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JMP Y2S1 > Week 43- Ascending Pathways and Sensation > Flashcards

Week 43- Ascending Pathways and Sensation Flashcards

1
Q

What is Nociception?

A

Signalling in the nervous system resulting from tissue damage

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2
Q

Is Nociception physiological or psychological?

A

Physiological

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3
Q

How does Nociception differ from pain?

A

It is physiological signalling in response to damage

Pain is a subjective feeling triggered by nociception signalling

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4
Q

Can there be nociception without pain?

A

Yes –> tissue damage triggers neural signals but no psychological distress eg anaesthesia , intoxication etc

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5
Q

Can there be pain without nociception?

A

Yes can be imagined pain and also hypnotised pain

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6
Q

What is the trigger for nociception?

A

Tissue damage/inflammatory response

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7
Q

What is the general pathway for nociception?

A

Tissue damage
Neural signal generation (nociceptors convert mechanical or chemical signals to neural)
Transmission –> ascending neural pathways to the brain
Perceptions/emotions/conceptualisations –> feed back to the transmission

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8
Q

What are the three classes of nociceptors?

A

Thermo
Chemo
Mechanical
–> Also polymodal –> nociceptors that react to multiple stimuli at once

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9
Q

What is the term for a pain producing chemical?

A

Algogenic

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10
Q

What is the Nociceptor reflex?

A

Reflex in which the body is able to move a limb out of harm without need of brain input

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11
Q

What is the steps in the nociceptor reflex?

A

Stimulus (e.g thermal receptor)
Afferent pathway to dorsal root ganglion and then to dorsal horn in spinal cord
Signals from afferent pathway travel ascending to brain as well as across to the ventral horn
Ventral horn efferent pathway
Effector organ targeted (muscle) –> response is movement (flexion away)

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12
Q

What is pain?

A

A defensive mechanism and a perceptual phenomenon

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13
Q

What is referred pain?

A

Pain perceived at a site that is different to the actual location of the nociceptive stimulus that is most commonly visceral

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14
Q

What is phantom pain?

A

The perception of pain in an absent leg –> possible mechanisms of activity in severed nerves

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15
Q

What are the different pain pathways?

A

Slow –> paleospino-thalamic

Fast –> neospino-thalamic

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16
Q

How does Slow and Fast pain pathways differ in fibre size?

A

Slow –> small fibres –> 0.2-5μm

Fast –> large fibres –> 6-20 μm

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17
Q

How does Slow and Fast pain pathways differ in sensation type?

A

Slow –> dull burning ache poorly localised

Fast –> sharp. Pricking well localised pain

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18
Q

How does Slow and Fast pain pathways differ in neurotransmitters?

A

Slow –> substance P

Fast –> glutamate

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19
Q

What location within the dorsal horn do slow and fast nociception pathways travel?

A

Slow –> deep dorsal horn

Fast –> superficial dorsal horn

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20
Q

What are the different types of pain?

A

Nociceptive
Inflammatory
Dysfunctional
Neuropathic

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21
Q

What is nociceptive pain?

A

Pain from legitimate noxious stimuli –> no nervous system lesion or inflammation

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22
Q

What are some features of nociceptive pain?

A

Evoked by high intensity stimuli
Pathway travels Painful stimulus –> nociceptor reaction Nociceptors –> nerves –> dorsal root ganglion, dorsal root, brainstem, thalamus, cortex

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23
Q

What is inflammatory pain?

A

Pain from active inflammation

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24
Q

What are some features of inflammatory pain?

A

Spontaneous and stimulus-dependant pain –> can happen with low and high stimuli
There is peripheral and central amplification

