Neurology Flashcards

1
Q

The main aims of a neurological examination. General system of examination and how to roughly do it

A
  • To find the anatomical site (level) of the lesion
  • Two People Cant Resist Sex

Tone:

  • How stiff something is
  • Increased Tone suggests UMN lesion
  • Decreased Tone suggests LMN lesion

Power:

  • Compare the two sides and try and compare with similiar forces
  • 0-5
  • 5 normal power
  • 0 complete paralysis

Coordination

  • Finger-nose command
  • With your right hand, touch your nose, then my finger then your nose as fast as you can

Reflexes:

  • Tap on knee tendon to initiate rapid muscle stretch
  • Hyper-reflexia= UMN
  • Hypo-reflexia= LMN

Sensation:

  • Light touch: use a piece of cotton wool to compare dermatomes on both sides
  • Proprioception: hold either side of finger tip then move up/down with the eyes closed
  • Vibration: tuning fork on bony prominences
  • Pain: use a neurotip- small disposable pin
  • Temperature: metal instrument as cold and the rubber part of this as hot
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2
Q

Why do all cranial nerves decussate and which CN is different

A

-Right side is controlled by the left brain and vice cersa

  • Occurs because of the way light and vision works
  • There needs to be an optic chiasm
  • The rest of the CNS swap over so everything stays consistent
  • If you saw a man on your right hand side (from left part of the brain), you would want to punch him on your right rather than your left

CNVII receives bilateral innervation from both sides of the brain

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3
Q

How to rate the severity of a coma

A
  • Glasgow Coma Scale assesses patient ability to open their eyes, move and speak
  • Minumum score of 3 to a maximum of 15
  • 8 or less is clinically defined as a coma
  • Motor Response
    6: Obeying commands
    5: Movement localised to stimulus
    2: Involuntary muscle straightening
    1: None
  • Vertbal Response:
    5: Orientated response
    4: Confused response
    3: Inappropriate words
    2: Incomprehensible
    1: None
  • Eye Opening
    4: Spontaneous
    3: To speech
    2: To pain
    1: None
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4
Q

Assessment for dementia

A
  • Abbreviated Mental Test Score (AMTS)
  • Score of 7-8/10 or less suggests cognitive impairment
  • Other tests are necessary to confirm a diagnosis of dementia, delirium or other causes of cognitive impairment
  • What is your age
  • What is the time to the nearest hour
  • Give pt address and get them to repeat it at the end of the test
  • What is the year
  • What is the name of the hospital where the pt is situated
  • Can you recognize two people (doctor and nurse)
  • What is your DOB
  • When did WW1 begin
  • Name present prime minister
  • Count backwards from 20 down to 1
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5
Q

Definition of a stroke and clinical features possibilities of a patient who has suffered a stroke

A
  • A focal neurological deficit that lasts longer than 24 hours
  • Results from a vascular lesion
  • Either ischaemic (due to lack of blood flow) or haemorrhagic
  • Paraplegia- impairment of motor or sensory function of the lower extremities
  • Hemiplegia- loss of motor or sensory control on one side of the body
  • Tetraplagia/Quadraplegia: Paralysis by illness/injury that results in partial or total loss of use of all 4 limbs and the torso
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6
Q

Increasing complexity/seriousness of strokes

A
  • If there is a focal deficit and full recovery in less than 24 hours, it is known as a transient ischaemic attack
  • if full recovery within a week with minimal/no deficit, then it is known as a Minor stroke
  • A stroke in evolution is where the signs and symptoms are worsening
  • Completed stroke is the point at which neurological deficit is at its worst
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7
Q

Types of Stroke and importance of distinguishing

A

15% of strokes are wet/haemorrhagic
85% of strokes are dry/ischaemic

  • First thing to do is to work out if wet or dry
  • Treatment option for the wrong type can be life threatening
  • If it as dry stroke, then you want to give anti coagulant drugs
  • Which could be disastrous if you did this in a patient with a wet stroke
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8
Q

Differential diagnosis of a stroke

A
  • Can be mimicked by fast expanding space occupying lesion such as tumour or an abscess
  • Hypoglycaemic patient
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9
Q

