Pbl Exam 3 Case 6

Front 1

1. What are the five basic types of sensory receptors, and what do they detect?

Back 1

1. Mechanorecetpors
-detect mechanical compression or stretching of the receptor or of tissues adjacent to the receptor
2. Thermoreceptors
-detect changes in temp, some receptors detecting cold and others warmth
3. Nociceptors
-pain receptors, which detect damage occurring in the tissue, whether physical or chemical damage
4. Electromagnetic receptors
-detect light on the retina of the eye
5. Chemoreceptors
-detect taste in the mouth, smell in the nose, O2 levels in the arterial blood, etc...

Front 2

2. How do two types of sensory receptors detect different types of sensory stimuli?

Back 2

By differential sensitivities.

Each type of receptor is highly sensitive to one type of stimulus for which it is designed and yet is almost nonresponsive to other types of sensory stimuli.

Front 3

3. What is the labeled line principle?

Back 3

Each nerve tract terminates at a specific point in the CNS, and the type of sensation felt when a nerve fiber is stimulated is determined by the point in the nervous system to which the fiber leads.

This specificity of nerve fibers for transmitting only one modality of sensation is called the labeled line principle.

Front 4

4. What do all sensory receptors have in common?

What is the basic cause of this?

Back 4

Whatever the type of stimulus that excites the receptor, its immediate effect is to change the membrane electric potential of the receptor.

This change in potential is called a receptor potential.

The basic cause of the change in membrane potential is a change in membrane permeability of the receptor, which allows ions to diffuse more or less readily thru the membrane and thereby to change the transmembrane potential.

Front 5

5. What are the four different ways to cause receptor potentials?

Back 5

1. By mechanical deformation of the receptor, which stretches the receptor membrane and opens ion channels

2. By application of a chemical to the membrane, which also opens ion channels

3. By change of the temp of the membrane, which alters the permeability of the membrane

4. By the effects of electromagnetic radiation, such as light on a visual receptor, which either directly or indirectly changes the receptor membrane characteristics and allows ions to flow thru membrane channels.

Front 6

6. What is the max receptor potential amplitude?

What is this max value similar to?

Back 6

The max amplitude of most sensory receptor potentials is about +100 mV, but this level occurs only at an extremely high intensity of sensory stimulus.

This is about the same max voltage recorded in action potentials and is also the change in voltage when the membrane becomes maximally permeable to sodium ions.

Front 7

7. Relation of the receptor potential to action potentials

Back 7

When teh receptor potential rises above the threshold for eliciting action potnetials in the nerve fiber attached to the receptor, then action potentials occur.

Also, the more the receptor rises above the threshold level, the greater becomes the action potential frequency.

Front 8

8. Relation between stimulus intensity and the receptor potential

What is the importance of this relationship?

Back 8

The frequency of repetitive action potentials transmitted from sensory receptors increases approximately in proportion to the increase in receptor potential.

This is important in that it is applicable to almost all sensory receptors. It allows the receptor to be sensitive to very weak sensory experience and yet not reach a maximum firing rate until the sensory experience is extreme. This allows the receptor to have an extreme range of response from very weak to very intense.

Front 9

9. Adaptation of receptors

Back 9

Sensory receptors adapt either partially or completely to any constant stimulus after a period of time.

That is, when a continuous sensory stimulus is applied, the receptor responds at a high impulse rate at first and then at a progressively slower rate until finally the rate of action potentials decreases to very few or often to none at all.

Front 10

10. Do all sensory receptors adapt to the same extent?

Back 10

No, so adapt extremely rapidly and others adapt slowly.

Furthermore, some adapt to a far greater extent than others.

For example, the pacinian corpuscles adapt to extinction within a few hundredths of a second, and the receptors at the bases of the hairs adapt to extinction within a second or more.

Front 11

11. How do the rods and cones adapt?

Back 11

They change the concentrations of their light sensitive chemicals

Front 12

12. What is one way by which mechanoreceptors adapt?

Back 12

The pacinian corpuscle is a viscoelastic structure so that when a distorting force is suddenly applied to one side of the corpuscle, this force is instantly transmitted by the viscous component of the corpuscle directly to the same side of the central nerve fiber, thus eliciting a receptor potential.

Within a few hundredths of a second, the fluid within the corpuscle redistributes, so that the receptor potential is no longer elicited.

Thus, the receptor potential appears at the onset of compression but disappears within a small fraction of a second even though the compression continues.

Front 13

13. What is another way by which mechanoreceptors adapt?

Back 13

A much slower mechanism, results from a process called accommodation, which occurs in the nerve fiber itself.

That is, even by chance the central core fiber should continue to be distorted, the tip of the nerve fiber itself gradually becomes "accommodated" to the stimulus.

This probably results form progressive inactivation of the sodium channels in the nerve fiber membrane, which means that sodium current flow thru the channels causes them gradually to close.

Front 14

14. How do slow adapting receptors work?

What are some examples of slow adapting receptors?

Back 14

They continue to transmit impulses to the brain as long as the stimulus is present.

Therefore, they keep the brain constantly apprised of the status of the body and its relation to its surroundings. AKA "tonic receptors"

Examples:
1. Receptors of the macula in the vestibular apparatus
2. Pain receptors
3. Baroreceptors of the arterial tree
4. Chemoreceptorso fthe carotid and aortic bodies

Front 15

15. How do rapidly adapting receptors work?

Back 15

The detect change in stimulus strength - AKA rate receptors, movement receptors or phasic receptors.

These receptors are useless for transmitting information about constant conditions in the body.

Front 16

16. What is the importance of rate receptors?

Back 16

Their predictive function.

If one knows the rate at which some change in bodily status is taking place, on can predict in one's mind the state of the body a few seconds or even a few minutes later.

Front 17

17. General classification of nerve fibers

Back 17

The fibers are divided into types A and C, and the type A fibers are further subdivided into α, β, γ, and δ fibers

Front 18

18. Type A fibers

Back 18

They are the typical large and medium sized myelinated fibers of the spinal nerves.

Front 19

19. Type C fibers

Back 19

They are the small unmyelinated nerve fibers that conduct impulses at low velocities.

The C fibers constitute more than one half of the sensory fibers in most peripheral nerves as well as all the postganglionic autonomic fibers.

Front 20

20. Group Ia fibers

Back 20

Fibers from the annulospiral endings of muscle spindles

They average about 17 microns in diameter; these are α-type A fibers in general classification.

Front 21

21. Group Ib fibers

Back 21

Fibers from the golgi tendon organs.

They average about 16 micrometers in diameter; these are also α-type A fibers.

Front 22

22. Group II fibers

Back 22

Fibers from most discrete cutaneous tactile receptors and from the flower-spray endings of the muscle spindles.

They average about 8 micrometers in diameter; these are β- and γ-type A fibers.

Front 23

23. Group III fibers

Back 23

Fibers carrying temperature, crude touch, and pricking pain sensations.

They average about 3 micrometers in diameter; they are δ-type A fibers.

Front 24

24. Group IV fibers

Back 24

Unmyelinated fibers carrying pain, itch, temperature, and crude touch sensations

They average about 0.5 to 2 micrometers in diameters; they are type C fibers.

Front 25

25. What are the two ways in which signal intensity is varied?

Back 25

1. Spatial summation
2. Temporal summation

Front 26

26. Spatial summation

Back 26

Increasing signal strength is transmitted by using progressively greater numbers of fibers.

Thus, the stronger signals spread to more and more fibers.

Front 27

27. Temporal summation

Back 27

Increasing signal strength is transmitted by increasing the frequency of nerve impulses in each fiber.

Front 28

28. What are the different neuronal pools in the CNS?

Back 28

1. Entire cerebral cortex
2. Basal ganglia
3. Specific nuclei in the thalamus, cerebellum, mesencephalon, pons, and medulla.
4. Entire dorsal gray matter of the spinal cord

Front 29

29. Neuronal pools

Back 29

Each pool has its own special organization that causes it to process signals in its own unique way, thus allowing the total consortium of pools to achieve the multitude of functions of the nervous system.

Front 30

30. Divergence of signals in neuronal pools

What are the type types of divergence?

Back 30

Often it is important for weak signals entering a neuronal pool to excite far greater numbers of nerve fibers leaving the pool.

Type types:
1. Amplifying
2. Divergence into multiple tract

Front 31

31. Convergence of signals in the neuronal pools

Back 31

Convergence means signals from multiple inputs uniting to excite a single neuron.

The importance of this is that neurons are almost never excited by an action potential froma single input terminal. But action potentials converging on the neuron from multiple terminals provide enough spatial summation to bring the neuron to the threshold required for discharge.

Front 32

32. What does convergence allow the nervous system to do?

Back 32

Allows summation of information from different sources, and the resulting response is a summated effect of all the different types of information.

It is one of the important means by which the central nervous system correlates, summates, and sorts different types of information.

Front 33

33. Reciprocal inhibition circuit

Back 33

Sometimes an incoming signal to a neuronal pool causes an output excitatory signal going in one direction and at the same time an inhibitory signal going elsewhere.

Think of reciprocal inhibition in OPP.

Front 34

34. How is inhibition achieved in a reciprocal inhibition circuit?

Back 34

The input fiber directly excites the excitatory output pathway, but it stimulates an intermediate inhibitory neuron, which secretes a different type of transmitter substance to inhibit the second output pathway from the pool.

This type of circuit is important in preventing overactivity in many parts of the brain.

Front 35

35. Afterdischarge

Back 35

In many instances, a signal entering a pool causes a prolonged output discharge, called afterdischarge, lasting a few ms to as long as many minutes after the incoming signal is over.

Front 36

36. What are the two mechanisms by which afterdischarge occurs?

Back 36

1. Synaptic afterdischarge
2. Reverberatory (oscillatory) circuits

Front 37

37. Synaptic afterdischarge

Back 37

When excitatory synapses discharge on the surfaces of dendrites or soma of a neuron, a postsynaptic electrical potential develops in the neuron and lasts for many milliseconds, especially when some of the long-acting synaptic transmitter substances are involved.

Front 38

38. Reverberatory (oscillatory) circuit

Back 38

Such circuits are caused by positive feedback w/in the neuronal circuit that feeds back to re-excite the input of the same circuit.

Consequently, once stimulated, the circuit may discharge repetitively for a long time.

Front 39

39. What causes the cessation of reverberation?

Back 39

Fatigue of synaptic junctions in the circuit.

Fatigue beyond a certain critical level lowers the stimulation of the next neuron in the circuit below threshold level so that the circuit feedback is suddenly broken.

Front 40

40. What two mechanisms cause neuronal circuits to emit output signals continuously w/o excitatory input signals?

Back 40

1. Continuous intrinsic neuronal discharge
2. Continuous reverberatory signals

Front 41

41. Continuous discharge caused by intrinsic neuronal excitability

Back 41

The membrane potentials of many neurons even normally are high enough to cause them to emit impulses continually.

This occurs especially in many of the neurons of the cerebellum, as well as in most of the interneurons of the spinal cord.

The rates at which these cells emit impulses can be increased by excitatory signals or decreased by inhibitory signals; inhibitory signals often can decrease the rate of firing to zero.

Front 42

42. Continuous signals emitted from reverberating circuits

Back 42

A reverberating circuit that does not fatigue enough to stop reverberation is a source of continuous impulses.

This type of information transmission is used by the autonomic nervous system to control such functions as vascular tone, gut tone, degree of constriction of the iris in the eye, and heart rate.

That is, the nerve excitatory signal to each of these can be either decreased or increased by accessory input signals into the reverberating neuronal pathway.

Front 43

43. Rhythmical signal output

Back 43

Many neuronal circuits emit rhythmical output signals, for instance, a rhythmical respiratory signal originates in the respiratory centers of the medulla and pons.

All or almost all rhythmical signals that have been studied have been found to result from reverberating circuits or a succession of sequential reverberating circuits that feed excitatory or inhibitory signals in a circular pathway from one neuronal pool to the next.

Front 44

44. How does the brain prevent inundation of information (i.e. epileptic seizures)?

Back 44

1. Inhibitory circuits
2. Fatigue of synapses

Front 45

45. Inhibitory circuits and stabilization of nervous system function

Back 45

Two types of inhibitory circuits in widespread areas of the brain help prevent excessive spread of signals:

1. Inhibitory feedback circuits that return from the termini of pathways back to the initial excitatory neurons of the same pathways

2. Some neuronal pools exert gross inhibitory control over widespread areas of the brain

Front 46

46. Fatigue of synapses and stabilization of nervous system function

Back 46

Means simply that synaptic transmission becomes progressively weaker the more prolonged and more intense the period of excitation.

