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BDS2; CHHD > Neurology > Flashcards

Neurology Flashcards

1. Have knowledge and be able to recognise signs and symptoms of neurological conditions 2. Have knowledge of cranial nerves and their associated pathologies 3. Be able to recognise the facial manifestations of neurological conditions 4. Be able to explain the dental relevance of neurological conditions and their management

1
Q

What are the common causes of neurological complaints (9)

A
  1. Headaches/orofacial pain
  2. Meningitis
  3. Cerebrovascular incidents (stokes, TIAs)
  4. Parkinsonism
  5. Multiple sclerosis
  6. Epilepsy
  7. Trigeminal neuralgia
  8. Herpes Zoster
  9. Tumours
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2
Q

What could be the cause of headaches/orofacial pain

A
  1. Local disease; dental disease or tumours in oronasal pharynx
  2. Vascular disease; vasculitis (inflamed temporal arteries causing pain on chewing), migraines
  3. Referred pain
  4. Neurological disorders; facial pain, herpetic neuralgia
  5. Psychogenic disorders; physical illness derived from emotions (e.g. stress causing headaches)
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3
Q

What is the cause of migraines

A

Intra and extra cranial blood vessel dilation and inflammation

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4
Q

What triggers can cause migraines

A
  • stress
  • caffeine, alcohol
  • weather
  • foods; chocolate and cheese
  • low blood sugar
  • bright light
  • lack of sleep
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5
Q

Outline the clinical features of migraines

A

Usually preceded by an aura (warning sign) such as visual symptoms

  • the headache is unilateral and throbbing
  • associated with nausea, vomiting, photophobia and phonophobia
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6
Q

How can migraines be managed

A
  1. Avoiding the triggers
  2. Triptans for acute attacks (stimulates serotonin which reduces inflammation by constricting blood vessels)
  3. B-blockers for recurrent frequent attacks = prophylactic e.g. propranolol
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7
Q

What is migrainous neuralgia/cluster headaches and what are the clinical symptoms

A

Less common than migranes, mainly affecting middle aged men and is characterised by unilateral pain around the eye, frontal, cheek and temporal area

There is ipsilateral lacrimation, photophobia, nasal stuffiness, rhinorrhoea

It happens in recurring separate bouts with daily or almost daily attacks for 4-12 weeks

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8
Q

How can migrainous neuralgia/cluster headaches be managed

A

High flow of oxygen (12-15L/min for 15 mins)

Triptans

Verapamil

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9
Q

How does verapamil work and what are the side effects of this drug

A

It is a Ca2+ channel blocker which prevents the recurrent migrainous neuralgia/cluster headaches

However this causes heart problems such as bradycardia and can also cause gingival hyperplasia

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10
Q

What is acute glaucoma

A

Where the optic nerve is damaged so there is a fluid build up increasing the intraocular pressure - this can lead to loss of vision if it isn’t diagnosed and treated early

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11
Q

What are the serious causes of headaches

A
  1. Acute glaucoma
  2. Acute hypertension
  3. Brain tumours
  4. Giant cell arteritis
  5. Meningitis
  6. Subarachnoid haemorrhage
  7. Subdural or epidural haemorrhage
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12
Q

What is giant cell arteritis

A

Inflammation of the temporal artery due to vasculitis, causing fever, temporal headaches, pain on chewing, lethargy, tender temporal artery and pulsating bulges

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13
Q

What can giant cell arteritis cause and what is used to treat it

A

The inflammation can extend to affect the ophthalmic artery which causes blockage and thus blindness

It is treated with high dose steroids e.g. prednisolone 40-60mg daily for 4 weeks along with aspirin

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14
Q

What is meningitis

A

A life threatening bacterial/viral infection causing inflammation of the meninges which is treated with IV antibiotics and antivirals

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15
Q

What is a subarachnoid haemorrhage

A

It causes stroke due to bleeding occurring on the brain surface (foetal) due to blood vessel rupture and this causes

  • sudden severe headache in occipital area
  • ‘hit in the head with bat’ pain
  • neck stiffness and nausea
  • photophobia and blurred vision
  • stroke like symptoms; slurred speech and weakness in one side of body
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16
Q

What is a subdural or epidural haemorrhage and what is the clinical presentation of this

A

Causes haematoma due to bleeding into the space between the skull and brain - damage to the blood vessel is a result of head injury

This is common in the elderly and those taking blood thinners or with an excessive alcohol intake

It causes

  • headaches
  • nausea
  • confusion
  • drowsiness on one side of face
  • visual disturbance
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17
Q