Dry stroke. Different aetiopathogenesis

A
  • Thrombosis at an atheroma plaque site
  • Local blood clot
  • Thrombi can move and form an emboli somewhere else in the body
  • Embolisation of this thrombi into an end artery
  • Important to work out where the embolus has come from
  • Typical end arteries include the vertebral basilar/carotids
  • Mural thrombi (thrombi attach in aorta) from left ventricle
  • Systemic hypotension and hypoperfusion (general decrease in blood pressure and supply)
  • Eg. in shock
  • Sudden stop in blood pressure
  • For a long period of time
  • Rarely (septic) vegetations from biscuspid/aortic valves in infective endocarditis (LHS of the heart)
  • If vegetations from the valve flick off, you may get a septic infarct
  • SI is an area of necrosis reesulting from vascular obstruction caused by emboli consisting of clumps of bacteria or infected materials
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10
Q

Which side of the heart are you more likely to get an embolus forming

A

Because as it leaves the right venticle, it is going straight to the lungs where it theoretically should get filtered

If leaving the LV, it is going around the rest of the body

So left side of the heart is where youre most likely to get an embolus

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11
Q

Common Stroke symptoms

A
  • Sudden numbness or weakness of face, arm or leg
  • Sudden confusion, trouble speaking or understanding
  • sudden trouble seeing in eyes
  • Sudden trouble walking, dizziness, loss of balance
  • Sudden severe headaches with no known cause

-call ambu asap

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12
Q

Main risks for a dry stroke

A
  • Diabetes
  • Smoking
  • Obesity
  • Alcohol
  • Oral Contraceptives (side effect of pro-coagulation)
  • Polycythaemia (high concentration of RBCs)
  • Atheroma (hypercholestrol/ lipid aemia)
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13
Q

Aetiopathogeneis and Risks for a wet stroke

A
  • Bleeding directly into the brain or into the space between the brains membranes
  • May occur due to a ruptured intra-cranial micro-aneurysm (Weakness in the wall of a cerebral artery or vein causing a localised dilation or balloning of a blood vessel)

-Often a hereitable, congenital defect
Such a Circle of Willis tendency to burst
Aortic aneurysm is the most life threatening
Also secondary to hypertension

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14
Q

Investigations and diagnosis of stroke

A
  • History of event (trauma to the side of the head may suggest wet)
  • Risk factors (IE, Rh Fever, Previous MI, Atrial Fib)
  • General signs evolving (wet strokes associated with vomiting and nausea)
  • Use INR to check if it is a warfarin bleed
  • Use LFTs
  • Use ESR to see if its vasculitis or endocarditis
  • Check glucose to rule out hypoglycaemic event
  • Use ECG to check AF/MI

-CT/MRI is the main differentiator to work out if it is a wet or dry stroke

Management is revolved around the diagnosis to see what type of stroke it is

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15
Q

Long-Term effects of a stroke and how the features develop

A
  • Most common lesion causes hemiplegia, where one side of the body is impaired
  • Often due to brain tissue death from the opposing side
  • Initially flaccid with reduced reflexes
  • In a few days, spasticity supervenes with a ‘typical stroke walk’ in which the arm is flexed and the leg is extended
  • Strength recovery takes over weeks to months
  • Can lead to one sided vision loss (hemianopic)
  • Or possibly apahasia (impairment of language)
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16
Q

L brain damage causes what and vice versa

A

Left Brain Damage

  • Paralyzed right side
  • Speech/langugage deficits
  • Slow, cautious behaviour
  • Memory Deficits

Right Brain Damage

  • Paralyzed left side
  • Spatial perceptual deficits
  • Quick, impulsive behavioral style
  • Memory deficits
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17
Q

Management of Dry stroke

A
  • Initially, make sure you diagnose the correct stroke
  • Use INR to check if it is a warfarin bleed
  • Use LFTs
  • Use ESR to see if its vasculitis or endocarditis
  • Check glucose to rule out hypoglycaemic event
  • Use ECG to check AF/MI
  • If confirmed dry stroke then:
  • Thrombolytic drugs
  • Aspirin
  • tPA- fibrin clot buster
  • Occasional Heparin (if DVT risk)
  • Slow reduction in BP- avoid a sudden crash and a second dry stroke
  • Support
  • Rehab, Physio
  • Nasogastral feeding
  • Hydration
  • Chair Lifts, Aids, OH adaptations, shower etc
  • Look for secondary risks
  • Carotid atheromas
  • Clotting screens
  • Hypertension
  • If appropriate, aspirin/chronic warfarin can be taken
  • Can also perform endarterectomy which is a surgical procedure to remove the atheromatous plaque in the lining of the material
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18
Q

