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BDS M5 Human Disease > Neurological disease > Flashcards

Neurological disease Flashcards

1
Q

How common is multiple sclerosis?

A
  • 80;100,000
  • most common CNS disorder of the young
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2
Q

What causes multiple sclerosis?

A
  • DEMYELINATION of axons
  • happens due to changes in the myelin sheath around the nerve axons
  • inflammatory change, can be seen in MRI scans
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3
Q

What category of patients with MS have it most severely?

A

women with 4th decade onset most severe

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4
Q

What is the aetiology of multiple sclerosis?

A
  • susceptibility acquired during childhood
  • ? altered host reaction to an infective agent ?
  • background genetic/immune factors
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5
Q

What groups is MS more common in?

A

identical twins and amongst immediate family members

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6
Q

In an MRI of an MS patient, what are the white areas?

A

plaques where there has been damage

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7
Q

In an MRI of an MS patient, what are the red areas?

A

inflammatory processes

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8
Q

What are the symptoms of MS?

A
  • muscle weakness
  • visual disturbance
  • paraesthesia
  • autonomic dysfunction
  • dysarthria
  • pain
  • balance/hearing loss
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9
Q

What are the signs of MS?

A
  • muscle weakness
  • spasticity
  • altered reflexes
  • tremor (intention)
  • optic atrophy
  • proprioceptive loss
  • loss of touch
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10
Q

In MS when does muscle spasticity occur?

A

happens when there is an upper motor neurone lesion

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11
Q

What are the MS investigations?

A
  • history and examination
  • MRI
  • CSF analysis
    • reduced lymphocytes
    • increased IgG protein
  • Visual Evoked Potentials
    • ALWAYS reduced after optic neuritis
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12
Q

When investigating MS what can an MRI show?

A

areas of plaques within the brain where there has been previous damage

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13
Q

What are the 2 types of MS?

A
  • relapsing and remitting
  • primary progressive type
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14
Q

What is relapsing and remitting type MS?

A

acute exacerbating and periods of respite
- damage builds up with each episode
- many will eventually develop progressive form (“secondary progressive”)

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15
Q

What is primary progressive type MS?

A

slow steady progressive deterioration
- cumulative neurological damage

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16
Q

What is the outcome of MS?

A
  • incurable
  • gradual decline
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17
Q

How is MS treated?

A
  • no effective treatment
  • acute exacerbations - steroid treatment
  • symptomatic management
    • antibiotics, antispasmodics, analgesia, physiotherapy and occupational therapy
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18
Q

What can be used to treat relapsing and remitting type MS?

A

Disease modifying therapies (may also slow some progressive forms)
- cladribine
- siponomod
- ocrelizumab

do not reverse damage that has already occurred

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19
Q

What can stem cell transplants be used for in MS?

A

‘reboot’ the immune system

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20
Q

What are the dental aspects of MS?

A
  • limited mobility and psychological disorders
  • treat under LA - GA may hasten onset of damage within the brain
  • orofacial motor and sensory disturbance
  • chronic orofacial pain possible
  • enhanced TRIGEMINAL NEURALGIA risk
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21
Q

What does motor neurone disease cause?

A

degeneration of the motor nerves in anterior horns of the corticospinal tract in the spinal cord

can also effect the motor nuclei in the brain stem, often called the bulbar motor nuclei in the cranial nerves

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22
Q

When do patient’s develop motor neurone disease?

A

30-60yrs

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23
Q

What is the progression of motor neurone disease?

A

unremitting and progressing, most patients die within 3 years of diagnosis

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24
Q

What does the progressive loss of motor function in MND affect?

A
  • limbs
  • intercostal
  • diaphragm
  • motor cranial nerves VII-XII
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25
Q

What is death in MND due to?

A
  • ventilation failure
  • aspiration pneumonia (swallowing/coughing difficulties)
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26
Q

What might the patient notice when they are first developing MND?

A
  • weakness (ankle or leg, tripping, difficulty with stairs)
  • slurred speech (difficulty swallowing)
  • a weak grip
  • muscle cramps and twitches
  • weight loss
  • emotional lability
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27
Q

What is the treatment for MND?

