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Medicine year 2 semester 1 > Case 19- Physiology > Flashcards

Case 19- Physiology Flashcards

1
Q

Motor unit

A
  • Alpha-motoneurons= activates skeletal muscle fibres

* Gamma-motoneurons= activates intrafusal fibres within the muscle spindle. Used in stretch

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2
Q

Henneman’s size recruitment principle

A
  • Motor neurons with large cell bodies tend to innervate fast-twitch, high-force, less fatigue-resistant muscle fibers
  • Motor neurons with small cell bodies tend to innervate slow-twitch, low-force, fatigue-resistant muscle fibers
  • Allows the CNS to recruit muscles to make contractions of differing strength and duration
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3
Q

Lower motor neuron organisation in the spinal cors

A
  • Distal musculature controls fine movements i.e. fingers. Within the dorsal lateral part of the spinal cord
  • Proximal and axial musculature controls position. Axial musculature controls the neck and head and is medial in the spinal cord
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4
Q

Lower motor neurons

A
  • Describes neurons of the brainstem and spinal cord that innervate muscles
  • Receive input from= sensory systems (reflex activity) and spinal cord interneurons (central pattern generators). Also from descending systems including upper motor neurons (corticospinal neurons and brainstem nuclei)
  • Motor unit- one lower motor neuron, its axon and all extrafusal muscle fibres it innervates
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5
Q

The pathways of the upper motor neurone

A

They have a direct pathway (lateral systems) and indirect pathway (medial system)

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6
Q

Upper motor neurons- direct pathway (lateral systems)

A
  • Corticospinal tract and Corticobulbar tract
  • Involves neurons of the cerebral cortex
  • Projects to the lower motor neurons (directly or indirectly)
  • Damage results in Babinski sign, Paralysis, Paresis (muscle weakness) exclusively of fine skilled movements
  • Segmental reflexes remain unaffected initially i.e. knee jerk reflexes
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7
Q

Upper motor neurons- Indirect pathway (medial system)

A
  • From brainstem nuclei to lower motor nucleus
  • Integrates supporting musculature during voluntary movements
  • Facilitates spinal reflex involved with balance, posture, equilibrium and gait
  • Damage results in spastic paralysis, hyperreflexia
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8
Q

Motor and descending (efferent pathways)

A

1) Pyramidal tracts= lateral/anterior corticospinal tracts

2) Extrapyramidal tracts= Rubrospinal tract, Reticulsopinal tracts, Olivospinal tract, Vestibulospinal tracts

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9
Q

Sensory and ascending (afferent pathways)

A

1) Dorsal column medial Lemniscus system- Gracile fasciculus, Cuneate fasiculus
2) Spinocerebellar tracts- posterior/anterior spinocerebellar tract
3) Anterolateral system- Lateral/Anterior Spinothalmic tract

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9
Q

Sensory and ascending (afferent pathways)

A

1) Dorsal column medial Lemniscus system- Gracile fasciculus, Cuneate fasiculus
2) Spinocerebellar tracts- posterior/anterior spinocerebellar tract
3) Anterolateral system- Lateral/Anterior Spinothalmic tract

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10
Q

Pathways into the spinal cord and basic function

A
  • Lateral corticospinal tract- Voluntary control of distal musculature
  • Anterior corticospinal tract- Voluntary control of proximal musculature
  • Reticulospinal tracts (pontine and medullary)- Regulate flexor reflexes and initiate patterned activity e.g. locomotion, swallowing
  • Rubrospinal tract- Motor control; excitation of flexor muscles
  • Tectospinal tract- Mainly cervical termination; orientation to visual stimuli
  • Vestibulospinal tracts- Lateral controls antigravity muscles – balance; medial regulates head movements
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11
Q

Organisation of descending pathways

A
  • Cerebral cortex projects directly to the spinal cord and motor nuclei of brainstem
  • Also projects to other brainstem centres i.e. corticorecticular projections
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12
Q

Exagerated reflexes following a corticospinal tract lesion

A

Babinski sign= following damage to descending corticospinal pathways on or before 2 years of age. Stroking the sole of the foot causes an abnormal fanning of the toes and the extension of the big toe.

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13
Q

Spasticity symptoms

A
  • Muscle stiffness, causing movements to be less precise and making certain tasks difficult to perform
  • Muscle spasms, causing uncontrollable and often painful muscle contractions
  • Involuntary crossing of the legs
  • Muscle and joint deformities
  • Muscle fatigue
  • Inhibition of longitudinal muscle growth
  • Inhibition of protein synthesis in muscle cells
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14
Q

Causes of muscle spasticity

A

Disruption of descending pathways leads to disordered spinal reflex pathways or inappropriate plasticity in uninjured descending pathways.

