1 and 2 - Neuroscience Review Flashcards

1
Q

Describe a lower motor neuron lesion

A

Results in IPSILATERAL deficits

  • Depending on number of neurons (in motor neuron pool) affected muscles can be weak or even paralyzed.
  • Decreased or absent muscle stretch reflexes. Since both tonic stretch and phasic (tendon tap) reflexes affected there is loss of muscle tone. Muscle shows flaccid weakness.
  • Either just one muscle or small group of muscles usually affected since lesion often in spinal root or peripheral nerve. Many muscles can be affected though if virus (example polio) targets anterior horn cells.
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2
Q

What symptoms will you see with a lower motor neuron lesion?

A

Signs of muscle denervation
• profound atrophy
• fasciculations
• fibrillations

Remember, lower motor neuron lesions result in ipsilateral deficits

Associated sensory loss patterns

  • Stocking & glove pattern if long peripheral nerves affected
  • Dermatome or fragments of dermatomes
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3
Q

Describe an upper motor neuron lesion

A

Results in CONTRALATERAL deficits

  • Immediately following the upper motor neuron lesion, spinal shock can cause hypotonia and a flaccid weakness/paralysis
  • This changes with time to a spastic weakness or spastic paralysis depending on the size of the lesion
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4
Q

What are the symptoms you will see with an upper motor neuron lesion?

A
  • Permanent, long-term effect is spastic weakness or paralysis
  • No signs of muscle denervation but can have disuse atrophy
  • Large groups of muscles will be affected (halves of the body or one whole limb)
  • Abnormal reflexes (Babinski sign or extensor plantar response)
  • Associated sensory loss also over large area, quadrants or halves of the body
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5
Q

Define upper motor neuron

A

Upper motor neurons (UMN)

An UMN is not actually a motor neuron since it does not synapse on skeletal muscle fibers. An upper motor neuron is a neuron in a higher motor area (e.g. motor cortex, premotor cortex, brainstem center) that synapses on a lower motor neuron or on an interneuron which synapses on a lower motor neuron.

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6
Q

Define lower motor neuron

A

Lower motor neurons -

They are the motor neurons of the spinal cord and brain stem that directly innervate skeletal muscle

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7
Q

Describe an upper motor neuron lesion

A

The patient would have flaccid paralysis due to spinal shock immediately after the lesion and then later develop spastic paralysis

  • Spasticity
  • Overactive deep tendon reflexes (DTR)
  • Positive Babinski sign (extensor plantar reflex)

Results in CONTRALATERAL deficits

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8
Q

Describe a lower motor neuron lesion

A
  • Atrophy
  • Decreased muscle tone
  • Weak or absent reflexes (hyporeflexia)
  • Fasiculations
  • Fibrillations
  • Paralysis of muscle if too many LMNs to that muscle are damaged

Results in IPSILATERAL deficits

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9
Q

There are two different classification systems of nerve fibers. What are they?

A
  • Roman number classification system

- Letter classification scheme

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10
Q

Describe the Roman system

A

Types I, II and III are myelinated, type IV is not.

If we exclude the A gamma fiber to the muscle spindles from the I to IV scheme, we can assign an “average” conduction velocity to each fiber type and the average conduction velocity

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11
Q

Type I

A

100 meters per second – A alpha

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12
Q

Type II

A

50 meters per second – A beta

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13
Q

Type III

A

20 meters per second – A gamma

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14
Q

Type IV

A

1 meter per second - C

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15
Q

Describe the letter classification scheme

A

A and B fibers are myelinated. C fibers are unmyelinated

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16
Q

A alpha function

A

Axon of alpha motor neuron; muscle spindle primary ending (Ia);

Golgi tendon organ afferent (Ib)

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17
Q

A beta function

A

Muscle spindle secondary ending (II)

And the axons of cutaneous mechanoreceptors

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18
Q

A gamma function

A

Axon of gamma motor neuron to muscle spindle fibers

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19
Q

A delta function

A

Fast pain, some temperature

receptors (Group III fibers)

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20
Q

B function

A

Sympathetic preganglionic axons

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21
Q

C function

A

Slow pain, some temperature (Group IV)
- and -
Sympathetic , postganglionic axons

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22
Q

Describe the role of enkephalin interneurons in nociceptive sensory transmission

A

An enkephalin is a pentapeptide involved in regulating nociception in the body. The enkephalins are termed endogenous ligands, as they are internally derived and bind to the body’s opioid receptors

It is one of three well-characterized families of opioid peptides produced by the body: enkephalins, endorphins, and dynorphins.

