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Phase 2- HNN > Week 3 > Flashcards

Week 3 Flashcards

1
Q

What is spinal shock?

A

Temporary suppression of all reflex activity below the level of the injury

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2
Q

When does spinal shock occur and how long does it last?

A

Occurs immediately after injury and intensity and duration vary with the level and degree of injury

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3
Q

How can you tell if spinal shock is over?

A

Return of the bulbocavernous reflex

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4
Q

What are the clinical effects of spinal shock?

A
  • Flaccid paralysis
  • Areflexia
  • Loss of sensation
  • Loss of bladder and bowel reflexes
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5
Q

What are the phases of spinal shock?

A
  • Areflexia
  • Initial reflex return
  • Initial hypperreflexia
  • Hyperreflexia and spasticity
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6
Q

What controls skeletal muscles?

A

Skeletal muscles are controlled by motor neurons in the ventral horn of the grey matter which are arranged segmentally

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7
Q

Where do motor neurons receive input from?

A

Local sources (segmental reflexes) and from several descending tracts form various parts of the brain (voluntary movement)

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8
Q

What does the corticospinal tract conduct?

A

Impulses for the control of muscles of the limbs and trunk

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9
Q

Axons from where form the corticospinal tracts?

A

Axons of upper motor neurons in the cerebral cortex form the corticopsinal tracts, and descend through the internal capsule of the cerebrum and cerebral peduncle of the midbrain

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10
Q

What happens to the corticospinal tracts in the medulla oblongata?

A

Axon bundles form ventral bulges known as pyramids, and about 85% of the corticospinal axons decussate to the contralateral-> lateral corticospinal tract

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11
Q

Describe the course of the corticospinal tract in the spinal cord:

A
  • Descend into the spinal cord where they synapse with a local circuit neuron or a lower motor neuron
  • 15% remain on the ipsilateral side where they eventually decussate at the spinal cord levels where they synapse with local circuit neuron or LMN -> anterior corticospinal tract
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12
Q

What does the right cerebral cortex control?

A

The left side of the body, and the left cerebral cortex controls the right side of the body

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13
Q

What does the anterior corticospinal tract control?

A

Trunk and proximal parts of the limbs

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14
Q

What does the lateral corticospinal tract control?

A

Responsible for precise, agile and highly skilled movements of the hands and feet

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15
Q

What does the corticobulbar tract conduct?

A

Impulses for the control of skeletal muscles in the head

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16
Q

What axons form the corticobulbar tract?

A

Axons of upper motor neurons from the cerebral cortex form the corticobulbar tract

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17
Q

Where does the corticobulbar tract descend?

A

Along with the corticospinal tract through the internal capsule of the cerebrum and cerebral peduncle of the midbrain

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18
Q

Where do axons of the corticobulbar tract terminate?

A

Axons terminate in the motor nuclei of nine pairs of cranial nerves in the brainstem:

  • oculomotor
  • trochlear
  • trigeminal
  • abducens
  • facial
  • glossopharyngeal
  • vagus
  • accessory
  • hypoglossal
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19
Q

What do lower motor neurons of the cranial nerves convey?

A

Impulses that control precise voluntary movement of the eyes, tongue and neck, plus chewing, facial expression, speech and swallowing

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20
Q

Describe the tectospinal pathway:

A
  • Maintenance of balance and posture
  • Project to cervical segments only
  • Modulates activity of alpha and gamma motor neurons innervating muscles of the neck
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21
Q

Describe the vestibulospinal pathway:

A
  • Maintenance of balance and posture
  • Runs entire length of cord
  • Modulates activity of alpha motor neurons
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22
Q

Describe the reticulospinal pathway:

A
  • Comprised of pontine (extensor) and medullar (flexor) tracts
  • Maintenance of balance and posture
  • Runs entire length of cord
  • Modulates activity of alpha motor neurons
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23
Q

Describe the rubrospinal tract:

A
  • Involved with subconscious regulation of upper limb muscle tone and movement
  • Upper motor neurons originate in the red nuclei in the midbrain
  • Decussates at the brainstem (midbrain)
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24
Q

How is sensory information from skin, muscles, joints and viscera transmitted?

A

Via dorsal roots of the spinal nerves and through certain cranial nerves to the spinal cord or brainstem

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25
Q

What ascends along the dorsal column-medial lemniscus pathway?