What are the indicators of a serious headache

A
  • abrupt, severe, bilateral headache
  • confusion, loss of consciousness, convulsions, fever, stiff neck, diplopia, weakness, numbness, dysarthria
  • following a recent sore throat or respiratory infection
  • persistance in someone who was usually headache free
  • preceded by head trauma
  • worsening after coughing, exertion, straining or sudden movement as this indicates an increased intracranial pressure
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18
Q

What is a stroke

A

A syndrome consisting of rapidly developing loss of focal CNS function which last > 24hr ; the two vascular mechanisms causing stroke are

  • ischaemic (embolic/thrombotic) due to atheroma formed in cerebral artery or emboli blocking blood vessels
  • haemorrhagic due to burst blood vessel

A CT scan is needed to distinguish between these two types and to eliminate differentials such as tumours and haematoma

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19
Q

What is the main cause of stoke

A

Atherosclerosis in carotid or intracerebral arteries with consequent thromboembolism

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20
Q

Describe the clinical presentations of stroke

A
  1. Facial weakness or numbness
  2. Hemiplegia = unilateral leg/arm weakness
  3. Speech disturbance
  4. Sudden visual deterioration
  5. Dysphagia
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21
Q

How are strokes treated

A
  • admission to a stroke unit
  • aspirin (300mg) given asap once diagnosis of primary haemorrhage has been excluded
  • thrombolysis (IV tissue plasminogen activator to breakdown the clot in ischaemic stroke)
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22
Q

Why can’t you give aspirin and IV tissue plasminogen activators to patients who have had a haemorrhagic stroke

A

Because it is contraindicated; these drugs will make the haemorrhage worse as they remove clots and so this will kill the patient

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23
Q

What are the dental aspects of patients who have previously had a stroke

A
  1. Impaired mobility and communication; speak slow and clear
  2. Oral hygiene deterioration on paralysed side; use electric toothbrush
  3. Modifications for treatment; upright seat, good suction to prevent objects entering pharynx (due to dysphagia)

BP and INR should be monitored if the patient is on warfarin

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24
Q

What is a transient ischaemic attack

A

The temporary disruption in blood supply to parts of the brain, commonly caused by thromboembolism from an atheroma in the carotid vessel causing sudden loss of focal CNS function which lasts minutes and is fully resolved within 24hrs

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25
Q

What are the risk factors of TIAs and what can be done to control them

A
  1. Smoking and alcohol cessation
  2. Hypercholesterolaemia - statins
  3. Atrial fibrillation/valvular disease - warfarin, NOAC (riveroxiban), aspirin, clopidogrel, dipyridamole
  4. Hypertension reduction
  5. Control diabetes mellitus
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26
Q

What is Parkinson’s disease

A

A degenerative condition affecting the substantia nigra of the basal ganglia where dopamine is the neurotransmitter

It is caused by gradual and progressive death of neurones in the substantia nigra and the loss of dopamine leads to lower stimulation of the motor cortex and slower onset of movements

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27
Q

What are the clinical features of Parkinson’s disease

A

Akinesia = impairment of movements

  • bradykinesia (slow)
  • poverty of facial expression
  • difficulty changing position
  • quiet and monotonous speech

Gait = shuffling

  • flexed or stooped posture
  • reduced arm swing on walking
  • postural instability (recurrent falls)

Tremor/rigidity

28
Q

How can Parkinson’s disease be treated and give examples of drugs for each category

A
  1. Dopamine replacement
    - L-Dopa and carbidopa = Co-careldopa
  2. Dopamine agonist (mimics action of dopamine)
    - Bromocriptine, Pergolide, Ropinirole
  3. Blocks dopamine metabolism
    - Selegiline (MAOB inhibitor)
  4. Inhibitors of Dopamine and L-dopa breakdown
    - Entacapone (COMT inhibitors)
  5. Anticholinergics
    - Procyclidine, Benzotropine = reduce resting tremor but causes dry mouth, flushing and dizziness
29
Q

Why is L-dopa and carbidopa given together as a dopamine replacement treatment for Parkinson’s disease

A

Because carbidopa inhibits the decarboxylase enzyme therefore less L-dopa is broken down to dopamine in the blood stream so there is a decrease in side effects; it allows time for L-dopa to cross the BBB before breakdown into dopamine occurs

30
Q

Outline the dental relevance of Parkinson’s disease

A
  1. Blank expressions and unresponsiveness should be taken as lack of intelligence
  2. Anxiety should be minimised as this can make tremors worse
  3. Avoid local anaesthesia with epinephrine as this can interact with L-dopa + dopa decarboxylase inhibits and COMT inhibitors causing tachycardia, arrhythmias and hypertension
  4. Anticholinergic drugs given for Parkinson’s may cause dry mouth and hallucinations
  5. Patients have compromised resorative care; involuntary movement and drooling
  6. They have worse oral health and incidence of; xerostomia, root caries, dysphagia, drooling and inability to keep good oral hygiene
31
Q