They behave in a similar way to opium in that they have an analgesic effect

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23
Q

Which areas of the nervous system excite the enkephalin interneurons?

A

Anterolateral system

The anterolateral system carries temperature, pain and “crude” touch sensations

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24
Q

What do you need to understand about descending pain control?

A
  • It is a regulatory mechanism used to control the descending pain pathways (occurs in the spinal cord)
  • It is complex, but you just need to know that this is an endogenous system that our bodies use to control pain
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25
Q

What types of medications utilize the descending pain control pathway?

A

Opioids

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26
Q

What are the two systems in the somatosensory system? (remember, this is the sensory system)

A
  • Dorsal column (posterior column) - medial lemniscus system

- Anterolateral system

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27
Q

What is the dorsal column responsible for?

A
  • Proprioception
  • Discriminative touch
  • Vibratory sense
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28
Q

What is the anterolateral system responsible for?

A
  • Temperature
  • Pain
  • “Crude” touch
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29
Q

What is the result of a spinal lesion affecting the dorsal column?

A

Loss of dorsal column mediated sensations ipsilaterally

Example: damage to right dorsal column would cause loss of proprioception, discriminative touch and vibratory sense in right foot.

This is because dorsal column fibers go up the spinal cord, cross in the medial lemniscus then go to the ipsilateral side of the brain, which controls the opposite side of the body.

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30
Q

What is the result of damage to the somatosensory area of the right thalamus?

A

Remember that fibers in the medial lemniscus (which have just crossed) synapse in the thalamus before going to the ipsilateral side of the brain.

This means that if there is a lesion of the right thalamus, the fibers won’t make it up to the right brain. The right brain controls the left side of the body.

This means damage to (somatosensory area of) right thalamus would cause loss of dorsal column mediated sensation in left foot.

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31
Q

What is the result of damage to the posterior limb of the internal capsule or the somatosensory cortex?

A

Both of these areas are located in the brain. Remember that the right brain controls the left side of the body.

This would cause contralateral deficits in dorsal column mediated sensations (proprioception, vibration, fine discriminative touch)

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32
Q

If there is a lesion in the somatosensory cortex, thalamus or medial lemniscus. what will be the effect on higher somatosensory function such as sterognosis and graphesthia?

A

These funcitons will be lost contralaterally to the lesion

This is because the lesion is after the fibers have already crossed in the medial lemniscus. After crossing they go straight up to that side of the brain. The right brain controls the left side of the body, so that means that the deficit will be on the contralateral side of the body compared to the lesion

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33
Q

What happens if there is a lesion lower than the medial lemniscus in terms of higher somatosensory function such as sterognosis and graphesthia?

A

These will be lost on the ipsilateral side of the dorsal column lesion

34
Q

What else does the dorsal column carry?

A

There is also some visceral pain pathways in the dorsal column (not the primary pain pathway)

35
Q

What is the anterolateral system responsible for again?

A
  • Temperature
  • Pain
  • “Crude” touch
36
Q

Where do singals in the anterolateral system cross?

A

In the spinal cord

37
Q

How is this different from the crossing of dorsal column fibers?

A

They cross in the medial lemniscus in the brainstem

38
Q

What is the clinical significance of pain and temperature information crossing in the spinal cord?

A

Since pain and temperature information cross in the spinal cord, midline lesions of the spinal cord (e.g. early syringomyelia ) cause bilateral loss of pain and temperature at the level of the lesion

39
Q

What about if there is a spinal cord lesion affecting only one side of the anterolateral system?

A

Spinal cord lesions of just one side of the cord cause contralateral loss of pain and temperature sensation.

40
Q

Where is the primary sensory cortex located?

A

Postcentral gyrus

41
Q

Where is the primary motor cortex located

A

Precentral gyrus

42
Q

Which parts of the body are represented by which areas of the postcentral gyrus (primary sensory cortex)?