A
  • NONE effective
  • pshyio and occupation therapy aim to maintain function for as long as possible
  • aspiration prevention - PEG tube feeding, reduce saliva
  • Riluzole - some get 6-9 months life extension
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28
Q

What are the dental aspects of MND?

A
  • difficulty in acceptance of dental care - muscle weakness of head and neck
  • realistic treatment planning - short life expectancy
  • drooling and swallowing difficulties
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29
Q

What is Parkinson’s disease due to?

A

lack of neurotransmitter dopamine in the brain

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30
Q

What causes Parkinson’s disease?

A

degeneration fo dopaminergic neurones in the basal ganglia of the substantia nigra leads to difficulty passing messages from the cortex (thinking) to the cerebellum and brain stem (doing)
- can lead to delays in the pt doing or understanding things

underlying cause for this unknown

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31
Q

What are the clinical signs of Parkinson’s disease?

A
  • bradykinesia - slow movement, and slow initiation of movement
  • rigidity - increased muscle tone
  • tremor - slow amplitude (tremor at rest)

can progress to on/off movement disorder after treatment

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32
Q

What are some of the non-motor effects of Parkinson’s disease?

A
  • impaired gait and falls
  • impaired use of upper limbs
  • mask-like face
  • swallowing problems
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33
Q

What are the treatments for Parkinson’s disease?

A

physio and occupational therapy
- work to maintain function at as high a level for as long as possible

medicinal

surgical

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34
Q

What can be one of the issues with Parkinson’s medications?

A

can cause abnormal compulsions and lead to issues with gambling

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35
Q

What medications can be used for the treatment of Parkinson’s disease?

A

dopamine
- levadopa

dopamine analogues
- tablets - promipexole, selegiline
- injection - apomorphine - SC
- infusion - duodopa - directly into the gut

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36
Q

What surgical treatment can be done for Parkinson’s disease?

A

stereotactic surgery - deep brain stimulation

stem cell transplant into substantia nigra?

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37
Q

What are the dental aspects of Parkinson’s disease?

A
  • difficulty accepting treatment
    • tremor at rest
    • often facial tremor reduces on purposeful movements e.g. mouth opening
    • difficulties with cooperation
  • dry mouth - anticholinergic effect of the drugs
  • drug interactions?
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38
Q

What is a stroke?

A

“acute focal neurological deficit resulting from cerebrovascular disease and lasting more than 24hrs or causing earlier death”

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39
Q

What does a stoke cause?

A
  • blockage of blood delivery of oxygen to the brain tissue leading to hypoxia and eventually death of brain tissue
  • infarction of tissue or haemorrhage into the brain tissue can also occur which increases pressure on brain
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40
Q

What are the types of stroke?

A
  • ischaemic stroke or haemorhhagic stroke
  • TIA (transient ischaemic attack)
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41
Q

What is a TIA?

A

Happens when there is a rapid loss of function but then a rapid recovery of function so that the patient within 24hrs has recovered all of the neurological issues which were lost

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42
Q

What do TIAs suggest?

A

issues within the blood vessels, increased risk of proper stroke in the future

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43
Q

What acronym is used to know what to look for when considering a stroke?

A

FAST - facial drooping, arm weakness, speech difficulty, time

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44
Q

What is the incidence of TIA compared to stroke?

A

25% that of stroke

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45
Q

What does a TIA cause?

A

localised loss of brain function, ischaemic event - not haemorrhage

46
Q

What is though to cause TIAs?

A

platelet emboli from vessels in the neck blocking blood flow to brain tissue causing ischaemia, but are rapidly removed and blood flow restored

47
Q

What is the % risk of having a stroke after having a TIA?

A

12% in 1yr

29% in 5yrs

2.4% risk of myocardial infarction

48
Q

What are the risk factors for stroke?

A
  • hypertension
  • smoking
  • alcohol
  • ischaemic heart disease
  • atrial fibrillation
  • diabetes mellitus
49
Q

What is the most common type of stroke?