A

Nerve impulses for touch, pressure, vibration and conscious proprioception from limbs, trunk neck and posterior head

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26
Q

Where does the name of the dorsal column-medial lemniscus pathway come from?

A

From the names of two white-matter tracts that convey the impulses;

  • dorsal column of the spinal cord
  • medial lemniscus of the brainstem
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27
Q

Where do first order neurons extend from, and where do they extend to?

A

First order neurons extend from sensory receptors in the limbs, trunk, neck and posterior head into the spinal cord and ascend to the medulla oblongata on the ipsilateral side

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28
Q

Where are cell bodies of the first order neurons of the dorsal column-medial lemniscus pathway found?

A

In the dorsal root ganglia of spinal nerves

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29
Q

What do the axons of the first order neurons of the dorsal column-medial lemniscus pathway form?

A

Dorsal columns, which consist of two parts:

  • gracile fasciculus
  • cuneate fasciculus
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30
Q

Where do the first order axons of the dorsal column-medial lemniscus pathway synapse with second order neurons?

A

They synapse with dendrites of second-order neurons whose cells bodies are located in the gracile nucleus or cuneate nucleus of the medulla

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31
Q

What nerve impulses are propagated along axons in the cuneate fasciculus to the cuneate nucleus?

A

Nerve impulses for touch, pressure, vibration and conscious proprioception from the upper limbs, trunk, neck and posterior head

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32
Q

What nerve impulses are propagated along axons in the gracile fasciculus to the gracile nucleus?

A

Nerve impulses for touch, pressure and vibration from the lower limbs and lower trunk

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33
Q

What do axons of second order neurons do before entering the medial lemniscus?

A

Cross to the opposite side of the medulla, and then enter the medial lemniscus

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34
Q

What is the medial lemniscus?

A

A thin-ribbon like projection that extends from the medulla to the central posterior nucleus of the thalamus

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35
Q

What happens to the dorsal column-medial lemniscus pathway in the thalamus?

A

The axon terminals of second-order neurons synapse with third-order neurons

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36
Q

Where do third-order neurons project?

A

Their axons project to the primary somatosensory area of the cerebral cortex

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37
Q

What nerve impulses travel in the spinothalamic tract?

A

Pain, temperature, itch and tickle from the limbs, trunk, neck and posterior head ascend to the cerebral cortex along the spinothalamic pathway

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38
Q

Describe first-order neurons of the spinothalamic tract:

A
  • Connect a receptor with the spinal cord
  • Cell bodies are located in the dorsal root ganglion
  • Axon terminals synapse with second-order neurons whose cell bodies are coated in the posterior grey horn of the spinal cord
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39
Q

Which axons of the spinothalamic tract decussate?

A

Second-order

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40
Q

Describe second-order neurons of the spinothalamic tract:

A
  • Cell bodies located in the posterior grey horn of the spinal cord
  • Decussate
  • Pass upward to the brain as the spinothalamic tract
  • End in the ventral posterior nucleus of the thalamus, where they synapse with third-order neurons to the primary somatosensory area on the ipsilateral side of the cerebral cortex as the thalamus
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41
Q

Describe ANS pathways:

A
  • Maintains homeostasis by regulating the function of many organs
  • Not independent and requires input from the CNS
  • Consists of a pre and postganglionic neuron
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42
Q

What structures have only a sympathetic supply?

A
  • Adrenal medulla
  • Hair follicles
  • Sweat glands
  • Spleen
  • Iris dilator -> pupil dilation
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43
Q

What structures have only a parasympathetic supply?

A
  • Ciliary muscles -> focussing of eyes

- Iris sphincter -> pupil constriction

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44
Q

What are the antagonistic actions by both SNS and PsNS

A
  • Provides delicate control over the functions of the viscera
  • HR -> sympathetic increases while parasympathetic decreases
  • Bronchus -> sympathetic dilates while Ps constricts
  • Pupil -> S dilates while Ps constricts
  • Genitalia -> S causes ejaculation while Ps causes erection
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45
Q

What is the basic principle of spinal injury?

A

Survival and extend of complications depends on the level of cut -> higher the transaction, the more serious the complication

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46
Q

What respiratory complications occur when the spinal injury is at or above C3, 4 or 5?

