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BDS3 - Diseases of the Human systems > Neurology > Flashcards

Neurology Flashcards

1
Q

what are degenerative brain diseases

A
  • slowly progressive diseases which stop proper neurological function
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2
Q

what are some examples of degenerative brain disease

A
  • Multiple sclerosis
  • Motor neurone disease
  • Parkinson’s disease
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3
Q

what is the most common CNS disorder fo the young

A
  • multiple sclerosis

- 80:100,000

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4
Q

how does multiple sclerosis happen

A
  • Demyelination of axons
  • Happens because of changes to myelin sheath around the nerve axons connecting different parts of the brain
  • Demyelination happens due to inflammatory change which can be seen on MRI scans as red changes
  • Typical of multiple sclerosis where the areas of the body affected change from time to time but enivitably the permanent changes which happen in the CNS lead to deficit in neurological knowledge and function
  • Affect any part of the body where nerves are involved
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5
Q

what patients have most severe MS

A
  • women with 4th decade onset
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6
Q

what is the aetiology MS

A

• Cause remains a mystery
• Susceptibility acquired during childhood
• Possible altered host reaction ot an infective agent
• Background genetic/immune factors
• More common in identical twins
• Certain genetic component
• Not clear if it an infective or environmental trigger
• Incidence increases the further from equator you are
- Led to suggestion that sunlight is involved and possibly the lack of vitamin D
• Symptoms can vary a lot from patient to patient
- Some more critical that others

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7
Q

what are the symptoms of MS

A
  • Muscle weakness
  • Visual disturbance
  • Paraethesia
  • Autonomic dysfunction
  • Dysarthria
  • Pain
  • Balance/hearing loss
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8
Q

what are the signs of MS

A 
•	Muscle weakenss
•	Spasticity 
•	Altered reflexes 
•	Tremor – intention 
•	Optic atrophy
•	Proprioceptive loss 
- 	Sudden loss of facial feeling must be considered as MS
•	Loss of touch
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9
Q

what is spasticity

A

• Muscle spasticity happens where there is an upper motor neuron lesion meaning damage to nerve is not in the nerve going from the spinal cord to muscle but in the spinal cord itself

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10
Q

what is optic atrophy

A
  • Optic nerve speed of conduction can be affected
  • If light shone onto the eye it can take a finite amount of time for that stimulation to reach occipital lobe in the brain
  • If patient has had inflammatory MS changes in the optic nerve, this conduction will be slowed and there will be a delay in receiving the signal
  • This can be measured and is a common test when assessing MS
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11
Q

what investigations are done for MS

A
  • history and examination
  • magnetic resonance and imaging
  • CSF analysis
  • visual evoked potentials
  • MRI useful to show areas of plaque in the brain
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12
Q

what will a patient with MS CSF be like

A
  • reduced lymphocytes

- increased IgG protein

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13
Q

what are the 3 different outcomes of MS

A
  • relapsing and remitting type
  • primary progressive type
  • symptomatic management
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14
Q

what is the relapsing and remitting type of MS like

A
  • Acute exacerbations and periods of respite
  • Damage builds up with each episode
  • Many will eventually develop progressive form – secondary progressive
  • Patient has episodes where there is active disease and loss of function, then after a few weeks it will settle and patient will enter period of stability
  • But the damage from these episodes builds and eventually the patient will become disabled from loss of function due to the collective damage within the CSF
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15
Q

what is the primary progressive type of MS like

A
  • Slow steady progressive deterioration

* Cumulative neurological damage

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16
Q

what is the symptomatic management for MS

A
  • Management at the time of an acute attack has to be symptomatic
  • Antibiotics, antispasmodics, analgesia, steroids
  • Physiotherapy and occupational therapy
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17
Q

what therapy is done for MS

A
  • physiotherapy and occupational therapy have a role with function loss
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18
Q