Management of Wet stroke

A
  • Pts may be offered meds that reduce BP and prevent further strokes
  • Surgery may be required to remove any blood from the brain and repair any burst blood vessels
  • Support
  • Rehab, Physio
  • Nasogastral feeding
  • Hydration
  • Chair Lifts, Aids, OH adaptations, shower etc
  • Similiarly look for secondary risks
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19
Q

Dental Relevance of Strokes

A
  • Need to teach patients how to brush teeth one handed
  • Severity and type of impairment is different for each patient so need to individualise
  • ID brushing
  • Getting to appointments on time
  • How can we make it easier for the patient
  • Dentures
  • Warfarin patient
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20
Q

Different types of wet strokes and explanation of each

A

Subarachnoid Haemorrhage

  • Inside the structure of the brain
  • Bleeding between arachnoid membrane and pia mater surrounding the brain
  • Circle of Willis Aneurysm Rupture usually
  • Sudden loss of conciousness
  • High pressure so fast onset
  • Often neurosurgery required
  • clip and tie bleeder

Subdural Haemorrhage

  • Collection of blood gathers between the inner layer of the dura mater and arachnoid mater
  • Usually venous with a slower onset
  • Lesion causes a mass effect- swells further with blood breakdown
  • Typically after a milder fall
  • Loss of consciousness a few hours/days later

Extradural haemorrhage

  • Typically middle meningeal artery bleed after blow to the side of the head
  • Typically in the temporal region
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21
Q

Definition of Epilepsy

A
  • Common condition that affects the brain and causes frequent seizures
  • Seizures are bursts of electrical activity in the brain that temporarily affect how it works
  • They can cause a wide range of symptoms

-Epilepsy means a patient may have a tendency to have seizures, but anyone can have a one-off seizure and not be epileptic

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22
Q

Causes of epilepsy

A
  • Not very well understood
  • Electrical signals in the brain become scrambled and there are sudden bursts of electrical activity
  • Often not clear why this happens

-Familial/genetic heritance: errors in genes affecting brain function

-Occasionally, epilepsy can be caused by damage to the brain, such as damage from:
Stroke
Brain tumour 
Severe Head Injury 
Drug/Alcohol abuse 
Brain infection 
Hypoxia during birth
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23
Q

Clinical Features of Epilepsy

A

-Seizures can affect people in different ways, depending on which part of the brain is involved

  • Uncontrollable jerking and shaking, called a fit
  • Losing awareness and staring blankly into space
  • Becoming stiff
  • Strange sensations, such as a rising feeling in the tummy, unusual smells or tastes, and a tingling feeling in your arms and legs
  • Collapsing/passing out
  • Main symptom is repeated seizures. Sudden bursts of electrical activity in the brain that temporarily affect how it works
  • Typically pass in a few seconds or minutes
  • Awake or asleep
  • Sometimes triggered by something, eg feeling very tired
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24
Q

Different types of seizures and explanation of eahch

A

Simple partial (focal) seizures or auras:

  • Strange feeling that is difficult to describe
  • Feeling that events have happened before (deja vu)
  • Intense feeling of fear or joy
  • Rising feeling in your tummy
  • Unusual smells or tastes/tingling in your arms and legs -Stiffness or twitching in part of your body, such as an arm or hand
  • Remain awake and aware while this happens
  • Considered warnings and may predispose to other types of seizures

Complex partial (focal) seizures:

  • Lose your sense of awareness and make random body movements
  • Smacking your lips
  • Rubbing your hands
  • Making random noises
  • Moving arms around
  • Picking at clothes or fiddling with objects
  • Chewing or swallowing
  • Pt won’t be able to respond to anyone and will not have any memory of it

Tonic-Clonic Seizures or grand mal:

