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Year 2 > HNN Week 3 > Flashcards

HNN Week 3 Flashcards

1
Q

Describe the anatomy and route of the facial nerve through the head and its branches and what fibres they carry/what they innervate:

A
  • the nerve actually carries three types of nerve fibres
    1 - somatic motor fibres: for facial muscles, posterior belly of digastric, stylohyoid and stapedius
    2 - sensory fibres: taste to anterior 2/3 of tongue
    3 - visceral parasympathetic motor supply: gives parasympathetic fibres
  • emerges from junction of pons and medulla as 2 divisions
  • > primary root: larger and innervates facial muscles
  • > intermediate root: has taste, sympathetic and parasympathetic fibres
  • enters skull through internal acoustic meatus and moves anteriorly in temporal bone in this canal for 1cm
  • then enters facial canal (still in temporal bone) and forms geniculate ganglion (the sensory ganglion of the facial nerve where the cell bodies of sensory neurons are)
  • the nerve then gives off three branches while in the facial canal:
    1) greater petrossal nerve - innervates lacrimal gland, exits temporal bone through greater petrossal foramen
    2) chorda tympani nerve - gives taste to anterior 2/3 of tongue, joins with lingual branch of trigeminal also
    3) stapedius nerve - motor supply to stapedius muscle which stabilises the stapes
  • facial nerve exits cranium at stylomastoid foramen, just posterior to the styloid process of the temporal bone
  • various EXTRACRANIAL branches are then given off the facial nerve:
    1 - posterior auricular branch
    2 - nerve to posterior belly of digastric muscle
    3 - nerve to stylohyoid muscle
  • the main trunk of the facial nerve (now all motor) continues anteriorly and inferiorly into the parotid gland and then gives off 5 branch types which innervate facial muscles controlling facial expression
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2
Q

Describe the anatomy and route of the vestibulocochlear nerve through the head and its branches and what fibres they carry/what they innervate:

A
  • function of this nerve is special sensory for hearing and balance
  • emerges from junction of pons and medulla
  • enters cranium via internal acoustic meatus
  • separates into:
  • fibres from the organ of corti in the cochlea leave the cochlea and join forming the cochlear nerve
  • fibres from the saccule, utricle and semi-circular canals uniting in the vestibular ganglion (on the vestibular nerve) and join forming the vestibular nerve
  • the vestibular ganglion contains bipolar neurons that have extensions to the utricle/saccule/semicircular canals
  • the vestibular ganglion is found at the outer part of the internal acoustic meatus
  • the vestibular nerve and cochlear nerve both travel through the internal acoustic meatus (a channel in the petrous part of the temporal bone)
  • the vestibulocochlear nerve then leaves the cranium via internal acoustic meatus and enters the brainstem at the junction of the pons and medulla
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3
Q

What is the innervation of the parotid gland?

A
  • glossopharyngeal nerve, NOT the facial nerve
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4
Q

What is tinnitus?

A
  • perception of sound in the absence of external auditory stimulus
  • hissing/buzzing/roaring sound in ears
  • can be constant/intermittent/unilateral/bilateral
  • caused by: head injury, inflammation, hypertension, atherosclerosis
  • subjective tinnitus = hearing a noise but no cochlear stimulation, due to medications/caffeine
  • objective tinnitus = sound is detectable by another observer, is an actual sound produced by a vascular structure near the ear e.g. turbulent bloodflow
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5
Q

What is vertigo?

A
  • disorder of vestibular function that creates a sense of movement
  • subjective vertigo: person is stationary but feels like surrounding environment is moving
  • objective vertigo: person feels like they are moving but their surrounding environment is stationary
  • patient has unstable gait as disordered vestibular function means balance is affected
  • may have autonomic signs:
  • > lowered BP
  • > tachycardia
  • > excessive sweating
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6
Q

What is Meniere’s disease and its signs/symptoms?

A
  • rare disorder affecting the inner ear
  • distension of the endolymphatic compartment causing a triad of symptoms: vertigo, tinnitus and hearing loss
  • other signs/symptoms: hyperacusis, distorted sound
  • hearing loss presents as 2-3hr long attacks which subside
  • as the disease progresses, hearing loss stops fluctuating and becomes worse, both ears become affected if not previously and there is risk of deafness
  • slightly more common in women and ages 20-60yrs
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7
Q

What is the cause of Meniere’s disease?