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15
Q

Treatments of muscle spasticity

A
  • Physical and occupation therapy to improve stretching, strength co-ordination and large and small muscle groups.
  • Oral medication that boost inhibitory neurotransmitter activity.
  • Intrathecal baclofecen to deliver boost to inhibition locally in the spinal cord.
  • Botox injections to weaken spastic muscles.
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16
Q

Corticospinal tracts

A

1) The lateral corticospinal tracts cross at the pyramidal decussation.
2) The anterior corticospinal tract crosses at the segmental level in the spinal cord.
3) The upper motor neurons of the corticospinal corticobulbar tact originate in the primary motor cortex (precentral gyrus).

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17
Q

Corticobulbar tracts

A

Corticobulbar fibres directly innervate motor nuclei V, VII, XI and XII. Generally bilateral except lower face (VII) and genioglossus (XII)

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18
Q

Corticobulbar fibres

A

Face, throat, eyes
• Direct innervation of lower motor neurons (α and γ) in motor nuclei of cranial nerves
• Indirect innervation mostly through pontine and medullary reticular formation (equivalent to interneurons of spinal cord)
• Bilateral (but predominantly crossed) projections to V, VII (upper face)
• Contralateral projections to VII (lower face)
• Ipsilateral projection to XI
• Bilateral to XII except mostly contralateral to genioglossus (protruder of tongue) therefore Upper motor neutron lesion results in tongue deviation contralateral to lesion whereas LMN lesion gives tongue deviation ipsilateral to lesion (e.g. right lesion of XII nucleus = tongue goes to right), (right lesion of corticobulbar pathway = tongue goes to left)

19
Q

Corticobulbar fibres- III, IV and VI (control movement of the eye)

A

Receives indirect, contralateral innervation from the frontal and parietal eye fields

20
Q

Tectospinal pathways

A

Controls neck movements in response to visual stimuli i.e. moving your head to track objects

21
Q

Direct rubrospinal pathways

A

Minor in humans- excites flexor activity and inhibit extensor activity. Most input is indirect via cerebellum and so may regulate learned movements.

22
Q

Reticulospinal tract

A
  • Originate from brain stem
  • Predominantly control axial muscles
  • Pontine and medullary reticulospinal tracts
23
Q

Vestibulospinal tracts

A
  • Originate from vestibular nucleus.
  • Lateral vestibulospinal tract – assist postural adjustments after angular and linear accelerations of head
  • Medial vestibulospinal tract – assist in head position to angular accelerations
24
Q

Summary of UMN and LMN pathways

A
  • Lower motor neurons (LMN) lie in the spinal cord (anterior horn) and discrete brainstem nuclei and innervate striated muscle
  • Upper motor neurons (UMN) originate in cerebral cortex, midbrain, pons or medulla and innervate lower motor neurons
  • Damage to LMN results in flaccid paralysis and areflexia while damage to UMN results in spastic paralysis with hyperreflexia
  • Corticospinal and corticobulbar fibres generally innervate LMN lying contralaterally (but learn exceptions)
  • UMN axons run in corticospinal, corticobulbar, rubrospinal, reticulospinal, tectospinal and vestibulospinal tracts
25
Q

Where do connections for pathways enter

A

The dorsal root ganglion

26
Q

Ascending tract

A

Sensory information from the peripheral nerve is transmitted to the cerebral cortex

27
Q

Damage or disease in the lower motor neuron can result in

A
  • Paralysis (loss of movement)
  • Paresis (weakness) of affected muscles
  • Loss of reflexes
  • Loss of muscle tone
  • Fibrillations (muscle fibre denervation) and fasciculations (motor neuron disease)
28
Q

Spinal nerves

A

Arise between two vertebrae, there are 31 spinal nerves in total

29
Q

Dermatome, Myotome

A

Dermatome- area of skin innervated by one spinal nerve. Cervical, Thoracic, Lumbar and Sacral
Myotome- muscles innervated by one spinal nerve

30
Q

Causes of spinal cord injury

A
  • Trauma
  • Slipped disk
  • Infection
  • Tumour growth
  • Ischaemia/Infarction
31
Q

Example of Trauma

A

Spinal cord Hemi-section (Brown Sequard syndrome). Damage to one side of the spinal cord. Motor and sensory pathways are damages. Multiple mixed motor and sensory signs and symptoms

32
Q

Slipped disk and herniation example

A

Spinal cord crush. The vertebral disk displaces and presses on the spinal cord. The severity depends on the level of the disk and level of compression. Often compresses spinal peripheral nerve. Causes loss/diminished pain, temperature and fine touch on one side.