  • Typical epileptic seizure
  • Initial tonic stage- lose conciousness, body goes stiff, and may fall to the floor
  • Second clonic stage- limbs jerk, lose control of your bladder or bowel, may bite tongue or inside of cheek and may have difficulty breathing
  • Typically stops after a few minutes, but some last longer
  • Difficulty remembering what happened

Absences, or petit mal

  • Lose awareness of surroundings for a short time
  • Mainly children
  • Stare blankly into space
  • Daydreaming
  • Flutter their eyes
  • Up to 15 seconds
  • Won’t be able to remember them

Myoclonic seizures

  • Some or all of your body suddenly twitches or jerks, like you’ve had an electric shock
  • Soon after waking up
  • Only last a fraction of a second, but several can sometimes occur in a short space of time
  • Normally remain awake during them

Clonic Seizures:

  • Body shakes and jerks like grand mal seizures
  • But you don’t go stiff at the start
  • Last a few minutes and may lose consciousness

Tonic seizures:

  • All muscles before very stiff
  • May lose balance and fall back

Atonic seizures:

  • All muscles suddenly relax
  • May fall to the ground (often forward)
  • Very brief
  • Usually you’ll be able to get up again straight away

Status epilepticus:

  • Any seizure that lasts a long time, or a series of seizures where the person doesn’t regain consciousness between
  • Medical emergency and needs to be treated as soon as possible
  • Call 999
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25
Q

Partial and generalized seizures definition and classify all the types of seizures

A

Partial Seizure: one hemisphere or lobe which can be further split into

  • Simple partial
  • Complex partial

Generalized Seizure: both hemispheres of the brain are affected

  • Tonic
  • Atonic
  • Clonic
  • Tonic-Clonic
  • Myoclonic
  • Absence
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26
Q

Significance of status epilepticus and management

A
  • if seizure lasts more than 5 mins
  • either ongoing or without returning to normal
  • no regaining conciousness between seizures
  • usually Tonic Clonic seizures
  • Medical emergency
  • Treated with benzodiazepines (enhance inhibitory NT GABA)
  • Call 999
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27
Q

Diagnosing and Investigations (along with explanation) of Epilepsy

A
  • MRI/Ct scan to look for abnormalities in the brain
  • eg unusual growth/brain tumour, damage to the brain, by stroke scarring in the brain
  • EEG (during and between seizures) detects electrical signals in the brain
  • Check for unusual electrical activity in the brain that can happen in people with epilepsy
  • Small sensors attached to the scalp to pick up the electrical signals produced when brain cells send messages to each other
  • Recorded by a machine and are looked at to see if unusual
  • As epilepsy varies considerably, diagnosis requires tests and examination of clinical history
  • Diagnosis can just be based on symptoms
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28
Q

When taking a history of epilepsy, or associating the epilepsy with a syndrome, what is important information/questions

A
  • Type or types of seizures
  • Age at which they began
  • Cause of the seizure
  • Whether the seizure are inherited
  • Part of the brain involved
  • Factors that provoke the seizure
  • How severe and how frequent
  • Ever hospitalized
  • ECG patterns during and between seizures
  • Brain imaging findings eg. MRI or CT scans
  • Genetic information
  • Other associated disorders
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29
Q

Triggers of epileptic seizure and how to identify the triggers

A

-Many people seizures occur randomly

  • Stress
  • Lack of sleep
  • Waking up
  • Drinking alcohol
  • Meds and illegal drugs
  • Monthly periods in women
  • Flashing lights (uncommon trigger)

-Keep a diary of when seizures occur and what happened before to identify and avoid possible triggers

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30
Q

Management of Epilepsy and aims of tx

A
  • Aim is to minimize or stop seizures completely
  • Take a diary everytime you have a seizure and see if you can spot a common trigger so you can avoid it. If strss is a trigger, then yoga and meditation can help
  • Anti-Epileptic Drugs/ Anti-Convulsants
  • Surgery to remove a small part of the brain that are causing the seizures
  • Procedure to put a small electrical device in the body that can help control seizures
  • Vagus nerve stimulation and deep brain stimulation
  • Ketogenic diet uses fat instead of carbs for energy. Ketone bodies used as an energy source for the brain rather than glucose. But atherosclerosis, diabetes and CVS disease
  • Some people may need to treatment for life, but some might be able to stop treatment if seizures disappear over time
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31
Q