What precautions should be taken when treating a patient with Parkinson’s disease

A
  • appointments when their medications have been taken
  • use rubber dam to protect airway as they have impaired swallowing reflexes
  • chair shouldn’t be reclined >45 and kept upright
  • provide physical support as there is increased risk of falling
32
Q

What is multiple sclerosis

A

Chronic relapsing neurological disorder more common in females 20-40y/o. It is an autoimmune disease in genetically susceptible individuals triggered by environmental agents e.g. EBV

33
Q

What is affected in multiple sclerosis

A

The white matter of the brain, spinal chord and optic nerves

  • multiple foci’s of inflammatory demyelination (plaques) which would normally protect and insulate axons to increase the speed of electrical transmissions
  • scarring (sclerosis)
34
Q

Outline the clinical features of multiple sclerosis

A
  1. Visual = nystagmus, diplopia, optic neuritis (inflammation of optic nerve)
  2. Speech = dysarthria
  3. Central = fatigue, cognitive impairment, depression, unstable mood
  4. Muscloskeletal = weakness, spasms, ataxia
  5. Sensation = pain, hypoesthesias, paraesthesias
  6. Bowel = incontinence, diarrhoea or constipation
  7. Urinary = incntinence or frequency retention
35
Q

What is relapse-remitting multiple sclerosis

A

Unpredictable attacks which may leave permanent deficits followed by periods of remission = most common type

36
Q

What is primary progressive multiple sclerosis

A

Steady increase in disability without attacks = uncommon

37
Q

What is secondary progressive multiple sclerosis

A

Initial relapsing-remitting MS that suddenly begins to decline without periods of remission

38
Q

What is progressive-relapsing multiple sclerosis

A

Steady decline since onset with super-imposed attacks

39
Q

What treatment is given to patients with MS

A

There is no cure but symptoms are managed

  1. Management of acute relapse
    - high dose corticosteroids (methylprednisolone)
  2. Modification of the disease course
    - Azathioprine, Methotrexate, Cyclophosphamide = immunosuppressants
    - Beta-interferons, glatiramer, Natalizumab, Mitoxantrone
  3. Control of symptoms
    - depression = SSRIs and tricyclics
    - spasms = muscle relaxants; benzodiazepine
    - bladder dysfunction = anticholinergic drugs
40
Q

What are the likely dental manifestations that are suggestive of advanced MS

A
  1. Trigeminal neuralgia (facial pain often bilateral)
  2. Facial para/anaesthesia = numb lower lip and chin
  3. Facial palsy
  4. Abnormal facial/intraoral pain and discomfort
  5. Difficulty swallowing
  6. Higher incidence caries, stomatitis, ulceration, candidiasis as a result of xerostomia
  7. Lhermitte phenomenon = tingling sensation in arms and legs on neck flexion (lesion of compression in upper cervical spinal chord)
41
Q

What is motor neurone disease

A

A degenerative condition that affects motor neurones and progressively leads to paralysis and eventual death - gradually muscles under voluntary control are affected and individuals lose strength, ability to speak, eat, move and breath

Cause is unknown but likely genetic, affects males more

42
Q

What are the clinical features of motor neurone disease

A
  1. Limb weakness
  2. Bulbar onset due to problems in brainstem or cerebellum; slurred speech, dysphagia, dysarthria, emotional liability
  3. Respiratory onset; dyspnoea and orthopnoea
43
Q

What is epilepsy

A

Seizures due to local discharges of the nerve cells in grey matter; it is a paroxysmal disorder characterised by intermittent, stereotyped attacks of altered consciousness, motor and sensory function, behaviour or emotion

44
Q

What are the classifications of epilepsy

A

Focal (partial) or generalised

  • Grand-mal or tonic clonic seizures (these have an aura and last <5 mins, adults)
  • Petit mal or absence seizures (children)
  • Status epileptics = uncontrolled series of seizures with no regain of consciousness; >5mins or 2 within 5 mins = medical emergency
45
Q

What precautions should be taken in dentistry when treating an epileptic patient

A
  • use of strong mouth props
  • keep mouth as free as possible from debris
  • ensure minimal equipments in the area around the patient
46
Q

What are the dental side effects of anticonvulsants (taken by patients with epilepsy)