Thus, fatigue and recovery from fatigue constitute an important short-term means of moderating the sensitivities of the different nervous system circuits. These help to keep the circuits operating in a range of sensitivity that allows effective function.

Front 47

47. What are the three physiologic categories of somatic senses?

Back 47

1. Mechanoreceptive somatic senses
2. Thermoreceptive senses
3. Pain senses

Front 48

48. Mechanoreceptive somatic senses

Back 48

Include both tactile and position sensations that are stimulated by mechanical displacement of some tissue of the body

Front 49

49. What do the tactile sensations include?

Back 49

1. Touch
2. Pressure
3. Vibration
4. Tickle

Front 50

50. What do the position sensations include?

Back 50

1. Static position
2. Rate of movement

Front 51

51. Exteroreceptive sensations

Back 51

Those sensations from the surface of the body

Front 52

52. Proprioceptive sensations

Back 52

Those sensations having to do w/the physical state of the body, including position sensations, tendon and muscle sensations of equilibrium.

Front 53

53. Three differences between the tactile sensations of touch, pressure and vibration

Back 53

1. Touch sensation generally results from stimulation of tactile receptors in the skin or in tissues immediately beneath the skin

2. Pressure sensation generally results from deformation of deeper tissues

3. Vibration sensation results from rapidly repetitive sensory signals, but some of the same types of receptors as those for touch and pressure are used.

Front 54

54. Six characteristics of tactile receptors

Back 54

1. Some free nerve endings can detect touch and pressure.
2. A touch receptor w/great sensitivity is the Meissner's corpuscle.
3. Fingertips and other areas that contain large numbers of Meissner's corpuscles usually also contain large numbers of expanded tip tactile receptors (i.e. Merkel's discs).
4. Slight movement of any hair on the body stimulates a nerve fiber entwining its base.
5. Located in the deeper layers of the skin and also in still deeper internal tissues are many Ruffini's end-organs.
6. Pacinian corpuscles lie both immediately beneath the skin and deep i the fascial tissues of the body.

Front 55

55. Meissner's corpuscle

Back 55

An elongated encapsulated nerve ending of a large (type Aβ) myelinated sensory nerve fiber.

These corpuscles are present in the nonhairy parts of the skin and are particularly abundant in the fingertips, lips, and other areas of the skin where one's ability to discern spatial locations of touch sensations is highly developed.

Front 56

56. Merkel's discs

Back 56

A type of expanded tip tactile receptor.

These receptors differ from Meissner's corpuscles in that they transmit an intially strong but partially adapting signal and then a continuing weaker signal that adapts only slowly.

Therefore, they are responsible for giving steady-state signals that allow one to determine continuous touch of objects against the skin.

Front 57

57. Iggo dome receptor

Back 57

Merkel's discs are often grouped together in a receptor organ called the Iggo dome receptor, which projects upward against the underside of the epithelium of the skin. This causes the epithelium at this point to protrude outward, thus creating a dome and constituting an extremely sensitive receptor.

Front 58

58. Hair end-organ

Back 58

Each hair and its basal nerve fiber, called the hair end-organ, are also a touch receptor.

This receptor adapts readily and, like Meissner's corpuscles, detains mainly movement of objects on the surface of the body or initial contact w/the body.

Front 59

59. Ruffini's end-organs

Back 59

Multibranched, encapsulated nerve endings that lie in the deeper layers of the skin and also in still deeper internal tissues.

These endings adapt very slowly, and therefore, are important for signaling continuous states of deformation of the tissues, such as heavy prolonged touch and pressure signals.

They are also found in joint capsules and help to signal the degree of joint rotation.

Front 60

60. Pacinian corpuscles

Back 60

Lie obth immediately beneath the skin and deep in the fascial tissues of the body.

They are stimulated only by rapid local compression of the tissues b/c they adapt in a few hundredths of a second.

Therefore, they are particularly important for detecting tissue vibration or other rapid changes in the mechanical state of the tissues.

Front 61

61. Transmission speed of tactile signals via Aβ nerve fibers

Back 61

Almost all specialized sensory receptors, such as Meissner's corpuscles, Iggo dome receptors, hair receptors, pacinian corpuscles, and Ruffini's endings, transmit their signals in velocities from 30-70 m/sec.

Front 62

62. Transmission speed of tactile signals via Aδ nerve fibers

Back 62

Free nerve ending tactile receptors transmit signals in fibers that conduct at velocities of only 5-30 m/sec.

Front 63

63. Transmission speed of tactile signals via type C unmyelinated fibers

Back 63

From a fraction of a meter up to 2 m/sec.

These send signals into the spinal cord and lower brain stem, probably subserving mainly the sensation of tickle.

Front 64

64. Summary of tactile nerve fiber transmission speeds

Back 64

Thus, the more critical types of sensory signals are all transmitted in more rapidly conducting types of sensory nerve fibers.

Conversely, the cruder types of signals, such as crude pressure, poorly localized touch, and especially tickle, are transmitted by way of much slower, very small nerve fibers that require much less space in the nerve bundle than the fast fibers.

Front 65

65. Detection of vibration

Back 65

Pacinian corpuscles can detect signal vibrations from 30-800 Hz b/c they respond extremely rapidly to minute and rapid deformations of the tissues, and they also transmit their signals of type Aβ nerve fibers, which can transmit as many as 1000 impulses/sec.

Lowe freq vibrations from 2-80Hz stimulate other tactile receptors, especially Meissner's corpuscles, which are less rapidly adapting than pacinian corpuscles.

Front 66

66. What is the purpose of the itch sensation

Back 66

To call attention to mild surface stimuli such as a flea crawling on the skin or a fly about to bite, and the elicited signals then activate the scratch reflex or other maneuvers that ride the host of the irritant.

Itch can be relieved by scratching if this removes the irritant, or if the scratch is strong enough to elicit pain.

The pain signals are believed to suppress the itch signals in the cord by lateral inhibition.

Front 67

67. What are the two sensory pathways by which sensory signals are carried?

Back 67

1. Dorsal column - medial lemniscal system

2. Anterolateral system

These two systems come back together partially at the level of the thalamus.

Front 68

68. Dorsal column-medial lemniscal system

Back 68

Caries signals upward to the medulla of the brain mainly in the dorsal columns of the spinal cord.

Then, after the signals synapse and cross to the opposite side in the medulla, they continue upward thru the brain stem to the thalamus by way of the medial lemniscus.

Front 69

69. Composition of the dorsal column-medial lemniscal system

Back 69

Composed of large, myelinated nerve fibers that transmit signals to the brain at velocities of 30-110 m/sec.

Front 70

70. Anterolateral system

Back 70

The signals, after entering the spinal cord from the dorsal spinal nerve roots, synapse in the dorsal horns of the spinal gray matter, then cross to the opposite side of the cord and ascend through the anterior and lateral white columns of the cord.

They terminate at all levels of the lower brain stem and in the thalamus.

Front 71

71. Composition of the anterolateral system

Back 71

Composed of smaller myelinated fibers that transmit signals at velocities ranging from a few meters per second up to 40 m/sec.

Front 72

72. Important difference between the dorsal column-medial lemniscal system and the anterolateral systems

Back 72

The dorsal column-medial lemniscal system has a high degree of spatial orientation of the nerve fibers w/respect to their origin, while the anterolateral system has much less spatial orientation.

These differences immediately characterize the types of sensory information that can be transmitted by the two systems.

Thus, info that must be transmitted rapidly and with temporal and spatial fidelity is transmitted mainly in the dorsal column-medial lemniscal system.

Front 73

73. Special capability of the anterolateral system

Back 73

The ability to trasnmit a broad spectrum of sensory modalities - pain, warmth, cold, and crude tactile sensations.

The dorsal system is limited to discrete types of mechanoreceptive sensations.

Front 74

74. Sensations transmitted in the dorsal column-medial lemniscal system

Back 74

1. Touch sensations requiring a high degree of localization of the stimulus
2. Touch sensations requiring transmission of fine gradations of intensity
3. Phasic sensations, such as vibratory sensations
4. Sensations that signal movement against the skin
5. Position sensations from the joints
6. Pressure sensations having to do w/fine degree of judgment of pressure intensity.

Front 75

75. Sensations transmitted in the anterolateral system

Back 75

1. Pain
2. Thermal sensations, including both warmth and cold sensations
3. Crude touch and pressure sensations capable only of crude localizing ability on the surface of the body
4. Tickle and itch sensations
5. Sexual sensations

Front 76

76. Pathway tracts in the dorsal column-medial lemniscal system

Back 76

On entering the spinal cord, the large myelinated fibers divide almost immediately to form a medial branch and a lateral branch.

The medial branch turns medially first and then upward in the dorsal column, proceeding by way of the dorsal column pathway all the way to the brain.

The lateral branch enters the dorsal horn of the cord gray matter, then divides many times to provide terminals that synapse with local neurons in the intermediate and anterior portions of the cord gray matter.

Front 77

77. The local neurons in the intermediate and anterior portions of the cord gray matter serve what three functions?

Back 77

1. A major share of them give off fibers that enter the dorsal columns of the cord and then travel upward to the brain.

2. Many of the fibers are very short and terminate locally in the spinal cord gray matter to elicit local spinal cord reflexes.

3. Others give rise to the spinocerebellar tracts

Front 78

78. Where do nerve fibers entering the dorsal columns pass to?

Back 78

They pass uninterrupted up to the dorsal medulla, where they synapse in the dorsal column nuclei (the cuneate and gracile nuclei).

From their, second-order neurons decussate immediately to the opposite side of the brain stem and continue upward thru the medial menisci to the thalamus.

In this pathway thru the brain stem, each medial lemniscus is joined by additional fibers from the sensory nuclei of the trigeminal nerve; these fibers subserve the same sensory functions for the head that the dorsal column fibers subserve for the body.

Front 79

79. Medial lemniscus fibers terminate where?

Back 79

In the thalamus, in the thalamic sensory relay area - called the ventrobasal complex.

From here, third-order nerve fibers project mainly to the postcentral gyrus of the cerebral cortex, which is called somatic sensory area 1.

Front 80

80. Spatial orientation of the nerve fibers in the DCML system

Back 80

In the dorsal columns of the spinal cord, the fibers from the lower parts of the body lie toward the center of the cord, whereas those that enter the cord at progressively higher segmental levels form successive layers laterally.

In the thalamus, distinct spatial orientation is still maintained, with the tail end of the body represented by the most lateral portions of the ventrobasal complex and the head and face represented by the medial areas of the complex.

*B/c of crossing over, there is contralateral representation in the thalmus.

Front 81

81. Brodmann's areas of the somatosensory cortex

Back 81

Areas 1, 2, and 3 are primary somatosensory are I

Areas 5 and 7 are somatosensory association areas.

Front 82

82. Somatosensory area I

Back 82

Much more extensive and much more important than somatosensory area II.

Has a high degree of localization of the different parts of the body; includes thigh, thorax, neck, shoulder, hand, fingers, tongue, and abdomen.

Front 83

83. Somatosensory area II

Back 83

Localization is poor, although roughly, the face is represented anteriorly, the arms centrally, and the legs posteriorly.

Requires somatosensory area 1 to function.

Includes the legs, arms, and face.

Front 84

84. Spatial orientation of signals from different parts of the body in somatosensory area I

Back 84

Lies immediately behind the central fissure, located in the postcentral gyrus of the human cerebral cortex.

The head is represented in the most lateral portion of somatosensory area I, and the lower part of the body is represented medially.

Front 85

85. Function 1 of the somatosensory cortex and the cortical layers

Back 85

1. The incoming sensory signal excites neuronal layer IV first, then the signal spreads toward the surface of the cortex and also toward deeper layers

Front 86

86. Function 2 of the somatosensory cortex and the cortical layers

Back 86

2. Layers I and II receive diffuse, nonspecific input signals from lower brain centers that facilitate specific regions of the cortex

This input mainly controls the overall levels of excitability of the respective regions stimulated.

Front 87

87. Function 3 of the somatosensory cortex and the cortical layers

Back 87

The neurons in layers II and III send axons to related portions of the cerebral cortex on the opposite side of the brain thru the corpus callosum.

Front 88

88. Function 4 of the somatosensory cortex and the cortical layers

Back 88

The neurons in layers V and VI send axons to the deeper parts of the nervous system.

Those in layer V are generally larger and project to more distant areas, such as to the basal ganglia, brain stem, and spinal cord where they control signal transmission.

From layer VI, especially large numbers of axons extend to the thalamus, providing signals from the cerebral cortex that interact w/and help to control the excitatory levels of incoming sensory signals entering the thalamus.

Front 89

89. How is the sensory cortex organized?

Back 89

Organized in vertical columns of neurons; each column detects a different sensory spot on the body w/a specific sensory modality.

