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KINE4505 > Topic 7 &8 > Flashcards

Topic 7 &8 Flashcards

1
Q

What is the primary function of descending spinal tracts from the cerebral cortex?

A

To modulate the actions of motor neurons in the brainstem and spinal cord.

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2
Q

Where does corticobulbar tract start and what is its function?

A

Starts in the cortex, ends in the motor nuclei of brain stem
Functions: control voluntary movements of muscles in the head, neck and face

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3
Q

How are the lower face muscles controlled by the corticobulbar tract?

A

The lower face muscles are controlled contralaterally, meaning the left brain affects the right side, and vice versa.

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4
Q

How are the upper face muscles controlled by the corticobulbar tract?

A

The upper face muscles are controlled bilaterally, with both sides of the brain affecting both sides of the upper face.

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5
Q

Origin of Corticospinal Tract +Function

A

Starts in cortex to spinal motor neurons innervating limbs/trunk, enables precise and fine motor control.

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6
Q

How does the location of damage in relation to the pyramidal decussation affect the side of the body that experiences problems?

A

Damage above the pyramidal decussation leads to problems on the contralateral (opposite) side of the body, while damage below the decussation causes issues on the ipsilateral (same) side.

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7
Q

What is the primary function of the medial corticospinal tract?

A

The primary function of the medial corticospinal tract is to manage proximal postural control.

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8
Q

How does the medial corticospinal tract project to muscles, and which muscles does it influence?

A

The medial corticospinal tract runs ipsilaterally and projects bilaterally to efferents, influencing muscles in the neck, shoulders, and trunk.

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9
Q

What is the function of the lateral corticospinal tract?

A

Primarily controls voluntary and fine motor movements, particularly those involving distal muscles.

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10
Q

What is the significance of the pyramidal decussation?

A

The pyramidal decussation is the point at which the lateral corticospinal tract crosses over at the junction of the medulla and spinal cord, determining whether damage will affect the body ipsilaterally or contralaterally.

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11
Q

What is the main input/output layer of the cerebral cortex? What cells are in layer 5

A

Layer 4; Layer 5 (corticopyramidal cells/betz cells)

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12
Q

What are the major inputs to the primary motor cortex (M1)?

A

Include the medial and lateral premotor areas, primary somatosensory cortex, parietal “area 5,” basal ganglia, thalamus, and cerebellum.

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13
Q

What are the major outputs from the primary motor cortex (M1)?

A

The corticospinal and corticobulbar tracts, which connect to various structures such as the basal ganglia, red nucleus, reticular formation, pons, cerebellum, and spinal cord.

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14
Q

Compare the somatotopic organization of M1 vs primary somatosensory cortex

A

M1: Motor cortex has a “homunculus” map, larger areas for precise motor control like hands and face.

Primary Somatosensory Cortex: Somatotopic organization represents sensory input, not motor control, with neighboring body parts mapped to adjacent cortical regions.

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15
Q

What is Intracortical Microstimulation (ICMS)?

A

An improved stimulation technique that involves inserting an electrode into cortical layer V and using electrical stimulation to observe response of muscles

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16
Q

What is TMS and its function?

A

A non-invasive technique that uses a magnetic field to stimulate the brain from outside the skull, used for r a wide range of applications, including studying brain function, investigating the effects of brain lesions or disorders, and even therapeutic purposes in conditions like depression

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17
Q

Convergence

A

Output from several regions converge on motor neuron pool of single muscle​

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18
Q

Divergence:

A

single corticospinal efferent projects to multiple motoneuron pools

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19
Q

How is the primary motor cortex (M1) organized in terms of body part mappings?

A

The primary motor cortex (M1) is organized functionally based on movement synergies, where multiple areas can represent the same body part for different functional movements.

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20
Q

What does somatotopic organization in the primary motor cortex (M1) indicate about the mapping of body parts, muscles, or movements?

A

Somatotopic organization in the primary motor cortex (M1) does not represent a direct one-to-one mapping of body parts, muscles, or movements.

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21
Q

What is revealed by injecting Horseradish Peroxidase (HRP) into a specific region of the motor cortex (M1)?

A

Injecting Horseradish Peroxidase (HRP) into a specific region of the motor cortex reveals horizontal connections between cortical areas.

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22
Q

What is the significance of horizontal connections between cortical areas in the motor cortex (M1)?

A

Facilitate information exchange between different regions of M1.

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23
Q

What are Upper motor neurons?

A

Upper motor neurons are cells that have their cell body originate in “higher” regions of the brain, such as the motor cortex, and travel along the corticospinal tract.

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24
Q

What are Lower motor neurons (alpha motor neurons)?

A

Directly innervate skeletal muscles, sending signals from the central nervous system to control muscle movement.

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25
Q

What is hypotonia? What conditions is it seen in?

A

Refers abnormally low resistance to stretch and is often seen in conditions such as cerebellar disorders, lower motor neuron (LMN) lesions, and acute upper motor neuron (UMN) lesions.

26
Q

What is Hypertonia? Which conditions is it associated with?

A

Hypertonia refers to abnormally strong resistance to stretch and is typically associated with chronic upper motor neuron (UMN) lesions

27
Q

What is hyperreflexia?

A

Exaggerated or heightened reflex response when specific reflexes are tested, indicating a more pronounced reflex than normal (in the spinal cord)

28
Q

What is hyporeflexia?

A

A condition characterized by reduced or diminished reflex responses when specific reflexes are tested, indicating a weaker or absent reflex.

29
Q

Spastic Hypertonia ​

A

Resistance to passive movement is velocity sensitive

30
Q

What is Rigidity?

