Somatic Nervous System Flashcards

1
Q

What are the classifications of the somatic nervous system?

A
  1. somatic afferent- somatosensory afferents within nerves – pain, touch, position, temperature, itch
    eg. localised pain (somatosensory fibres/nerves – pain, touch,
  2. somatic efferent- motor axons within nerves
    eg. skeletal muscle activation
  3. visceral afferent- viscerosensory afferents within nerves of the viscera and blood vessels
    eg. GI pain
  4. visceral efferent- smooth and cardiac motor (ie. gland- and gut wall-innervating) axons within nerves
    eg. GI muscle activation (vomiting)
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2
Q

How do the CB, CS and pyramidal tracts project?

A

Lateral M1 neurons controlling the face project down the corticobulbar tract and medial M1 neurons controlling the body project down the corticospinal tract. These pyramidal tracts project through the genu (CBT) and posterior limb (CST) of the internal capsule

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3
Q

What is the corticospinal tract?

A

The CS tract(s) convey motor commands to lower motor neurons in the ventral horn of the spinal cord via the internal capsule, cerebral peduncles, medullary pyramids, and lateral funiculus

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4
Q

What is the corticotubular tract?

A

The CB tract is the functional equivalent of the CS tract, but it synapses with the cranial motor nuclei – the brainstem analogue of the ventral horn in the spinal cord. Clinically, the pattern of innovation is particularly important for the facial motor nucleus (VII), since it controls facial motor tone, and that is very diagnosable.

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5
Q

What is Bell’s palsy and how can it be distinguished from UMN lesions?

A

Bell’s palsy is a common condition that results from damage to the facial nerve. Bell’s palsy, a lower motor neuron lesion (C, right), can be distinguished from upper motor neuron lesions (A, B, right) based upon whether the whole face or just the lower face loses its muscle tone. The ‘upper’ motor neurons innervate the superior face ‘lower’ MNs bilaterally, but the inferior face LMNs predominantly unilaterally, so if there is an UMN lesion, only lower face tension is lost

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6
Q

Lower vs upper motor neurons

A

Lower motor neurons- are motor neurons that directly innervate muscle eg. the ⍺ motor neurons of the ventral horn or cranial motor neurons

Upper motor neurons- control lower motor neurons. An example are the layer 5 Betz neurons of the primary motor cortex, whose axons form the corticospinal and corticobulbar tracts.

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7
Q

What happens in proprioception?

A

Proprioceptive afferents sense muscle tension. While extrafusal muscle fibres cause muscle tension, intrafusal muscle fibres are innervated by proprioceptors (type Ia and type II afferents) to sense tension. Tendon tension is sensed by type Ib proprioceptors innervating golgi tendon organs

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8
Q

Intramural fibres vs GTOs

A
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9
Q

What is the action of alpha and gamma motor neurons?

A

𝞪 motor neurons innervate extrafusal fibres, which generate contractile force of the muscle;
𝞬 motor neurons innervate intrafusal fibres, and stimulate them to contract, maintaining the sensitivity of proprioception.

  • Modulation of the levels of γ motor contraction relative to α motor contraction controls the sensitivity of proprioception – this sensitivity is called gain. Gain is controlled by lower (spinal cord) subconscious circuits and upper (brain) conscious circuits
  • By tensing the intrafusal fibres so that as the muscle gets shorter, they contract, maintaining the proprioceptors’ ability to detect tension in them.
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10
Q

Why does an UMN lesion cause clonus?

A

Loss of inhibition of inter neurons. The action of inhibitory neurons ensures that muscle contraction does not occur simultaneously (= prevents spasticity).

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11
Q

What is the reticular system?

A

is an enormously complex collection of nuclei in the brainstem. It is responsible for lots of subconscious motor control (eg. posture, breathing).

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12
Q

What is the vestibular system and the reflexes?

A

Vestibular sensation is the sense of balance/head position.
Vestibulospinal reflex: stops you falling over by innervating spinal cord LMNs.
Vestibulocollic reflex: keeps your head up by innervating cervical LMNs.
Vestibulo-ocular reflex: keeps your gaze fixed by innervating cranial nuclei of III, IV, and VI (extra-ocular nerves)

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13
Q

What is the tectospinal tract?

A

It’s the ‘roof’ over the cerebral aqueduct between the 3rd and 4th ventricles. Tectum = superior colliculus (responsible for visual reflex movements) + inferior colliculus (auditory reflex movements)

sends motor signals to coordinate with eye and head movements (neck and shoulder LMNs + nuclei of III, IV, and VI).

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14
Q

What do somatosensory pathways consist of?

A

Consist of 3 Order Ascending Neurons:

  • Sensory neurons
  • Spinal cord/brain stem
  • Thalamus
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15
Q

What are the somatosensory receptors and their function?

A
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16
Q

What are the somatosensory nerve fibres and what sensation are they responsible for?

A
17
Q

Pain vs nociception

A

Pain- is an experience, commonly a response to nociception but is possible without nociception

Nociception- neural process of encoding noxious stimuli

18
Q

What is the physiology of pain?

A
19
Q

What is transduction?

A

Transforming noxious stimuli into electrical activity. Nociceptors are polymodal. Capable of creating an AP from different stimuli:

  • Temperature extremes
  • Trauma
  • Hypoxia
  • Chemicals
  • Mechanically gated Na & Ca ion channels
  • Heat sensitive ions channels
  • Mast Cells: 5HT/Histamine
  • Damaged Cells:
    → Bradykinin on G-protein coupled receptors
    → ATP on ATP-sensitive K channels
    → Potassium
    → Prostagladins
20
Q

What is transmission?