Front 90

90. What signals play a major role in controlling the effluent motor signals that activate sequences of muscle contractions?

Back 90

In the most anterior 5-10mm of the postcentral gyrus, located deep in the central fissure in Brodmann's area 3a, an especially large share of the vertical columns respond to muscle, tendon, and joint stretch receptors.

Many of the signals from these sensory columns then spread anteriorly, directly to the motor cortex located immediately forward of the central fissure.

Front 91

91. As one move from anterior to posterior in the somatosensory area I, what are the differences in sensory modalities?

Back 91

As one moves posteriorly, more and more of the vertical columns respond to slowly adapting cutaneous receptors, and then still farther posteriorly, greater numbers of the columns are sensitive to deep pressure.

Front 92

92. What happens in the most posterior portion of somatosensory area I?

Back 92

About 6% of the vertical columns respond only when a stimulus moves across the skin in a particular direction.

Thus, this is still a higher order of interpretation of sensory signals; the process becomes even more complex as the signals spread farther backwards into the somatosensory association area I.

Front 93

93. Lesions causing bilateral excision of the somatosensory area I causes loss of what types of sensory judgment?

Back 93

1. Unable to localize discretely the different sensation in the different parts of the body.
2. Unable to judge critical degrees of pressure against the body.
3. Unable to judge the weights of objects.
4. Unable to judge shapes or forms of objects. This is called astereognosis.
5. Unable to judge texture of material.

*No loss of pain and temp in these regions, but the sources of pain and temp will be poorly localized.

Front 94

94. Somatosensory association areas

Back 94

Brodmann's areas 5 & 7 of the cerebral cortex.

Play important roles in deciphering deeper meanings of the sensory information in the somatosensory areas.

This area combines information arriving from multiple points in the primary somatosensory area to decipher its meaning.

Front 95

95. The somatosensory association areas receive signals from where...?

Back 95

1. Somatosensory area I
2. Ventrobasal nuclei of the thalamus
3. Other areas of the thalamus
4. Visual cortex
5. Auditory cortex

Front 96

96. What happens if one removes the somatosensory association area from one side of the brain?

Back 96

Amorphosynthesis

The person loses the ability to recognize complex objects and complex forms felt on the opposite side of the body.

In addition, he or she loses most of the sense of form of his or her own body or body parts on the opposite side.

Front 97

97. Basic neuronal circuit pattern in the DCML system

Back 97

At each synaptic stage, divergence occurs.

Thus, a weak stimulus causes only the centralmost neurons to fire. A stronger stimulus causes still more neurons to fire, but those in the center discharge at a considerably more rapid rate than do those farther away from the center.

Front 98

98. Two point discrimination in the DCML system

Back 98

The capability of the sensorium to distinguish the presence of two points of stimulation is strongly influenced by another mechanism, lateral inhibition.

Front 99

99. Effect of lateral inhibition

Back 99

Increases the degree of contrast in the perceived spatial pattern.

It does this by blocking lateral spread of the excitatory signals and, therefore, increases the degree of contrast in the sensory pattern perceived in the cerebral cortex.

As a result, the peaks of excitation stand out, and much of the surrounding diffuse stimulation is blocked.

Front 100

100. Transmission of rapidly changing and repetitive sensations

Back 100

The dorsal column system is also of particular importance in apprising the sensorium of rapidly changing peripheral conditions.

This system can recognize changing stimuli that occur in as little as 1/400 of a second.

Front 101

101. Vibratory sensation

Back 101

Transmitted only in the dorsal column pathway.

For this reason, application of vibration to different peripheral parts of the body is an important tool used by neurologists for testing functional integrity of the dorsal columns.

Front 102

102. What is the ultimate goal of sensory stimulation?

Back 102

To apprise the psyche of the state of the body and its surroundings.

Front 103

103. Weber-Fechner principle

Back 103

Gradations of stimulus strength are discriminated approximately in proportion to the logarithm of stimulus strength.

For ex:
A personal already holding 30g of weight in his hand can barely detect an additional 1g increase in weight.

Front 104

104. Equation for Weber-Fechner principle

Back 104

Interpreted signal strength =

Log (stimulus) + constant

Front 105

105. Limitations of Weber-Fechner principle

Back 105

It is quantitatively accurate only for higher intensities of visual, auditory, and cutaneous sensory experience and applies only poorly to most other types of sensory experience.

However, it still is a good point to remember that the greater the background sensory intensity, the greater an additional change must be for the psyche to detect the change.

Front 106

106. Power law

Back 106

Interpreted signal strength =

K x (Stimulus - k)^y

The exponent y and the constants K and K are different for each type of sensation.

Front 107

107. Positional senses

Back 107

AKA proprioceptive senses

Divided into two types:
1. Static position sense
2. Rate of movement sense, AKA kinesthesia

Front 108

108. Positional sensory receptors - muscle spindles

Back 108

Determines joitn angulation in mid ranges of motion.

They are exceedingly important in helping to control muscle movement,.

The net stretch information from the spindles is transmitted into the computational system of the spinal cord and higher regions of the dorsal column system for deciphering joint angulations.

Front 109

109. Which types of receptors are especially adapted for detecting rapid rates of change?

Back 109

1. Pacinian corpuscles
2. Muscle spindles

Front 110

110. Two categories of DCML system thalamic neurons that respond to joint rotation

Back 110

1. Those maximally stimulated when the joint is at full rotation

2. Those maximally stimulated when the joint is at minimal rotation

Front 111

111. Pathway of the anterolateral fibers

Back 111

The spinal cord anterolateral fibers originate mainly in dorsal horn laminae I, IV, V, and VI.

The anterolateral fibers cross immediately in the anterior commissure of the cord to the opposite anterior and lateral white columns, where they turn upward toward the brain by way of the anterior spinothalamic and lateral spinothalamic tracts.

Front 112

112. Upper terminus of the two spinothalamic tracts

Back 112

Mainly twofold:
1. Throughout the reticular nuclei of the brain stem
2. In two different nuclear complexes of the thalamus, the ventrobasal complex and the intralaminar nuclei

Front 113

113. Ventrobasal complex and the intralaminar nuclei

Back 113

In general, the tactile signals are transmitted mainly into the ventrobasal complex, terminating in some of the same thalamic nuclei where the dorsal column tactile signals terminate.

From here, the signals are transmitted to the somatosensory cortex along with the signals from the dorsal columns.

Front 114

114. Pain transmission in the anterolateral tract

Back 114

Only a small fraction of the pain signals project directly to the ventrobasal complex of the thalamus.

Instead, most pain signals terminate in the reticular nuclei of the brain stem and from there are relayed to the intralaminar nuclei of the thalamus where the pain signals are further processed.

Front 115

115. Transmission speed in the anterolateral pathway

Back 115

1. The velocities of transmission are only 1/3 to 1/2 those in the DCML system, ranging between 8-40 m/sec.
2. The degree of spatial localization of signals is poor.
3. The gradations of intensities are also far less accurate, most of the sensations being recognized in 10-20 gradations of strength, rather than as many as 100 gradations of the dorsal column system.
4. The ability to transmit rapidly changing or rapidly repetitive signals is poor.

Front 116

116. Function of thalamus in tactile sensation

Back 116

When the somatosensory cortex is destroyed, the person loses most critical tactile sensibilities, but a slight degree of crude tactile sensibility does return.

Therefore, it must be assumed that the thalamus has a slight ability to discriminate tactile sensation, even though the thalamus normally functions mainly to relay this type of info to the cortex.

Front 117

117. Loss of the somatosensory cortex and its effect on pain and temp sensation

Back 117

Has little effect on one's perception of pain sensation and only a moderate effect on the perception of temperature.

Thus, there is much reason to belive that the lower brain stem, the thalamus, and other associated basal regions of the brain play dominant roles in discrimination of these sensibilities.

Front 118

118. Corticofugal signals

Back 118

Transmitted from the periphery to the brain, they control the intensity of sensitivity of the sensory input.

These signals are almost entirely inhibitory, so that when sensory input intensity becomes too great, the corticofugal signals automatically decrease transmission in the relay nuclei.

Front 119

119. Two effects of corticofugal signals

Back 119

1. Decreases lateral spread of the sensory signals into adjacent enurons and, therefore, increases the degree of sharpness in the signal pattern.

2. It keeps the sensory system operating in a range of sensitivity that is not so low that the signals are ineffectual nor so high that the system is swamped beyond its capacity to differentiate sensory patterns.

Front 120

120. What is glycolysis?

Back 120

The catabolism of glucose to pyruvate or lactate

It is one of the principal pathways for generating ATP in cells and is present in all cell types.

The role of glycolysis in fuel metabolism is related to its ability to generate ATM with, and without, oxygen.

Front 121

121. Glycolysis and biosynthetic precursors

Back 121

Glycolysis is an anabolic pathway that provides biosynthetic precursors.

For example, in liver and adipose tissue, this pathway generates pyruvate as a precursor for fatty acid biosynthesis.

This pathway also provides precursors for the synthesis of compounds such as amino acids and ribose 5-phosphate, the precursor of nucleotides.

Front 122

122. Difference between aerobic and anaerobic glycolysis

Back 122

AEROBLICALLY:
Glucose → Pyruvate
ATP produced by both oxidative and substrate-level phosphorylation

ANAEROBICALLY:
Glucose → Lactate
ATP produced by substrate-level phosphorylation ONLY

Front 123

123. What are the reactions of glycolysis?

Back 123

1. Conversion of glucose to glucose 6-phosphate
2. Conversion of glucose 6-P to the triose phosphates
3. Oxidation and substrate level phosphorylation

Front 124

124. Overall net reaction in the glycolytic pathway

Back 124

Glucose + 2NAD⁺ + 2ADP + 2 Pi →
2 pyruvate + 2NADH + 2H⁺ + 2ATP + 2H₂O

Front 125

125. What are the two phases of glycolysis?

Back 125

1. Preparative phase
2. ATP generating phase

Front 126

126. What occurs in the preparative phase?

Back 126

Glucose is phosphorylated twice by ATP and cleaved into two triose phosphates.

The ATP expenditure in the beginning of the preparative phase is sometimes called "priming the pump", b/c this initial utilization of 2 mol ATP per mole of glucose results in the production of 4 mol of ATP per mole of glucose in the ATP-generating phase.

Front 127

127. What occurs in the ATP generating phase?

Back 127

Glyceraldehyde 3-phosphate is oxidized by NAD⁺ and phosphorylated using inorganic phosphate.

The high energy phosphate bond generated in this step is transferred to ADP to form ATP.

B/c 2 mole of triose phosphate were formed, the yield from the ATP generating phase is 4 ATP and 2 NADH.

The result is a net yield of 2 mol of ATP, 2 mol of NADH, and 2 mol of pyruvate per mole of glucose.

Front 128

128. Step 1: conversion of glucose to glucose 6-P

Back 128

Begins w/a transfer of a phosphate from ATP to glucose to form glucose 6-P via hexokinase.

Phosphorylation of glucose commits it to metabolism w/in the cell b/c glucose 6-P cannot be transported back across the plasma membrane.

Front 129

129. Importance of glucose 6-P

Back 129

Glucose 6-P is a branch point in carb metabolism. It is a precursor for almost every pathway that uses glucose, including glycolysis, the pentose phosphate pathway, and glycogen synthesis.

Front 130

130. Hexokinases

Back 130

The enzyems that catalyze the phosphorylation of glucose. They are a family of tissue-specific isoenzymes that differ in their kinetic properties.

The isoenzyme found in liver and beta-cells of the pancreas has a much higher Km than other hexokinases and is called glucokinase.

Front 131

131. Step 2: conversion of glucose 6-P to the triose phosphate

Part 1

Back 131

Glucose 6-P is isomerized to fructose 6-P via phosphoglucose isomerase.

Front 132

132. Step 2: conversion of glucose 6-P to the triose phosphate

Part 2

Back 132

Phosphorylation of fructose 6-P to fructose 1,6-bis-P by phosphofructokinase-1 (PFK-1).

*This is considered the first committed step of the glycolytic pathway.

Front 133

133. Why is it the first committed step?

Back 133

This phosphorylation requires ATP and is thermodynamically and kinetically irreversible.

Therefore, PFK-1 irrevocably commits glucose to the glycolytic pathway.

Front 134

134. Step 2: conversion of glucose 6-P to the triose phosphate

Part 3

Back 134

Fructose 1,6-bis-P is cleaved into two phosphorylated three-carbon compounds (glyceradehyde 3-P and dihydroxyaceptone-P) by aldolase.

