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CHHD > Neurology For Dentists > Flashcards

Neurology For Dentists Flashcards

1
Q

Name a few types of common neurological complaints

A 
Headaches/Orofacial pain
Meningitis
Cerebrovascular accidents
Parkinsonism
MS
Epilepsy
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2
Q

What is the most common neurological complaint

A

Headaches (often chronic)

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3
Q

What are headaches usually caused by

A
  • Local Disease (tumour maybe)
  • Vascular Disease
  • Referred Pain
  • Neurological disorders
  • Psychogenic disorders
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4
Q

What are migraines most commonly caused by

A

Intra and extra cranial blood vessels dilatation and inflammation

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5
Q

What are some triggers for migraines

A

Stress, caffeine, alcohol, weather, certain foods (choice/cheese), low blood sugar, bright light, lack of sleep

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6
Q

What are the clinical features of a migraine

A

Headache usually unilateral and throbbing

Associated Sx = nausea, vomiting, photophobia and phonophobia

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7
Q

What management options are there for migraines

A

Avoid the triggers
Acute attacks with triptans
Frequent attacks with B-blocker i.e. propranolol

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8
Q

What are the clinical features of migrainous neuralgia/cluster headaches

A
  • Unilateral pain around the eye, frontal, cheek and temporal area
  • Ipsilateral lacrimation, photophobia, nasal stuffiness and rhinorrhorea
  • Recurrent in separate bouts with daily or almost daily attacks for weeks/months
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9
Q

What are the management options for migrainous neuralgia/ cluster headaches

A
  • High flow oxygen
  • Triptans
  • Verapamil
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10
Q

How does triptans work to reduce migraines

A
  • Releases Serotonin in the brain that reduces inflammation and constricts the blood vessels
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11
Q

What serious conditions can cause a headache

A
  • Acute glaucoma
  • Acute hypertension
  • Brain tumours
  • Giant cell arteritis
  • Meningitis
  • Subarachnoid haemorrhage
  • Subdural or epidural haemorrhages
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12
Q

What are the indicators of seriousness in headaches

A
  • Abrupt, severe/bilateral headache
  • Confusion, neck stiffness, diplopia, weakness/numbness
  • Disruption of normal life and over age of 55
  • Preceded head injury
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13
Q

What are some of the clinical features of giant cell arteritis

A
  • Fever
  • Temporal headache
  • Pain in the jaw and chewing
  • Tenderness of the temporal artery
  • Recurrence in children
  • Worsening after coughing or exertion
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14
Q

What does a strokes onset like

A

Rapidly developing symptoms/signs of loss of focal CNS function - like unilateral weakness in the arm

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15
Q

How long do stroke symptoms last for

A

More than 24 hours or they lead to death

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16
Q

What are the 2 types of stroke

A

Ischaemic

Haemorrhagic

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17
Q

What causes ischaemic stroke (most common)

A

Atheroma formation in the carotid artery or intracerebral artery or an emboli that comes from the heart and travels to the brain and blocks a blood vessel

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18
Q

What causes haemorrhagic stroke

A

Burst blood vessels in the brain

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19
Q

What are the risk factors for a stroke

A
  • Hypertension
  • Diabetes Mellitus
  • Hyperlipidaemia
  • Heart Disease
  • Atrial Fibrillation
  • Excess alcohol
  • Smoking
  • Carotid artery occlusion
  • Polycythaemia vera
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20
Q

What changes in lifestyle factors can be made to reduce the risk of stroke

A
  • Maintain a healthy weight
  • Eat healthily
  • Regular exercise
  • Reduce alcohol intake
  • Stop smoking
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21
Q

What targets of drug treatment can be used to reduce the risk of stroke

A
  • Treat hypertension
  • Treat high cholesterol (diet and statins)
  • Atrial fibrillation (beta blockers and anticoagulants
  • Keep good glycemic control if diabetic
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22
Q

What do the clinical manifestations of a stroke depend on

A

On the vascular territory affected

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23
Q

What are some typical clinical features of stroke

A
  • Facial weakness or numbness
  • Hemiplagia (unilateral leg or arm weakness of both)
  • Speech disturbance
  • Sudden visual deterioration
  • Dysphagia
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24
Q

What investigations would be done if you suspect a stroke

A
  • Assess the patients risk factors - hypertension and ECG, smoking, drinking etc.
  • CT head scan to distinguish ischaemic and haemorrhagic and other differentials like tumours or hematomas
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25
Q