A
  • Phrenic nerve -> innervates the diaphragm
  • Section above this level results in disconnection of all the motor neurons innervating the respiratory muscles from the respiratory centres in the mid and hindbrain
  • Breathing ceases and patient dies if artificial ventilation is not administered
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47
Q

What respiratory complications occur when the spinal injury is at or above C6 and 7?

A
  • Innervates the intercostal muscles
  • Severing the spinal cord below the origin of phrenic but above thoracic at C6 and 7 segments cause disconnection of the motor neurons that innervate the intercostal muscles
  • Innervation to the diaphragm remains -> breathing remains intact
  • Paradoxical breath (chest moves out upon expiration and in upon inspiration) is present
  • Thorax is sucked in during inspiration instead of being expanded by contraction of external intercostal muscles
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48
Q

What complications are there in the limbs with spinal injury?

A

Patients need constant monitoring and prophylaxis -> increased risk of pressure sores and DVT

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49
Q

When is there complete function loss?

A

When there is a complete spinal lesion there is complete functional loss below the level of injury (no sensation or voluntary movement and both sides are equally affected)

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50
Q

When is there partial function loss?

A

When there is an incomplete spinal lesion, there is partial function loss (can move one limb more than the other or have some sensation in a paralysed limb)

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51
Q

What does reappearance of any sensation or voluntary movement of a limb indicate?

A

Cord injury is incomplete

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52
Q

What level of function loss occurs after complete spinal injury to high cervical levels?

A

Quadriplegia

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53
Q

What level of function loss occurs after complete spinal injury to C5 segment?

A

Control of shoulder and biceps but no wrist or hand control

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54
Q

What level of function loss occurs after complete spinal injury to C6 segment?

A

Wrist control but no hand control

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55
Q

What level of function loss occurs after complete spinal injury to C7 and T1 segment?

A

Straighten arms but may have problems with dexterity of hands and fingers

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56
Q

What level of function loss occurs after complete spinal injury to T1-8 segment?

A
  • Paraplegia with hands not affected
  • Poor control of trunks as abdominal muscles are affected
  • Balance while sitting is still very good
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57
Q

What level of function loss occurs after complete spinal injury to lumbar and sacral segments?

A

Decreased control of hip flexors and legs

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58
Q

How do some patients with spinal injury learn when they need to void urine?

A
  • As bladder fills, input to the cord from bladder wall stretch receptors produces reflex rise in BP by spinal mechanism
  • BP regulation is deficient in the patient and hence the rise is greater than in normal people -> appears as flushing of face and signals patient to go to the toilet
  • Scratching of thigh increases sensory bombardment of sacral regions -> facilitates micturition reflex and bladder empties
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59
Q

What issues surround emptying of bladder in spinal injury patients?

A
  • Incomplete emptying of bladder increases the risk of UTIs that may lead to kidney damage and hypertension due to the release of renin
  • Patients who have retained use of their arms can be taught to compress the bladder to improve emptying
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60
Q

What does normal reflex depend on?

A

Normal reflex depends on the participation of supraspinal mechanisms (not spinal reflexes)

61
Q

Describe somatic reflexes:

A
  • Never regain voluntary control of skeletal musculature
  • Reflex activity gradually recovers together with autonomic activity
  • Flexor reflexes return first -> ankle, knee and hip in sequence
  • Extensor reflexes return about 6 months after transection -> tend to be exaggerated leading to spastic paralysis
  • Final stage is a predominant extensor activity with extensor spasms
  • Extensor tendon reflexes are exaggerated -> hyperreflexia
62
Q

What is spastic paralysis?

A

A chronic pathological condition in which the muscles are affected by persistent spasms and exaggerated tendon reflexes because of damage to the central nervous system.

63
Q

Describe autonomic reflexes:

A
  • Mass reflex (autonomic dysreflexia) occurs -> stage of reflex activity that follows the primary flaccidity of the shock due to massive sympathetic discharge
  • Trivial stimulus to groin or soles of feet -> flexion of legs, defecation, micturition and erection in men -> socially embarrassing
  • Profound sweating that can be triggered by cutaneous stimulation
  • Primitive control of autonomic function by spinal mechanisms is re-established but BP control remains more unstable than in normal people
  • BP rises with filling of bladder -> stretch receptor bombardment
  • Change in posture from lysing to standing causes pooling of blood in legs and causes a reduction in venous return but autonomic compensation is inadequate -> BP rises and subject may faint (orthostatic hypotension)
64
Q

Describe the plantar reflex:

A
  • Maintains a standing position
  • Tested by the babinski response: lateral aspect of the sole is firmly stroked with a blunt object, normal adults respond with plantar flexion of the toes
  • Test for damage of the pyramidal tract in adults
65
Q

What are the results of the plantar reflex?