Anti-Epileptic Drugs how they work, type and side effects

A
  • Most commonly used tx for epilepsy
  • Work by changing the levels of chemicals in your brain. Don’t cure epilepsy but can stop seizures occuring
  • Must be used every day. Sudden cessation can provoke a seizure so cessation is a slow withdrawal
  • Phenytoin
  • Sodium valproate
  • Carbamazepine
  • Lamotrigine

-Depends on epilepsy type, age and if female (pregnant) Sodium valproate can harm an unborn baby

  • Drowsiness
  • Lack of energy
  • Uncontrollable shaking (tremor)
  • Rashes
  • Serious allergic reaction
  • Headaches
  • Muscle cramps
  • Hair loss or unwanted hair growth
  • Swollen gums- phenytoin
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32
Q

When is surgery indicated in the treatment of epilepsy procedure, recovery and risks

A
  • If AEDs are not controlling the seizures
  • EEG, MRI show focal lesion accessible/emendable to surgery without serious side efffects
  • Surgery under GA
  • Cut through scalp and lift bone flap to open skull and remove the brain lesion
  • Takes a few weeks or months after surgery
  • Seizures may not stop straight away- might need to keep taking AEDs for a year or two

-Risks of complications from surgery, problems with your memory, mood, vision

33
Q

What would you do if AEDs and surgery is contraindicated

A

Vagus Nerve Stimulation

  • Electrical device like a pacemaker under the chest skin
  • Stimulation of vagus nerve to control seizure by influencing the electrical signs in the brain
  • Doesnt stop seizures completely, but helps make them less severe and less frequent

Deep Brain Stimulation

  • Similiar to VNS but device placed in chest and connected to wires that run directly into the brain
  • Helps prevent seizures by changing the elctrical signs of the brain
  • New procedure- not used often so efficacy not yet clear for epilepsy
34
Q

Every-day life for epileptics

A
  • if seizures are not well controlled, avoid driving, swimming and cooking
  • Avoid driving and swimming until you have seen a specilist
  • Guards on heaters and radiators to stop you falling on them
  • Furniture edges or corners should be covered
  • Shower instead of bath
  • Back burners of saucepan with handles turned away from the edge
  • Don’t lock the door
  • Teachers must be aware of what meds children take, spotting and dealing with seizure and absence seizures
  • Pregs pt must avod sodium vaproate
  • Employer make reasonabel adjustments to work tasks
35
Q

Sudden unexpected death epilepsy

A
  • Sometimes a person dies unexpectedly
  • Rare but important to be aware of the danger because it may sometimes be preventable
  • Reduce your risk is to make sure your epilepsy is well controlled by taking your medication as recommended and avoiding seizure triggers when possible
36
Q

Multiple Sclerosis Definition and mini pathogenesis

A
  • Common neurological condition characterised by areas of demyelination in CNS
  • Autoimmune to oligodendrocytes
  • Type IV Hypersensitivity
  • Loss of myelin fatty sheath in the brain and spinal chord
  • Loss of insulator around the nerves
  • Demyelination leads to loss of salutatory conduction between Nodes of Ranvier
  • Everything slows down
  • Also nerves can excite nearby nerves that they wouldn’t normally excite
37
Q

Aetiology of MS

A
  • Unknown
  • Virsus perhaps
  • Autoimmune mechanism
  • Less common in the tropics
  • Female?Male
38
Q

Pathology of MS and types of nerves affected

A

-Immune system inappropriately attacks the body’s oligodendrocytes

  • Loss of myelin fatty sheath in the brain and spinal chord
  • Loss of insulator around the nerves
  • Demyelination leads to loss of salutatory conduction between Nodes of Ranvier

-Classically peri-venular plaques of demyelination (around the veins)
-Predeliction for:
Optic nerves
Periventricular white matter
Brainstem and cerebellar connections
Cervical spinal cord- corticospinal and dorsal columns

-Never involves peripheral nerves- Guillan Barre Syndrome

  • Early on in MS, the oligodendrocytes can heal and extend out new myelin (remyelination)
  • However, later on, remyelination will stop. Damage becomes irreversible with a loss of axons
39
Q

