Spinal Nociception Flashcards

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1
Q

What is the spinal cord and its function?

A

The spinal cord is a rope-like structure located in the vertebral column, with a diameter of about one centimetre. It sends pairs of nerves from each vertebral level, totalling 31 pairs of spinal nerves. The spinal cord is crucial for transmitting sensory and motor information between the brain and the rest of the body.

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2
Q

What is seen in the transversal view of the spinal cord regarding pain transmission?

A

In the transversal view, the spinal cord appears white due to myelinated tracts surrounding the inner grey matter, which has a butterfly-like shape. The anterolateral system (spinothalamic tract) in the white matter transmits nociceptive information to the brain, while the dorsal column system transmits tactile information via A-beta fibers and can also transmit pain under certain conditions.

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3
Q

What are Rexed’s laminae in the spinal cord?

A

Rexed’s laminae, classified in 1952, divide the grey matter of the spinal cord into 10 layers. In the context of pain, only laminae 1, 2, and 5 are relevant, as they are key zones involved in nociceptive processing.

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4
Q

What is the role of lamina I in nociception?

A

Lamina I is a thin layer that contains nociceptive specific neurons, which directly receive inputs from C fibers and A-delta fibers. Neurons from the dorsal root ganglion synapse in lamina I, making it an essential area for receiving and processing pain signals.

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5
Q

What is the function of lamina II (substantia gelatinosa) in nociception?

A

Lamina II, also known as the substantia gelatinosa, receives inputs from C and A-delta fibers and contains numerous interneurons. These interneurons modulate incoming signals, switching them from excitatory to inhibitory, making lamina II crucial for pain modulation.

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6
Q

What are the characteristics of lamina V and its role in nociception?

A

Lamina V houses wide dynamic range (WDR) neurons that respond to various stimuli, including pain, pressure and touch. These neurons that respond to various stimuli, including pain, pressure and touch. THese neurons are polymodal, meaning they are not strictly pain specific and can process information from different types of sensory inputs.

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7
Q

What is the significance of laminae VII and VIII in nociception?

A

Although laminae VII and VIII are not directly involved in nociception, they receive inputs from interneurons in lamina II and neurons in lamina V. They contain motor neurons that convert pain perception into reflexive actions or behaviours.

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8
Q

How do nociceptive specific (NS) and WDR neurons differ?

A

Nociceptive specific neurons respond only to specific pain modalities, such as pinpricks or pressure, and their action potentials end abruptly. WDR neurons respond to both noxious and non-noxious stimuli, such as brushing or tapping, and generate a sustained sequence of action potentials following a stimulus.

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9
Q

What are the primary mediators of spinal nociception?

A

Glutamate and substance P are important mediators of nociceptive transmission, while GABA is the main inhibitory mediator, often working with glycine to achieve optimal inhibition. There are approximately 30 neurotransmitters involved in pain processing at the spinal cord level, making it challenging to develop effective drugs for chronic pain.

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10
Q

What is temporal summation of pain (wind-up)?

A

Temporal summation of pain, also known as wind-up, involves an increasing sensation of pain due to repeated non-painful stimulation. This occurs when multiple stimuli accumulate without sufficient time for decay, resulting in amplified pain perception. It is associated with the activity of WDR neurons and depends on the activation of C fibers.

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11
Q

What is the role of C fibers in temporal summation of pain?

A

C fibers have a slow response rate that allows action potentials to accumulate, contributing to temporal summation of pain. This phenomenon is important in understanding mechanisms of chronic pain and helps study receptor systems involved in pain modulation.

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12
Q

What is central sensitisation?

A

Central sensitization occurs when a strong or long-lasting stimulus sensitizes the spinal cord, causing sub-threshold stimuli to be perceived as painful. It involves sensitization of neurons in the dorsal horn, leading to expanded receptive fields and heightened pain sensitivity.

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13
Q

How does central sensitisation differ from temporal summation?

A

Temporal summation involves increased pain from repeated stimulation over a short period, while central sensitization refers to longer-lasting sensitization resulting from strong or prolonged stimuli. Central sensitization typically results in ongoing changes in spinal cord neurons, leading to chronic pain.

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14
Q

What is secondary hyperalgesia?

A

Secondary hyperalgesia is a manifestation of central sensitization where pain occurs in the area surrounding an injury. It is characterized by decreased sensitivity to heat and increased sensitivity to mechanical stimuli, involving central nervous system components like dorsal horn neurons.

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15
Q

What are the two types of secondary hyperalgesia?

A

The two types of secondary hyperalgesia are allodynia and punctate hyperalgesia. Allodynia involves pain from a gentle tactile stimulus, while punctate hyperalgesia is caused by blunt pressure on the affected area. Both involve sensitized wide dynamic range neurons in the spinal cord.

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16
Q

What is dynamic mechanical hyperalgesia (allodynia)?

A

Allodynia is pain produced by a gentle tactile stimulus, such as cloth movement, which can be intolerable for chronic pain patients. It is caused by sensitization of dorsal horn neurons due to crosstalk between A-beta afferents and nociceptors, involving NMDA receptor activity.

17
Q

What is punctate hyperalgesia?

A

Punctate hyperalgesia is caused by blunt pressure on the affected skin area. It differs from allodynia in that it affects a larger area, lasts longer, and is less responsive to local cooling. Sensitized wide dynamic range neurons interpret non-painful pressure as noxious.

18
Q

How does spinal cord plasticity contribute to pain perception?

A

Intense and long-lasting pain sensitizes wide dynamic range neurons, causing them to interpret non-painful stimuli as painful. This plasticity leads to temporal summation, where repeated non-painful stimuli gradually increase the sensation of pain, and central sensitization, which involves prolonged effects on the spinal cord.

19
Q

What is the Gate Control Theory of pain?

A

The Gate Control Theory, introduced by Melzack and Wall in 1965, suggests that pain perception is modulated in the spinal cord by the interplay between transmission cells (T cells), substantia gelatinosa (SG), and large (L) and small (S) fibers. Descending fibers from the brain can influence this process, allowing psychological factors to affect pain perception.

20
Q

How does the Gate Control Theory explain pain modulation?

A

According to the Gate Control Theory, L fibers strengthen SG neurons, which inhibit T cells, reducing pain signals, while S fibers reduce this inhibition, allowing pain signals to pass. Descending fibers from the brain can further modulate the activity of SG and T cells, enabling emotional and attentional states to influence pain.

21
Q

What are the limitations of the Gate Control Theory?

A

The Gate Control Theory has been criticized for oversimplifying pain modulation, not accounting for multiple pathways and neurotransmitters involved. It also does not adequately explain the influence of temporal factors, such as temporal summation, on pain perception, and presynaptic inhibition from SG cells is not always observed in all contexts.