A
  • Negative Babinski response -> plantar flexion

- Positive Babinski response -> dorsiflexion of great toe and fanning of other toes

66
Q

When is the Babinski sign different?

A
  • Postural reflex of normal person is replaced with the primitive withdrawal reflex
  • In babies, Babinski sign is positive -> pyradimal tracts not fully developed
  • After transection, Babinski response is lost with other reflexes and when is reappears it assumes the abnormal form -> sign that spinal shock is wearing off
67
Q

Describe abdominal reflexes in patients recovering from spinal transection:

A
  • If belly is scratched, muscles of the belly wall contract by reflex and pull theumbilxcus towards the stimulus
  • After spinal transection, the reflex is abolished bilaterally, but if the corticospinal projections are interrupted on one side, ipsilateral reflex is abolished
68
Q

Describe the cremasteric reflex in patients recovering from spinal transection:

A
  • Inner thigh is scratched -> reflex contraction of cremaster muscle that elevates the ipsilateral testicle
  • After spinal transection -> reflex is absent
69
Q

What are upper motor neurons?

A

Neurons in the primary motor cortex, that have axons in the spinal cord and excite alpha motor neurons directly or via spinal interneurons

70
Q

What are lower motor neurons?

A

Alpha motor neurons that run from the spinal cord to the periphery (PNS)

71
Q

What are lesions, in reference to UMN and LMN?

A

Neurons may be destroyed, functioning abnormally or only a proportion is functioning

72
Q

What are UMN lesions?

A

Indicate that the lesion is above the anterior horn cell

73
Q

What are LMN lesions?

A

Indicate that the lesion is either in the anterior horn cell or distal to the anterior horn cell

74
Q

What are the clinical features of a LMN lesion?

A

Muscle wasting, fasiculations, flaccid tone, weakness and paralysis due to loss in muscle in bulk, reduced or absent tendon jerk reflex and negative Babinski sign

75
Q

What are the clinical features of a UMN lesion?

A
  • No muscle wasting
  • No fasiculations
  • Spastic tone
  • Weakness or paralysis due to inefficient recruitment of alpha motor neurons
  • Hyperreflexic tendon jerk reflex
  • Positive Babinski sign
76
Q

What is tinnitus?

A
  • Perception of sounds in the absence of external auditory stimulus
  • May be constant, intermittent and uni or bilateral
77
Q

What is tinnitus a result of?

A

Hearing loss, sounds produced by adjacent structures or other disease processes

78
Q

How is tinnitus divided?

A

Objective and subjective tinnitus

79
Q

Describe objective tinnitus:

A
  • Sound is detected or potentially detectable by another observer
  • Typical causes are vascular abnormalities or neuromuscular disorders
  • In some vascular disorders, sounds generated by turbulent blood flow are conducted to the auditory system -> pulsatile form
80
Q

Describe subjective tinnitus:

A
  • Noise perception when there is no noise stimulation of the cochlea
  • Intermittent periods of mild, high-pitched tinnitus lasting several minutes in normal-hearing people
  • Impacted cerumen is a benign cause of tinnitus -> resolves after removal
  • Medication such as aspirin and stimulants such as nicotine and caffeine can cause transient tinnitus
81
Q

What conditions are more associated with persistent tinnitus?

A
  • Noise-induced hearing loss
  • Prebycusis -> sensorineural hearing loss that occurs with ageing
  • Hypertension
  • Atherosclerosis
  • Head injury
  • Cochlear or labyrinthine infection
  • Inflammation
82
Q

What are the proposed causes of subjective tinnitus?

A
  • Abnormal firing of auditory receptors
  • Dysfunction of cochlear neurotransmitter function or ionic balance
  • Alterations in central processing of the signal
83
Q

What is vertigo?