A

conduction of electrical impulse through the nervous system

1stOrder Neurone

  • A-beta/A-delta & C
  • Dorsal Horn: Laminae I-V

2ndOrder Neurone

  • Decussate
  • Ascend in thelatspinothalamic tract

3rdOrder Neurone

  • Thalamus
  • Sensory Cortex
21
Q

What is perception?

A

subjective sensation of pain

  • Thalamus/Sensory cortex: localisation
  • Limbic Cortex: emotional response
  • Reticular Formation: alertness
  • Autonomic interconnections
22
Q

What is modulation?

A

process of alterations in the pain signals along the transmission pathway of pain

23
Q

What are the excitatory and inhibitory neurotransmitters and neuropeptides?

A
24
Q

Where do analgesics work?

A
25
Q

How is pain classified?

A

Based on Duration
- Acute (less than 3 months)
- Chronic (more than 3-6 months)
- Acute on Chronic

Based on nature of pain
- Nociceptive
- Neuropathic
- Mixed
- Visceral
- Malignant / Cancer pain

26
Q

What are the domains of chronic pain?

A
27
Q

Nociceptive vs neuropathic pain

A
28
Q

What are the Neuropathic pain proposed Pathophysiologies?

A

Excitotoxicity: nerve damage results in a barrage of nociceptive input released into the spinal cord that can damage inhibitory cells and result in a disinhibited pain system.
Sodium channels: in damaged nerves, abnormal sodium channels may be produced that result in a hyperexcitable nerve.
Ectopic discharge: damaged nerves produce ectopic, or abnormal, nerve impulses that may promote pain perceptions.
Deafferentation: if the central nervous system (CNS) is deprived of normal nerve input, as in the case of amputation or plexus avulsion, pain may result. The classic picture is severe pain in an insensate (or absent) limb.
Central sensitization: with repeated sensory input, the CNS may become hyperresponsive (sensitized) to peripheral input, a so-called facilitated state. This state is caused by long-term or permanent changes in the anatomy or physiology of the CNS produced by pain.

29
Q

Peripheral vs central mechanisms of neuropathic pain

A

Peripheral mechanisms:

  1. Sensitization by spontaneous activity by neurons, lowered threshold for activation, increased response to given stimulus.
  2. Formation of ectopic neuronal pacemakers along nerve and increased expression of sodium channels and voltage gated calcium channels. (α 2 delta subunit- where gabapentin acts)
  3. Adjacent demyelinated axons can have abnormal electrical connections channels and increased neuronal excitability.

Central mechanisms:

Sustained painful stimuli results in spinal sensitization (neurons within dorsal horn)

  1. Increased spontaneous activity of dorsal horn neurons, reduced activation thresholds and enhanced responsiveness to synaptic inputs.
  2. Expansion of receptive fields, death of inhibitory interneurons (intrinsic modulatory systems).
  3. Central sensitization mediated by NMDA receptors that further release excitatory amino acids and neuropeptides.
  4. Sprouting of sympathetic efferents into neuromas and dorsal root and ganglion cells.
30
Q

How is pain assessed?

A
  • Numerical Rating Scale (NRS)
  • Visual Analog Scale (VAS)
  • Defense and Veterans Pain Rating Scale (DVPRS)
  • Adult Non-Verbal Pain Scale (NVPS)
  • Pain Assessment in Advanced Dementia Scale (PAINAD)
  • Behavioral Pain Scale (BPS)
  • Critical-Care Observation Tool (CPOT)
31
Q

What is the WHO pain ladder?

A
32
Q

What are multimodal therapies?

A

Synchronous administration of ≥ 2 pharmacological agents or approaches, each with a distinct mechanism of action which allows dose reduction of individual agents to reduce the risk for adverse effects

33
Q

What are the perioperative techniques in pain management?

A

Nonopioid systemic analgesics- paracetamol, NSAIDs, gabapentinoids
Systemic opioids- IM injections, IV injections, PCA
Central regional analgesia- epidural opioid, clonidine
Peripheral regional analgesia- peripheral nerve blocks, intra-articular blocks, opioids

34
Q

What are pain treatment goals?

A
  • Reduce and manage pain
  • Decreased subjective pain reports
  • Decreased objective evidence of disease
  • Optimize medication use
  • Increase function & productivity
  • Restore life activities
  • Increase psychological wellness
  • Reduce level of disability
  • Stop cure seeking
  • Reduce unnecessary health care
  • Prevent iatrogenic complications
  • Improve self-sufficiency
  • Achieve medical stabilization
  • Prevent relapse / recidivism
  • Minimize costs - maintain quality
  • Return to gainful employment
35
Q

What is the mechanistic approach to pain therapy?

A
36
Q

What is interventional pain management?

A
  • Epidural or Perineural injections of local anesthetics/steroids - Precision (USG)
  • Sympathetic nerve blocks.
  • Neural ablative procedures (RF/Rhizotomy)
  • Peripheral Neural Stimulation - PENS
  • Spinal cord stimulation (PNFS/DRG).
  • Implantation of intrathecal drug delivery systems.
37
Q

What is spinal cord stimulation (SCS)

A

Implanted medical device that delivers electrical pulses to nerves in the dorsal aspect of the spinal cord that can interfere with the transmission of pain signals to the brain and replace them with a more pleasant sensation called paresthesia