Front 135

135. Step 2: conversion of glucose 6-P to the triose phosphate

Part 4

Back 135

Then, dihydroxyacetone phosphate (DHAP) is isomerized to glyceradehyde 3-P, which is a triose phosphate via triose phosphate isomerase.

For every mole of glucose that enters glycolysis, 2 mol of glyceraldehyde 3-P continue thru the pathway.

Front 136

136. Step 3: oxidation and substrate level phosphorylation

Part 1

Back 136

Glyceraldehyde 3-P is oxidized and phosphorylated to form
1,3-bisphosphoglycerate via glyceraldehyde-3-P dehydrogenase.

This enzyme oxidizes the aldehyde group of glyceradehyde 3-P to an enzyme-bound carboxyl group and transfers the electrons to NAD⁺ to form NADH.

Front 137

137. What is this oxidation step dependent upon?

This marks the beginning of what...?

Back 137

Dependent upon a cysteine residue at the active site of the enzyme, which forms a high energy thioester bond during the course of the reaction.

This high-energy intermediate accepts an inorganic phosphate to form the high-energy acyl phosphate bond in 1,3-bis-phosphoglycerate, releasing the product from the cysteine residue on the enzyme.

*This high-energy phosphate bond is the start of substrate level phosphorylation.

Front 138

138. Importance of NAD⁺

Back 138

Since NAD⁺ is required for the
oxidation step in this reaction, NAD⁺ must be continually replenished within the cytosol to maintain
flux through glycolysis.

This is accomplished aerobically in the mitochondrial matrix by the electron transport chain, or anaerobically in the cytosol by the enzyme lactate dehydrogenase which
converts pyruvate to lactate.

Front 139

139. Step 3: oxidation and substrate level phosphorylation

Part 2

Back 139

The energy of the phosphate in the bond is transferred to ADP to form ATP by 3-phosphoglycerate kinase. 3-Phosphoglycerate is also a product of this reaction.

The energy of the acyl phosphate bond is high enough so that the 3-phosphoglycerate kinase can harness the energy to transfer to ADP to form ATP.

Front 140

140. Step 3: oxidation and substrate level phosphorylation

What needs to occur next?

Back 140

To transfer the remaining low energy phosphoester on 3-phosphoglycerate to ADP, it must be converted to a high energy bond.

This conversion is acccomplished by moving the phosphate to the second carbon (forming 2-phosphoglycerate) and then removing the water to form phosphoenolpyruvate (PEP).

Front 141

141. Step 3: oxidation and substrate level phosphorylation

Part 3: moving the phosphate

Back 141

Phosphoryl shift in 3-phosphyglycerate to form 2-phosphoglycerate by phosphoglycerate mutase.

Front 142

142. Step 3: oxidation and substrate level phosphorylation

Part 4: Dehydration

Back 142

Dehydration of 2-phosphoglycerate to form phosphoenolpyruvate (PEP) by enolase

Front 143

143. Step 3: oxidation and substrate level phosphorylation

Part 4: Generation of pyruvate

Back 143

Substrate level phosphorylation to generate ATP in the conversion of
phosphoenolpyruvate to pyruvate by pyruvate kinase

In this reaction, the high phosphoryl
transfer potential of
phosphoenolpyruvate is used by the
enzyme pyruvate kinase to generate
pyruvate, the end product of
glycolysis, and 2 ATP are formed for
every glucose molecule entering the
pathway

Front 144

144. What are the two alternate routes for oxidation of cytosolic NADH?

Back 144

1. Aerobic, involving shuttles that transfer reducing equivalents across the mitochondrial membrane and ultimately to the electron transport chain and oxygen.

2. Anaerobic, where NADH is reoxidized in the cytosol by lactate dehydrogenase, which reduces pyruvate to lactate.

Front 145

145. Fate of pyruvate

Back 145

Depends on the route used for NADH oxidation.

If NADH is reoxidized in a shuttle system, pyruvate can be used for other pathways, one of which is oxidation to acetyl CoA and entry into the TCA cycle for complete oxidation.

Alternatively, in anaerobic glycolysis, pyruvate is reduced to lactate and diverted away from other potential pathways.

Front 146

146. So, in essence, what do the shuttle systems allow the body to do?

Back 146

Allows for more ATP to be generated than by anaerobic glycolysis, by both oxidizing the cytoplasmically derived NADH in the electron-transport chain and by allowing pyruvate to be oxidized completely to CO₂.

Front 147

147. Why are the shuttles required for the oxidation of cytosolic NADH by the electron transport chain?

Back 147

The inner mitochondrial membrane is impermeable to NADH, and no transport protein exists that can translocate NADH across this membrane directly.

Front 148

148. Reoxidization of NAD⁺

Back 148

Consequently, NADH is rexodized to NAD⁺ in the cytosol by a reaction that transfers the electrons to DHAP in the glycerol 3-P shuttle and oxaloacetate in the malate-aspartate shuttle.

The NAD⁺ that is formed in the cytosol returns to glycolysis, which glycerol 3-P or malate carry the reducing equivalents that are ultimately transferred across the inner mitochondrial membrane.

Thus, these shuttles transfer electrons and not NADH per se.

Front 149

149. Glycerol 3-phosphate shuttle

Part 1

Back 149

The glycerol 3-phosphate shuttle is the major shuttle in most tissues.

In this shuttle, cytosolic NAD⁺ is regenerated by cytoplasmic glycerol 3-phosphate dehydrogenase, which transfers electrons from NADH to DHAP to form glycerol 3-phosphate.

Front 150

150. Glycerol 3-phosphate shuttle

Part 2

Back 150

Glycerol 3-phosphate then diffuses thru the outer mitochondrial membrane to the inner mitochondrial membrane, where the electrons are donated to a membrane bound flavin adenine dinucleotide (FAD)-containing glycerophosphate dehydrogenase.

This enzyme donates electrons to CoQ, resulting in an energy yield of approx 1.5 ATP.

Dihydroxyacetone phosphate returns to the cytosol to continue the shuttle.

Front 151

151. What is the malate-aspartate shuttle?

Back 151

Cytosolic NAD⁺ is regenerated by cytosolic malate dehdyrogenase, which transfers electrons from NADH to cytosolic oxaloacetate to form malate.

Malate is then transported across the inner mitochondrial membrane by a specific translocase, which exchanges malate for α-ketoglutarate.

In the matrix, malate is oxidized back to oxaloacetate and NADH is generated. However, the newly formed oxaloacetate cannot pass back thru the inner mitochondrial membrane, so aspartate is used to return it to the cytosol.

Front 152

152. What is the sum of reactions in the malate-aspartate shuttle?

Back 152

NADH(cytosol) + NAD⁺(matrix) → NAD⁺(cytocol) + NADH (matrix)

Front 153

153. Anaerobic glycosis

Back 153

When the oxidative capacity of a cell is limited, the pyruvate and NADH produced from glycolysis cannot be oxidized aerobically. The NADH is, therefore, oxidized to NAD⁺ in the cytosol by reduction of pyruvate to lactate.

This reaction is catalyzed by lactate dehydrogenase.

Front 154

154. What is the net reaction in anaerobic glycolysis?

Back 154

Glucose + 2 ADP + 2 Pi →
2 lactate + 2 ATP + 2 H₂O + 2 H⁺

Front 155

154. Comparison of ATP production in aerobic vs. anaerobic glycolysis

Back 155

Aerobic: 30-32 mol of ATP can be produced from 1 mol of glycose oxidized to CO₂

Anaerobic: 2 mol of ATP per mole of glucose

Thus, anaerobic glycolysis must occur approx 15x faster and use approx 15x more glucose.

Front 156

155. Acid production in anaerobic glycolysis

Back 156

Anaerobic glycolysis results in acid production in the form of H⁺. At an intracellular pH of 7.35, lactic acid dissociates to form the carboxylate anion, lactate, and H⁺ (the pKa for lactic acid is 3.85).

Lactate and the H⁺ are both transported out of the cell into interstitial fluid by a transporter on the plasma membrane and eventually diffuse into the blood.

Can result in lactic acidosis is too much lactate is generated.

Front 157

156. What tissues are dependent on anaerobic glycolysis?

Back 157

1. RBCs and WBCs (no mitochondria)
2. Kidney medulla
3. Tissues of the eye
4. Skeletal muscles (some of the time)

Front 158

157. Characteristics of tissues that are dependent on anaerobic glycolysis

Back 158

1. Have low ATP demand
2. High levels of glycolytic enzymes
3. Few capillaries, such that O₂ must diffuse over a greater distance to reach target cells.

Front 159

158. Tissues that use both aerobic and anaerobic glycolysis

Back 159

In tissues with some mitochondria, both aerobic and anaerobic glycolysis occur simultaneously.

The relative proportion of the two pathways depends on the mitochondrial oxidative capacity of the tissue and its oxygen supply and may vary among cell types within the same tissue b/c of cell distance form the capillaries.

Front 160

159. When would a tissue switch from aerobic to anaerobic glycolysis?

Back 160

When a cell's energy demand exceeds the capacity of the rate of the electron transport chain and oxidative phosphorylation to produce ATP, glycolysis is activated, and the increased NADH/NAD⁺ ratio directs excess pyruvate into lactate.

Front 161

160. What is the fate of lactate?

Back 161

Lactate released from cells that undergo anaerobic glycolysis is taken up by other tissues (primary the liver, heart, and skeletal muscle) and oxidized back pyruvate.

In the liver, pyruvate is used to synthesize glucose (gluconeogenesis), which is returned to the blood. The cycling of lactate and glucose between peripheral tissues and liver is called the Cori cycle.

Front 162

161. The heart and lactate utilization

Back 162

The heart, w/its huge mitochondrial content and oxidative capacity is able to use lactate released from other tissues as a fuel.

Front 163

162. Lactate dehydrogenase (LDH)

Back 163

LDH is a tetramer composed of A subunits and B subunits.

Different tissues produce different amounts of the two subunits, which then combine randomly to form five different tetramers (M4, M3H1, M2H2, M1H3, and H4).

These isoenzymes differ only slightly in their properties, but the kinetic properties of the M4 form facilitate conversion of pyruvate to lactate in skeletal muscle, whereas the H4 facilitates conversion of lactate to pyruvate in the heart for energy generation.

Front 164

163. Bis-phosphogycerate shunt

Back 164

This is a side reaction of the glycolytic pathway in which 1,3-bis-phosphoglycerate is converted to 2,3-BPG).

RBCs form 2,3-BPG to serve as an allosteric inhibitor of oxygen binding to heme.

2,3-BPG re-enters the glycolytic pathway via dephosphorylation to 3-phosphoglycerate.

Front 165

164. What are the two major regulatory enzymes in ATP homeostasis?

Back 165

1. Phosphofructokinase-1 (PFK-1)
2. Pyruvate dehydrogenase (PDH)

Both these regulatory sites respond to feedback indicators of the rate of ATP utilization.

Front 166

165. Relationships among ATP, ADP, and AMP concentrations

Back 166

The AMP levels within the cytosol provide a better indicator of the rate of ATP utilization than the ATP concentration itself.

The equilibrium is such that hydrolysis of ATP to ADP in energy-requiring reactions increases both the ADP and AMP contents of the cytosol.

However, ATP is present in much higher quantities than AMP or ADP, so a small decrease of ATP concentration in the cytosol causes a much larger percentage increase in the small AMP pool.

*ATP levels do NOT fall significantly
until the approach of fatigue

Front 167

166. Regulation of hexokinases

Back 167

In most tissues, hexokinase is a low Km enzyme w/a high affinity for glucose.

It is inhibited by physiologic concentrations of its product, glucose 6-P. If glucose6-P does not enter glycolysis or another pathway, it accumulates and decreases the activity of hexokinase.

Front 168

167. Regulation of PFK-1

Back 168

PFK-1 is switched ON by: AMP, ADP (and fructose-2,6-bisP in liver and adipose tissue)

PFK-1 is switched OFF by: ATP and Citrate

(AMP activation overrides ATP inhibition)

Front 169

168. How is glycolysis switched on to make fat when [ATP] and [citrate] are high and AMP levels remain low?

Back 169

PFK-1 is switched ON by
FRUCTOSE 2,6-BISPHOSPHATE

Fructose-2,6-bisphosphate is particularly important in activation of glycolysis

Front 170

169. Insulin/glucagon levels and Fructose-2,6-bisphosphate

Back 170

High [insulin/glucagon] activates PFK-2:
- increases production of F-2,6-bisP

High [insulin/glucagon] switches on synthesis of key enzymes of glycolytic pathway:
-hexokinase
-phosphofructokinase-1
-pyruvate kinase

Front 171

170. Lactic acidemia

Back 171

Lactate levels > 5 mM → blood pH < 7.2

Result of increased NADH/NAD⁺
- decreased pyruvate oxidation
- increased production of lactate

Typical causes
- alcoholism, hypoxia, inhibition of electron transport chain.