A
  • Illusion of motion associated with disorders of vestibular function
  • Sensation of spinning, “to-and-fro” motion or falling
84
Q

What is subjective vertigo?

A

Person is stationary and the environment is in motion

85
Q

What is objective vertigo?

A

Person is in motion and the environment is stationary

86
Q

What is presyncope and what causes it?

A

A feeling of light-headedness or blacking out is commonly caused by postural hypotension or a stenotic lesion in the cerebral circulation that limits blood flow

87
Q

What may cause unstable gait?

A
  • disorders of sensory input
  • peripheral neuropathy
  • gait problems
88
Q

What can vertigo result from?

A

Central (mild and constant) or peripheral (severe in intensity and episodic) vestibular disorders

89
Q

Describe motion sickness:

A
  • Normal physiological vertigo
  • Caused by repeated rhythmical stimulation of the vestibular system -> car, air or boat travel
  • Vertigo, malaise, nausea and vomiting are the principle symptoms
  • Autonomic signs may occur including;
    • lowered BP
    • tachycardia
    • excessive sweating
  • Hyperventilation produces changes in blood volume and pooling of blood in the lower extremities -> postural hypotension
90
Q

What does Meniere’s disease cause a triad of?

A

Vertigo, tinnitus and hearing loss

91
Q

Why does Meniere’s disease occur?

A

Due to distension of the endolymphatic compartment of the inner ear

92
Q

What are the suggested mechanisms of Meniere’s?

A
  • Increased production of endolymph
  • Decreased production of perilymph accompanied by a compensatory increase in volume of the endolymphatic sac
  • Decreased absorption of endolymph caused by malfunction of the endolymphatic sac or blockage of endolymphatic pathways
93
Q

What is thought to cause Meniere’s?

A
  • Infection -> syphilis
  • Trauma
  • Immunological
  • Endocrine -> adrenal-pituitary insufficiency and hypothyroidism
  • Vascular disorders
94
Q

What is Meniere’s characterised by?

A
  • Fluctuating episodes of tinnitus, feelings of ear fullness, violent rotatory vertigo that often renders the person unable to sit or walk
  • There is a need to lie quietly with the head fixed in a comfortable position, avoiding all head movements that aggravate the vertigo
95
Q

What ANS symptoms are often present in Meniere’s?

A
  • Pallor, sweating, nausea and vomiting

- More severe the attack, more prominent the ANS manifestations

96
Q

How does the disease progress?

A
  • Fluctuating hearing loss occurs with a return to normal after the episode subsides
  • Initially the symptoms tend to be unilateral, resulting in rotatory nystagmus caused by an imbalance in vestibular control of the eye movements
  • Because initial involvement is usually unilateral and sense of hearing is bilateral -> many people are not aware of the full extent of their hearing loss
  • As the disease progresses, the hearing loss stops fluctuating and progressively worsens, with both ears tending to be affected -> prime disability becomes deafness
  • Episodes of vertigo diminish and disappear, although the person may be unsteady, especially in the dark
97
Q

What are the differential diagnoses for Meniere’s?

A 
ENT:
- acoustic neuroma
- otitis media
- earwax
- ototoxic drugs
Intracranial Pathology:
- vertebrobasilar insufficiency
- intracranial tumours
- migraine
Systemic Illness
- anaemia
- hypothyroidism
- diabetes mellitus
- autoimmune disease
- syphilis
98
Q

What is acoustic neuroma?

A

Benign Schwann cell tumour affecting CN VIII

99
Q

What does acoustic neuroma cause?

A

Unilateral sensorineural hearing loss

100
Q

What causes hearing loss in acoustic neuroma?

A

Compression of cochlear nerve or interfering with the blood supply to the nerve and cochlea

101
Q

What is thought to cause tumour growth?

A

Tumour suppressor gene abnormalities on chromosome p22 (merlin or schwannomin protein)

102
Q

What do patients with acoustic neuroma present with?

A

Dizziness or vertigo

103
Q

What characterises unilateral hearing loss?

A

Difficulty in locating sound and find it difficult to find a voice in

104
Q

What happens as the tumour enlarges?

A

Other nerves become affected and the symptom that is most common is facial numbness

105
Q

What is found in larger tumours?

A

Nystagmus and gait abnormalities

106
Q

What is affected late, and what happens when it is affected?