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25
What is dysfunctional pain?
Pain but with no known structural nervous system lesion or active peripheral inflammation
26
What are some features of dysfunctional pain?
Spontaneous and stimulus dependant Present with lack of stimulus Peripheral and central amplification
27
What is neuropathic pain?
Pain from nervous system lesion or disease --> marked neuroimmune response
28
What are some features of neuropathic pain?
Evoked by low and high intensity stimuli | Peripheral amplification and central amplification and neuroimmune interactions in periphery and in CNS
29
What is neuropathic pain?
Pain from nervous system lesion or disease --> marked neuroimmune response Neuropathic pain is pain caused by damage or disease affecting the somatosensory nervous system.
30
What are some features of neuropathic pain?
Evoked by low and high intensity stimuli | Peripheral amplification and central amplification and neuroimmune interactions in periphery and in CNS
31
What is the pathway of nociceptive pain?
Nociceptor --> dorsal root ganglion --> 1st neuron (pseudo unipolar (DRG)) --> dorsal horn of spinal cord --> 2nd neuron --> ascending
32
What are the three branches of the trigeminal nerve and where do they sensory innervate the face?
Ophthalmic --> forehead eyes and nose Maxillary --> upper jaw and cheeks Mandibular --> lower jaw
33
What other structures apart from the face does the trigeminal nerve give sensory innervation?
Large cerebral vessels Pial vessels Large venous sinuses Dura mater
34
How can the physiology of a migraine be described?
Vicious circle --> pain drives inflammation --> inflammation drives pain and back around
35
What is the difference between a headache and a migraine?
Headaches --> can include migraine, tension headaches, cluster headaches Migraines --> neurovascular disorder --> starts in brain and moves to vessels --> has trigeminal involvement
36
What is the name for diseases of the peripheral nerves?
Neuropathies
37
How do neuropathies commonly clinically manifest?
Sensory or motor abnormalities
38
What is the 3 main pathological types of damage to peripheral nerves?
Primary axon degeneration Primary demyelination Destruction of both axon and myelin
39
What needs to remain for potential repair and regeneration of the peripheral axon and myelin?
The cell body (soma) of the nerve
40
During axonal degeneration what happens to axon distal to point of transection?
They degenerate (Wallerian degeneration)
41
What cell type is important for removing axon and myelin debris?
Macrophages
42
What happens to the target tissue of damaged nerves?
It is denervated and commonly atrophies
43
What is the general stages in nerve regeneration?
Regeneration starts at site of transection --> with formation of growth cone Schwann cells guide the sprouting axons in the growth cone Nerve cell body becomes swollen Axon growth of 1-3mm per day Tissue is reinnervated Sprouting axons pruned to remove misguided branches Schwann cells create new myelin sheaths around axons
44
What is the growth cone in nerve regeneration?
Outgrowth of new branches from the stump of the proximal axon
45
What determined if axon repair will be successful?
The distance between the 2 transected ends needs to remain in close proximity
46
What is a Traumatic neuroma?
It is a nonneoplastic proliferation of axonal processes and associated Schwann cells --> results in a painful nodule
47
What causes a traumatic neuroma?
Failure of the outgrowth axons to find their distal targets
48
What happens during primary or segmental demyelination?
Schwann cells and myelin sheaths targets of damage --> axons relatively intact Myelin sheaths degenerate In response to damage Schwann cells and Schwann cell precursors proliferate Repair is imitated through formation of new myelin sheaths
49
What is needed for regeneration and recovery of nerves?
Cell bodies intact No scarring of the nerve Myelin is able to regenerate
50
What is normally characteristic of regenerated myelin?
They tend to be shorter and thinner in comparison to the original Leads to slower nerve conduction velocity
51
What is wrong in mononeuropathy?
Affects single nerve: | Results in deficits in a restricted distribution dedicated by normal anatomy
52
What is common causes of mononeuropathy?
Trauma Entrapment Infections
53
What is wrong in polyneuropathy?
Generalised symmetrical involvement --> affects multiple nerves Axons affected in length dependant fashion (deficits subsequently start in feet and ascend during disease progression)
54
What is wrong in focal peripheral neuropathy/ mononeuritis multiplex?
Disease that affects peripheral nerves in a haphazard manner: Mononeuropathy --> one nerve affected Multi mononeuropathy --> asymmetrical disease of several nerves
55
What is a common cause of peripheral neuropathy?
Vasculitis
56
What is wrong in radiculopathy/polyradiculoneuropathies?
Disease affecting nerve roots as well as peripheral nerves --> leads to diffuse symmetric symptoms in proximal and distal parts of the body
57
What is the result from a neuronopathies?
Destruction of neurons --> leads to secondary degeneration of axons - -> damage at level of the neuronal cell body - ->peripheral nerve dysfunction equally likely to affect proximal and distal parts of the body
58
What are some examples of causes of neuronopathies?
Herpes zoster | Toxins like platinum compounds
59
What are some examples of nutritional/metabolic neuropathies?
Diabetes Mellitus Uraemia Vitamin deficiencies --> Thiamine, Vit B6, Vit B12
60
What are some examples of toxic neuropathies?
Drugs --> wide range | Toxic --> alcohol, lead, aluminium, arsenic, mercury, acrylamide
61
What is the normal presentation of neuropathy in most toxins?
"Dying back" axonal neuropathy Symmetrical sensory and motor neuropathy "glove and stocking" distribution