How does a haemorrhage appear in a CT scan

A

Dense and white

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26
Q

How does ischaemia appear in a CT scan

A

Darker

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27
Q

What treatments are there for stroke

A
  • Admission to a stroke unit for rapid clinical assessment
  • Aspirin (300mg) should be given as soon as possible after the onset of stroke symptoms once a diagnosis of primary haemorrhage has been excluded
  • Thrombolysis (intravenous tissue plasminogen activator) - eligible for ischaemic stroke and ineligible for haemorrhagic stroke - risk of haemorrhage
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28
Q

How fast should treatment be given after the onset of stroke symptoms

A

4 hours

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29
Q

What are the dental aspects of treating someone who has had a stroke in the past

A
  • Impaired mobility and communication - speak slower and simply
  • Oral hygiene deterioration on paralysed side - suggest electric toothbrush or manual with adapted holder
  • Modifications during dental treatment- treatment in upright position and good suction to prevent foreign objects from entering the pharynx
  • Monitor BP and anticoagulation status
30
Q

What is a Transient Ischaemic Attack (TIAs)

A

Mini strokes commonly caused by thromboembolism from an atheroma in the carotid vessels

31
Q

What symptoms of Transient Ischaemic Attacks (TIAs) are there

A

Sudden loss of focal CNS function
Speeh disturbance
Weakness and numbness in limbs

32
Q

How long do the clinical manifestations of Transient Ischaemic Attacks last for

A

Minutes/hours that fully resolve within 24 hours

33
Q

What are some risk factors for Transient Ischaemic Attacks (TIAs)

A
  • Smoking/alcohol
  • Hypercholesterolaemia
  • Atrial fibrillation/valvular disease
  • Hypertension
  • Diabetes Mellitus
34
Q

What are some preventative measures for Transient Ischaemic Attacks (TIAs)

A
  • Stop drinking/smoking
  • Reduce cholesterol by diet or drugs (statins)
  • Anticoagulant (warfarin, NOAC)
  • Antiplatelet (aspirin, clopidogrel)
  • Treat hypertension
  • Keep blood sugar under control
35
Q

What does Parkinson’s disease affect the most

A

The substantia nigra of the basal ganglia where dopamine is the neurotransmitter

36
Q

What is Parkinson’s caused by

A

Gradual and progressive death of neutrons in the substantial nigra - loss of dopamine leads to less stimulation of the motor cortex and slower onset of movements

37
Q

When do symptoms for Parkinson’s appear

A

When 60-80% of dopaminergic neurones are lost

38
Q

What does the substantia nigra normally do

A

Sends dopamine releasing signals to the cordic nucleus? basal ganglia and this sends signals to the motor cortex and neurones to do movement

39
Q

What are the clinical features of Parkinson’s

A 
Akinesia:
- Bradykinesia
- Poverty of facial expression
- Difficulty changing position
- Quiet monotonous speech
Gait:
- Flexed or stooped posture
- Reduced arm swing on walking
- Postural instability 
Tremor/Rigidity
40
Q

How does dopamine replacement therapy work for Parkinson’s

A

L-Dopa + Carbidopa = Co-careldopa

L-Dopa is broken down into Dopamine and travels in a vesicle to the synapse where dopamine is released and will bind to receptors and stimulate motor cortex to move

41
Q

How does dopamine agonist therapy work for Parkinson’s, include named examples

A

Bromocriptine, Pergolide, Ropinirole

These binds directly to the dopamine receptors

42
Q

What does selegiline do to treat parkinson’s

A

Inhibits dopamine metabolism by inhibiting monoamine oxidase type B

43
Q

What does entacapone do to treat parkinson’s

A

Inhibits Dopamine and L-dopa breakdown by inhibiting Cathechol-O-methyl transferase

44
Q

Name some anticholinergic drugs and how they help to treat Parkinson’s

A

Procyclidine and benzotropine

These reduce tremors at rest but have side effects like dry mouth

45
Q

Why can’t L-dopa be given alone

A

As 97%+ will only be present in the peripheral circulation and can’t enter the brain and this will cause a lot of side effects like nausea, vomiting, arrhythmia and postural hypertension

46
Q

Why do we give carbidopa along with L-dopa for dopamine replacement

A

It inhibits the DOPA decarboxylase enzyme so less Dopamine is released into the peripheral circulation so less side effects

47
Q

What are the dental aspects relating to Parkinson’s disease

A
  • Lack of expression doesn’t mean lack of reaction or intelligence
  • Minimise anxiety as it increases tremor that may affect the tongue/lip
  • Avoid LA with epinephrine that can interact with L-dopa + Dopa decarboxylase inhibitor and COMT inhibitors
  • Anticholinergic drugs - dry mouth and hallucinations
48
Q

What can be caused by the interaction between epinephrine and L-Dopa + Dopa decarboxylase inhibitor and COMT inhibitors