what therapy can be done for relapsing and remitting type of MS

A
  • disease modifying therapies
  • cladribine, siponomod, ocrelizumab
  • drugs don’t help the damage but slow down the rate at which new lesions occur
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19
Q

how does a stem cell tranplstn help MS

A
  • ‘reboot’ the immune system
  • Effectively if the problem is an unhelpful inflammatory response to an environmental stimulus, then the immune system recognition of this can be changed by changing immune system
  • Not without their own risks however
  • Any existing disability will not be reversed from this however
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20
Q

what are the dental aspects of MS

A

• Limited mobility and psychological disorders
• Difficulty accessing care but also for oral hygiene reasons
• Treat under LA
• Orofacial motor and sensory disturbance
- Suspect in younger patients?
• Chronic orofacial pain possible
• Enhanced trigeminal neuralgia risk
- Suspect in younger patients!

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21
Q

why do we not do GA for MS patients

A
  • if did under GA it has been suggested to cause damage n the brain
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22
Q

what is motor neurone disease (MND)

A
  • degeneration of the motor nerves in the spinal cord
  • corticospinal tracts/anterior horns
  • bulbar motor nuclei can also be affected - in the brainstem
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23
Q

what age are patients with MND

A
  • 30-60 years
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24
Q

what is the prognosis of MND

A
  • 3 years within diagnosis
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25
Q

who is more likely to get MND

A
  • males

- 2.5:1 female

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26
Q

what happens in MND

A
  • progressive loss of motor function
  • limbs
  • intercostal
  • diaphragm = impair ventilation
  • motor cranial nerves = VII-XII
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27
Q

what is death due to in MND

A
  • ventilation failure = leading to hypoxia

- aspiration pneumonia

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28
Q

what will the patient notice in MND

A
  • weakness in ankle or leg
  • slurred speech, develop into difficulty swallowing food
  • a weak grip
  • muscle cramps and twitches
  • weight loss
  • emotional lability = crying or laughing in appropriate situations
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29
Q

what is the treatment for MND

A
  • none effective
  • physiotherapy and occupational therapy
  • riluozole = some get 6-9 months life extension
  • PEG tube feed to prevent aspiration pneumonia
  • reduce salivation
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30
Q

what are the dental aspects of MND

A
  • difficulty in acceptance of dental care = muscle weakness of head and neck
  • realistic treatment planning = be sensible, shorter life expectancy so we give treatment to help self-image, not complicated treatment
  • drooling and swallowing difficulties = give anticholinergics and botox injections into saliva glands
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31
Q

what is Parkinson’s

A
  • quite common
  • disabling
  • progressive
  • due to a lack of a neurotransmitter dopamine int eh substantia nigra of brain
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32
Q

who is most likely to get Parkisons

A
  • older people

- mostly affects over 50’s

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33
Q

what happens as Parkinson’s progresses

A
  • marker for dopamine is gradually lost
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34
Q

what is the cause of Parkinson’s

A
  • unknown
  • repeated head trauma
  • degeneration of dopaminergic neurones in the basal ganglia of the brain
  • shortage of dopamine results in difficulty of message passaging from ‘thinking’ to ‘doing’ brain = from cortex to cerebellum
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35
Q

what are some clinical signs of Parkinson’s

A
  • bradykinesia = slow movement
  • rigidity = increased muscle tone, more stiff
  • tremor = slow amplitude, resting tremor (key features of Parkinson’s)
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36
Q

what is the effect of Parkinson’s

A
  • can lead to problems with posture and also communication and cognition
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37
Q

what are clinical observations of Parkinson’s

A
  • impaired gait and falls = walking is unsteady
  • impaired use of upper limbs
  • mask-like face
  • swallowing problems
  • dementia, psychosis
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38
Q

what are the treatment options for Parkinson’s

A
  • physical support
  • medical
  • surgery
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39
Q