Front 172

171. If cerebral oxygen supply were completely interrupted, the brain would last for how long?

Back 172

10 seconds.

The only reason that consciousness lasts longer during anoxia or asphyxia is that there is still some oxygen in the lungs and in circulating blood.

A decrease of blood flow to approximately 1/2 of the normal rate results in a loss of consciousness.

Front 173

172. Hypoxia inducible factor-1 (HIF-1)

Back 173

Released in response to hypoxemia.

HIF-1 is a gene transcription factor found in tissues throughout the body that plays a homeostatic role in coordinating tissue responses to hypoxia.

HIF-1 increases transcription of the genes for many of the glycolytic encymes, including PFK-1, enolase, LDH, etc.

HIF-1 also increases synthesis of a number of proteins that enhance oxygen delivery to tissues, including erythropoietin, VEGF, and NO synthase.

Front 174

173. What are the two major contributors to cavities in the mouth in low pH environments?

Back 174

Lactobacilli and S. mutans

Front 175

174. Type I skeletal muscle fibers

Back 175

AKA fast glycolytic fibers, or white muscle fibers

Front 176

175. Type IIb skeletal muscle fibers

Back 176

AKA slow oxidative fibers, or red muscle fibers.

Front 177

176. Differences between type I and type IIb muscle fibers

Back 177

The designation fast or slow refers to their rate of shortening, which is determined by the level of the isoenzyme of myosin ATPase present.

Compared w/glycolytic fibers, oxidative fibers have a higher content of mitochondria and myoglobin, which gives them a red color.

Front 178

177. Ischemic conditions, AMP levels, and the heart

Back 178

Under ischemic conditions, AMP levels within the heart increase rapidly b/c of the lack of ATP production via oxidative phosphorylation.

The increase in AMP levels activates an AMP-dependent protein kinase (protein kinase B) which phosphorylates the heart isoenzyme of PFK-2 to activate its kinase activity.

This results in increased levels of fructose 2,6-bis-P, which activates PFK-1 along with AMP so that the rate of glycolysis can increase to compensate for the lack of ATP production via aerobic means.

Front 179

178. MI and lactate production

Back 179

The absence of oxygen for oxidative phosphorylation would decrease levels of ATP and increase those of AMP, resulting in a compensatory increase of anaerobic glycolysis and lactate production.

However, obstruction of a vessel leading to her heart would decrease lactate removal, resulting in a decrease of intracellular pH.

Under these conditions, at very low pH levels, glycolysis is inhibited and unable to compensate for the lack of oxidative phosphorylation.

Front 180

179. Where is the primary motor cortex located?

Where is the somatosensory cortex located?

Back 180

These areas are located on either side of the central sulcus.

The primary motor cortex (Brodmann's area 4) is in the precentral gyrus, while the primary somatosensory cortex (Brodmann's areas 3,1 and 2) is in the postcentral gyrus.

Front 181

180. Posterior, intermediate, and anterior horns of the gray matter in the spinal cord.

Back 181

Posterior horn is involved mainly in sensory processing

Intermediate horn contains interneurons and certain specialized nuclei.

Anterior horn contains motor neurons.

Front 182

181. White matter vs. gray matter in the spinal cord levels

Back 182

The white matter is thikest in the cervical levels, where most ascending fibers have already entered the cord and most descending fibers have not yet terminated on their targets.

The sacral cord is mostly gray matter.

The spinal cord has more gray matter at the cervical and lumbosacral levels than at the thoracic levels, particularly in the ventral horns, where lower motor neurons for the arms and legs reside.

Front 183

182. Blood supply to the spinal cord

Back 183

Arises from branches of the vertebral arteries and spinal radicular arteries.

The vertebral arteries give rise to the anterior spinal artery that runs along the ventral surface of the spinal cord.

In addition, two posterior spinal arteries arise from the vertebral or posterior inferior cerebellar arteries and supply the dorsal surface of the cord.

Front 184

183. Spinal arterial plexus

Back 184

The anterior and posterior spinal arteries are variable in prominence at different spinal levels and form a spinal arterial plexus that surrounds the spinal cord.

Front 185

184. Radicular arteries

Back 185

31 segmental arterial branches enter the spinal canal long its length; most of the branches arise from the aorta and supply the meninges.

Only 6-10 of these reach the spinal cord as radicular arteries, arising at variable levels.

Front 186

185. Great radicular artery of Adamkiewicz

Back 186

There is usually a prominent radicular artery arising from the left side, anywhere from T5 to L3, but usually between T9 and T12.

This is called the great radicular artery of Adamkiewicz, and provides the major blood supply to the lumbar and sacral cord.

Front 187

186. Which zone of the spinal cord is vulnerable to decreased perfusion?

Back 187

The mid-thoracic region, at approx T4-T8 lies between the lumbar and vertebral arterial supplies and is vulnerable to decreased perfusion.

This region is most susceptible to infarction during thoracic surgery or other conditions causing decreased aortic pressure.

Front 188

187. Batson's plexus

Back 188

The epidural veins of the spinal cord, called Batson's plexus, do not contain valves, so elevated intra-abdominal pressure can cause reflux of blood carrying metastatic cells (such as prostate cancer) or pelvic infections into the epidural space.

Front 189

188. Apraxia

Back 189

Lesion of the regions of motor association cortex can cause apraxia, in where there is a deficit in higher-order motor planning and execution despite normal strength.

Front 190

189. Upper motor neurons vs. lower motor neurons

Back 190

UMNs carry motor system outputs to LMNs located in the spinal cord and brainstem, which in turn, project to muscles in the periphery.

Front 191

190. Descending UMN pathways

Back 191

Arise from the cerebral cortex and brainstem. These descending motor pathways can be divided into lateral motor systems and medial motor systems based on their location in the spinal cord.

Front 192

191. Lateral motor systems

What are the two lateral motor systems?

Back 192

Lateral motors systems travel in the lateral columns of the spinal cord and synapse on the more lateral groups of ventral horn motor neurons and interneurons.

Include:
1. Lateral corticospinal tract
2. Rubrospinal tract

*Both pathways cross over from their site of origin and descend in the contralateral lateral spinal cord to control contralateral extremities.

Front 193

192. Importance of the lateral corticospinal tract

Back 193

Essential for rapid, dextrous movements at individual digits or joints.

Front 194

193. Medial motor systems

What are the four medial motor systems?

Back 194

Medial motor systems travel in the anteromedial spinal cord columns to synapse on medial ventral horn motor neurons and interneurons.

Include:
1. Anterior corticospinal tract
2. Vestibulospinal tract
3. Reticulospinal tract
4. Tectospinal tract

Front 195

194. Importance of medial motor systems

Back 195

These pathways control the proximal axial and girdle muscles involved in postural tone, balance, orienting movements of the head and neck, and automatic gait-related movements.

The medial motor systems descend ipsilaterally or bilaterally.

Front 196

195. Unilateral lesions of the medial motor systems vs. lateral corticospinal tract

Back 196

The medial motor systems tend to terminate on interneurons that project to both sides of the spinal cord, controlling movements that involve multiple bilateral spinal segments.

Thus, unilateral lesions of the medial motor systems produce no obvious deficits.

In contrast, lesions of the lateral corticospinal tract produce dramatic deficits.

Front 197

196. Role of the rubrospinal tract

Back 197

Role is small is its clinical importance in uncertain, but it may participate in taking over functions after corticospinal injury.

It may also play a role in flexor (decorticate) posturing of the upper extremities, which is typically seen w/lesions above the levels of the red nuclei, in which the rubrospinal tract is spared.

Front 198

197. What is the most clinically important descending motor pathway in the nervous system?

Back 198

The lateral corticospinal tract.

This pathway controls movement of the extremities, and lesions along its course produce characteristic deficits that often enable precise clinical localization.

Front 199

198. Betz cells

Back 199

About 3% of the corticospinal neurons are giant pyramidal cells called Betz cells, which are the largest neurons in the human nervous system.

Front 200

199. Corona radiata

Back 200

Axons from the cerebral cortex enter the upper portions of the cerebral white matter, or corona radiata, and descend toward the internal capsule.

In addition to the corticospinal tract, the cerebral white matter conveys bidirectional information between different cortical areas, and between cortex and deep structures such as the basal ganglia, thalamus, and brainstem.

Front 201

200. What are the three parts of the internal capsule?

Back 201

1. Anterior limb
-separates the head of the caudate from the glubus pallidus and putamen

2. Posterior limb
-separates the thalamus from the glubus pallidus and putamen
-the corticospinal tract lies here*

3. Genu
-is at the transition between the anterior and posterior limbs, at the levels of the foramen of Monro.

Front 202

201. Somatotopic organization in the internal capsule

Back 202

Motor fibers for the face are most anterior, and those for the arm and leg are progressively more posterior.

Despite this, the fibers of the internal capsule are compact enough that lesions at this level generally produce weakness of the entire contralateral body (face, arm and leg).

Front 203

202. Corticobular means what...?

Back 203

Fibers projecting from the cortex to the brainstem, including motor fibers for the face, are called corticobulbar instead of corticospinal because they project from the cortex to the brainstem, or bulb.

Front 204

203. Cerebral peduncles and basis pedunculi

Back 204

The internal capsule continues into the midbrain cerebral peduncles, meaning literally "feet of the brain".

The white matter is located int eh ventral portion of the cerebral peduncles and is called the basis pedunculi.

Front 205

204. Middle one-third of the basis pedunculi contains...?

Back 205

Contains corticobulbar adn corticospinal fibers w/the face, arm, and leg axons arranged from medial t lateral, respectively.

The other portions of the basis pedunculi contain primarily corticopontine fibers.

Front 206

205. Medullary pyramids

Back 206

The corticospinal tract fibers next descend thru the ventral pons, where they form somewhat scattered fascicles. These collect on the ventral surface of the medulla to to form the medullary pyramids.

For this reason the corticospinal tract is sometimes referred to as the pyramidal tract.

Front 207

206. Cervicomedullary junction & pyramidal decussation

Back 207

The transition from medulla to spinal cord is called the cervicomedullary junction, which occurs at the level of the foramen magnum.

At this point about 85% of the pyramidal tract fibers cross over in the pyramidal decussation to enter the lateral white matter columns of the spinal cord, forming the lateral corticospinal tract.

Front 208

207. Somatic efferents

Back 208

Anterior horn cells or cranial nerve motor nuclei project directly from the CNS to skeletal muscle.

Front 209

208. Autonomic efferents

Back 209

There is a peripheral synapse located in a ganglion interposed between the CNS and the effector gland or smooth muscle.

The autonomic nervous system itself consists of only efferent pathways.

Front 210

209. Where are preganglionic neurons of the sympathetic nervous system located?

Back 210

In the intermediolateral cell column in lamina VII of spinal cord levels T1 to L2 or L3.

Front 211

210. Sympathetic postganglionic neurons release _______ onto end organs.

Parasympathetic postganglionic neurons release predominantly ______ on end organs.

What is the exception to this rule?

Back 211

Sympathetic: Norepinephrine

Parasympathetic: Acetylcholine

*One exception to the rule is the sweat glands, which are innervated by sympathetic postganglionic neurons that release acetylcholine

Front 212

211. What are the signs of lower motor neuron lesions?

Back 212

1. Muscle weakness
2. Atrophy
3. Fasciculations
4. Hyporeflexia

Front 213

212 What are fasciculations?

Back 213

Abnormal muscle twitches caused by spontaneous activity in groups of muscle cells.

Front 214

213. What are the signs of upper motor neuron lesions?

Back 214

Muscle weakness and a combination of increased tone and hyperreflexia sometimes referred to as spasticity.

Also seen are abnormal Babinski's sign, Hoffmann's sign, posturing, and so on.

*There may initially be flaccid paralysis w/decreased tone and decreased reflexes, which gradually, over hours or even months, develops into spastic paresis.

Front 215

214. What is the most important functional consequences of both upper and lower motor neuron lesions?

Back 215

Weakness.

Weakness can be caused by lesions or dysfunction at any level in the motor system,

Front 216

215. Unilateral face arm, and leg weakness or paralysis w/no sensory deficits

Where would the lesion be located?

Back 216

AKA hemiparesis or hemiplegia; pure motor weakness.

Locations ruled in: corticospinal and corticobulbar tract fibers below the cortex and above the medulla: posterior limb of the internal capsule, basis pontis, or middle third of the cerebral peduncle

Side: contralateral to the weakness

Front 217

216. Unilateral face arm, and leg weakness or paralysis w/no sensory deficits

Where would the lesion NOT be located?