A
  • exact cause unclear but thought to be due to pressure changes in the inner ear
  • > increased endolymph production in the cochlear duct between the scala vestibuli and the scala tympani
  • > decreased endolymph absorption
  • > decreased perilymph production in the scala vestibuli (ascending to apex of cochlea) and scala tympani (descending to base of cochlea)
  • trauma
  • infection
  • endocrine disorder
  • usually idiopathic due to a viral injury in the fluid transport system of the inner ear
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8
Q

What are risk factors of Meniere’s disease?

A
  • autoimmunity
  • genetics
  • viral infection
  • chemical imbalances of inner ear fluid (high Na/K)
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9
Q

How can you investigate/diagnose Meniere’e disease?

A
  • audiogram (patient listens to transmitted sound and presses button when they hear it and results plotted on graph)
  • X-ray of temporal bone (petrous pyramid radiograph)
  • administration of hyperosmolar substances (glycerine/urea) can provide temporary hearing improvement = sign of meniere’s disease
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10
Q

How is meniere’s disease managed and treated?

A
  • symptomatic control
  • Aim is to reduce distension in the endolymphatic space either medically or surgically
    MEDICALLY:
  • suppressant drugs (prochlorperazone/diazepam) act centrally to decrease activity of vestibular system
  • diuretics reduce fluid endolymph volume
  • low Na diet
  • steroid hormones (prednisolone) - maintain satisfactory hearing and reduce dizziness

SURGERY:
- create endolymphatic shunt to drain XS endolymph from the inner ear and into the subarachnoid space/mastoid

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11
Q

What is another name for a Schwannoma?

A

Neurofibroma

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12
Q

What is a Schwannoma?

A
  • solid, benign tumour arises from Schwann cells in the cerebellopontine angle (structure at margin of pons and cerebellum)
  • grows on nerve sheath of 8th CN
  • tumour can enlarge and cause compression of cranial nerves 7 and 8 and obstructive hydrocephalus may be a complication
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13
Q

What is the cause of a Schwannoma?

A
  • tumour grows due to TSG abnormalities on chromosome p22 (abnormalities with the merlin/schwannomin protein)
  • is mostly sporadic without a known cause
  • there is a familial autosomal dominant form where patients have bilateral tumours and other intracranial tumours
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14
Q

What are signs and symptoms of a Schwannoma?

A
  • assymetrical hearing loss
  • facial numbness
  • progressively common episodes of hearing loss
  • tinnitus
  • vertigo
  • difficulty localising sounds
  • headache
  • hydrocephalus
  • reduced taste
  • slower blink
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15
Q

What is the pathophysiology of a Schwannoma?

A
  • tumour grows around the CN8 (vestibulocochlear nerve)
  • degree of hearing loss unrelated to size of tumour
  • minimal symptoms initially as the tumour is slow growing (2-3mm/year) and the brain can compensate
  • other nerves may become affected as the tumour enlarges (especially facial nerve function)
  • large masses can compress the 4th ventricle (as it is posterior to the pons) and cause hydrocephalus
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16
Q

How can you investigate a Schwannoma?

A
  • audiogram
  • MRI/CT
  • Gadolinium enhanced MRI
  • Biopsy
  • PET scans (useful for looking at primary tumour and any metastases)
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17
Q

How can you treat a Schwannoma non-surgically?

A
  • monitoring only (if patient is older and there are risks associated with surgery)
  • stereotactic radiosurgery = highly targeted radiation, if surgery is not an option
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18
Q

How do you treat a Schwannoma surgically?

A

3 goals of surgery are:

  • remove tumour
  • maintain facial nerve
  • preserve hearing on the affected side

tumour can be approached from 3 sites:
1) suboccipital retrosigmoid approach (most versatile)
2) middle fossa
3) translabyrinthine
the choice of which depends on the size and severity of the tumour

Suboccipital retrosigmoid approach:

  • portion of occipital bone behind the ear is removed
  • during the surgery an audiologist attaches an electrode to the face/ear to monitor facial nerve and brainstem during the surgery to prevent damage
  • complications commonly arise as the CN7 and CN8 have a common course through the internal auditory meatus and are in close proximity
  • removal of posterior wall of internal auditory canal
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19
Q

What is a common side effect of the suboccipital retrosigmoid approach to remove a schwannoma?