A

Remember the homunculus and recall that the right side of the brain controls the left side of the body

  • Feet = medial
  • Torso, arms, hands = middle
  • Face, mouth, eyes = lateral
43
Q

We already went over the types of motor fibers (UMN, LMN). Describe how you determine whether or not the effects of a lesion will be ipsilateral or contralateral

A
  • Any lesion in the motor cortex, internal capsule or descending motor tract in the brain will cause upper motor neuron lesion symptoms contralateral to the lesion
  • Any lesion of the spinal cord (still UMN) can cause upper motor neuron symptoms for ipsilateral muscles which are innervated by neurons below the level of the lesion
44
Q

Define fasciculation

A

Fasciculations - visible twitches of muscle that can be seen as ripples under the skin. Can involve one or more motor units.

Benign fasciculations are not a sign of lower motor neuron disorder. An example of a benign fasciculation is the eyelid twitching often seen during periods of fatigue or eye strain.

45
Q

Define fibrillation

A

Fibrillations - spontaneous activity within single muscle fibers. They are not visible clinically since they are too small to be seen as movement through the skin.

Fibrillations can be recognized only by electromyography.

46
Q

Define motor neuron pool

A

The group of motor neurons that innervate a muscle

47
Q

Define motor unit

A

Motor unit definition - one alpha motor neuron plus all the skeletal muscle fibers it innervates

48
Q

Define hemiparesis

A

Hemiparesis is weakness of both arm and leg on same side

49
Q

Define paraparesis

A

Weakness of the lower limbs

50
Q

Define quadriparesis

A

Weakness affecting all four limbs

51
Q

Define paraplegia

A

Paralysis caused by illness or injury that results in the partial or total loss of use of the lower extremities

Caused by transection below the cervical level but above the lumbar enlargement - you get paralysis of both legs

52
Q

Define quadriplegia

A

Paralysis caused by illness or injury that results in the partial or total loss of use of all their limbs and torso

Caused by a high cervical lesion - you get paralysis of all four limbs

53
Q

Define ataxia

A

The loss of full control of bodily movements

54
Q

Define cerebellar ataxia

A

Ataxia is commonly associated with cerebellar lesions

55
Q

Define sensory ataxia

A

Sensory ataxia - damage to ascending sensory input to cerebellum can cause ataxia even if cerebellum itself intact

56
Q

Define intention tremor

A

Commonly associated with cerebellar lesions

The amplitude of an intention tremor increases as an extremity approaches the endpoint of deliberate and visually guided movement

57
Q

Define tremor of rest, resting tremor

A

shaking of the limb, even when the person is at rest. Often, the tremor affects only the hand or fingers. This type of tremor is often seen in patients with Parkinson’s disease

58
Q

Define lead pipe rigidity

A

Leadpipe rigidity results when an increase in muscle tone causes a sustained resistance to passive movement throughout the whole range of motion, with no fluctuations

59
Q

Define cogwheel rigidity

A

Cogwheel rigidity is a combination of lead-pipe rigidity and tremor which presents as a jerky resistance to passive movement as muscles tense and relax

60
Q

Define bradykinesia

A

Slowness in the execution of movement (bradykinesia)

61
Q

Define akinesia

A

Lack of movement

Difficulty in initiating movement is sometimes called akinesia, sometimes called bradykinesia

62
Q

Define dysdiadochokinesia

A

Commonly associated with cerebellar lesions

An impaired ability to perform rapid, alternating movements

63
Q

Define dysmetria

A

Commonly associated with cerebellar lesions

A lack of coordination of movement typified by the undershoot or overshoot of intended position with the hand, arm, leg, or eye. It is a type of ataxia. It is sometimes described as an inability to judge distance or scale.

64
Q

Define hypermetria

A

Commonly associated with cerebellar lesions

Specifically an “overshoot”

65
Q

Define chorea

A

Jerky involuntary movements affecting especially the shoulders, hips, and face

“Dance like”

66
Q

Define dystonia

A

Sustained muscle contractions cause twisting and repetitive movements or abnormal postures

67
Q

Define athetosis

A

Abnormal muscle contractions cause involuntary writhing movements. It affects some people with cerebral palsy, impairing speech and use of the hands.