Demyelination of Peripheral Nerves

A
  • Guillan Barre Syndrome of demyelination

- Post virus illness

40
Q

What is myelin and what produces it

A
  • Protective sheath of axons allowing them to quickly send electrical impulses
  • Produced by oligodendrocytes in CNS
41
Q

Clinical Features of MS

A
  • Vary a lot from person-person
  • Largely dependent on location of plaques
  • Symptoms worsen over weeks and linger for months without treatment
  • Typically associated with periods of chronic fatigue

3 common symptoms include:

  • Difficulty or unclear speech caused by plaques in the brainstem
  • May interfere with eating, talking and swallowing
  • Involuntary rapid eye movements (Nystagmus)
  • Optic Neuritis
  • Plaques in the nerves of the eye
  • If optic nerve, then loss of vision and optic neuritis
  • If nerve controlling ocular movements, then pain and double vision (dyplopia)
  • Intention Tremor
  • Caused by plaque along motor pathways int he SC
  • Affect outbound signals like skeletal muscle control
  • Muscle weakness and spasms
  • Tremors
  • Also commonly numbness and pins and needles
  • Spastic paraparesis- gradual weakness with muscle spasms in the legs
42
Q

Diagnosis of MS

A
  • Suspected where there are multiple neurologic symptoms separated in space which is attributed to damage to different locations of the NS as well as time
  • Separate bowts/flare ups and remission
  • MRI scan shows white matter plaques due to bundles of myelin
  • Electrophysiology: flash lights in someone’s eyes and watch for an impulse arrival at the back of the skull on the optical cortex. Check if impulse is slightly delayed or distorted
-Cerebrospinal Fluid shows high levels of antibodies which is an indication of an autoimmune process
Lumbar puncture (oligoclonal bands of IgG protein is characteristic of inflammation 

-Doppler Ultrasound can eliminate vascular problems

43
Q

Types of Multiple Sclerosis

A
-Primary Progressive:
Constantly getting worse
No chill 
Neurological deficit accumulations 
First major event and it never tops 

-Secondary Progressive
One episode
Period of remission
Resurgence and decline

-Relapse Remitting 
Most common 
Random demyelinating episodes 
No pattern 
Tired/stress provoked 
Full/partial Recovery
Slow accumulation of deficit 

-Benign MS:
One episode
Full recovery
No return

44
Q

Management of MS

A
  • Support/Counselling. Massive psychological effect
  • No cure but medications can lessen severity and reduce frequency of relapses
  • Intravenous corticosteroids such as methyl prednisolone very useful during relapses
  • Also ACTH as it causes increased production of cortisol from adrenal gland which prevents release of substances in the body that cause inflammation
  • Beta Interferon: prevents cell signalling between nerves
  • Physio
  • Muscle relaxants such as benzodiazepines and baclofen
  • Self catheterisation
  • Multiple disciplinary approach required with physio, neuro, chest physician, GMP and GDP
45
Q

Differential Diagnosis of MS

A
  • Single CNS demyelination plaque
  • Transverse myelitis
  • Mononeuropathies
46
Q

Dental Relevance of MS

A
  • Trigeminal Neuralgia
  • Recurrent facial plsies
  • Increased caries rate due to spasticity or ataxic movements of upper limbs making OH more difficult
  • Inability to tolerate dental procedure due to spastic head, limbs or tongue movements
  • Dental pain of no specific origin with no underlying dental problem
  • Difficulty in swallowing and emotional lability due to pseudobulbar palsy
  • Oral dysaesthesia (burning in the mouth
  • Mobility issues (can be mild symptoms or pt may be severely incapacitated)
  • Recurrent UTIS and are often on frequent courses of antibiotics
  • Vision can be affected during active episodes
  • Hot environments, anxiety and stress can exaccerbate active disease
  • Polypharmacy
47
Q