A

Facial nerve function- results in a slower blink, altered taste and altered tearing

107
Q

What may present with larger masses?

A

Hydrocephalus

108
Q

What is the differential diagnosis for acoustic neuroma?

A

Meningioma, epidermoid, facial nerve schwannoma and trigeminal schwannoma

109
Q

Where does the facial nerve attach to the brainstem?

A

The lateral surface, between the pons and medulla oblongata

110
Q

What roots does the facial nerve consist of?

A

Large motor root and a smaller sensory root (intermediate nerve)

  • large motor root contains general visceral efferent fibres
  • intermediate nerve contains special afferent fibres for taste, parasympathetic general visceral efferent and general somatic afferent fibres
111
Q

Where do the nerve roots leave the cranial cavity?

A

They cross the posterior cranial fossa and leave the cranial cavity through the internal acoustic meatus

112
Q

Where do the nerve roots fuse to form the facial nerve?

A

In the petrous part of the temporal bone, as they enter the facial canal

113
Q

What does the facial nerve do in the facial canal?

A

Enlarges to form the geniculate ganglion

114
Q

What does the geniculate ganglion give off?

A

The greater petrosal nerve, which carries mainly preganglionic parasympathetic fibres

115
Q

What does the facial nerve give off as it continues along the bony canal?

A

The nerve to stapedius and the chorda tympani

116
Q

Where does the facial nerve exit the skull?

A

Stylomastoid foramen

117
Q

What is the chorda tympani?

A

Nerve that carries taste fibres from the anterior two-thirds of the tongue and preganglionic fibres destined for the submandibular ganglion

118
Q

Where does the facial nerve pass after exiting the skull?

A

Into the parotid gland, where there is further branching and anastomosing of the nerved

119
Q

Where are the 5 terminal branches of the facial nerve that emerge from the upper, anterior and lower border of the parotid gland?

A
  • Temporal
  • Zygomatic
  • Buccal
  • Marginal Mandibular
  • Cervical
120
Q

What does the vestibulocochlear nerve carry fibres for?

A

Special afferent fibres for hearing and balance

121
Q

What are the two divisions of the vestibulocochlear nerve?

A
  • Vestibular component -> balance

- Cochlear component -> hearing

122
Q

Where does the vestibulocochlear nerve attach to the brainstem?

A

Lateral surface of the brainstem between the pons and medulla

123
Q

What happens after the vestibulocochlear nerve emerges from the internal acoustic meatus?

A

It crosses the posterior cranial fossa and the two divisions combine into the single nerve seen in the posterior cranial fossa and within the substance of the petrous part of the temporal bone.

124
Q

What happens to the vestibular nerve?

A
  • Enlarges to form the vestibular ganglion
  • Divides into superior and inferior parts
  • Distributes to the three semicircular ducts and the utricle and saccule
125
Q

What happens to the cochlear nerve?

A
  • Enters the base of the cochlea and passes upwards through the modiolus
  • Ganglion cells of the cochlear nerve are in the spiral ganglion at the base of the lamina of the modiolus as it winds round the modiolus
  • Branches of the cochlear nerve pass through the lamina of the modiolus to innervate receptors in the spiral organ
126
Q

What is a neoplasm?

A
  • Abnormal mass of tissue
  • Growth is uncoordinated and exceeds that of normal tissues
  • Persists in the same excessive manner after cessation of the stimuli which caused it to start
127
Q

What is the growth pattern of benign tumours?

A
  • Expansive
  • Capsule
  • Localised
128
Q

What is the growth pattern of malignant tumours?

A
  • Infiltrative
  • No capsule
  • Metastasises
129
Q

What is the histology of malignant tumours?

A
  • Loses resemblance to tissue of origin

- Pleomorphism

130
Q

What is the histology of benign tumours?

A
  • Resembles tissue of origin
  • Nuclei normal
  • Uniform cells
131
Q

What are the sequelae of enlarging space occupying regions?

A
  • Brain and spinal cord are enclosed by bone
  • Expansion of their contents by a space-occupying lesion that leads to compression and distortion of the tissues of the CNS
  • Slowly enlarging SOL- atrophy of adjacent brain or spinal tissue
  • Rapid enlargement -> rise in pressure in the affected compartment from the normal level of <15 mmHg and herniation of tissue into adjacent compartment where the pressure is lower
132
Q

What are the clinical signs of early space occupying lesion?