62
How does glucose impact peripheral nerves?
Thought to cause microvascular injuries to small blood vessels These small blood vessels can no longer supply nerves
63
What is the impact of alcohol on peripheral nerves?
Long term alcohol consumption can lead to malnutrition | Direct toxic affects --> acetylaldehyde, ethanol etc
64
What is Paracetamol?
Weak COX inhibitor --> site of action in CNS
65
What is the action of Paracetamol?
Good analgesic Antipyretic NO anti-inflammatory action
66
What is the target of NSAIDs in pain management?
Prostaglandins sensitise nociceptive neurons --> lowering their threshold for activation Prostaglandins also promote bradykinin release --> also activate nociceptive neurons NSAIDs reduce prostaglandin production --> hence lower pain
67
What is the mechanism of opioids in pain management?
Prevents AP generation Activate PRE-synaptic u opioid receptors AND POST-synaptic u opioid receptors PRE mechanism: 1. Inhibits AdCy to reduce cAMP 2. Inhibits voltage-gated Ca2+ channels 3. Reduces synaptic vesicle mobilisation 4. Reduces neurotransmitter release POST mechanism: 1. Activates G protein to activate K+ channels 2. K+ channels cause K+ efflux --> hyperpolarises cell
68
How is neuropathic pain managed long term?
Treatment must involve constant reassessment of residual or on-going pain
69
What are some options for invasive treatments for management of neuropathic pain?
Intrathecal opioids Spinal cord stimulation Deep brain stimulation Neurosurgical techniques
70
What is the mechanisms of tricyclic antidepressants?
Promotes activity of descending inhibitory pathways at the spinal cord Reduces nociception = reduces pain
71
What does Gabapentin and Pregabalin?
Reduces nociception --> reduces pain BUT gabapentin appears to also increase GABA release AND gabapentin prevents central sensitisation of nociception pathways
72
What does carbamazepine and other anti-epileptic drugs do in pain management?
Block action potential generation --> hence reduces nociception and pain
73
What is the gold standard for trigeminal neuralgia?
Carbamazepine
74
What is the mechanism of Ketamine?
Polyamine --> competitive antagonist
75
How does Capsaicin work for pain management?
Agonist at transient receptor potential vanilloid type 1 (TRPV1 receptor) --> ligand gated non-selective cation channel (Ca2+ and Na+) --> initial activation leads to drainage of substance P Analgesic duration depends on rate of replacement of substance P
76
Why can capsaicin be more effective post nerve injury?
TRPV1 receptors are upregulated following peripheral nerve injury
77
How does Lignocaine function for nerve damage?
It is a voltage-gated sodium channel blocker | Reduce nociception
78
How can lidocaine be administered?
IV or spinally
79
What is the idea behind the WHO ladder for pain management?
Assess pain first THEN choose drug from appropriate level --> do not start from the bottom option and work up to success
80
What is the normal clinical pattern of sensory loss in glove and stocking distributions?
Sensory loss starts normally in the toes --> feet --> distal legs and fingers --> wrist --> forearm etc
81
What is the clinical pattern of sensory loss with specific peripheral nerves?
There is sensory loss in the areas in which only that nerve innervates (can be both muscular and sensory depending on nerve)
82
What is normally the clinical pattern of sensory loss within specific dermatomes?
There is usually a sensory loss in corresponding dermatomes to where there has been a nerve root lesion --> eg herniation of a vertebrae --> will lead to the dermatome for that vertebrae to losing sensory information
83
What happens to sensory information in complete spinal cord transection?
The dermatomes of the level and below of the transection will lose sensory information
84
What is the effect on sensory ability in a stroke?
Contralateral sensory loss
85
What is the pattern of sensory loss in Mononeuropathies? 
Localised sensory disturbance in the area supplied by the damaged nerve.
86
What is the pattern of sensory loss in Peripheral neuropathy? 
Symmetrical sensory deficits in a ‘glove and stocking’ distribution in the peripheral limbs.
87
What are the most common causes of peripheral neuropathies?
diabetes mellitus and chronic alcohol excess.
88
What is the pattern of sensory loss in Radiculopathy?
occurs due to nerve root damage (e.g. compression by a herniated intervertebral disc), resulting in sensory disturbances in the associated dermatomes.
89
What is the pattern of sensory loss in Spinal cord damage?
Sensory loss both at and below the level of involvement in a dermatomal pattern due to its impact on the sensory tracts running through the cord.
90
What is the pattern of sensory loss in Thalamic lesions (e.g. stroke)?
Contralateral sensory loss.
91
What is the pattern of sensory loss in Myopathies? 
Often involve symmetrical proximal muscle weakness.
92
What are some red flags for clinical presentation of back pain for possible fracture?
major trauma | minor trauma in elderly/osteoporotic
93
What are some red flags for clinical presentation of back pain for possible tumour/infection?
``` age (<20 or >50) Hx of cancer Fever weight loss recent bacterial infection immunosuppression pain worse at night/when supine ```
94
What are some red flags for clinical presentation of back pain for possible neurological deficit?
severe/progressive sensory loss/weakness | bladder or bowel dysfunction
95
What is trigeminal neuralgia?
It is pain caused by disruption of the trigeminal nerve which supplies facial sensation Pain can be caused by even mild stimulation of the face
96
What is the causes of trigeminal neuralgia?
Nerve compression --> vascular, tumour Demyelination --> MS Brain lesion --> surgical trauma, stroke, facial trauma

JMP Y2S1 (24 decks)

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