what physical support is offered for Parkinson’s

A
  • physiotherapy and occupational therapy

- work to maintain function at as a high level for as long as possible

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40
Q

what medical treatment is given for Parkinson’s

A
  • dopamine = levodopa

- dopamine analogues

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41
Q

what is the problem with levodopa for Parkinson’s

A
  • very effective treatment initially but the dose needs to be continually increased to keep the benefit and therefore the consequences of the side effects eventually becomes intolerable
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42
Q

what are the different types of dopamine analogues for Parkinson’s

A
  • Mimic the effect of dopamine
  • Tablets - promipexole, selegiline
  • Injection - apomorphine – subcutaneous
  • Infusion - duodopa – directly into the gut
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43
Q

what surgery is offered for Parkinson’s

A
  • stereotactic surgery = becoming more common

- stem cell transplant to produce dopamine = not majorly used yet

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44
Q

how is stereotactic surgery done

A
  • Deep brain stimulation
  • Using 3-dimensional technique to locate electrode in part of the brain and this deep brain stimulation can help some patients return to a much more normal function so that the medical dose they require is much lower
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45
Q

what are the dental aspects of Parkinson’s

A

specialist area

  • difficulty accepting treatment = tremor (but should go away when open mouth)
  • dry mouth from anticholinergic drugs
  • drug interactions
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46
Q

what is a stroke?

A

acute focal neurological deficit resulting from cerebrovascular disease and lasting more than 24 hours or causing earlier death
- death of brain tissue from hypoxia

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47
Q

what can lead to a stroke

A
  • no local cerebral blood flow
  • infarction of tissue
  • haemorrhage into the brain tissue
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48
Q

what is a TIA

A
  • transient ismchaemic attack
  • rapid loss of function but also rapid recovery
  • suggests a worse stroke will occur later on
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49
Q

what is the acronym for signs of stroke

A
  • FAST
  • facial drooping
  • arm weakness
  • speech difficulty
  • time
50
Q

what happens in a TIA

A
  • localised loss of brain function
  • ischaemic event = not haemorrhage
  • get full recovery within 24 hours = most recover in 30 mins
51
Q

how do TIA’s happen

A
  • thought hat these happen from platelet emboli from the vessels in the neck
  • block blood flow causing ischaemia rapidly removed and blood flow returns before any drastic damage has occurred
52
Q

what is the risk of a proper stroke after a TIA

A
  • 12% in 1 year
  • 29% in 5 years
  • 2.4% risk of myocardial infarction
53
Q

what are risk factors for a stroke

A
  • hypertension = if diastolic >110mmHg then a x15 risk compared to diastolic <80
  • smoking
  • alcohol
  • ischaemic heart disease
  • atrial fibrillation
  • diabetes mellitus
54
Q

what is the commonest cause of adult disability

A
  • stroke
55
Q

what is the lifetime risk of a stroke

A
  • 1 in 6

- more likely in males

56
Q

what is the incidence of a stroke

A
  • 2 in 1000 population/year
57
Q

how does the incidence of stroke increase with age

A
  • 0.5/1000 population over 50

- 15/1000 population age 80

58
Q

what is the most common type of stroke

A
  • infarction 85%
  • haemorrhage 10%
  • subarachnoid haemorrhage 5%
  • venous thrombosis <1%
59
Q

what are the causes of an ischaemic stroke

A
  • uncertain

- most of the time due to narrowing of the vessels and plaques forming and ischaemic happening

60
Q

what is the cause of an intracranial bleed

A
  • aneurysm rupture
61
Q

what is the causes of embolic stroke

A
  • embolism from left side of the heart
  • atrial fibrillation
  • heart valve disease
  • recent MI
62
Q

what does atheroma of blood vessels usually cause

A
  • usually TIAs
  • but sometimes full strokes
  • atheroma of carotid bifurcation, internal carotid artery, vertebral artery
63
Q

what are berry aneurysms

A
  • weak points that can rupture leading to bleeding

- can be genetic so patient presenting with these, should have family members checked to