A

Headache, papilloedema and vomiting

133
Q

What are the pathological mechanisms of early space occupying lesions?

A
  • Distortion of meninges and blood vessels (headache)
  • Compression of optic nerve (papilloedema)
  • Disruption of medulla (vomiting)
134
Q

What are the pathological mechanisms of late space occupying lesions?

A
  • Compression of oculomotor nerve (pupillary constriction and then dilation)
  • Traction of abducens nerve (abducens palsy)
  • Compression of posterior cerebral artery (occipital infarction)
  • Compression of cerebral peduncle (hemiparesis)
  • Compression and reduced perfusion of medulla (increased BP, decreased HR, pulmonary oedema)
  • Traction on brainstem arteries (fatal infarction of brainstem/haemorrhage)
135
Q

Which is the most extensive venous sinus, and where does it run?

A

Superior sagittal sinus -> runs in the midline below the bony vault (at the top of the fall cerebri) from front to back and ends where the upper margin of the falx cerebri joins the tentorium cerebelli (a region at which several sinuses come together to form the confluence of sinuses)

136
Q

What does the splitting of dura mater enclose?

A

Venous channels, called intracranial venous sinuses which drain much of the venous blood from the brain

137
Q

Where does most of the blood drain to from the superior sagittal sinus?

A

The right transverse sinus which courses transversely until, in the region of the mastoid process, it turns downwards to become the sigmoid sinus

138
Q

What happens to the sigmoid sinus?

A

It leaves the skull via the jugular foramen to become the right internal jugular vein

139
Q

Where is the inferior sagittal sinus?

A

In the lower margin of the falx cerebelli

140
Q

What do the great cerebral vein and inferior sagittal sinus join to form and where does this vessel run?

A

Straight sinus which runs in the junction between the falx and the tentorium cerebelli

141
Q

What happens to the straight sinus at the confluence of sinuses?

A

It turn to the left as the left transverse sinus, in turn becoming the sigmoid sinus and internal jugular vein on the left side

142
Q

What do the sagittal and sigmoid sinuses receive apart from the small cranial veins from the skull itself?

A

Numerous cerebral veins from the brain

143
Q

Where do the cavernous sinuses lie?

A

On each side of the pituitary gland and the adjacent part of the sphenoid bone

144
Q

What passes through the cavernous sinus, and why is this important?

A
  • Internal carotid artery, the three nerves that supply the eye muscles and the ophthalmic and mandibular branches of the trigeminal nerve
  • Important because among their tributaries are veins from the orbit and the face which act as possible pathways for infection from the outside to the inside of the skull
145
Q

What are consequences of surgery on the vestibulocochlear nerve?

A
  • Vestibulocochlear nerve and facial nerve have a common course in the internal auditory canal
  • Note in close proximity to each other so therefore there is a risk that any surgery carried out on the vestibulocochlear nerve may damage the facial nerve
  • Consequence is facial palsy
146
Q

What is the presentation of facial palsy?

A
  • Weakness of the muscles of facial expression and eye closure
  • Face sags and is drawn across to the opposite side on smiling
  • Voluntary eye closure may not be possible and can produce damage to the conjunctiva and cornea
  • In partial paralysis, the lower face is generally more affected
  • In severe cases, there is often demonstrable loss os taste over the front of the tongue, and intolerance to high-pitched or loud noises
  • May cause mild dysarthria and difficulty eating
147
Q

How can facial palsy caused by a LMN be recognised?

A
  • Patient can’t wrinkle their forehead -> final common pathway to the muscles is destroyed
  • Lesion must be either in the pons, or outside the brainstem
148
Q

How can facial palsy caused by an UMN be recognised?

A
  • Upper facial muscles are partial spared because of alternative pathways in the brainstem
  • Patient can wrinkle their forehead (unless there is a bilateral lesion) and the sagging of the face seen with LMN palsies is less prominent
  • There appear to be different pathways for voluntary and emotional movement
149
Q

What is tarsorrhaphy?

A
  • Surgical procedure in which the eyelids are partial sewn together to narrow the opening
  • May be done to protect the cornea in cases of corneal exposure

Phase 2- HNN (6 decks)

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