L4 - Locating CNS lesions Flashcards

1
Q

Define syndrome

A

Syn = same

Drome = run

A constellation of signs and symptoms that are frequently associated with each other and suggests the signs and symptoms have a common origin

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2
Q

Define hemiparesis

A

Hemi = half

par = paralysis

esis = condition of

Weakness or incomplete paralysis on one side of the body

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3
Q

Define hemiplegia

A

Hemi = half

plegia = stroke/stricken

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4
Q

Define hemianesthesia

A

Hemi = half

Anaesthesia = lack of sensation

Loss of sensation on one side of the body

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5
Q

Define spasticity

A

Is increased, involuntary, velocity-dependent muscle tone that causes resistance to movement

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6
Q

Define flaccidity

A

Weakness or paralysis and reduced muscle tone

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7
Q

Define hyperreflexia

A

Overactive or over-responsive reflexes

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8
Q

Define hyporeflexia

A

Underactive or non-responsive reflexes

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9
Q

What is a focal process?

A

A neurological deficit, based on a single geographical contiguous lesion, e.g. focal right foot weakness/numbness.

Or like my current issue with my lateral femoral cutaneous nerve. God that bastard hurts

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10
Q

What are the most common causes of focal deficits/focal processes of neurological disease?

A

Most common = stroke, ischemia caused by a lack of blood supply leading to neural tissue infarction in a well-defined area

Also, less commonly, solitary brain tumors

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11
Q

What is a multifocal process of neurological disease?

A

Damage to numerous sites

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12
Q

What is the most common cause of multifocal deficits/processes of neurological disease?

A

Most common is multiple sclerosis

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13
Q

What is a diffuse deficit/process of neurological disease?

A

Widespread dysfunction of the nervous system

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14
Q

What is the most common cause of diffuse deficits/processes of neurological disease?

A

Most common = produced by toxins or metabolic abnormalities

e.g. toxin build-up in hepatic encephalopathy

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15
Q

Why is neuroanatomical understanding helpful in trying to determine lesion location?

A

The brain and spinal cord contain tracts and nuclei that are very close to each other; due to their proximity, many pathological lesions are larger than any single nuclei or tract

Combinations of signs and symptoms may help localise the lesion

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16
Q

What are the major pathways to consider in the rostrocaudal location of a lesion? (3)

A
  1. Dorsal column medial lemniscal pathway
  2. Spinothalamic tract
  3. Lateral corticospinal tract
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17
Q

What general things should be considered in rostrocaudal localisation of a lesion? (3)

A
  1. Where tracts travel
  2. Where they decussate fro one side of the neuroaxis to the other
  3. What type of information does it carry
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18
Q

What should be considered in transverse localisation of a lesion?

A

Consider the placement of structures in a transverse plane in the brainstem and spinal cord. Tracts and nuclei are located in predictable locations medially to laterally

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19
Q

What is a negative manifestation?

A

When something that is normally there no longer is, e.g. when you lose sensation or control over an area, there has been a loss and thus it is a negative manifestation

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20
Q

What is a positive manifestation?

A

When something that previously wasn’t there now is, e.g. smelling smells that aren’t there, seeing things that aren’t there, spasticity increasing motor tone from loss of inhibition

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21
Q

Spasticity is directly correlated with?

A

Upper motor neuron damage

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22
Q

Flaccidity is directly correlated with?

A

Lower motor neuron damage

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23
Q

Where specifically in the thalamus do the SON synapse with the TON in the DCML pathway?

A

Ventral posterolateral (VPL) part of the thalamus

The posterolateral part of the ventral thalamus, annoying name I know. Could easily be misinterpreted

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24
Q

FON enter the spinothalamic tract and travel up _ or _ segments within ______ _____ before synapsing with SON in the _____ _____ of the above segment

Describe the * that is needed when stating that the FON synapse on the SON

A

FON enter the spinothalamic tract and travel up 1 or 2 segments within Lissauer’s tract before synapsing with SON in the substantia gelatinosa of the above segment

​The FON will synapse directly on the SON if it occurs at the same level, if the FON enters the dorsal horn
inhibitory interneurons if the pathway moves up 1 or 2 segments

Citation needed about this, as one slide says the SON are Inhibitory interneurons whilst another says the SON go directly to the thalamus

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25
Q

As the branches of the ascending STT travel through the brainstem, they send branches off to?

However, most neurons continue onto?

A

Send branches off to the reticular formation

However, most neurons continue onto intralaminar thalamic nuclei and the ventral posterolateral thalamus

26
Q

The VPL nuclei receives pain/temperature input regarding?
Whilst the VPM nuclei receives pain/temperature input regarding?

A

Ventral posterolateral nuclei receives pain/temperature input from the body
Ventral posteromedial nuclei receives pain/temperature input from the face

Both in the ventral part of the thalamus

27
Q
A
28
Q

Where does the corticospinal tract originate? What % does each section contribute? (3)

A
  1. Premotor/supplementary motor areas (30%)
  2. Precentral gyrus (30%)
  3. Postcentral gyrus (40%)
29
Q

Where does the corticospinal tract decussate?