64
Q

what type of stroke is harder to see on a CT image

A
  • infarction worse than haemorrhage
  • CT scans not good at showing lesion early after onset
  • MRI scan much easier to use to see infarction
65
Q

what are some causes of venous thrombosis

A
  • use of contraceptiive pill
  • polycythaemia
  • thrombophilia
66
Q

what are the causes of border zone infarction

A
  • severe hypotension
  • cardiac arrest
  • get poor brain perfusion for a period of time which has led to brain injury
67
Q

how can vasculitis affect strokes-

A
  • vasculitic disorders may narrow blood vessels in the brain and cause limitation of oxygen delivery and therefore stroke
68
Q

ow can stroke be prevented

A
  • reduce risk factors = smoking, diabetes, control hypertension
  • antiplatelet action = aspirin, dipyridamole, clopidogrel
  • anticoagulants = warfarin, apixaban
  • carotid endarterectomy = severe stenosis, previous TIA’s
  • <85
  • preventative neurosurgery
69
Q

how is a carotid endarterectomy done

A
  • on some occasions is completely excised
  • removing artery and collateral blood supply of the brain and head and neck is very good and can cope with this
  • but, in some occasions surgeons will try remove plaque itself making vessel more patent so patient can still perfuse the area
70
Q

what different strokes do we need to differentiate when investigation

A
  • infarct
  • bleed
  • subarachnoid haemorrhage
71
Q

what needs to be done for best treatment outcome

A
  • need to differentiate which type of stroke it is quickly
72
Q

what imaging is used to investigate a stroke

A
  • CT scan
  • MRI scan
  • digital subtraction angiography (DSA)
73
Q

what is good and bad about CT scanning for strokes

A
  • rapid, easy access

- poor for ischaemic stroke = the most common

74
Q

what is good and bad about MRI scan for investigation strokes

A
  • difficult to obtain quickly
  • better at visualising early changes of damage
  • MRA (MR angiography) is the best investigation for visualising the brain circulation
75
Q

what can a DSA be used for when investigating strokes

A
  • if MRA not available

- good for looking at blood flow in the brain

76
Q

what do we look for in a carotid ultrasound when investigation strokes

A
  • look for evidence of atherosclerosis in carotid artery

- LV thrombus

77
Q

why do we do an ECG when investigating stroke

A
  • looking for changes such as and A fib
78
Q

what investigations do we do to assess risk factors for a stroke

A
  • carotid ultrasound
  • ECG
  • blood pressure
  • diabetes screen
  • thrombophilia screen = in young patients
79
Q

what are some of the effects of a stroke

A
  • loss of functional brain tissue
  • gradual or rapid loss of function
  • inflammation in tissue surrounding the infarct/bleed
80
Q

how do strokes cause loss of functional brain tissue

A
  • immediate nerve cell death

- nerve cell ischaemic in penumbra around infarction

81
Q

what is penumbra

A
  • areas surrounding tissues in stroke
82
Q

how do strokes cause gradual or rapid loss of function

A
  • stroke may evolve over minute or hours
  • strokes don’t appear fully formed
  • over time of an hour, can gradually lose function
83
Q

can there be some recovery from stroke

A
  • as inflammation settles there can be recovery
84
Q

what are some complications of s stroke

A
  • motor function loss
  • sensory loss
  • cognitive impairment
85
Q

what motor function loss can be caused by a stroke

A
  • cranial nerve or somatic
  • autonomic in brainstem lesions
  • dysphonia
  • swallowing = aspiration of food and saliva, pneumonia and death
86
Q

what sensory loss effects can a stroke cause

A
  • cranial nerve or somatic

- body perception = neglect, phantom limbs, don’t associate parts of their body as their own