Neuralgia definition, classification and example

A
  • Pain in the distribution of a nerve
  • Either primary (nerve-based pain) or secondary (nerve-related pain)
  • Primary neuralgia is pain in the distribution of a nerve (nerve-based pain)
  • Secondary neuralgia is nerve-related pain
  • For example, in trigeminal neuralgia:
  • Primary TN is caused by an artery/vein compressing on CNV
  • Secondary TN is when trigeminal neuralgia has been caused by another medical condition for example tumour, cyst, MS, facial injury
48
Q

Importance of Facial Pain

A
  • Damage warning
  • Protective response
  • Pain is initially a good thing
  • Body’s way of telling you to not use something
  • As pain lasts for longer, the value of it exceeds its merit
49
Q

Chronic Pain defintiion

A
  • Present for >3 months
  • Outlives its usefulness
  • May not go
  • May not be able to cure pain but aim is to limit associated disabilities so often more realistic
50
Q

Allodynia

A

pain from normally non-painful stimuli

51
Q

Hyperalgesia

A

increased response to normally painful stimulus

52
Q

Dysaesthesia

A

Unpleasant sensation spontaneous or evoked

53
Q

Paraesthesia

A

Abnormal sensation- spontaneous or evoked

Not unpleasant

54
Q

Hypoalgesia

A

-Diminished pain response to a painful stimuli

55
Q

Anaesthesia

A

No pain from a painful stimulus

56
Q

Neuralgia

A

Pain from nerve distribution

57
Q

Neuropathic

A

Pain associated with damage or disease

58
Q

Pain-sensing structure of the face

A
Teeth
Gingiva 
Mucosa
Skin 
TMJ
Sinuses 
Eyes
59
Q

Effects of Chronic Facial Pain

A
  • Anxiety/depression
  • Decreased capacity for activities of daily living
  • Sleep disturbance
  • Taking time off work
  • Impact directly relates to perceived not necessarily actual severity
  • Medicalisation can make it worse
60
Q

Neuropathy

A

-Term used to designate an abnormality or pathology in a peripheral nerve

61
Q

Different ways to measure pain

A

VAS (Visual Analogue Scale)
-Literally rates pain from 0-10 from good to agony

Brief Pain Inventory (BPI)

  • Intensity of pain
  • QoL

HAD (Hospital Anxiety and Depression Score)

McGill Pain Questionaires
-Characteristics of pain

62
Q

Most common pain associated with TN

A

-Sharp

63
Q

Most common pain associated with atypical facial pain

A
  • Burning

- Heaviness

64
Q

Primary Neuralgia definition. What is a good clue that the neuralgia is primary
Classic nerves affected

A
  • Corresponds to pain going along a nerve distribution and nowhere else
  • Pain corresponds exactly to the anatomical distribution of a cranial nerve

If it crosses the midline, it is unlikely to be primary TN as CNS does not cross over

-Usually either glossopharyngeal nerve or v2/3 branches of trigeminal

65
Q

Clinical features of general primary neuralgias

A
  • Unilateral
  • Trigger zones
  • Severe stabbing/electric/sudden lacinating pain
  • Paroxysmal (short episodes)
  • No sensory/motor impairment
  • Long remission intervals
66
Q

Trigeminal Neuralgia definition, history and clinical features

A
  • Unclear single aetiology
  • If under 50yo, suspect brain mass/MS/significant lesion
  • Arise in one or more divisions of the trigeminal nerve but rarely in V1

-Classically have a trigger zone: wind/touch/shave precipitates pain. An area of the face if touched will cause extreme pain

Diagnosis made on history

  • No physical signs
  • Recurrent, brief, painful jabs lasting approximately 30 seconds
  • Characteristic trigger zones
  • Middle aged
  • No associated sensory changed
  • No facial weakness
67
Q

Management of neuralgia

A
  • Management
  • Support and care
  • AEDs often used eg carbamazepine
  • Oxcarbazepine
  • Lamotrigine
  • LA injections give temporary relief
  • Open cranial surgery can be used for vascular decompression
68
Q

Post-Herpetic Neuralgia definition and clinical features

A
  • Occurs after herpes zoster infection
  • Pain is steady and sustained
  • Pain may be dermatomal
  • Associated with a paroxysmal shooting pain
  • Pain is felt superficially in the area of an acute attack
  • May persist for several months
69
Q

