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Minor Oral Surgery > Neurological Complications > Flashcards

Neurological Complications Flashcards

1
Q

Neurological complications can be divided into…

A
  • those that occur as a direct result of the procedure itself (IANB or posterior superior alveolar nerve block)
  • those that arise due to toxicity of the agents used
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2
Q

What is the most common neurological complication following an IANB?

A

facial nerve palsy

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3
Q

The facial nerve exits the skull through the …

A

stylomastoid foramen

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4
Q

After leaving the skull, the facial nerve is divided into two main branches. Name them

A
  • temporal
  • cervical
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5
Q

The facial nerve enters the parotid gland. What are the further divisions of the facial nerve that arise here? What is the function of these nerves ?

A
  • temporal
  • zygomatic
  • buccal
  • mandibular
  • cervical

They supply the muscles of facial expression

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6
Q

Before the facial nerve exists the skull, what structure is present ?

A

chorda tympani

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7
Q

Briefly outline the functions of the chorda tympani

A
  • supplies preganglionic secretomotor fibres to submandibular and sublingual glands
  • carries efferent taste fibres from the anterior two thirds of the tongue except for the vallate papillae
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8
Q

What are the clinical signs of a patient with peripheral facial nerve palsy?

A
  • generalised weakness of the ipsilateral side of the face
  • inability to close eyelids
  • obliteration of the nasolabial fold
  • drooping of the corner of the mouth
  • deviation of the mouth to the unaffected side
  • may complain of pain in the retroauricular area
  • may complain of decreased taste sensation
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9
Q

What is bells sign?

A

this is an upward and outward movement of the eye when an attempt to close the eyes is made. The (white) sclera and not the iris is exposed as a result

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10
Q

Facial nerve palsies may be _____ or _____ in origin

A

central or peripheral

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11
Q

Central facial nerve palsies are an indication of …

A

upper motor neuron lesions

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12
Q

What is a classic signs of an upper motor neuron lesion as pertains to facial nerve palsies? Suggest a reason for this

A
  • the muscles of the forehead in the affected area are spared; thus a smooth appearing forehead
  • this is because this area receives innervation from both cerebral hemispheres due to the crossover of fibres in the corticonuclear tracts
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13
Q

Peripheral nerve palsy is an indication of … lesions. What is the clinical implication of these types of facial nerve palsies?

A

lower motor neuron lesions

  • they affect all the muscles of the face e.g. no forehead sparing
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14
Q

Facial nerve palsy following IANB may appear immediately or delayed. True or false

A

true

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15
Q

What is the general recovery time for immediate/transient palsy?

A

within 3 hours of LA administration

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16
Q

What are the postulated causes of immediate/transient palsy?

A
  • anaesthesia of the facial nerve trunk as a result of abnormal anatomy e.g. passage of the nerve along the deep surface of the parotid gland
  • congenital abnormality where the gland fails to envelop the nerve and its divisions thus increasing its exposure to the LA solution
  • capsule of the parotid gland may prevent escape of any LA inadvertently deposited within the gland thus maintaining a high concentration of solution in contact with passing branches of the facial nerve
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17
Q

The current postulated causes of immediate/transient palsy do not account for certain characteristics of the condition. Outline these characteristics

A
  • they do not explain the involvement of the chorda tympani and the associated taste disturbance
  • occurence of facial nerve palsy following posterior superior alveolar nerve block
  • delayed onset of palsy hours after anaesthetics has worn off
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18
Q

Delayed onset facial palsy occurs several hours and in some cases many days after the administration of the anaesthetic. True or false

A

true

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19
Q

Outline the 3 hypotheses that have been put forward to explain delayed-onset facial palsy

A
  • anasthetic solution or its break down products stimulate the sympathetic plexus associated with the external carotid artery : * from the external carotid artery, fibres of this plexus continue in association with the stylomastoid artery as it passes the parotid gland. The stimulation of the stylomastoid sympathetic plexus causes vasa nervorum of the facial nerve leading to ischaemic neuritis and secondary oedema.
  • the mechanical action of the needle itself may lead to stimulation of the sympathetic plexus associated with the external carotid artery
  • reactivation of a latent viral infection due to trauma of the procedure may be responsible for the neural sheath inflammation and subsequent disturbance of function
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20
Q

The stylomastoid artery is a branch of …

A
  • occipital artery (66% of cases)
  • auricular artery (34% of cases)
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21
Q

What is the origin of the fibres of the stylomastoid sympathetic plexus ?

A

superior cervical ganglion

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22
Q

The superior cervical ganglion gives rise to … branches

A

lateral, medial and anterior branches

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23
Q

What branch (originating from the superior cervical ganglion) gives rise to the plexuses that accompany the common and external carotid arteries?

A

the anterior branch

24
Q

What does amaurosis refer to?

A

blindness (vision loss) or weakness that occurs without any apparent weakness to the eye

25
Q

Suggest a possible cause of total body hemiparesis following IANB

A

inadvertent intravascular injection of LA with subsequent retrograde internal movement in branches of the internal carotid artery

26
Q

What does total body hemiparesis comprise of?

A
  • ptosis
  • occipital and neck stiffness
  • anaesthesia of the right side of the face with dysphasia (speech impairment) which leads to complete aphasia and right hemiparesis
27
Q

Total body hemiparesis can be attributed to excess ____ created during the administration of the injection leading to retrograde flow into the internal carotid artery

A

pressure

28
Q

What does barbing refer to?

A

needle tip distortion/deformation

29
Q

Post- injection parasthesia has been atrributed to …

A
  • barbing of the needle which upon withdrawal from the tissues may damage said tissues e.g IAN
30
Q

Suggest other causes of persistent post injection parasthesia

A
  • injection of LA contaminated with sterilizing agents
  • development of haemorrhage or haematoma around the nerve sheath leading to necrosis of the neural tissue
31
Q

What is a sign/symptom of direct IAN trauma ? How can this be managed?