87
Q

what cognitive impairment is caused by stroke

A
  • worse affect for patient
  • appreciation
  • processing = understanding of information, speech and language = dysphasia, dyslexia, dysgraphia, and dyscalculia
  • memory impairment
  • emotional lability and depressions
88
Q

what can a stroke be managed in an acute phase

A
  • limit damage = reduce amount of tissue lost by managing penumbra effectively
  • reduce future risk = also important to institute treatment at this point to minimise future risk
89
Q

what can a stroke be managed in a chronic phase

A
  • rehabilitation

- reduce future risk

90
Q

what are the acute phase treatment of a stroke

A
  • reduce damage = calcium channel blockers (nimodipine)
  • improve blood flow/oxygenation = thrombolysis possible within 3 hours (alteplase), maintain perfusion to brain tissue
  • normoglycemia = hyper/hypo harmful
  • remove haematoma = subarachnoid haemorrhage only
  • prevent future risk = aspirin 300mg daily, anticoagulant if indicated
91
Q

why is brain glucose level important

A
  • brain is solely dependent on glucose for its energy stores and therefore it if it not available patient will have more or exaggerated damage from stroke
92
Q

what is the chronic phase management of a stroke

A
  • nursing and rehabilitation
  • speech and language therapy
  • occupational tehrapy
  • making the most of patients residual function and trying to improve speech and language and communication
93
Q

what are the dental aspect of a stroke

A
  • problems often around mobility
  • impaired mobility and dexterity
  • communication difficulties
  • risk of cardiac emergencies
  • loss of protective reflexes = anticholinergic drugs could help
  • loss of sensory information
  • stroke pain
94
Q

what is stroke pain

A
  • CNS generated pain perception
  • poorly recognised feature where damage to the brain can change the way the brain understands its environment
  • patient can report pain, but it is coming from the damaged CNS and not from any peripheral stimulation which they think it is
95
Q

what is epilepsy associated with

A
  • reduced GABA levels in the brain

- group of conditions which happen from abnormal discharge from neurones within the brain

96
Q

what does reduced GABA levels cause in epilepsy

A
  • leads to abnormal cell-cell message propagation
  • takes less stimulation for a neutron to fire and pass a message on to another cell
  • abnormal chain reaction set up which causes discharge of lots of neurons either in one area of the brain or throughout
97
Q

what are febrile seizures

A
  • patient has same symptoms as someone having a tonic clonic epilepsy
  • largely in children and only when child has a fever
  • above 38 degrees
  • if have it once, likely to have it again
  • doesn’t mean child is epileptic, just means they are prone to these
98
Q

how are febrile seizures controlled

A
  • managed acutely the same way as any tonic clonic seizure
  • in preventative stage, it is important that when a child has an illness and they are systemically unwell, that their temperature should be monitored
  • cool hot children
99
Q

what is the treatment of febrile seizures

A
  • antipyretic medication = paracetamol, ibuprofen
  • remove clothes
  • cool sponging
  • cool bath
100
Q

what are the classification of epilepsy

A
  • generalised = tonic/clonic, absence (petit mal), mycologic/atonic
  • partial = simple partial, complex partial
  • simple sensory
101
Q

what are the triggers for epilepsy

A
  • cryptogenic/idiopathic = mainly
  • vascular disease
  • alcohol
  • cerebral tumour
  • trauma
  • infection
  • other
102
Q

what CNS disease can cause epilepsy

A
  • tumour, stroke

- CJD, meningitis, encephalitis

103
Q

what social activities can cause epilepsy

A
  • late night, alcohol, hypoglycaemia

- flashing lights

104
Q

what can epileptic focus be

A
  • generalised or partial
105
Q

what is generalised epileptic focus

A
  • there is often a central focus which spreads the signal to all parts of the cortex which means all parts of the body are involved in seizure
106
Q

what is partial epileptic focus

A
  • if the focus is only at one particular part of the cortex, then this will primarily be the area affected by the seizure
107
Q