33
Q

What defecits are caused when the tracts are damaged

A
  • Lateral corticospinal tract- paralysis, hyperreflexia- left below lesion
  • Anterior corticospinal tract- proximal muscles (trunk)
  • Rebrospinal, Reticulospinal, Vestibulospinal- balance, spasticity, abnormal reflexes
  • Dorsal column- fine touch, proprioception- left below lesion
  • Spinothalmic tract- pain, temperature- right below lesion
  • Spinocerebellar tracts- balance, unsteady gait
34
Q

SSymptoms of herniated disk- depends on the severity of the crush

A
  • Weakness and pain in myotome/dermatome at level of injury
  • Potential reflexes reduced at level of injury
  • Symptoms caused by pressure of disk on spinal cord/nerve at a single spinal level
35
Q

Nerve damage- infection example

A

Syphilis at the Tabes Dorsalis/ Syphilitic myelopathy stage. Demyelination of the dorsal column neurons. Caused by the spirochete bacterium Treponema pallidum. Form of tertiary syphilis.

36
Q

Infection- Which tracts cause which deficit

A
  • Dorsal column= Hypoaesthesia- reduced touch i.e. sensations. Sensory ataxia- poor coordication, positive Romberg sign. Paraesthesia- pina and needles
  • Dorsal horn= diminishes reflexes i.e. deep tendon reflexes, muscle hypotonia
37
Q

Damge to nerves- Tumour growth

A

Syringomyelia. Cyst that grows inside the spinal cord. Can be congenital or acquired. If the cyst is in the central canal there is loss/diminished pain and temperature on both sides at the level of the cyst. Signs include back pain, muscle weakness and stiffness

38
Q

Tumour growth- Which tracts cause which symptoms

A
  • Spinothalamic tract= gradual loss of pain and temperature bilaterally
  • Spread to ventral horn= muscle weakness, lower motor neurone signs
39
Q

Damage t nerves- Ischaemia/Infarction

A

Anterior spinal cord syndrome. Occlusion of anterior spinal artery. Loss of blood and oxygen to the anterior portion of the spinal cord. Damages pathways in the anterior portion of the spinal cord.These include:
• Ventral horns (LMN)
• Anterior and lateral spinothalamic tracts
• Anterior spinocerebellar tracts (masked)

40
Q

Barriers to regeneration- following injury to the spinal cord

A

• Infiltration of immune cells- inflammation
• Release of chemicals from damaged cells- further spread of damage i.e. Excitotoxicity
• Formation of Glial scar- reactive astrocytosis
• Inhibitory debris- proteins
The main barriers to regeneration are the glial scar and debris

41
Q

Events after injury

A
  • Injury eg. Crush
  • Cell death, Microglia, Astrocytes react, OPC’s react, infiltration Macrophages after damage to blood vessels
  • Inflammation leads to further death and spreading of the damage
  • Excitotoxicity
  • 7-10 days fibrotic scar tissue forms in the cyst
  • Astrocyte, OPC, Microglia- glial scar
  • Mature around 2 weeks after injury
42
Q

Why no regeneration in the CNS- Myelin debris and glial scar inhibitory proteins

A
  • Debris not fully cleared by microglia
  • Myelin debris contains inhibitory proteins= Nogo (membrane protein), Oligodendrocyte myelin glycoprotein, Myelin associated glycoprotein
  • Glial scar/astrocytes inhibitory proteins- Chondroitin sulphate proteoglycans
43
Q

Name some of the cardinal symptoms of neurological disease

A

1) Headaches
2) Nausea and vomiting
3) Visual changes
4) Hearing changes
5) Vertigo/dizziness
6) Speech and language difficulty
7) Swallowing difficulty
8) Altered consciousness
9) Psychological changes
10) Gait
11) Co-ordination changes

44
Q

Central signs

A

Brisk reflexes, increased tone and pale optic disc. These suggest damage to the spinal cord. Pale disc suggests optic nerve

45
Q

Syringomyelia

A

Cavity in the central canal of the spinal cord
Damages crossing fibres of the spinothalamic tract
Affects motor neurones in the medial aspect of ventral horn and long motor pathways in the cortico-spinal tract in lateral spinal cord.

Medicine year 2 semester 1 (53 decks)

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