Neurology for dentistry Flashcards

1
Q

What is Bell’s Palsy?

A

Inflammation or viral inflammation of the facial nerve that causes one sided weakness or the entire face.

Slow onset of symptoms

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2
Q

What is multiple sclerosis?

A

A neuromuscular disorder that results in uncoordinated movement.

It is caused by the damage of myelin sheath on brain/spinal cord.

Occurs over the course of days-weeks relapses an occur.

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3
Q

What is myasthenia gravis?

A

Chronic condition that relapses

It is an autoimmune condition with the production of autoantibodies against Acetylcholine receptors at NMJ, meaning there is less stimulation of muscles by ACh which increases fatiguability of muscles and causes them to be weak.

  • symptoms can include - eyes moving slowly, tongue movement disordered.
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4
Q

Does bells palsy affect lower motor neurones or upper motor neurones?

A

Lower motor neurones (facial nerve)

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5
Q

What is fasciculation?

A

involuntary twitching of muscle fibres

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6
Q

What does damage to an upper motor neurone cause? (muscle tone, weakness, reflexes)

A

Causes an increased in reflex firing as they are no longer under inhibitory control.

Causes an increase in spasticity and pyramidal weakness.

Pyramidal weakness is weak extensors in arms and weak flexors in legs.

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7
Q

What may LMN damage to a nerve which is supplying the tongue cause?

A

Fasciculation
Atrophy
Weakness
Wasting

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8
Q

How can we test for damage in trigeminal (v) cranial nerve?

A

open mouth (control muscles of mastication)

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9
Q

How can we test the function of facial (VII) cranial nerve?

What is the disease called when facial nerve is damaged and what is its effects?

A

Smile (controls muscles of facial expression)

Bells palsy is when VII is damaged and it causes unilateral paralysis of one side of the face.

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10
Q

How can we test the function of the vagus (X) cranial nerve?

A

Cough, swallow (motor to muscles of soft palate).

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11
Q

How can we test the function of the hypoglossal nerve?

A

Move tongue (motor to tongue muscles)

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12
Q

What will happen to someone with damaged trigeminal nerve when they are trying to open their mouth and protrude their jaw?

A

Their jaw will move towards the side where there is a damaged trigeminal nerve as the pterygoid muscles won’t be contracting on the damaged side so the chin will deviate.

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13
Q

What will happen to someone with a damaged vagus nerve when they try to swallow, cough or say ‘aaaa’?

A

Uvula will be pulled up unequally towards the side which is functioning correctly.

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14
Q

What will happen to someone with a damaged hypoglossal nerve when they go to protrude their tongue?

A

It will turn toward the damaged side as there will be no protrusion on that side.

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15
Q

How may we, as dentists, manage pts with myasthenia gravis?

A

Dental treatment early in day when not fatigued.

Do not use procaine antibiotics.

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16
Q

How can we manage a pt with bells palsy as a dentist?

A

Protect eye (eye protection) during dental treatment as can’t move.

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17
Q

How may we manage pts which have had a stroke as a dentist?

A

Stroke may cause dysphagia (TACS) which may cause aspiration risk/drooling.

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18
Q

What is epilepsy?

A

People who are prone to having frequent recurrent seizures.

19
Q

What is the main type of seizure seen in younger people?

A

Generalised seizures

20
Q

What is the main type of seizure seen in older people?

A

focal seizures

21
Q

What are the main two types of focal seizures?

A

Aware (simple) and impaired consciousness (impaired awareness).

22
Q

How do we diagnose epilepsy?

A

Take history, consider differential diagnosis.

MRI brain scan to look for lesions.

EEG (electroencephalogram) - records brain electrical activity.

23
Q

How can we manage epilepsy?

A

If just single seizure - not medicated unless it’s likely there is going to be a recurrent seizure.

Anti-epileptic drugs
- lamotrigine, carbamazepine, valproate.
(choice based on efficacy, tolerability, safety (teratogenic effects, cost).

24
Q

What are some common dental side effects of common anti-epileptic drugs? (valproate, phenytoin, carbamazepine)?

A

valproate = affects platelets which can increase bleeding during procedures.

phenytoin - causes gingival hyperplasia

carbamazepine = causes xerostomia

25
Q

When may neurosurgery be good for patients with epilepsy?