A

infarction (85%)

50
Q

What is the cause of ischaemic stroke?

A

often unclear, usually to do with narrowing of vessels, plaque formation

51
Q

What causes haemorrhagic stroke?

A

usually the result of small inter cranial bleed such as from a ruptured aneurysm

52
Q

What causes embolic stroke?

A

embolism from the left side of the heart
- atrial fibrillation
- heart valve disease
- recent MI

atheroma of cerebral vessels
- carotid bifurcation
- internal carotid artery
- vertebral artery

53
Q

What are less general causes of stroke?

A

venous thrombosis
- OCP use
- polycythaemia
- thrombophilia

‘borderzone’ infarction
- severe hypotension
- cardiac arrest

vasculitis

54
Q

How can strokes be prevented?

A
  • reduce risk factors
  • antiplatelet action (secondary prevention only)
    • aspirin, dipyridamole, clopidogrel
  • anticoagulants - bellicose risk - AF, LV thrombus
    • warfarin, apixaban
55
Q

When may surgery be used in the prevention of stroke?

A

particularly where the carotid artery is heavily involved, atherosclerosis around the carotid furcation
- in some occasions this is completely excised taking some of the artery away, or only the plaque itself is removed

56
Q

What surgeries may be used in the prevention of stroke?

A
  • carotid endarterectomy
  • preventative neurosurgery
    • aneurysm clips, AV malformation correction
57
Q

Why is it important to differentiate the type of stroke occurring?

A

EARLY information needed to assess treatment options

58
Q

What imaging techniques are used to investigate stroke?

A

imaging
- CT scan
- MRI scan
- Digital Subtraction angiography (DSA)

59
Q

What are the pros and cons of CT scan when investigating stroke?

A
  • rapid, easy access
  • poor for ischaemic stroke
60
Q

What are the pros and cons of MRI scan when investigating stroke?

A
  • difficult to obtain quickly
  • better at visualising early changes of damage
  • MRA (MR angiography) is the best investigation for visualising the brain circulation
61
Q

When is digital subtraction angiography (DSA) used?

A

investigation of stoke if MRA is not available

62
Q

Other than imaging, what is used to investigate stroke?

A

assess risk factors
- carotid ultrasound
- cardiac ultrasound (LV thrombus)
- ECG (arrhythmias and AF)
- blood pressure
- diabetes screen
- thrombophilia screen (young patients)

63
Q

What are the effects of stroke?

A
  • loss of functional brain tissue
  • gradual or rapid loss of function
  • inflammation in tissue surrounding the infarct/bleed
64
Q

How is functional brain tissue lost during a stroke?

A
  • immediate nerve cell death
  • nerve cell ischaemia in penumbra around infarction which will die if not protected
  • stroke may ‘evolve’ over minutes of hours
  • recovery of some function with time
65
Q

What are the complications of stroke?

A
  • motor function loss
  • sensory loss
  • cognitive impairment
66
Q

What can motor function loss following a stroke affect/cause?

A
  • cranial nerve or somatic
  • autonomic in brainstem lesions
  • dysphonia
  • swallowing
    • aspiration of food and saliva
    • pneumonia and death
67
Q

What can sensory loss after a stroke affect/cause?

A
  • cranial nerve or somatic
  • body perception
    • neglect
    • phantom limbs
68
Q

What can cognitive impairment after a stroke affect/cause?

A
  • appreciation - special sensation
  • processing - understanding, speech and language
  • memory impairment
  • emotional lability and depression
69
Q

What are the phases of management of stroke?

A
  • acute phase
  • chronic phase
70
Q

What does the acute phase of stroke management involve?

A
  • limit damage
  • reduce future risk
71
Q

What does the chronic phase of stroke management involve?

A
  • rehabilitation
  • reduce future risk
72
Q

What is done to limit damage during acute phase of stroke management?

A
  • penumbra region - survivable ischaemia
    - calcium channel blockers
    • improve blood flow/oxygenation
      • thrombolysis possible within 3hrs
      • maintain perfusion pressure to brain
    • normoglycaemia - hyper/hypo harmful
    • remove haematoma
      • subarachnoid haemorrhage only
73
Q

What is done to reduce future risk during acute phase of stroke management?