A

Facial palsy

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20
Q

What are the clinical features of facial palsy?

A
  • temporary weakness or paralysis of the muscles in one side of the face
  • due to compression/swelling/damage of the facial nerve
  • muscles for facial expression and eye closure are weak
  • face sags and is drawn to the opposite side on smiling
  • voluntary closure of eye not possible
  • dysarthia
  • loss of taste over anterior 2/3 of tongue
  • there is a difference in the paralysis of the face depending on if the cause is an upper motor neuron/lower motor neuron lesion
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21
Q

What is dysarthia?

A

difficult/unclear articulation of linguistically normal speech

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22
Q

How is facial palsy managed?

A
  • most common in 15-60yr olds
  • symptoms tend to improve in 2-3 weeks, but may take up to 9 months for full recovery
  • tarsorrhaphy
  • corticosteroids (prednisolone) to reduce inflammation of CN7 and speed up recovery
  • plastic surgery (cannot restore function but can improve appearance)
  • Botulinum toxin injection (to relax tight facial muscles)
  • acupuncture
  • physiotherapy (relaxation techniques and relaxation of facial muscles)
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23
Q

What are the facial signs of a lower motor neuron lesion?

A
  • forehead cannot be wrinkled as the final common pathway to the muscles is destroyed
  • the lesion is either in the pons or outside the brainstem
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24
Q

What are the facial signs of an upper motor neuron lesion?

A
  • upper facial muscles are partially spared due to alternative pathways in the brainstem
  • facial sagging less prominent
  • forehead CAN wrinkle
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25
Q

What is tarsorrhapy and why is it carried out?

A
  • surgical procedure where eyelids are partially sewn together to narrow opening of the eye
  • is done if blinking control is damaged to prevent the cornea drying out and becoming damaged
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26
Q

What is CN1 and how do you test its function?

A

Olfactory - sensory, for smell

- test ability to smell with coffee/cinnamon etc.

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27
Q

What is CN2 and how do you test its function?

A

Optic - sensory, for vision

  • visual acuity with letters
  • colour vision
  • pupillary reflexes
  • peripheral fields and blind spot
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28
Q

What is CN3 and how do you test its function?

A

Occulomotor - motor, pupil constriction (sphincter pupillae), eyeball (superior and inferior rectus, inferior and medial oblique) and eyelid movement (levator palpabrae superioris muscle)
- look in H shape to check all eye movements, horizontal and vertical planes

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29
Q

What is CN4 and how do you test its function?

A

Trochlear - motor, superior oblique muscle

- eye movements

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30
Q

What is CN5 and how do you test its function?

A

Trigeminal - both, sensory supply to face and motor supply to muscles of mastication
- test facial sensation with cotton wool, pin and feel side of face for temporalis, masseter and move jaw side to side

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31
Q

What is CN6 and how do you test its function?

A

Abducens - motor, lateral rectus muscle

- eye movements

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32
Q

What is CN7 and how do you test its function?

A

Facial - both, muscle of facial expression, taste anterior 2/3 tongue, salivary and lacrimal secretions, sensory of external ear
- facial expression tests

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33
Q

What is CN8 and how do you test its function?

A

Vestibulocochlear - sensory, hearing and balance

1) Rinne’s test - to prove air conducts sound better than bone, vibrating tuning fork placed on mastoid process until sound can no longer be heard, and then hold fork outside the ear and sound should be heard
2) Weber’s test - vibrating tuning fork placed on centre of forehead and subject asked if one side is louder than the other

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34
Q

What is CN9 and how do you test its function?

A

Glossopharyngeal - both: sensory - posterior 1/3 tongue and carotid body and sinus, motor - swallowing, speech and saliva from parotid
- test by asking subject to say ‘aahh’

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35
Q

What is CN10 and how do you test its function?

A

Vagus - both: motor - swallowing and speech, Provides motor innervation to the majority of the muscles of the pharynx, soft palate and larynx.

parasympathetic innervation - Innervates the smooth muscle of the trachea, bronchi and gastro-intestinal tract and regulates heart rhythm

sensory - Innervates the skin of the external acoustic meatus and the internal surfaces of the laryngopharynx and larynx. Provides visceral sensation to the heart and abdominal viscera.

