus (DM) associated polyneuropathies

A

~Death and destruction of peripheral nerve axons (both sensory, motor, and autonomic) especially of feet and hands
~Results from the DM mediated decrease in peripheral blood flow resulting in diminished oxygen and nutrient supplies being delivered to the peripheral nerves

64
Q

Median Neuropathy (Carpal Tunnel Syndrome-CTS)

A

~Compression of the median nerve within the carpal tunnel in the wrist
~Chronic marked by pain, paresthesia, numbness, and weakness in the distribution of the median nerve
~Repetitive tasks determined by position of the hand and degree of load

65
Q

CTS Incidence

A

~Top reasons for lost workdays
~70% of women
~Surgery peak btw 45-55 year-old in women, 65 years for men
~Prevalence increases with gripping, holding tools that vibrate, lifting more than 12 kg, or working in an extremely cold environment

66
Q

CTS Etiology and Risk Factors

A

~Median nerve most superficial and vulnerable to changes of the palm
~Neuropathic conditions, including diabetes mellitus, alcoholism, and toxic exposure
~People with osteoarthritis of the CMC joint of the thumb, rheumatoid tenosynovitis, edema, pregnancy, hypothyroidism, congestive heart failure, physically inactive, and obese, smoking

67
Q

CTS Pathogenesis

A

~Schwann cell changes underlie the initial mechanism of CTS and are independent of axonal damage
~Compressed nerve segments show thinner myelin sheaths
~If the mechanical pressures are high enough, compression can create an axonotmesis in which axon continuity is lost and wallerian degeneration occurs

68
Q

CTS Symptoms

A

~Pain (distal forearm, wrist and thumb, index and middle fingers-can radiate into arm, shoulder, neck)
~Thenar weakness
~Loss of grip strength

69
Q

Aging and the CNS

A

~Senescence, or aging, results from changes in DNA, RNA. and proteins
~Simple loss of cells is common, nerve cell shrinking, causing possible changes in functional efficiency, may be a more important effect of old age than cell loss
~Inner structure of the nerve cell changes with aging

70
Q

Aging and the PNS

A

~Structural changes
~Reduction in content
~Increased dysfunction
~Motor changes
~Sensory changes
~Causes

Patho (13 decks)

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