A
  • aspirin 300mg daily
  • anticoagulation if indicated (delay 2 weeks)
    • AF
    • LV thrombus
74
Q

What is involved in rehabilitation during chronic phase stroke management?

A

nursing and rehabilitation
- immobility support
- prevention of bed sores
- physio to prevent contractures

  • speech and language therapy
    • communications
    • swallowing and eating
  • occupational therapy
75
Q

What are the dental aspects of stroke?

A
  • impaired mobility and dexterity (attendance, OH)
  • communication difficulties
  • risk of cardiac emergencies
  • loss of protective reflexes (aspiration, saliva)
  • loss of sensory information (difficulty with new dentures etc)
  • ‘stroke pain’ (CNS generated pain perception)
76
Q

What is epilepsy?

A

a group fo conditions that happen because of abnormal discharge of neurones within the brain

77
Q

What is epilepsy associated with?

A

reduced GABA levels in the brain which leads to abnormal cell-cell propagation
- this means less stimulation is needed for a neurone to fire and pass the message on to another cell

78
Q

What are febrile seizures?

A

seizures that largely happen in children and only happen when the child has a fever
- if a child has a febrile seizure once they are likely to have one again

79
Q

How can febrile seizures be prevented?

A

when children are ill monitor their temperature and cool them down in above 38 degrees

  • paracetamol
  • ibuprofen
  • remove clothes
  • cool sponging
  • cool bath
80
Q

What are the 2 classifications of epilepsy?

A
  • generalised
  • partial
81
Q

What are the main types of generalised epilepsy?

A
  • tonic/clonic
  • absense (petit mal)
  • myoclonic/atonic
82
Q

What are the types of partial epilepsy?

A
  • simple partial
  • complex partial
  • simple sensory
83
Q

What are the triggers for epilepsy?

A
  • idiopathic
  • trauma - head injury
  • CNS disease - tumour, stroke, CJD, meningitis, encephalitis
  • social - late nights, alcohol, hypoglycaemia, flashing lights
84
Q

What is the epileptic focus in generalised epilepsy?

A

often a central focus which then spreads the signal out to all parts of the cortex, means that all parts of the body are involved in the seizure

85
Q

What is the epileptic focus in partial epilepsy?

A

focus in one particular part of the cortex, this will be the area primarily affected by the seizure, may effect motor, perception, or sensation

86
Q

What happens during tonic clonic seizures?

A
  • prodromal aura
  • loss of consciousness/continence
  • initial tonic (stiff)
  • clonic (contraction/relaxation)
  • post-ictal drowsiness
87
Q

In most cases, after how long does a tonic/clonic seizure terminate?

A

usually terminates spontaneously after 1-3mins

88
Q

What is status epilepticus?

A

recurrent seizures, or prolonged seizure that hasn’t stopped

89
Q

What happens during petit mal (absence) seizures?

A
  • short lived episodes (5-15 seconds)
  • loss of awareness - eyelids flutter, vacant stare, stops activity, loss of response
  • CHILDHOOD usually
  • can be ultimate attacks in a single day
90
Q

What are the medical problems with tonic-clonic seizures?

A
  • INJURY - protect where possible
    • protect from surroundings
    • remove objects from the mouth IF POSSIBLE
  • asphyxia
    • USE SUPPLEMENTAL OXYGEN
    • GUEDEL airway IF POSSIBLE
    • SUCTION any secretions
91
Q

What are the social problems with tonic-conic seizures?

A
  • pregnancy
    • metabolism upset, drug reactions
  • sudden death
    • asphyxiation/aspiration
  • social
    • driving, employment
92
Q

What things can precipitate tonic-clonic seizures?

A
  • withdrawal/poor medication compliance
  • epileptogenic drugs
    • some GA agents
    • alcohol
    • tricyclics
  • fatigue/stress
  • infection
  • menstruation
93
Q

What is a Jacksonian seizure?