Back 217

Unlikely to be cortical b/c the lesion would have to involve the entire motor strip.

Also unlikely to be muscle or peripheral nerve because in that case conincidental involvement of only half the body would be required.

Also not the spinal cord or medulla b/c in that case the face would be spared.

Front 218

217. Unilateral face arm, and leg weakness or paralysis w/no sensory deficits

What are the common causes?

Back 218

1. Lacunar infarct of the internal capsule or of the pons
2. Infarct of the cerebral peduncle

Front 219

218. Unilateral face arm, and leg weakness or paralysis w/no sensory deficits

What are the symptoms?

Back 219

1. Upper motor neuron signs are usually present

2. Dysarthria (dysarthria-pure motor hemiparesis)

3. Ataxia (ataxia-hemiparesis)

Front 220

219. Unilateral face arm, and leg weakness or paralysis w/sensory deficits

Where would the lesion be located?

Back 220

Ruled in: entire primar motor cortex, including face, arm, and leg representations of the precentral gyrus, or corticospinal and corticobulbar tract fibers above the medulla.

Side: Contralateral to the weakness

Front 221

220. Unilateral face arm, and leg weakness or paralysis w/sensory deficits

Where would the lesion NOT be located?

Back 221

Unlikely to be below the medulla

Front 222

221. Unilateral face arm, and leg weakness or paralysis w/sensory deficits

What are the common causes?

Back 222

Numerous, including infarct, hemorrhage, tumor, trauma, herniation, post-ictal state, and so on...

Front 223

222. Unilateral arm and leg weakness or paralysis

Where would the lesion be located?

Back 223

AKA hemiplegia or hemiparesis sparing the face

Location: Arm and leg area of the motor cortex; corticospinal tract from the lower medulla to the C5 level of cervical spinal cord

Side:
-Motor cortex or medulla: contralateral to the weakness
-Cervical spinal cord: ispilateral to weakness

Front 224

223. Unilateral arm and leg weakness or paralysis

Where would the lesion NOT be located?

Back 224

Unlikely to be the corticospinal tract below the motor cortex above the medulla b/c the corticobulbar tract fibers are very nearby, and the face would thus usually be involved.

Unlikely to be muscle or peripheral nerve b/c in that case coincidental involvement of only half of the body would be required.

Also, not below C5 in the cervical cord b/c in that case some arm muscles would be spared.

Front 225

224. Unilateral arm and leg weakness or paralysis

Associated features/symptoms?

Back 225

Upper motor neuron signs are usually present. Cortical lesions sparing the face are often in a watershed distribution, and they affect proximal more than distal muscle (man in the barrel syndrome).

Cortical lesions may be associated w/aphasia or hemineglect. In medial medullarly lesions there may be loss of vibration and joint position sense on the same side as the weakness, and tongue weakness on the opposite side.

In lesions of the spinal cord, the Brown-Sequard syndrome may be present.

Front 226

225. Unilateral arm and leg weakness or paralysis

Common causes?

Back 226

1. Watershed infarct (anterior cerebral-middle cerebral watershed)
2. Medial or combined medial and lateral medullary infarcts
3. Multiple sclerosis
4. Lateral trauma
5. Compression of the cervical spinal cord.

Front 227

226. Unilateral face and arm weakness or paralysis

Where is the lesion located?

Back 227

AKA faciobrachial paresis or plegia.

Location: face and arm areas of the primary motor cortex, over the lateral frontal convexity.

Side: Contralateral to weakness

Front 228

227. Unilateral face and arm weakness or paralysis

Where is the lesion NOT located?

Back 228

Ruled out: Unlikely to be muscle or peripheral nerve b/c in that case coincidental involvement of the face and arm would be required. Uncommon in lesions at the internal capsule or below b/c the corticobulbar and corticospinal tracts are fairly compact, resulting in leg involvement w/most lesions

Front 229

228. Unilateral face and arm weakness or paralysis

What are the symptoms?

Back 229

Upper motor neuron signs and dysarthria are usually present.

In dominant-hemisphere lesions, Broca's aphasia is common; in non dominant-hemisphere lesions, hemineglect may occasionally be present.

Sensory loss can occur if the lesion extends into the parietal lobe.

Front 230

229. Unilateral face and arm weakness or paralysis

What are the common causes?

Back 230

Middle cerebral artery superior division infarct is the classic cause.

Tumor, abscess, or other lesions may also occur in this location.

Front 231

230. Unilateral arm weakness or paralysis

Where is the lesion located?

Back 231

AKA Brachial monoparesis or monoplegia

Arm area of primary motor cortex, or pheripheral nerves supplying the arm

Side:
-Motor cortex: contralateral to weakness
-Peripheral nerves: ipsilateral to weakness

Front 232

231. Unilateral arm weakness or paralysis

Where is the lesion NOT located?

Back 232

Ruled out: Unlikely, anywhere along the corticospinal tract, b/c in that case the face and/or lower extremity would also likely be involved.

Rare cases of foramen magnum tumors may initially affect one arm.

Front 233

232. Unilateral arm weakness or paralysis

What are the symptoms if it is a motor cortex lesion?

Back 233

There may be associated upper motor neuron signs, cortical sensory loss, aphasia, or subtle involvement of the face or leg.

Occasionally none of these are present. The weakness pattern may be incompatible w/a lesion of peripheral nerves.

For example, marked weakness of all finger, hand, and wrist muscles w/no sensory loss and normal proximal strength does not occur w/peripheral nerve lesions.

Front 234

233. Unilateral arm weakness or paralysis

What are the symptoms if it is a peripheral nerve lesion?

Back 234

There may be associated lower motor neuron signs.

Weakness and sensory loss may be compatible w/a known pattern for a peripheral nerve lesion.

Front 235

234. Unilateral arm weakness or paralysis

What are the common causes?

Back 235

Motor cortex lesion: infarct of a small cortical branch of the middle cerebral artery, or a small tumor, abscess, or the like.

Peripheral nerve lesion: compression injury, diabetic neuropathy, and so on.

Front 236

235. Unilateral leg weakness and paralysis

Where is the lesion located?

Back 236

AKA crural monoparesis or monoplegia

Leg are of the primary motor cortex along the medial surface of the frontal lobe, lateral corticospinal tract below T1 in the spinal cord, or peripheral nerves supply the leg.

Side: Contralateral to weakness if lesion in motor cortex; ipsilateral if spinal cord or peripheral nerve lesion.

Front 237

236. Unilateral leg weakness and paralysis

Where is the lesion NOT located?

Back 237

Ruled out: Unlikely to be in the corticospinal tract above the upper thoracic cord, b/c in that case the face and or upper extremity would usually also be involved.

Rarely, cervical cord tumors can initially cause leg weakness only.

Front 238

237. Unilateral leg weakness and paralysis

What are the symptoms if it is a motor cortex lesion?

Back 238

There may be associated upper motor neuron signs, cortical sensory loss, frontal lobe signs such as a grasp reflex, or subtle involvement of the arm or face.

Occasionally none of these are present. The weakness pattern may be incompatible w/a lesion of the peripheral nerves - for example, diffuse weakness of all muscles in one leg.

Front 239

238. Unilateral leg weakness and paralysis

What are the symptoms if it is a spinal cord lesion?

Back 239

There may be associated upper motor neuron signs, a Brown-Sequard syndrome, a sensory level, or some subtle spasticity of the contralateral leg. Sphincter function may be involved.

The weakness pattern may be incompatible w/a lesion of the peripheral nerves.

Front 240

239. Unilateral leg weakness and paralysis

What are the symptoms if it is a peripheral nerve lesion?

Back 240

There may be associated lower motor neuron signs.

Weakness and sensory loss may be compatible w/a known pattern for a peripheral nerve lesion.

Front 241

240. Unilateral leg weakness and paralysis

What are the common causes?

Back 241

Motor cortex lesion: infarct in the anterior cerebral artery territory, or a small tumor, abscess, etc..

Spinal cord lesion: unilateral cord trauma, compression by tumor, multiple sclerosis

Peripheral nerve lesion: compression injury, diabetic neuropathy, etc...

Front 242

241. Unilateral facial weakness or paralysis

Where is the lesion located?

Back 242

AKA Bell's palsy (peripheral nerve); isolated facial weakness

Common: peripheral facial nerve (CN VII)

Uncommon: lesions in the face area of the primary motor cortex or in the genu of the internal capsule; facial nucleus and exiting the nerve fascicles in the pons or rostral lateral medulla.

Front 243

242. Unilateral facial weakness or paralysis

Where is the lesion NOT located?

Back 243

Ruled out: Unlikely w/lesions below the rostral medulla

Front 244

243. Unilateral facial weakness or paralysis

What are the symptoms if there are facial nerve or nucleus lesions (LMN)?

Back 244

The forehead and orbicularis oculi are not spared. With facial nerve lesions (e.g. Bells) there may be hyperacusis, decreased taste, and pain behind the ear on the affected side.

In facial nucleus lesions in the pons there are usually deficits associated w/damage to nearby nuclei and pathways such as CN VI, CN V, or the corticospinal tract.

In rostral lateral medullary lesions, a lateral medullary syndrome will be present.

Front 245

244. Unilateral facial weakness or paralysis

What are the symptoms if there are motor cortex or capsular genu lesions (UMN)?

Back 245

The forehead is relatively spared.

Dysarthria and unilateral tongue weakness are common. There may be subtle arm involvement.

In cortical lesions, sensory loss or aphasia may be present.

Front 246

245. Unilateral facial weakness or paralysis

What are the common causes?

Back 246

Facial nerve: Bell's palsy, trauma, surgery.

Motor cortex, capsular genu, pons, or medula: infarct.

Front 247

246. Facial diplegia

Back 247

Facial weakness may be difficult to detect in cases in which it occurs bilaterally, called facial diplegia, since the weakness is symmetrical.

Causes include motor neuron disease, bilateral peripheral nerve lesions (such as in Guillain-Barre syndrome or in bilateral Bell's palsy), or bilateral white matter abnormalities caused by ischemia or demyelination (such as in pseudobulbar palsy).

Front 248

247. Bilateral arm weakness or paralysis

Where is the lesion located?

Back 248

AKA brachial diplegia

Medial fibers of both lateral corticospinal tracts; bilateral cervical spine ventral horn cells; peripheral nerve or muscle disorders affecting both arms.

Front 249

248. Bilateral arm weakness or paralysis

Where is the lesion NOT located?

Back 249

Ruled out: Unlikely to be in the corticospinal tract b/c in that case the face and/or legs would also be involved.

Front 250

249. Bilateral arm weakness or paralysis

What are the symptoms?

Back 250

A central cord syndrome or anterior cord syndrome may be present.

Front 251

250. Bilateral arm weakness or paralysis

What are the common causes?

Back 251

Central cord syndrome:
1. Syringomyelia
2. Intrinsic spinal cord tumor
3. Myelitis

Anterior cord syndrome:
1. Anterior spinal artery infarct
2. Trauma
3. Myelitis

Peripheral nerve:
1. Bilateral carpal tunnel syndrome
2. Disc herniations

Front 252

251. Bilateral leg weakness or paralysis

Where is the lesion located?

Back 252

AKA Paraparesis or paraplegia

Bilateral leg areas of the primary motor cortex along the medial surface of the frontal lobes

Lateral corticospinal tracts below T1 in the spinal cord

Cauda equina syndrome or other peripheral nerve or muscle disorders affecting both legs.

Front 253

252. Bilateral leg weakness or paralysis

Where is the lesion NOT located?

Back 253

Ruled out: unlikely to be in the corticospinal tracts above the upper thoracic cord, b/c in that case the face and/or upper extremities would also be involved.

Rarely, cervical cord tumors can initially cause bilateral leg weakness w/o arm involvement.

Front 254

253. Bilateral leg weakness or paralysis

Symptoms associated w/bilateral medial frontal lesions?

Back 254

Upper motor neuron signs may be present.

There may also be frontal lobe dysfunction, including confusion, apathy, grasp reflexes, and incontinence.

Front 255

254. Bilateral leg weakness or paralysis

Symptoms associated w/spinal cord lesions?

Back 255

Upper motor neuron signs, sphincter dysfunction, and autonomic dysfunction may be present.

A sensory level or loss of specific reflexes may also help to determine the segmental level of the lesion.

Front 256

255. Bilateral leg weakness or paralysis

Symptoms associated w/bilateral peripheral nerve or muscle disorders?

Back 256

Cauda equina syndrome is associated w/sphincter and erectile dysfunction, sensory loss in lumbar or sacral dermatomes, and lower motor neuron signs.