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36
Q

What is CN11 and how do you test its function?

A

Spinal accessory - motor

  • sternocleidomastoid and trapezius muscle
  • move head to test sternocleidomastoid
  • lift shoulders against resistance to test strength of trapezius muscle
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37
Q

What is CN12 and how do you test its function?

A

Hypoglossal - motor

  • tongue movement
  • ask subject to protrude tongue and if there is nerve damage, it will move to the injured nerve side (as there is no muscle opposition)
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38
Q

What is the function of the frontal lobe?

A

reasoning, behaviour and mood

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39
Q

What is the function of the parietal lobe?

A

sensory pathways

40
Q

What is the function of the occipital lobe?

A

sight

41
Q

What is the function of the temporal lobe?

A

hearing, memory in the hipocampus

42
Q

Describe the arterial supply of the brain:

A
  • internal carotid arteries and vertebral arteries lie in the subarachnoid space
    INTERNAL CAROTIDS
  • enter cranial cavity through carotid canal in the temporal bone
  • has two terminal branches (anterior cerebral artery and middle cerebral artery)
  • both anterior cerebral arteries are connected by an anterior communicating artery
    VERTEBRAL ARTERIES:
  • ascend in the neck and join forming the basilar artery
  • the basilar artery enters through the pons and divides into 2 posterior cerebral arteries
43
Q

Describe the venous drainage of the brain:

A
  • cerebral and cerebellar veins drain into venous sinuses
44
Q

In which cerebral artery are strokes most common?

A

Middle cerebral artery

45
Q

What parts of the brain do the anterior cerebral arteries supply?

A

frontal lobe

superior and medial brain surfaces

46
Q

What parts of the brain do the middle cerebral arteries supply?

A

temporal lobe

lateral brain surfaces

47
Q

What parts of the brain do the posterior cerebral arteries supply?

A

occipital lobe

inferior brain surfaces

48
Q

What is the difference between primary and secondary brain injuries?

A

primary - caused by direct impact

  • > diffuse axonal injury
  • > contusions
  • > haemorrhage
  • > lacerations

secondary - often diffuse or as a result of the primary injury

  • > infection
  • > concussion
  • > hypoxia
  • > chemical/free radical injury
49
Q

Describe diffuse axonal injury:

A
  • shearing of fragile axons due to acceleration/deceleration forces at the time of trauma
  • microscopic findings show axon swelling
  • common in white matter of hemishperes, upper brain stem and corpus callosum
  • there tends to be 2 categories of forces involved:
    1) contact as there is a momental impact
    2) inertial - as there is acceleration of the brain linearlly and rotationall after the impact
  • can cause cerebral impairment ranging from confusion -> coma -> death
  • diagnosed by immediate onset of unconsciousness and no intracranial lesion seen on scan
50
Q

Describe haemorrhage and haematoma:

A
  • haemorrhage can lead to haematoma formation

HAEMORRHAGE TYPES:

  • extradural
  • subdural
  • intracerebral
51
Q

Describe an extradural haemorrhage:

A

EXTRADURAL HAEMATOMA:

  • between inner side of skull and dura
  • usually due to tearing of middle meningeal artery
  • associated with SKULL FRACTURE
  • common in young as the dura is less fixed
  • presents with history of head trauma and unconsciousness, and then lucid period with temporary improvement followed by deterioration and unconsciousness
  • haematoma compresses brain structures -> increased intracranial pressure -> death
52
Q

Describe an subdural haemorrhage:

A

SUBDURAL HAEMATOMA:
- more common in elderly as the brain shrinks away from the dura and the bridging veins become more fragile
- due to tearing of small bridging veins that connect the veins on the surface of the cortex into dural sinuses (these veins pass from pial vessels through arachnoid space, through arachnoid and dura mater and empty into intradural spaces)
- is a slower developing haematoma as bleeding is venous (rather than extradural)
- fibroblastic activity causes the haematoma to become capsulated
- fluid in the encapsulated area has high osmotic pressure and draws in fluid from the surrounding subarachnoid space = mass expands and exerts pressure on surrounding cranial areas
Classifications:
a) acute = haematoma symptoms seen within 24hrs injury
b) subacute = symptoms appear in 2-10 days after initial trauma
c) chronic = symptoms do not arise until several weeks after initial trauma

53
Q

Describe an intracerebral haemorrhage:

A
  • can occur in any brain lobe but mainly the frontal and temporal lobes due to the bony prominences on the inner skull
  • common in elderly/alcoholics where their cerebral vessels are weaker
54
Q

How can herniation of the brain occur and what are the two main herniation categories?