Glossopharyngeal neuralgia definition, possible cause, location, triggers

A
  • Paroxysmal pain: ear, base of the tongue, tonsillar fossa or angle of jaw
  • Sensory areas of the IX nerve
  • Triggers include chewing, swallowing, talking, yawning and coughing
  • Possible bradycardia, hypotension, or asystole
  • Possible causes: compression by neoplasms, infections or blood vessels
  • May be seen in patients with MS
70
Q

Causes of Facial Pain

A
  • Trigeminal Neuralgia
  • Post-herpetic neuralgia
  • Glossopharyngea neuralgia
  • Geniculate neuralgia
  • Facial pain associated with diabetic neuropathy
  • Occipital neuralgia
  • Atypical facial pain
  • Schwannoma
  • Local Dental pain
  • Trauma
  • Sinusitis
  • Migraine
  • TMJ
  • Giant Cell arteritis
  • Atypical facial pains
71
Q

Example, explanation and tx of intra-cranial secondary neuralgia

A

Schwannoma (acoustic neuroma)

  • Tumour
  • Typical CNV and CNVIII nerves
  • Unilateral deafness +/- tinitus
  • If CNV, corneal reflex is lost
  • Early diagnosis vital
  • Excision/gamma knife required as treatment
72
Q

Example and explanation, investigations, treatment and differential diagnosis of cranial base secondary neuralgia

A

Pagets Bone Disease

-Clinical features vary with severity and site

  • Often affects frontal and/or occipital regions
  • Can progress to involve the entire skull
  • Narrowing of auditory canal can lead to deafness

-Activity demonstrated by a bone scan

  • Calcitonin- inhibits bone resorption
  • Bisphosphonates- inhibits bone resorption by binding to hydroxyapatite crystals
  • Mithramycin- cytotoxic agent

-Differential diagnosis could be osteoblastic metastases, fibroud dysplasia or lymphoma

73
Q

Causes of local dental pain

A
  • Acute/chronic pulpitis
  • Abscess
  • Dentine sensitivity
  • Periodontitis
  • High filling
  • Pulp exposure
  • Chemical/thermal irritation of pulp
  • Cracked cusp
  • Lateral canals?
74
Q

Example of vascular facial pain, precipitating factors, clinical features and treatment

A

Migraine

  • Precipitating actors include cheese, chocolate and alcohol
  • Sleep too little or too much
  • Heat/noise/light
  • Hormonal OCP
  • Stress
  • High impact episodic headache
  • Nausea and lathargia
  • Vasospasm causing pain
  • Blinding pain over unilateral forehead
  • Urge to sleep in the dark

Migralieve
Anti-emitics
Tryptans (zolmitriptan)
Beta blockers and amitriptyline as prophylaxis

and Giant Cell arteritis

75
Q

Giant Cell Arteritis definition, clinical features, investigations and treatment

A
  • Crushing headache
  • Granulomatous inflammation of mid-sized arteries causing ischaemia
  • Risk of optic arterial occlusion leading to blurring and even blindness
  • Biopsy, ESR
  • High dose prednisolone required as treatment
76
Q

TMJ Pain classification and causes

A
-Intracapsular:
Degenerative conditions 
Neoplasia 
Trauma 
Inflammatory 

-Capsular:
Trauma
Joint dysfunction

-Muscles of Mastication
Joint dysfunction
Arythromyalgia

77
Q

If trying to diagnose bruxism, facial arthomyalgia (muscular pain associated w a joint) or TMDs, what else should you look for clinically

A
  • Attrition
  • Crenated lateral tongue
  • Tenderness of the TMJ
  • Tenderness of muscles of mastication
  • Stress anxiety
78
Q

Trigeminal Autonomic cephalgias definition and clinical features

A
  • TN like history
  • Localised to V1
  • Recurrent episodic headaches
  • Periods of remisssion between with no pain
  • Typically male 20-50 yo
  • Classically peri-orbital pain
  • Fast onset
  • Red eye, Horners Syndrome

1) Cluster headache
2) Paroxysmal hemicranias
3) Short acting Neuralgiform Headache with conjunctival injection and tearing

79
Q

FACIAL PAIN HAS NOT BEEN COVERED PROPERLY IN THESE FLASHCARDS

A

so look in the textbook a