A

Rigidity is a condition in which resistance to passive movement remains constant regardless of velocity. It can be associated with abnormal postures (Decorticate and Decerebrate) and movements observed in neurological disorders.

31
Q

Upper motor neuron sydrome symptoms

A

1) Increased Muscle Stretch Reflexes
2) Sign of babinski: neurological response where the big toe extends upward and the other toes fan out when the sole of the foot is stroked with a blunt object
3) Weakness with an Increase in Muscle Tone manifesting as spasticity

32
Q

What is muscle tone determined by?

A
  1. Intrinsic elastic properties of muscle​ (structure of muscle itself)
  2. Neural input
33
Q

What characterize Decerebrate Rigidity?

A

Characterized by stiff arms and legs, upper arms are turned inwards and feet are point downwards

34
Q

What is Decerebrate Rigidity caused by?

A

Damage or dysfunction in the brainstem, often at a lower level within the brainstem.

35
Q

What characterizes Decorticate Rigidity?

A

The arms are flexed (bent towards the body) and the legs are extended (straight).

36
Q

What causes Decorticate Rigidity?

A

Damage to the cerebral cortex or its connections, above the level of the brainstem.

37
Q

What is the Hoffman Reflex used for?

A

Used to examine the reflexes of the upper extremities by stimulating 1a afferents and motor neurons,

38
Q

How is the Hoffman Reflex test conducted?

A

The Hoffman Reflex test involves stimulating a nerve with a small electrode and then measuring the time it takes for the stimulus to elicit a response in the muscle, observing the ‘M wave’ and ‘H wave’.

39
Q

What characterizes spinal shock?

A

Spinal shock is characterized by a complete absence of reflexes following an acute spinal cord injury, possibly due to the withdrawal of descending inputs.

40
Q

What might you observe when testing someone in the acute stage of spinal shock?

A

In the acute stage of spinal shock, you might observe a normal M wave but an absence of the H wave, indicating that the lower motor neuron and muscle are functional, but the spinal cord isn’t processing information.

41
Q

How do reflexes change after recovery from spinal shock?

A

After recovery from spinal shock, reflexes can become oversensitive, which may lead to increased muscle tone and hyperreflexia.

42
Q

Treatments for Spasticity and Hyperactive Reflexes

A

Baclofen is administered to the spinal cord as a GABA B receptor agonist, which helps to inhibit synaptic activity, particularly between Ia fibers and motor neurons.

43
Q

What are “hyperactive” reflexes? What causes them?

A

Hyperactive reflexes are spasm-like muscle bursts that occur in response to mild stimuli

44
Q

What causes hyperactive reflexes?

A

Hyperactive reflexes are caused by a loss of descending inhibition, which normally helps to modulate and restrain reflex activity.

45
Q

What is the Babinski sign? What can reverse this response?

A

1)The Babinski sign is a reflex test where stroking across the plantar surface of the foot normally causes flexion of the toes. 2) Upper motor neuron damage can reverse this response​

46
Q

What is a primary injury in the context of spinal cord injuries?

A

A primary injury refers to the initial mechanical damage to the neuronal apparatus of the spinal cord.

47
Q

What is a secondary injury following a spinal cord injury?

A

A secondary injury is the damage that occurs over hours post-injury

48
Q

What are the “3 D’s” of spinal cord injury mentioned in the context of secondary injury?

A

The “3 D’s” of spinal cord injury in the context of secondary injury are death, demyelination, and damage.

49
Q

Neuroprotective Strategies to protect spinal cord tissue:

A

block glutamate receptors​

​

  • antioxidants​ to combat free radical damage

​

  • block Na+ channels​
50
Q

What causes glutamate Excitotoxicity? What does this lead to?

A

Neurons deprived of oxygen can release large amounts of glutamate, causing a sodium and calcium ion influx causing cell swelling and triggering destructive enzymes which may initate apoptosis (cell death)

51
Q

What does Wallerian Degeneration result from and what does it affect?

A

Results from axotomy, the cutting or crushing of an axon, and it leads to the degeneration of the axon as well as surrounding pre-synaptic, post-synaptic cells, and glia.

52
Q

Possible long term therapies for spinal cord injury:

A

Regeneration of damaged axons​

Remyelination – Schwann cell transplants​

Cell replacement – stem cells​

53
Q

What is Poliomyelitis? (Polio)

A

Caused by the poliovirus and is characterized by an acute infection of the ventral horn of the spinal cord.

54
Q

How does Poliomyelitis affect neurons?

A

Poliomyelitis selectively destroys lower motor neurons, leading to the denervation of muscles.

55
Q

What is Amyotrophic Lateral Sclerosis (ALS)?

A

ALS, or Amyotrophic Lateral Sclerosis, is a neurodegenerative disease characterized by the degeneration of both “upper” and “lower” motor neurons.

56
Q

How does ALS affect muscles?

A

ALS leads to neurogenic atrophy of muscles, causing muscle weakness and wasting.

57
Q

What are two symptoms that can be seen in ALS?

A

Fasciculations; Small, visible or felt muscle twitches or contractions

Fibrillations: Fine and rapid muscle contractions that are not visible externally, detected using specialized tests like EMG,

58
Q

What are upper vs. lower motor signs?

A

UMN: hyperactive reflexes, babinsky sign
LNM: Atrophy or fasiculation

59
Q

How do the electrical properties of axons change in multiple sclerosis?

A

Normally, voltage-gated potassium (K+) channels are present in the internodes, and voltage-gated sodium (Na+) channels are densely packed in the region of the node of Ranvier. However, after demyelination in multiple sclerosis, these electrical properties are altered, leading to impaired nerve conduction.

60
Q
A

KINE4505 (16 decks)

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