A

Electric shock

practitioner should immediately cease the injection

32
Q

How does Horners syndrome result from LA delivery?

A

penetration of the LA through pharyngeal spaces and prevertebra spaces causing blockade of the stellate ganglion

33
Q

Outline the features of horners syndrome

A
  • flushing of the face on the same side
  • ptosis of the eye
  • vasodilation of the conjuctiva
  • pupillary constriction
  • occasionally a rash over the neck, face, shoulder and arm of the ipsilateral side
34
Q

Horners syndrome with reports of a hoarse voice and difficulty breathing are due the involvement of what nerve ?

A

recurrent laryngeal nerve

(these effects were transient in the case reported)

35
Q

Gow- gates injection where access to the cavernous sinus was gained results in inadvertent intravenous injection. Transient paralysis of cranial nerves has been reported as a result of this. State the cranial nerves

A
  • III (3)
  • IV (4)
  • VI (6)
36
Q

What are the clinical implications of transient paralysis of the cranial nerves following GG technique?

A
  • immobility of the ipsilateral eyeball
  • diplopia
  • ptosis of eyelid
  • dilated pupil (this is in contrast to horners syndrome!)
37
Q

How can complications from GG technique be avoided?

A
  • careful aspiration
  • direction of the needle should be to an area with fewer large bore blood vessels such as the lateral aspect of the condyle
38
Q

Explain how sudden unilateral deafness may occur following LA injection

A
  • the venous systems within the mandible provide access for the anaesthetic to the middle ear
  • the vasoconstrictor results in localised vasospasm of the cochlear division of the internal auditory artery
  • this leads to the dysfunction of the cochlear nerve
39
Q

Outline the route via the posterior superior alveolar artery that leads to peripheral nerve palsy

A

LA injected into the posterior superior alveolar artery is transported via the middle meningeal artery and subsequent petrosal artery branches to the facial nerve

40
Q

What are the signs/symptoms of abducens nerve palsy?

A
  • double vision
  • limitation of abduction of ipsilateral eye
  • parasthesia of lateral side of the upper and lower eyelids
41
Q

Suggest potential causes for abducens nerve palsy

A
  • inadvertent depositon of LA which passes through the inferior orbital fissure to cause direct anaesthesia of abducens nerve
  • LA solution reaches the inferior opthalamic vein via the pterygoid plexus or communicating branches
  • deposition of anaesthetic solution within the posterior superior alveolar artery which causes backflow into connecting maxillary artery and subsequently the middle meningeal artery
  • LA reaches the abducens nerve within the cavernous sinus, arrividing via the infratemporal fossa and pterygoid plexus and its connecting emissary veins passing through the foramen ovale and lacerum
42
Q

Palsy of the lateral rectus recovers well before the effects of the LA has subsided. True or false

A

True

43
Q

Abducens nerve palsy has been postulated to be potentially causes by LA solution passing through the infraorbital fissure. Why is this an unlikely cause?

A

this is because the abducens nerve lies within the common tendinous ring, medial to the lateral rectus muscle and some distance from the potential needle entry point

44
Q

Outline some features of the inferior opthalamic vein

A
  • no valves
  • connects directly to the extrinsic muscles of the eye via the inferior orbital foramen
45
Q

What kind of injection can easily reverse the flow of blood within the inferior opthalamic vein? What is the potential effect of this?

A

Intramluminal injection

predisposition of the muscles to LA solution

46
Q

There is a constant anastomosis between the orbital branch of the opthalamic artery and the …

A

recurrent meningeal divsion of the lacrimal branch of the opthalamic artery

47
Q

What is the cause of temporary blindness following posterior superior alveolar LA delivery?

A

large quantity LA under great pressure diffusing through the inferior orbital fissure and coming into contact with the optic nerve

48
Q

High concentrations of LA in the brain are usually a result of …

A

rapid injection into a blood vessel

(reverse carotid flow?)

49
Q

What type of patients are at risk of toxic accumulation of LA ?

A
  • impaired liver function
  • impaired renal function (for final step of elimination)
50
Q

What are the distinct phases following the build up of LA or its breakdown products in the brain?

A
  • initial CNS stimulation
  • cerebral depression
51
Q

The initial CNS stimulation caused by LA/LA breakdown product build up is marked the following symptoms:

A
  • anxiety
  • restlessness
  • hallucinations to increased depth and rate of respiration
  • gagging
  • vomiting
  • risk of severe cortical stimulation resulting in seizures and convulsions
52
Q

What are the hallmarks of medullary/cerebral depresssion following a build up of LA/LA breakdown products?

A
  • lapse into unconsciousness
  • drop in blood pressure
  • marked reduction in respiratory rate
  • death resulting from repsiratory failure
53
Q

How can you treat convulsions resulting from build up of LA/LA breakdown products ?

A
  • slow IV infusion of 10mg diazepam (over 2 minute period)
  • rectal route can be used if IV access is difficult
54
Q

What is flumazenil ?

A

BZD antagonist

55
Q

How is cerebral depression managed?

A
  • elevation of the foot of the dental chair
  • administration of oxygen and respiratory and circulatory support
  • hospital based treatment- methoxamine hydrochloride
56
Q

What is responsible for psychomotor reactions to LA? What is the implication of this biologically?

A

fear of the injection

  • fear leads to reflex dilation of the splanchnic blood vessels with concomitant cerebral anaemia and hypoxia
  • pallor, cold skin and perspiration + low blood pressure and a rapid but weak pulse
  • convulsive movements may accompany these symptoms

Minor Oral Surgery (36 decks)

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