A

90% decussate in the medullary pyramids

The remaining 10% remains ipsilateral to the level of the spinal cord, where 8% of the remainder decussates, with only 2% remaining ipsilateral

30
Q

Describe the path the corticospinal tract takes from the cortex to muscles

A

Travels from cortex through posterior limb of internal capsule

from there, some projections are sent via thalamus and cerebral peduncles into brainstem. (NOT CEREBELLAR - that would be too posterior)

Some projections to red nucleus and reticular formation before 90% decussate in medullary pyramids, travelling down contralaterally in lateral fasciculus

31
Q

What is the name of the area where the descending corticospinal tract pathway goes in the spinal cord?

A

Lateral fasciculus if they did decussate at the medullary pyramids
Anterior fasciculus if they didn’t decussate and remained ipsilateral

32
Q

The corticobulbar tract provides voluntary motor control for? (8. Ooft)

A
  1. Facial muscles
  2. Muscles of mastication
  3. Laryngeal muscles
  4. Palatal muscles
  5. Pharyngeal muscles
  6. Tongue muscles
  7. Upper trapezius muscles
  8. Smooth muscles/glands
33
Q

Where does the corticobulbar tract originate? Also give %s contributed (4)

A
  1. Premotor/supplementary motor areas (50%)
  2. Precentral gyrus relating to face/head (5%)
  3. Postcentral gyrus (30-35%)
  4. Other frontal and parietal cortical areas (10-15%)
34
Q

Describe the corticobulbar pathway to the cranial nerves and where control is bilateral or unilateral

A

Travels from the cortical area through the internal capsule, then cerebral peduncles into the brainstem.

From there, projects to cranial nerve nuclei mostly bilaterally except lower muscles of facial expression/tongue, upper trapezius

35
Q

Which areas controlled by the corticobulbar tract are not innervated bilaterally?

A

All bilateral except lower muscles of facial expression/tongue, upper trapezius

36
Q

Which cranial nerves are not part of the corticobulbar tract? (3)

A
  1. Oculomotor
  2. Trochlea
  3. Abducens

(the above are in midbrain and pons)

37
Q

Define an upper motor neuron

Give examples of locations of upper motor neurons

A

Any motor neuron that resides entirely within the CNS

E.g. Cortex, internal capsule, brainstem, or white matter tracts in spinal cord

38
Q

What would upper motor neuron damage clinically manifest with?

A

Spastic paralysis and hyperactive deep tendon reflexes due to loss of descending inhibitory input

As well as diminished or absent superficial reflexes and pathological reflexes, such as + Babinski response (normally inhibited by a mature corticospinal tract)

39
Q

What is hypertonia?
What causes hypertonia?

A

Too much muscle tone causing affected areas to be difficult to move

Damage to upper motor neurons.
Lower motor neurons normally want to activate and do things but are actively inhibited by UMN, however, when UMN are damaged the LWN are disinhibited, causing excessive tone and spastic paralysis

40
Q

What is a LMN?

Where would be a location of a LMN and what would happen if it was damaged?

A

Lower motor neuron

Cranial and spinal nerves (part of the final common motor pathway)
e.g. Ventral horn, or cranial nerve nuclei, neurons in axon as they leave SC, or in the periphery

Would cause flaccid paralysis, muscle atrophy, if damaged
Diminished or absent deep tendon reflexes (hyporeflexia/areflexia)

41
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A
42
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43
Q

Where does the corticospinal tract travel in the spinal cord?

A
44
Q

Where does the spinothalamic tract travel in the spinal cord?

A
45
Q

What are some key questions to ask in spinal cord lesions? (6)

A
46
Q
A

Spinal cord transection

47
Q
A

Small central lesion

Likely caused by commissural syndrome (targets fibres that decussate in SC)

As the STT decussates in the SC, a small central lesion would stop both sides experiencing pain/temperature in dermatomal distribution of the spinal cord segments (the dermal areas provided for by the affected spinal cord levels)

48
Q
A

Small central lesion

Likely caused by commissural syndrome (targets fibres that decussate in SC)

As the STT decussates in the SC, a small central lesion would stop both sides experiencing pain/temperature in dermatomal distribution of the spinal cord segments (the dermal areas provided for by the affected spinal cord levels)

49
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50
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51
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52
Q
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53
Q
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54
Q

What are the major long pathways of clinical significance in event of a lesion?

A
55
Q

What pathway provides somatosensation for the face?

(Touch, pressure, vibration, proprioception)

A

Trigeminothalamic tract

56
Q

Describe where the 3 neurons of the trigeminothalamic tract go

A

The FON enters the pons in trigeminal nerve, terminating by synapsing in the pons principle (chief) trigeminal nucleus

SON decussates in the pons and ascends in trigeminothalamic tract to VPM (ventroposterior medial nucleus) of the thalamus

TON leaves the thalamus and enters the posterior limb of the internal capsule, heading to the postcentral gyrus

57
Q

Where are the FONs and where do they synapse in the trigeminothalamic tract?

A

FON enter the pons in the trigeminal nerve, terminating by synapsing pons principle (chief) trigeminal nucleus

58
Q

Where are the SON of the trigeminothalamic tract?

A

Originate in the pons principle (chief) trigeminal nucleus, decussating within the pons and ascending in the trigeminothalamic tract to synapse with TON in the ventroposterior medial thalamus

59
Q

Where are the TON and where do they go in the trigeminothalamic tract?

A

TON originates in the ventroposterior medial nucleus of the thalamus, where it leaves the thalamus and enters the posterior limb of the internal capsule, heading to the postcentral gyrus

60
Q
A