A
  1. Phenytoin
    - gingival hypertrophy
    - folic acid deficiency (as phenytoin inhibits the enzyme involved in its absorption) which leads to macrocytic anaemia
  2. Sodium valproate
    - thrombocytopenia
    - inhibits platelet aggregation
    - increases bleeding tendencies
47
Q

Which drugs are taken for tonic clonic seizures

A
  1. Carbamazepine
  2. Phenytoin
  3. Sodium valporate
  4. Gabapentin

These potentiate hepatic enzyme inducers at therapeutic levels and affects the level of pain medications and sedatives that are required

48
Q

Which drugs are taken for absence seizures

A
  1. Sodium valporate

2. Ethosuximide

49
Q

Which drugs are taken for partial seizures

A
  1. Carbamazepine

2. Sodium valporate

50
Q

Which drugs are commonly used in dentistry that can potentiate anticonvulsants activity and how

A
  1. Aspirin; increases bleeding tendencies by valporate
  2. Azole antifungals; interfere with carbamazepine and phenytoin, increase bleeding with valproate
  3. Metronidazole antibiotic; interferes with phenytoin, increases bleeding with valporate
  4. NSAIDs; increase bleeding tendencies with valproate
51
Q

How should patients with epilepsy be treated during a medical emergency

A

Prevent injury during tonic, clonic and flaccid phases

  • Flaccid = put in recovery position and use suction to remove excess secretions from airways
  • monitor vital signs
  • administer oxygen (15L/min)
  • administer midazolam (buccal/intranasal) during flaccid phase to stop constant seizure activity
  • in Status epileptics call ambulance
52
Q

Describe the clinical presentation of Right CNIII palsy

A

Oculomotor nerve palsy

Right eye = down and outward gaze as there is paralysis of the superior, inferior and medial rectus and the inferior oblique muscles, dilated pupil, and ptosis

Lest eye= normal

53
Q

Describe the clinical presentation of Left CNIV palsy

A

Trochlear nerve palsy

Paralysis of the superior oblique muscle which moves the eye down and outwards; causes double vision on looking down and inwards = vertigo diplopia

54
Q

Describe the clinical presentation of Left CNVI palsy

A

Abducens nerve palsy

Paralysis of the lateral rectus so the eye cannot abduct, causing horizontal diplopia

55
Q

What is Bell’s palsy

A

Acute paralysis of the facial nerve near the stylomastoid foramen (presents as LMN lesion) - it is unilateral and runs in the family and affects CNVII

56
Q

How does Bell’s palsy affect the muscles of facial expression

A

All of the muscles are affected unilaterally because the lesion is occurring in the lower motor neurone; this causes

  • the angle of the mouth to fall
  • weakness of frontalis so can’t raise eyebrows
  • weak eye closure
57
Q

Describe the clinical presentation of Bell’s palsy

A
  1. Pain around jaw/ear prior to paralysis
  2. Unilateral facial paralysis
  3. Hyperacusis (sound sensitive), loss of taste on anterior tongue, changes in salivation
58
Q

How is Bell’s palsy managed

A
  • high dose prednisolone
  • antivirals (acyclovir)
  • protection of the exposed cornea to prevent drying out
59
Q

What is trigeminal neuralgia

A

Severe and sudden pain on one side of face lasting for a few seconds/minutes; paroxysms may occur in quick succession
- most = idiopathic
- some = structural cause e.g. MS or posterior fossa tumour which compresses the nerves
The onset of attacks is provoked by mild stimuli to trigger zones

60
Q

How is trigeminal neuralgia treated

A

Carbamazepine is the first choice

- gabapentin and lamotrigine are additional agents

61
Q

What is herpes zoster infection

A

It lies dormant in dorsal root ganglia cells after the initial chickenpox infection; reactivation results in herpes zoster = shingles

62
Q

Describe the clinical presentation of herpes zoster

A
  • localised pain and itching
  • unilateral vesicular rash affecting a single dermatome which doesn’t cross the midline
  • there is persistent pain post eruption and healing = post-herpetic neuralgia
63
Q

What is herpes zoster treated with

A

It is self-limiting but is also treated with acyclovir (antiviral) especially in those who have a weakened immune system

64
Q

What risk is posed by zoster ophthalmicus

A

Risk of corneal damage leading to blindness

65
Q

What is Hunt syndrome, the clinical presentations and how is it treated

A

VZV infection of facial nerve near the ear

  • lower motor neurone facial palsy
  • rash in vesicles in EAM and hearing loss
  • severe ear pain

It is treated with high dose prednisolone and antiviral aycylovir

BDS2; CHHD (32 decks)

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