A

Tachycardia
Arrhythmias
Hypertension

49
Q

Why might you need to protect the airways of a patient with Parkinson’s

A

They may have dysphagia and trouble swallowing so might need rubber dam or some shit

50
Q

What is multiple sclerosis and who is it common in

A
  • Chronic relapsing neurological disorder affecting young adults, thought to be autoimmune
  • More common in females than males
  • Can develop at any age
  • Usually presents between 20 and 40 years
  • More common in temperate areas than tropical climate
51
Q

What parts of the body are affected by multiple sclerosis

A

Affects the white matter of the brain, spinal cord and optic nerves
- Forms multiple foci of inflammatory demyelination (plaques) and scarring (sclerosis)

52
Q

What are the consequences of multiple sclerosis

A

Reduction in conduction velocity, loss of information conveyed by impulse traffic along various pathways

53
Q

What is the most common form of multiple sclerosis and how does the level of disability develop over time

A

Relapsing-remitting MS

Unpredictable attack that may or may not leave permanent deficits followed by periods of remission

54
Q

What is the 2nd most common form (10-20%) of MS and how does the level of disability develop over time

A

Primary progressive MS

Steady increase in disability without attacks

55
Q

What is the 3rd most common form of MS and how does the level of disability develop over time

A

Secondary progressive MS

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

56
Q

What is the least common form of MS and how does the level of disability develop over time

A

Progressive relapsing MS

Steady decline since onset with super-imposed attacks

57
Q

What are some clinical features of MS

A

Central - Fatigue, depression, unstable mood
Visual - optic nerve inflammation, diplopia
Musculoskeletal - weakness, spasms, ataxia
Bowel - incontinence, diarrhoea or constipation

58
Q

What is done to manage acute relapses of MS

A

High dose corticosteroids e.g. methylprednisolone

59
Q

What drugs can be given to modify the number of relapses

A

Immunosuppressants - azathioprine, methotrexate and cyclophosphamide
Disease Modifying Therapies 0 Beta-interferons, glatiramer, natalizumab and mitoxantrone

60
Q

What can be done to treat the depression, spasms and bladder dysfunction of MS

A

Depression - SSRIs, tricyclics
Spasms - Muscle relaxants - benzodiazepine
Bladder dysfunction - anticholinergic drugs

61
Q

What symptoms are likely manifestations suggestive of advanced MS

A

Trigeminal neuralgia - often bilateral
Facial para/anaesthesia - numbest of lower lip and chin
- Facial Palsy
Abnormal facial or intraoral pain and discomfort
Difficulty swallowing
Lhermitte phenomenon - tingling sensation (arms or legs) on neck flexion

62
Q

What are the dental aspects to consider of MS

A
  • Shorter appointments - unable to keep mouth open for long
  • Treat in morning - fatigue is less pronounced
  • Treat in semi-supine position - respiratory problems
  • Emphasis on preventative care
63
Q

What does motor neurone disease do

A

Leads to progressive paralysis and eventual death, gradually muscles under voluntary control are affected

64
Q

What are the clinical features of Motor neurone disease

A

Limb weakness - usually affects the upper limbs and/or lower limbs
Bulbar onset - Slurred speech, dysphagia, accompanying emotional liability
Respiratory onset - dyspnoea and orthopnoea

65
Q

What’s done to diagnose motor neurone disease

A

Clinical examinations
EMG/nerve conduction studies
CT/MRI brain and spinal cord - excludes other pathologies

66
Q

What can be done to manage motor neurone disease

A
  • No cure
  • Supportive care, MDT + management of symptoms
  • Drug: riluzole - disease modifying efficacy
67
Q

What dental aspects are there relating to motor neurone disease

A
  • Impaired oral hygiene
  • Poor mobility and co-ordination
  • Protection of airway may be impaired
68
Q

What happens to the grey matter in epilepsy

A

Recurrent occasional, sudden, excessive, rapid and local discharges of the nerve cells in grey matter

69
Q

What kind of disorder is epilepsy and what characterises it

A

It is a paroxysmal disorder characterised by intermittent, stereotyped attacks of altered consciousness, motor or sensory function, behaviour or emotion

70
Q

What happens in a grand-mal/tonic clonic seizure and who is this most common in

A

Aura - becomes irritable and loses consciousness
Tonic phase - rigidity
Clonic phase - jerking movements, lots of salivation
Recovery phase - confused and stuff

Common in adults

71
Q

What happens in a petit-mal/absence seizure and who is this most common in

A

Common in children

Presents with repetitive rapid blinking, child stares into space

72
Q

What is status epilepticus

A

Medical emergency where the seizure lasts more than 5 minutes or patient gets 2 or more seizures within 5 minutes with no regain of consciousness

CHHD (27 decks)

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