Distal symmetrical polyneuropathies tend to preferentially affect distal muscles, and may have associated distal "glove-stocking" sensory loss and lower motor neuron signs.

Neuromuscular disorders and myopathies often affect proximal more than distal muscles.

Front 257

256. Bilateral leg weakness or paralysis

Common causes?

Back 257

Bilateral medial frontal lesions:
-parasagital meningioma
-bilateral anterior cerebral artery infarcts
-cerebral palsy

Spinal cord lesions: numerous, including tumor, trauma, myelitis

Front 258

257. Bilateral leg weakness or paralysis

Common causes of bilateral peripheral nerve or muscle disorders?

Back 258

Cauda equina syndrome:
-tumor, trauma disc herniation

Other peripheral nerve or muscle disorders:
-The lower extremities are often clinically affected before the arms in Guillain-Barre syndrome
-Lambert-Eaton syndrome
-numerous muscle disorders
-distal symmetrical polyneuropathies (caused by diabetes and other toxic, metabolic, congenital and inflammatory conditions).

Front 259

258. Bilateral arm and leg weakness or paralysis

Where is the lesion located?

Back 259

AKA quadriparesis, quadriplegia, tetraparesis, tetraplegia

Bilateral arm and leg areas of the motor cortex; bilateral elsions of the corticospinal tracts from the lower medulla to C5.

Peripheral nerve motor neuron or muscle disorders severe enough to affect all four limbs usually also affect the face, although in some cases face involvement may be relatively mild.

Front 260

259. Bilateral arm and leg weakness or paralysis

Where is the lesion NOT located?

Back 260

Unlikely to be below the motor cortex and above the medulla b/c the face would then be involved.

Unlikely to be in the spinal cord below C5 b/c the arms would then be partly spared.

Front 261

260. Bilateral arm and leg weakness or paralysis

What are the symptoms in a bilateral motor cortex lesion?

Back 261

Cortical lesions sparing the face are often in a watershed distribution and affect proximal more than distal muscles (man in the barrel syndrome).

Upper motor neuron signs are usually present and there may be associated aphasia, neglect, or other cognitive disturbances.

Front 262

261. Bilateral arm and leg weakness or paralysis

What are the symptoms in a bilateral upper cervical cord lesion?

Back 262

Upper motor neuron signs are usually present.

There may be a sensory level, sphincter dysfunction, or autonomic dysfunction.

High cervical lesions may cause respiratory weakness and may involve the spinal trigeminal nucleus, causing decreased facial sensation.

Front 263

262. Bilateral arm and leg weakness or paralysis

What are the symptoms in a lower medullary lesion?

Back 263

Upper motor neuron signs are usually present.

There may be occipital headache, tongue weakness, sensory loss, hiccups, respiratory weakness, autonomic dysfunction, sphincter dysfunction, or abnormal eye movements.

Front 264

263. Bilateral arm and leg weakness or paralysis

What are the common causes

Back 264

Motor cortex lesions:
-bilateral watershed infarcts (anterior cerebral-middle cerebral watershed)

Upper cervical cord and lower medullary lesions:
-tumor
-infarct
-trauma
-MS

Peripheral nerve or muscle disorders: numerous

Front 265

264. Generalized weakness or paralysis

Where is the lesion located?

Back 265

Bilateral lesions of the entire motor cortex; bilateral lesions of the corticospinal and corticobulbar tracts anywhere from corona radiata to pons; diffuse disorders involving all lower motor neurons, peripheral axons, neuromuscular junctions, or muscles.

Front 266

265. Generalized weakness or paralysis

Where is the lesion NOT located?

Back 266

Small focal or unilateral lesions do not produce generalized weakness.

Lesions of the lower medulla or spinal cord spare the face or upper extremities.

Front 267

266. Generalized weakness or paralysis

Symptoms associated?

Back 267

Bilateral cerebral or corticospinal lesions may be associated w/upper motor neuron signs.

Lesions of the peripheral nerves may be associated w/lower motor neuron signs.

Sensory loss, eye movement abnormalities, pupillary abnormalities, autonomic disturbances, or impaired consciousness may be present, and these features help determine the location and nature of the lesion.

Respiratory depression is common w/sever generalized weakness.

Front 268

267. Generalized weakness or paralysis

Common causes?

Back 268

Global cerebral anoxia, pontine infarct or hemorrhage, advanced amyotrophic lateral sclerosis, Guillain-Barre syndrome, myasthenia, botulism, and numerous other diffuse neopalstic, infectious, inflammatory, traumatic, toxic, or metabolic disturbances.

Front 269

268. Spastic gait

Back 269

Unilateral or bilateral

Stiff-legged circumduction, sometimes with scissoring of the legs and toe-walking (form increased tone in calf muscles), decreased arm swing unsteady, falling toward side of greater spasticity.

Front 270

269. Localization and cause of spastic gait

Back 270

Unilateral or bilateral corticospinal tract

Causes:
-cortical, subcortical, or brainstem infarcts affecting upper motor neuron pathways
-cerebral palsy
-degenerative conditions
-multiple sclerosis
-spinal cord lesions

Front 271

270. Ataxic gait

Back 271

Wide based, unsteady, staggering side to side, and falling toward side of worse pathology.

Subtle deficit can be detected with tandem hell-to-to gait testing.

Front 272

271. Localization and cause of ataxic gait

Back 272

Cerebellar vermis or other midline cerebellar structures

Causes:
-toxins such as alcohol
-tumors of cerebellar vermis
-infarcts or ischemia of cerebellar pathways
-cerebellar degeneration

Front 273

272. Vertiginous gait

Back 273

Looks similar to ataxic gait, wide based and unsteady.

Patients sway and fall when attempting to stand w/feet together and eyes closed (Romberg sign)

Front 274

273. Localization and cause of vertiginous gait

Back 274

Vestibular nuclei, vestibular nerve, or semicircular canals

Causes:
-toxins such as alcohol
-infarcts or ischemia of vestibular nuclei
-benign positional vertigo
-Meniere's disease

Front 275

274. Frontal gait

Back 275

Slow, shuffling, narrow or wide based, magnetic, unsteady.

Sometimes resembles Parkinsonian gait.

Some patients can perform cycling movements on their back much better than they can walk, giving rise to the term "gait apraxia" in this condition

Front 276

275. Localization and cause of frontal gait

Back 276

Frontal lobes or frontal subcortical white matter

Causes:
-hydrocephalus
-frontal tumors such as glioblastoma or meningioma
-bilateral anterior cerebral artery infarcts
-diffuse subcortical white matter disease

Front 277

276. Parkinsonian gait

Back 277

Slow, shuffling, narrow based.

Difficulty initiating walking. Often stooped forward, with decreased arm swing, and "en bloc turning".

Unsteady, with retropulsion, taking several rapid steps to regain balance when pushed backward

Front 278

277. Localization and cause of Parkinsonian gait

Back 278

Substantia nigra or other regions of basal ganglia

Causes:
-Parkinson's disease
-other parkinsonian syndromes, such as progressive supranuclear palsy, or use of neuroleptic drugs.

Front 279

278. Dyskinetic gait

Back 279

Unilateral or bilateral dance-like (choreic), flinging, or writhing movements occur during walking and may be accompanied by some unsteadiness.

Front 280

279. Localization and cause of dykinetic gait

Back 280

Subthalamic nucleus, or other regions of basal ganglia

Causes:
-Huntington's disease
-infarct of subthalamic nucleus or striatum
-side effect of levodopa
-other familial or drug-induced dyskinesias

Front 281

280. Tabetic gait

Back 281

High-stepping, foot flapping gait, with particular difficult walking in the dark or on uneven surfaces.

Patients sway and fall in attempts to stand with feet together and eyes closed (Romberg sign).

Front 282

281. Localization and cause of tabetic gait

Back 282

Posterior columns or sensory nerve fibers

Causes:
-posterior cord syndrome
-severe sensory neuropathy

Front 283

282. Paretic gait

Back 283

Exact appearance depends on location of lesion.

With proximal hip weakness there may be a waddling, Trendelenburg gait.

Severe thigh weakness may cause sudden knee buckling.

Foot drop can cause a high-stepping, slapping gait with frequent tripping.

Front 284

283. Localization and cause of paretic gait

Back 284

Nerve roots, peripheral nerves, neuromuscular junction, or muscles.

Causes:
Numerous peripheral nerve and muscle disorders.

Front 285

284. Painful (antalgic) gait

Back 285

Pain may be obvious based on patient's report or facial expression.

Tends to avoid putting pressure on affected limb.

Front 286

285. Localization and cause of painful gait

Back 286

Bones, joints, tendons, ligaments, and muscles.

Causes:
-arthritis
-fractures
-dislocations
-contractures
-soft tissue injuries

Front 287

286. Functional gait disorder

Back 287

Can be hard to diagnose. Sometimes patients say they have poor balance, yet spontaneously perform highly destabilizing swaying movements while walking, without ever falling.

Localization: psychologically based

Causes: conversion disorder or factitious disorder.

Front 288

287. Multiple sclerosis part 1

Back 288

An autoimmune inflammatory disorder affecting CNS system myelin.

The cause is unknown, although there is mounting evidence that T lymphocytes may be triggered by a combination of genetic and environmental factors to react against oligodendroglial myelin. Myelin in the peripheral nervous system is not affected.

Front 289

288. Multiple sclerosis part 2

Back 289

Multiple plaques of demyelination and inflammatory response can appear and disappear in multiple locations in the CNS over time, eventually forming sclerotic glial scars.

Demyelination causes slowed conduction velocity, dispersion or loss of coherence of action potential volleys, and ultimately conduction block.

B/c dispersion increases w/temp, some patients have worse symptoms when they are warm.

Front 290

289. Prevalence of MS

Back 290

about .1% in the US, witha higher worldwide prevalence in whites from northern climates, and about a 2:1 female to male ratio.

Lifetime risk of developing MS goes up 3-5% if a first degree relative is affected. Peak age of onset is 20-40 years. Onset before 10 or after 60 is rare but not unheard of.

Front 291

290. Clinical features of MS

Back 291

Two or more deficits separated in neuroanatomical space and time.

In practice, the Dx is based on the presence of typical clinical features, together with MRI evidence of white matter lesions, slowed conduction velocities on evoked potentials, and the presence of oligoclonal bands in CSF obtained via lumbar puncture.

Front 292

291. Oligoclonal bands

Back 292

Abnormal discrete bands seen on CSF gel electrophoresis.

They result from the synthesis of large amounts of relatively homogeneous immunoglobulin by individual plasma cell clones in the CSF.

These bands are present in over 85% of patients with clinically definite MS.

Front 293

292. MRI findings in MS

Back 293

MRI finding suggestive of MS include multiple T2-bright areas, representing demyelinative plaques located in the white matter.

The plaques tend to extend into the white matter from periventricular locations, and they occur in both supratentorial and infratentorial structures.

Front 294

293. Amyotrophic lateral sclerosis AKA Lou Gehrig's disease or ALS

Back 294

Characterized by gradually progressive degeneration of both upper motor neurons and lower motor neurons, leading eventually to respiratory failure and death.

ALS has an incidence of 1-3 per 100,000 and is slightly more common in men. The usual age of onset is in the 50-60's. Most cases occur sporadically, but there are also inherited forms that can have autosomal dominant, recessive, or X-linked transmission.

Front 295

294. Initial symptoms in ALS

Back 295

Usualy weakness or clumsiness, which often begins focally and then spreads to involve adjacent muscle groups.

Painful msucel cramping and fasciculations are also common. Some patients present with dysarthria, and dysphagia, or with respiratory symptoms.

A head droop is often present b/c of weakness of the neck muscles.

Front 296

295. Werdnig-Hoffmann disease

Back 296

Spinal muscular atrophy occurring in infancy is known as Werdnig-Hoffmann disease and usually leads to death by the second year of life.

Front 297

296. What does a motor unit consist of?

Back 297

1. A single lower motor neuron (spinal anterior horn cell)
2. The axon of that neuron
3. The muscle fibers it innervates

Front 298

297. Relationship between muscle fibers and muscle movements

Back 298

There are more muscle fibers per motor unit in muscles w/coarse movements (such as calf muscles) than in those w/refined movements (such as extraocular eye muscles(.

Front 299

298. Peripheral nerves and nerve sheaths

Back 299

Composed of myelinated and unmyelinated axons and their investing Schwann cells grouped into fascicles by connective tissue sheaths:

1. Epineurium - encloses the entire nerve
2. Perineurium - encircles each fascicle
3. Endoneurium - surrounds individual nerve fibers

Front 300

299. Schwann cells

Where does protein synthesis occur?