68
Q

Give the lesion responsible for Parkinson’s disease

A

Degeneration of dopaminergic projection to striatum from substantia nigra

Though loss of dopamine primary pathology also loss of

i. Noradrenergic neurons in locus ceruleus
ii. Serotonergic neurons in the raphe nuclei

69
Q

What are the symptoms associated with Parkinson’s disease?

A
  • Tremor at rest
  • Muslce tone/rigidity (cogwheel type)
  • Bradykinesia (slowness)
  • Can evolve to akinesia (lack of motion)
  • Difficulty initiating movement
  • Postural reflex impairment
  • Freezing of gait (sudden become unable to start walking or just stop moving forward while walking - first appears as hesitation to start walking or turn)
70
Q

Give the lesion responsible for Huntington’s disease

A
  • First selective loss of GABA/enkephalin projection from striatum to GPe
  • Later more widespread degeneration of striatal neurons
  • Also loss of cortical neurons
71
Q

What are the symptoms associated with Huntington’s disease?

A
  • Chorea (involuntary movement)
  • Dementia
  • Voluntary movements slower than normal
72
Q

Describe the genetic basis of Huntington’s disease

A
  • Autosomal dominant disease
  • High penetrance
  • Genetic defect repeated trinucleotide (CAG) of 40 or more repeats on Chromosome 4
  • Age of onset dependent on length of repeats
  • As repeat length increases, age of onset decreases
73
Q

When given a list of patient’s neurological symptoms, be able to state the location of lesions that would cause those symptoms. If told a patient has an ischemic stroke involving the right (or left) anterior (or middle) cerebral artery be able to state which part of the body will be affected.

A

Last objective

74
Q

What does the anterior cerebral artery supply?

A

Anterior cerebral artery

  • Medial aspect of the frontal and parietal lobes
  • Medial sensorimotor cortex

Just know medial brain

75
Q

What happens if there is an occlusion in the anterior cerebral artery?

A

Motor and somatosensory deficits will be evident on the CONTRALATERAL leg and foot

Think about the homonculus

Everything below the belt (genitals, hip, legs, feet)

76
Q

What does the middle cerebral artery supply?

A

Its another branch directly off the internal carotid artery

Supplies virtually the entire lateral surface of the cerebral hemispheres

77
Q

What happens if there is an occlusion in the middle cerebral artery?

A

Deficits on the CONTRALATERAL side

Hands and head/face

78
Q

Describe the deficits seen in a spinal hemisection (sensory loss of Brown-Sequard syndrome)

A
  • The loss of fine tactile sensation is on the side of the lesion (dorsal column - because it hasn’t crossed yet)
  • This is because the lesion is in the back, the fibers go up to the medial lemniscus can cross, they then go straight up to the brain and the brain affects the contralateral ide of the body
  • The loss of pain and temperature (anterolateral column) is on the contralateral side of the lesion because it hasn’t crossed yet
79
Q

If a patient is able to shut both eyes, but is not able to turn up one edge of their mouth to smile, where is the lesion?

A

In the contralateral brain - upper motor neuron

Contralateral because the right brain controls the left body

Doesn’t affect the top half of the face because there is dual innervation from the other side

80
Q

If a patient is unable to shut their eye or turn up the edge of their mouth to smile, both on the same side, where is the lesion?

A

In the facial nucleus - lower motor neuron on the ipsilateral side

ipsilateral because the lesion is not in the brain, it is after the signal has left the brain

81
Q

With brown-sequard syndrome, what happens to motor function?

A

There is a lesion in the spinal cord

  • Pain and temperature have already crossed - contralateral symptoms
  • Fine touch and proprioception has not yet crossed - ipsilateral symptoms
  • Motor function has already crossed - it is descending, so it is ipsilateral (monoplegia and Babinski sign will be present)
  • This makes it easy - the ONLY thing that is contralateral to the lesion is pain and temperature ***
82
Q

When you have damage to the cerebellum, will the symptoms be ipsilateral or contralateral?

A

IPSILATERAL

Same side as the lesion

Need to know this