what is a tonic clonic seizure

A
  • has a prodromal aura = patient has awareness sf change in their brain function
  • loss of consciousness/continence
  • initial tonic = stiff (all voluntary muscles in the body react together, puts strain on skeleton and particularly the spin and can lead to damage)
  • clonic = contraction/relaxation (intermittent contraction and relaxation of muscles)
  • in most cases, the tonic/clonic seizure will spontaneously terminate in 1-3 minutes
  • can have post-ictal drowsiness
108
Q

what is status epilepticus

A
  • to do with tonic/clonic seizures
  • recurrent seizures
  • in small number of cases tonic clonic will be followed by this
  • if this process goes on for a long time it is very dangerous for patient as normal breathing muscles cannot operate during the seizure and patient becomes hypoxic
109
Q

what are the medical risks of tonic/clonic seizures

A
  • injury = protect where possible, remove objects from mouth

- asphyxia = use supplemental oxygen, suction any secretions

110
Q

what are social risks of tonic/clonic seizures

A
  • pregnancy = metabolism upset, drug reactions
  • sudden death = asphyxiation/aspiration, aspiration of gut contents which are refluxed and can lead to acute lung damage
  • social = driving/employment, need to be free of seizures for a year before driving
111
Q

what are the precipitators for tonic/clonic seizures

A
  • most idiopathic
  • withdrawal/poor medication compliance = patient doesnt like side effects of drugs so don’t take them
  • epileptogenic drugs = some GA agents, alcohol, tricyclics and SSRIs
  • fatigue/stress
  • infection
  • menstruation
112
Q

what is petit Mal stroke

A
  • short lived episodes = 5-15seconds
  • loss of awareness = eyelids flutter, vacant stare, stops activity, loss of response
  • usually in childhood
  • can be multiple attacks in one day
  • patient won’t seem to have any changes unless you are watching them carefully
  • in some cases, it can be put down to daydreaming in class
113
Q

what are partial seizures

A
  • motor localised to one region of the brain
  • may move spread to other motor areas = Jacksonian seizure, start with a small tremor at upper limb and it will progressively start to move along limb
  • sensory = visual or auditory hallucinations
  • often there is an aura, and may have deja vu
114
Q

what are complex partial seizures

A
  • automatism = repetitive purposeless movements, lip smacking/grimacing
  • happens when different areas of the brain are affected which produce connected movements
  • movements stop at end of seizure
115
Q

what is the treatment for epilepsy

A
  • preventative = anticonvulsant drugs
  • emergency = most require supportive treatment only if unconscious, status epilepticus benzodiazepines
  • need airway and oxygen to prevent hypoxia
116
Q

what anticonvulsant drugs are used for tonic clonic seizures

A
  • valproate, carbamazepine, phenytoin, gabapentin, phenobarbitone, lamotrigine
117
Q

what anticonvulsant drugs are used for absence seizures

A
  • levetiracetam
118
Q

what drugs are used for epilepsy

A
  • GABA receptor actions = valproate, benzodiazepines
  • sodium channel actions = carbamazepine, phenytoin
  • because these drugs all work on different systems in the body, it allows them to be used in combination
119
Q

what surgery can be done for epilepsy

A
  • removal of focal neurological lesions = brain tumours
  • focal seizures = identifiable point of origin within brain, not well controlled by mediation
  • some surgeries involved removing entire lobes of the brain while others only remove the damaged areas
120
Q

how do you determine the focus site

A
  • stereotactic surgery in 3 dimensions to remove that one part through a craniotomy through the skull can be helpful
121
Q

what are the dental aspects of epilepsy

A
  • need to ask about compliance with medication
  • complication of fits = oral soft tissue, dental injury/fracture
  • complications of treatment = gingival hyperplasia (phenytoin), bleeding tendency (valproate), folate deficiency (rare)
  • know emergency care
  • assess risk of fit = good and bas phases, as when last 3 fits took place, good to know if they are likely to have on soon or not
  • ideally treat at times of ‘low risk’

BDS3 - Diseases of the Human systems (4 decks)

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