A

partial seziure which starts localised to one motor region of the brain but them moves/spreads to other motor areas - starts as small tremor at extremity of upper limb and progressively moves up to the elbow, shoulder, neck

94
Q

What can a sensory partial seizure cause?

A
  • any sensory modality - visual, auditory, taste, smell
  • often aura and may involve déjà vu
95
Q

What are complex partial seizures?

A

happen when different areas of the brain are affected which produces connected repetitive purposeless movements e.g. grimacing, lip smacking

96
Q

What is used to preventatively treat epilepsy?

A

anticonvulsant drugs
- tonic-clonic
- valproate, carbamazepine, phenytoin, gabapentin, phenobarbitone, lamotrigine
- absence
- levitiracetam

97
Q

What is involved in the emergency management of a seizure?

A
  • most require SUPPORTIVE treatment ONLY if UNCONSCIOUS - airway and oxygen
  • status epilepticus requires BENZODIAZEPINES
98
Q

How do epilepsy drugs work?

A

GABA receptor actions (most)
- valproate
- Gaba transaminase inhibtor
- benzodiazepines
- GABA a receptor action on Cl- enhanced

Sodium channel actions
- carbamazepine
- stabilises
- phenytoin
- ? unsure of action

99
Q

When may surgery be used to treat epilepsy?

A

when there is a single focus which is clearly identified and poorly controlled

100
Q

What are the dental aspects of epilepsy?

A

complications of fits
- oral soft tissue injury
- dental injury/fracture

complications of treatment
- gingival hyperplasia (phenytoin)
- bleeding tendency (valproate)
- folate deficiency (rare)

KNOW EMERGENCY CARE

101
Q

How should you assess the risk of a pt having a seizure during dental care?

A
  • good and bad phases
  • ask when last three seizures took place
  • ask about compliance with medication
  • ask about changes in medication
  • treat at times of ‘low risk’ if possible
102
Q

What is cerebral ataxia?

A

A broad-based stance with truncal instability during walking, causing falls to either side. The steps are irregular, and the feet may be lifted too high

103
Q

What is intention tremor?

A

characterized by coarse, low frequency oscillation. Increases inamplitude as the extremity approaches endpoint of deliberate, visually‐guided movement

104
Q

What is resting tremor?

A

a tremor not associated with voluntary muscle contraction and occurring in a body part supported against gravity. Typically seen in Parkinson’s disease as a “pill-rolling” action of the hand (slow oscillation at wrist with fingers curved into the palm)

105
Q

What is essential tremor?

A

a tremor occurring during voluntary contraction of the musclesand not associated with any other neurological disorder. Tremor may occur maintaining a posture, moving a limb or in purposeful movement toward a target (i.e. essential tremor is in fact a disorder comprising one or more different tremors)

106
Q

What is festination?

A

quickening and shortening of normal gait pattern seen in Parkinson’s. Makes patient appear to hurry but is a very inefficient way of moving

107
Q

What is bradykinesia?

A

slowness of movement. A key feature of Parkinson’s which isresponsible for the mask‐like face, loss of arm swing, festination and difficulty initiating and stopping an action (e.g. turning a corner or starting to walk)

108
Q

What is paralysis?

A

loss of motor control in a part of the body. Sometimes associated withsome sensory impairment. It may be flaccid (floppy) or spastic (rigid)

109
Q

What is spasticity?

A

aused by hypertonia or stiffness of the muscles. A common finding in patients who recover from a stroke. Causes typical features of flexed adducted upperlimb and extended lower limb with foot drop. If untreated spasticity can lead to contractures in the limb with resulting fixed deformity.

110
Q

What is automatism?

A

automatic, repetitive, involuntary behaviour e.g. lip smacking, chewing, swallowing, grasping, skin rubbing

111
Q

What is post-ictal?

A

events after a seizure. Patients may be drowsy, confused, unable to speak and have a headache. Duration varies with type of seizure (most marked witha prolonged generalised tonic‐clonic seizure)

BDS M5 Human Disease (13 decks)

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