A
  • brain is supported by the skull and 2 supporting non-expandable septa (falx cerebri and tentorium cerebelli) which divide the brain into compartments
  • large semi-circular opening in the tentorium cerebelli called tentorial notch where brainstem and blood vessels pass through
  • > supratentorial herniation: happen above tentorium cerebelli
  • > infratentorial herniation: happen below tentorium cerebelli
55
Q

Describe supratentorial herniations:

A

1) CINGULATE
- displacement of the cingulate gyrus (area out from the corpus callosum) and hemisphere tissue to the opposite side of the falx cerebri
- can cause ISCHAEMIA due to compression of cerebral arteries

2) TRANSTENTORIAL
- causes CENTRAL and UNCAL syndromes
a) CENTRAL
- downwards displacement of cerebral hemispheres, basal ganglia, diencephalon and midbrain through tentorial notch
- SMALL REACTIVE PUPILS and DROWSY

b) UNCAL
- medial part of temporal lobe called UNCUS is pushed towards the tentorium and puts pressure on the midbrain of the brainstem
- CN3 may get caught (which normally controls pupil constriction) therefore pupils dilated
- midbrain compressed = unconsciousness and coma

56
Q

Describe intratentorial herniation:

A
  • increased ICP in infratentorial compartment
  • herniation can be upwards or downwards

UPWARDS DISPLACEMENT
- cerebral aqueduct blocked = hydrocephalus and coma

DOWNWARDS DISPLACEMENT

  • midbrain pushed through tentorial notch
  • cerebellum pushed through foramen magnum
  • normally results in death as lower brainstem centres are involved in compression and they control vital cardiopulmonary function
57
Q

Describe brain contusions:

A
  • bruising due to bleeding of the brain from direct force, depressed skull fracture or closed acceleration/deceleration injury
  • contusions are normally found along the rough inner surfaces of the brain in a closed injury
58
Q

Describe hypoxia of the brain:

A
  • deprivation of O2 with maintained blood flow e.g. in anaemia, decreased atmospheric pressure, CO poisoning or failure of the lungs to oxygenate blood
  • fairly well tolerated as neurons are capable of substantial anaerobic metabolism and normally patient gets symptoms of drowsiness
  • severe hypoxia = cardiac arrest and ischaemia
59
Q

Describe ischaemia of the brain:

A
  • conditions where there is low bloodflow and therefore a lack of O2
  • can be
    a) focal e.g. stroke
    b) global e.g. due to cardiac arrest
  • prolonged ischaemia = infarction of brain tissue
  • location and extent of damage depends on brain collateral bloodflow
  • watershed areas = at borders of areas supplied by major cerebral arteries) are vulnerable and ischaemia can occur here producing focal neurological deficits and can cause a spectrum of neurological disorders
  • injury from ischaemia is irreversible
60
Q

Describe chemical injury on the brain:

A
  • inappropriate release of excitatory amino acid neurotransmitters like glutamate can cause neuron injury
  • prolonged ischaemia -> metabolic depletion of ATP -> inapproproate glutamate release -> XS Ca ion influx through glutamate gated NMDA channels -> calcium cascade
  • the calcium cascade initiated cell damage by causing protein breakdown and free radical formation
  • DNA fragmentation and mitochondrial injury also occur = eventually cell death
61
Q

What is the difference between communicating and non-communicating hydrocephalus?

A 
Communicating = impaired CSF absorption from subarachnoid space into the venous system
Non-communicating = an obstruction in the ventricular system prevents CSF reaching the subarachnoid villi
62
Q

Describe the importance of maintaining ICP (intracranial pressure) and how it is determined:

A
  • contents of cranial cavity are 80% brain tissue, 10% CSF and 10% blood
  • each of these three compartments contributes to maintenance of normal ICP = 0-15mmHg
  • the volumes of the three compartments must be balances and tissue cannot compensate well
    Factors determining ICP:
    1) Monro-Kellie hypothesis: a change in one of the three compartments must be balanced by the other
    -> CSF can be absorbed
    -> a degree of venous compression can occur as most blood in the venous system of the brain is at low pressure
  • the brain tissue itself has poor compliance and a poor ability to buffer changes in ICV
  • once the compensatory mechanisms of the CSF and blood reach their limits, any further increase of ICP can alter brain function
63
Q

What is cerebral perfusion pressure?