A

When pt is suffering from unstable epilepsy with recurring seizures even whilst receiving medication.

Surgery may be used to remove lesion seen on MRI scan.

26
Q

What are some potential complications of seizures?

A

Accidents/suicide

Status epilepticus
- seizure persisting longer than 5 minutes - need status epilepticus treatment.

Prolonged neuronal activity >30mins may cause irreversible neurological damage and death.

SUDEP - sudden unexpected death in a patient with epilepsy (with no structural or toxic cause)

27
Q

As a dentist what can we do if a pt has seizure in our chair?

A

Call for help

Damage limitation(recover position, pillows to limit fall damage, remove objects)

Oxygen

Look at clock as most seizures will terminate <3 mins

28
Q

What is the pathophysiology of idiopathic Parkinson’s disease?

A

Destruction of dopaminergic neurones of substantia nigra (so no dopamine production)

Causes the basal ganglia to have reduced domaine levels because dopamine in the basal ganglia is responsible for preparing the brain to be in a ready state to allow movement to happen easily and effortlessly.

This causes poverty of motion (bradykinesia) - the body isn’t in a ready state to move quickly so there is more effort required for any given movement.

29
Q

What are some other causes of parkinsons disease apart from ideopathic parkinsons disease?

A

Anti-psychotic drugs (dopamine blockers)

/ Head injury

post encephalitis (inflammation of the CNS may have caused damage to dopaminergic neurones).

30
Q

What are the micro and macro ways we can identify parkinsons disease in the midbrain?

A

Macro:
Reduced melanin pigment in substantia nigra
- dopamine if made from a precursor of melanin. so reduced melanin = reduced dopamine.

Micro:
- degeneration of dopaminergic neurones from the substantia nigra to the basal ganglia.

31
Q

What is the clinical history if iPD?

A

Insidious onset
Resting tremor (pill rolling motion with hands).
Slowness of movement (bradykinesia).
Smaller handwriting ( as hands more effort to move).
insomnia

32
Q

What would we expect to see whilst examining someone with iPD?

A

Pill rolling resting tremor
Rigidity
Bradykinesia

33
Q

What are some non motor signs of iPD?

A

Hyposmia (impaired smell)
Constipation
Sleep disturbance
Depression/dementia (executive dysfunction).

34
Q

How can we investigate & treat iPD?

A

Clinical diagnosis (investigations rule out other diagnosis)

We treat using trials of medications:
initially
- lovodopa + dopa decarboxylase inhibitor (stop breakdown of dopamine)
- dopamine agonists

Advanced therapies
- dopamine directly into duodenum
Continuous s/c apomorphine (which is a dopamine agonist)
Deep brain electrical stimulation of the basal ganglia.

35
Q

How is parkinsons related to dentistry?

A

Dry mouth

Tooth wear due to bradykinesia

Lack of muscular control (may be difficult to brush due to bradykinesia, difficulty with dentures)

Lack of facial expression - need to use limb/eye movement to signal comfortability etc.

36
Q

What affect does dopamine have on the basal ganglia?

A

Increases the readiness potential for the brain for movement allowing for quicker, easier movement.

Normally the pallidum is spontaneously active and other parts of the basal ganglia inhibit the pallidum to allow controlled movement.

Dopamine allows the release of the pallidum from inhibition to allow movement to occur.

37
Q

Name some differential diagnosis for epilepsy

A

Cardiogenic syncope, psychogenic

38
Q

What is the parkinsonism clinical triad?

A

Bradykinesia, resting tremor, rigidity.

39
Q

What is a side effect of tx with dopamine?

A

uncontrolled or excess dopamine can cause dyskensia - uncontrolled movement.

40
Q

Give an example of some drugs to treat parkinsons disease?

A

Lovadopa or dopa decarboxylase inhibitor

Augment effects of existing dopamine (dopamine agonists - apomorphine)

41
Q

What are some advanced therapies to treat dopamine?

A

Dopamine directly into duodenum

Deep brain stimulation

Continuous subcutaneous apomorphine

42
Q

What are some differential diagnosis for parkinsons disease?

A

thyroid

structural brain lesions.

43
Q

What are some differential diagnosis for parkinsons disease?

A

thyroid

structural brain lesions.