Back 300

Single Cchwann cells myelinate axonal segments (internodes) separated by nodes of Ranvier.

Protein synthesis does not occur in the axon; rather, axoplasmic flow delivers proteins and other substances synthesized int he perikaryon, and a retrograde transport system serves as a feedback to the cell body.

Front 301

300. Perineurial barrier and blood-nerve barrier

Back 301

The perineurial barrier is formed by the tight junctions between the perineurial cells.

Endoneurial capillaries complete the blood-nerve barrier.

Front 302

301. Skeletal muscle fibers

Back 302

They are syncytial cells w/multiple nuclei located beneath the plasma membrane (sarcolemma); they contain identical repeating units (sarcomeres) of actin and myosin contractile proteins delimited by perpendicularly disposed Z bands.

Front 303

302. Segmental demyelination

Back 303

Loss of myelin occurs along discrete regions of axons from dysfunction of the Schwann cell or damage to the myelin sheath.

With sequential episodes of demyelination and remyelination, layers of Schwann cell processes accumulate around the axon (onion bulbs).

Front 304

303. Axonal degeneration and muscle fiber atrophy

Back 304

Primary destruction of the axon occurs, with secondary disintegration of its myelin sheath.

In the slowly evolving neuronopathies or axonopathies, evidence of myelin breakdown is scant b/c only a few fibers degenerate at a time.

Wallerian degeneration is the acute reaction distal to a cut axon and consists of axonal and myelin breakdown with phagocytosis by macrophages.

Front 305

304. Nerve regeneration and reinnervation of muscle

Back 305

Proximal stumps of degenerated axons can regrow, guided by Schwann cells vacated by degenerated axons.

Regeneration occurs at a rate on the order of 2 mm per day and shows multiple, closely aggregated, thinly myelinated small caliber axons (regenerating cluster).

This regrowth of axons is a slow process, apparently limited by the rate of the slow component of axonal transport and the movement of tubulin, actin, and intermediate filaments.

Front 306

305. Denervation atrophy

Back 306

Breakdwon of myosin and actin, and shrinkage of muscle fibers to small, angulated shapes occur as a result of loss of innervation.

Front 307

306. Reinnervation of muscle fibers

Back 307

This occurs after nerve regeneration or, more commonly, when surviving axons sprout around denervated muscle cells and incorporate the fibers into their motor unit, imparting the same histochemical type to a group of contiguous fibers - type grouping.

Front 308

307. Group atrophy

Back 308

This occurs when a type group becomes denervated.

Front 309

308. Myopathic changes in muscle fibers

Back 309

Varied patterns occur, including segmental necrosis, myophagocytosis, myocyte regeneration via satellite cells, increased central nuclei, and variation in fiber size.

Front 310

309. Segmental necrosis of muscle fibers

Back 310

Destruction of a portion of a myofiber may be followed by myophagocytosis as macrophages infiltrate the region.

Front 311

310. Regeneration of muscle fibers

Back 311

Peripherally located satellite cells proliferate and reconstitute a destroyed portion of the fiber.

The regenerating fiber shows large internalized nuclei, prominent nucleoli, and basophilic cytoplasm laden with RNA.

Front 312

311. Hypertrophy of muscle fibers

Back 312

In response to increased load, large fibers may divide along a segment (muscle fiber splitting) so that, in cross-section, a single large fiber contains a cell membrane traversing its diameter, often with adjacent nuclei.

Front 313

312. Guillain-Barré syndrome

Back 313

AKA acute inflammatory demyelinating polyradiculoneuropathy

This is a life-threatening ascending paralysis, with weakness beginning in the distal limbs but rapidly advancing to affect proximal muscles.

Annual incidence in the US is 1/100,000 to 3/100,000

Front 314

313. Clinical features of Guillain-Barré syndrome

Back 314

Nerve conduction velocity is slowed and cerebrospinal fluid protein is elevated in the absence of increase cells.

Front 315

314. Pathologic features in Guillain-Barré syndrome

Back 315

Segmental demyelination and chronic inflammatory cells involving the nerve roots and peripheral nerves.

Guillain-Barré syndrome appears to be an immune-mediated disorder, often following a viral infection (CMV, Epstein-Barr virus) or Campylobacter jejuni.

Front 316

315. Chronic inflammatory demyelinating polyradiculoneuropathy

Back 316

A mixed sensorimotor polyneuropathy similar to Guillain-Barré syndrome, but it follows a subacute or chronic course, usually with relapses and remission.

Peripheral nerves show recurrent demyelination and remyelination and "onion bulb" histologic changes.

Front 317

316. Infection polyneuropathies; Leprosy

Back 317

Direct infections of Schwann cells occur in leprosy; the host response can be either limited (lepromatous leprosy) or vigorous (tuberculoid leprosy)

Front 318

317. Varicella-zoster virus

Back 318

After chickenpox, varicella-zoster virus produces latent infection of neurons in the sensory ganglia of the spinal cord and brain stem.

Subsequent reactivation leads to a painful vesicular skin eruption in the distribution of sensory dermatomes (shingles), most frequently thoracic or trigeminal.

Front 319

318. Diphtheria

Back 319

Diphtheritic neuropathy results from the effects of the diphtheria exotoxin.

It beings clinically with paresthesias and weakness and is characterized pathologically by segmental demyelination.

Front 320

319. Hereditary motor and sensory neuropathy type I (HMSN I)

Back 320

This is the most common form (AKA Charcot-Marie-Tooth disease, hypertrophic form) and typically presents in young adults with weakness and calf atrophy.

The disease is autosomal dominant, with multiple genetic forms.

Front 321

320. What is the most common genetic variant of HMSN I?

Back 321

HMSN, type Ia.

This is the most common genetic variant; it involves duplication of a portion of chromosome 17, including myelin-specific protein gene, PMP-22.

Less commonly, there is mutation of a gene on chromosome 1, coding for myelin protein zero (HMSN, type Ib.

Also, an X-linked form involves gap junction protein connexin-32.

Front 322

321. Pathologic features in HMSN I

Back 322

The disease shows segmental demyelination and "onion bulb" histologic changes.

The underlying common pathogenic feature involves repetitive demyelination.

Front 323

322. HMSN II

Back 323

HMSN II is clinically similar, but exhibits axonal loss without demyelination, and it usually presents at a later age.

This neuronal type is also autosomal dominant (locus on chromosome 1).

Nerves show axonal loss w/o nerve enlargement and no onion bulb histologic changes.

Front 324

323. HMSN III AKA Déjérine-Sottas disease

Back 324

AKA Déjérine-Sottas disease

This is an infantile, autosomal recessive neuropathy that may involve either PMP-22 or myelin protein zero.

The onset is in infancy, with progressive upper and lower extremity weakness and muscle atrophy and greatly enlarged palpable nerves.

Segmental demyelination is severe w/prominent onion bulbs.

Front 325

324. Symptoms in hereditary sensory and autonomic neuropathies

Back 325

Symptoms are usually limited to numbness, pain, and autonomic dysfunction, such as orthostatic hypotension.

Some hereditary neuropathies are notable for the deposition of amyloid within the nerve; these familial amyloid polyneuropaties have a clinical presentation similar to that of the hereditary sensory and autonomic neuropathies.

In other cases, inborn errors of metabolism cause prominent peripheral nerve manifestations.

Front 326

325. HSAN I

Back 326

Autosomal dominant

Predominantly sensory neuroapthy, presenting in young adults; axonal degeneration (mostly myelinated fibers)

Gene and locus: Serine palmitoyl-transferase, long chain base, subunit 1 (SPTCL1) gene

Front 327

326. HSAN II

Back 327

Autosomal recessive (some cases are sporadic)

Predominantly sensory neuropathy, presenting in infancy; axonal degeneration (mostly myelinated fibers)

Gene and locus: unknown

Front 328

327. HSAN III

Back 328

AKA Riley-Day syndrome; familial dysautonomia

Occurs most often in Jewish children. It is autosomal recessive.

Predominantly sensory neuropathy, presenting in infancy; axonal degeneration (mostly myelinated fibers); atrophy and loss of sensory and autonomic ganglion cells.

Front 329

328. What are the three principal patterns of neuropathy that occur in diabetes mellitus?

Back 329

1. Distal symmetric sensory or sensorimotor neuropathy (most commonly a chronic axonal neuropathy w/dramatic reduction of small myelinated and unmyelinated fibers).

2. Autonomic neuropathy (affects about 20-40% of diabetics)

3. Focal or multifocal asymmetric neuropathy (mononeuropathy or multiple mononeuropathy), such as unilateral ocular nerve palsies with a sparing of reflexes.

Front 330

329. Metabolic and nutritional peripheral neuropathies

Back 330

Neuropathies are encountered in patients w/renal failure (before dialysis), chronic liver disease, chronic respiratory insufficiency, and hypothyroidism.

Axonal neuropathies also occur w/deficiencies of thiamine, vitamin B12, B6, and E.

The neuropathy caused by excessive EtOH consumption is often associated w/thiamine deficiency.

Front 331

330. Neuropathies associated w/malignancy

Back 331

Direct effects: infiltration or compression of peripheral nerves by tumor may cause a mononeuropathy, brachial plexopathy, cranial nerve palsy, or polyradiculopathies involving the lower extremities when the cauda equina is involved by meningeal carnicomatosis.

Front 332

331. Paraneoplastic syndromes

Back 332

Progressive sensorimotor neuropathy is most pronounced in the lower extremities, particularly w/small cell lung carcinoma.

Less commonly, a pure sensory neuropathy occurs as a result of loss of dorsal root ganglion cells and axonal loss in the posterior columns of the spinal cord.

Patients often have a circulating polyclonal antibody directed against a neuronal protein (anti-Hu)

Front 333

332. Plasma cell dyscrasias

Back 333

Peripheral neuropathy w/deposition of light chain amyloid in peripheral nerves (AL type) occurs in patients w/plasma cell dyscrasias.

Neuropathy may also be related to the binding of monoclonal IgM to myelin-associated glycoprotein (MAG) independent of amyloid deposition.

Front 334

333. Adrenoleukodystrophy

Back 334

Metabolic disease that is X-linked; 4% of female carriers are symptomatic.

Mixed motor and sensory neuropathy, adrenal insufficiency, spastic paraplegia.

Onset is between 10-20 years for males with leukodystrophy and between 20-40 years for females with myeloneuropathy.

Front 335

334. Pathologic findings in adrenoleukodystrophy

Back 335

Segmental demyelination, with onion bulbs; axonal degeneration (myelinated and unmyelinated)

Electron microscopy; linear inclusions in Schwann cells

Front 336

335. Familial amyloid polyneuropathies

Back 336

Autosomal dominant metabolic disease that leads to sensory and autonomic dysfunction.

Age of onset varies with site of mutation.

Front 337

336. Pathological findings in familial amyloid polyneuropathies

Back 337

Amyloid deposits in vessel walls and connective tissue w/axonal degeneration

Front 338

337. Porphyria, acute intermittent (AIP) or variegate coproporphyria

Back 338

Autosomal dominant metabolic disease in which there are acute episodes of neurologic dysfunction, psychiatric disturbances, abdominal pain, seizures, proximal weakness, autonomic dysfunction; attacks may be precipitated by drugs

Front 339

338. Pathologic findings in porphyria, acute intermittent (AIP) or variegate coproporphyria

Back 339

Acute and chronic axonal degeneration; regenerating clusters

Front 340

339. Refsum disease

Back 340

Autosomal recessive metabolic disease in which there are mixed motor and sensory neuropathy with palpable nerves; ataxia, night blindness, retinitis pigmentosa, ichthyosis.

Age of onset is before 20 years (a genetically distinct infantile form also exists)

Pathologic findings: SEVERE onion bulb formation

Front 341

340. Neuropathies and lacerations

Back 341

Neuropathies can follow cutting injuries or bone fractures in which sharp fragments of bone lacerate a nerve.

Front 342

341. Avulsions and neuropathies

Back 342

Following application of tension to a nerve, neuropathies can occur as the result of a force applied to one of the limbs.

Front 343

342. Traumatic neuromas

Back 343

Painful nodules of tangled axons and connective tissue form regenerating axonal sprouts of the proximal stump may occur after nerve transection.

Front 344

343. Compression neuropathy AKA entrapment neuropathy

Back 344

Most commonly seen w/the median nerve at the level of the wrist within the compartment delimited by the transverse carpal ligament (carpal tunnel syndrome).

This neuropathy is observed w/any condition that can cause decreased space within the carpal tunnel, such as tissue edema; additional factors include pregnancy, degenerative joint disease, hypothyroidism, amyloidosis (especially that related to β₂-microglobulin deposition in renal dialysis patients), and excessive wrist usage.