A

CPP = the difference between mean arterial pressure (MAP) and intracranial pressure (ICP)

  • it is the net pressure gradient that causes cerebral blood flow
  • CPP must be maintained within narrow limits as too low (ischaemia) and too high (increased intracranial pressure)
64
Q

Describe usage of the Glasgow Coma Scale (GCS) and its different components:

A
  • used as a diagnostic tool to determine and record the degree of someone’s coma
  • the test has three components and scores from each are added to produce a score between 15 (the best possible score) or 3 (worst possible score)
Eye opening:
4 = spontaneous
3 = on calling
2 = on pain
1 = none
Motor response:
6 = obeyes commands
5 = localises pain
4 = normal flexion
3 = abnormal flexion
2 = extension
1 = none (flaccid)
Verbal response:
5 = orientated
4 = confused conversation
3 = inappropriate words
2 = incomprehensible sounds
1 = none
65
Q 
Describe the GCS results of a 
a) minor TBI
b) moderate TBI
c) severe TBI
and therefore the % mortality of patients in these categories.
A

a) 13-15 = 0.1% mortality
b) 9-12 = 10% mortality
c) <9 = 40% mortality

66
Q

What is plasticity?

A

Umbrella term describing lasting change to an individuals brain throughout their life. Tissue that has been partially (not fully) damaged has the potential to partially recover.

67
Q

Describe the regeneration potential of the brain:

A
  • CNS neurons have limited regeneration capacity compared to PNS neurons
  • oligodendrocytes synthesise glycoproteins which inhibit axon growth
  • there can be substantial recovery after a TBI as partly damaged tissue can recover
  • there can also be ADAPTATION of uninjured tissue in the brain to undertake some of the functions of the damaged tissue
68
Q

Describe the examinations and diagnostic tests you would use to diagnose a TBI:

A

1) history:
- details of the traumatic incident
- mechanism of injury
- drug/alcohol use
- PMH
- medications
- age

2) physical examinations
- head and neck
- cardiovascular status
- respiratory status

3) GCS and pupillary examinations

4) lab investigations
- > FBC
- > serum electrolytes and urea
- > urine analysis
- > blood analysis (toxicity/alcohol)

5) Imaging
- > CT (fastest)
- > if a skull fracture is suspected, do not bother carrying out an X-ray but take a CT straight away as there is a very high risk of intracranial trauma, which you examine for using CT anyway

69
Q

Describe the management and treatment of TBI:

A

IMMEDIATE

  • Airway
  • Breathing
  • Circulation
  • Disability/neurological status
  • Exposure
  • assisted ventilation, adequate O2 supply
  • protect cervical spine to prevent further injury

MANAGE SECONDARY COMPLICATIONS

  • intracranial haematoma needs to be surgically removed
  • induced coma (as after a TBI metabolism in the brain has been significantly altered and some areas of the brain may have inadequate blood flow, so by reducing brain activity and the amount of energy that different areas of the brain needs it can help reduce swelling and at risk areas can be protected
  • antibiotics given to prevent meningitis
  • mannitol (diuretic) is given to reduce the viscosity of the blood and relive raised ICP
  • steroids given to reduce inflammation

REHABILITATION

  • skilled, prolonged energetic support
  • special rehabilitation units
  • use of the MDT
70
Q

What are the important impacts of a TBI on a patient and their family?

A 
Cognitive issues
- amnesia
- neglect
- disordered attention and motivation
Behavioural and cognitive issues
- grief
- depression
- temperature dyscontrol
Incomplete recovery
- paralysis
- hemiparesis
  • post-traumatic epilepsy
  • hydrocephalus
  • punch-drunk syndrome
  • carers
  • financial issues
  • stress on entire family
  • long periods of unknowning and poor prognosis
71
Q

What is punch-drunk syndrome?

A
  • repeated head injury and concussions causes a type of cognitive impairment typically seen in boxers characterised by:
  • lower limb weakness
  • gait unsteadiness
  • slow muscular movements
  • hand tremors
  • speech hesitancy
72
Q

What is central cord syndrome?

A
  • typically in older patients
  • hyperextension injury after banging head
  • cord is compressed
  • > anteriorly by osteophytes
  • > posteriorly by ligamentum flavum
73
Q

What is anterior cord syndrome?

A
  • most common spinal cord infarction
  • where the anterior spinal artery that supplies blood to the anterior portion of the spinal cord is interrupted and there is ischaemia of anterior 2/3 of spinal cord and possibly medula
74
Q

What is posterior cord syndrome?

A

due to interruption of posterior spinal artery

75
Q

What is Brown-Sequard syndrome?

A
  • hemi-section of the spinal cord is injured due to
  • > penetrating stab wound
  • > gunshot wound
  • there is paralysis on the affected side (as corticospinal tract mostly decussates in the medulla)
  • loss of proprioception and fine discrimination on the affected side
  • loss of sensation of pain and temperature on the OPPOSITE SIDE as the spinothalamic tract decussates at the level of the spinal cord
76
Q

What is cauda equina syndrome?

A
  • due to bony protrusion/dics protrusion in the lumbar or sacral region
  • signs:
  • > non-specific lower back pain
  • > bowel and bladder dynfunction
  • > leg numbness and weakness
  • > saddle paraesthesia (tingling and numbness in the lower groin and buttock regions)
77
Q

What is the typical triad of presenting features in neurogenic shock?

A

Due to the body’s sudden loss of sympathetic control after a spinal injury to T6 or above

  • hypotension (no vascular tone in blood vessels)
  • bradycardia (no sympathetic input to keep HR up)
  • hypothermia (no shivering and dilation of blood vessels so heat escapes)
78
Q

What can be used to treat sexual and fertility impairment in

a) males
b) females after a SCI?

A

a) - viagra
- cialis
(both treat erectile dysfucnction once a man is sexually aroused)
- electro-ejaculation

b) assisted conception and pregnancy

79
Q

Can concussion get diagnosed?

A

No, it is a clinical opinion but always be safe and cautious and do not allow sports players to continue playing if you suspect concussion as this can worsen their injury/there could be a serious underlying injury

80
Q

What are the immediate consequences to the patient of a TBI?

A
  • headache
  • difficulty thinking
  • memory issues
  • mood swings
  • attention deficit
81
Q

What are the long term consequences to the patient of a TBI?

A
  • limited limb function
  • abnormal speech and language
  • loss of thinking ability
  • emotional problems
82
Q

What is a ‘sensory unit’?

A

A single sensory nerve fibre and the receptors with which it is connected

83
Q

What is a receptive field?

A

The area in which a sensory nerve picks up stimulation

84
Q

Define the term ‘brain stem’:

A

The brain stem controls more vital functions than any other equivalent volume of the nervous system.
Anatomical components of the brain stem are: medulla, pons and midbrain (cerebellum is not included)

85
Q

Describe the bones that make up the cranial cavity:

A

See colouring book page 2-2 and 2-3

86
Q

Where does CN1 leave the cranial cavity?

A

Olfactory nerve bundles leave through the foramina of the cribriform plate

87
Q

Where does CN2 leave the cranial cavity?

A

optic canal

88
Q

Where does CN3 leave the cranial cavity?

A

superior orbital fissure

89
Q

Where does CN4 leave the cranial cavity?

A

superior orbital fissure

90
Q

Where does CN5 leave the cranial cavity?

A

V1 (ophthalmic nerve) = superior orbital fissure
V2 (maxillary nerve) = foramen rotundum
V3 (mandibular nerve) = foramen ovale

91
Q

Where does CN6 leave the cranial cavity?

A

superior orbital fissure

92
Q

Where does CN7 leave the cranial cavity?

A

Internal acoustic meatus

93
Q

Where does CN8 leave the cranial cavity?

A

Internal acoustic meatus

94
Q

Where does CN9 leave the cranial cavity?

A

Jugular foramen

95
Q

Where does CN10 leave the cranial cavity?

A

Jugular foramen

96
Q

Where does CN11 leave the cranial cavity?

A

Jugular foramen

97
Q

Where does CN12 leave the cranial cavity?

A

Hypoglossal canal

Year 2 (22 decks)

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