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Finals > Neurology > Flashcards

Neurology Flashcards

1
Q

What is a TIA

A

Transient neurological dysfunction secondary to ischaemia without infarction

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2
Q

What is a crescendo TIA?

A

2 or more TIAs in one week

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3
Q

List some stroke RF

A 
CVD - angina, MI, PVD 
Previous stroke/TIA
AF
Carotid artery disease
HTN
DM
Smoking 
Vasculitis
Thrombophilia
COCP
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4
Q

Describe the management of stroke

A

Head CT to exclude haemorrhage

Exclude hypoglycaemia

Do not try to lower BP - risk of hypoperfusion

Aspirin 300mg STAT and continued for 2 weeks

Thrombolysis with Alteplase <4.5hrs symptom onset

Thrombectomy <24hrs

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5
Q

Describe the secondary prevention of stroke

A

Treat modifiable RF
Clopidogrel 75mg OD (or dipyridamole 200mg BD)
Atorvastatin 80mg
Carotid endarterectomy fi stenosis

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6
Q

What is a cerebral venous sinus thrombosis

A

Blood clot in veins that drain the brain resulting in venous congestion and tissue hypoxia

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7
Q

What are the two types of haemorrhage

A

Intracerebral - bleeding into the brain secondary to ruptured vessel - interventricular or intraparenchymal

Subarachnoid haemorrhage - bleeding outside the brain between pia mater and arachnoid mater

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8
Q

Describe a total anterior circulation stroke

A

All 3:
Unilateral weakness (and/or sensory deficit)
Homonymous hemianopia
Higher cerebral dysfunction

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9
Q

Describe partial anterior circulation stroke

A

2 of the TACS

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10
Q

Describe posterior circulation stroke

A

Cranial nerve palsy with a contralateral motor/sensory deficit
Bilateral motor or sensory deficit
Conjugate eye movement disorder
Isolated homonymous hemianopia

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11
Q

Describe lacunar stroke

A

Subcortical stroke that occurs secondary to small vessel disease
No loss of higher cerebral function

Pure motor
Pure sensory
Sensori-motor
Ataxic hemiparesis

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12
Q

List the layers under the skull

A

Dura mater
Arachnoid mater
Pia mater

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13
Q

List some risk factors of intracranial bleeds

A 
Head injury 
HTN
Aneurysms 
Ischaemic stroke 
Brain tumour 
Anticoagulants
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14
Q

Describe the presentation of an intracerebral bleed

A 
Sudden onset headache 
Seizures 
Weakness
Vomiting
Reduced consciousness
Sudden onset neurological symptoms
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15
Q

Describe the glasgow coma scale

A 
Max = 15
Min = 3

Eyes

  • spontaenous = 4
  • speech = 3
  • Pain = 2
  • None = 1

Verbal response

  • Orientated = 5
  • Confused conversation = 4
  • Inappropriate words = 3
  • Incomprehensible sounds = 2
  • None = 1

Motor response

  • obeys commands = 6
  • Localises pain = 5
  • Normal flexion = 4
  • Abnormal flexion = 3
  • Extends = 2
  • None = 1
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16
Q

Describe subdural haemorrhage

A

Rupture of bridging veins
Between dura and arachnoid mater
Crescent shape on CT
Not limited by cranial sutures - cross over suture lines
More frequent in eldely and alcoholic patients

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17
Q

Describe extradural haemorrhage

A

Rupture of the middle meningeal artery in the temporo-parietal region - can be associated with fracture of the temporal bone

Between the skull and dura mater

Bi-convex shape and are limited by cranial sutures (do not cross the suture lines)

Young patient with traumatic head injury and ongoing headache

Brief period of improved neurological symptoms and consciousness followed by a rapid decline over hours as the haematoma gets large enough to compress the intracranial contents

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18
Q

Describe intracerebral haemorrhage

A

Bleeding into brain tissue

Can occur spontaneously or as the result of bleeding into an ischaemic infarct or tumour or rupture of aneurysm

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19
Q

Describe a subarachnoid haemorrhage

A

Bleeding into the subarachnoid space, where the CSF is located between the pia mater and arachnoid membrane - usually the result of cerebral aneurysm

Sudden onset occipital headache that occurs after strenuous activity such as weight lifting or sex. Thunderclap headache

Associated with cocaine and sickle cell disease

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20
Q

Describe the management of intracerebral bleeds

A

Immediate head CT
Check FBC and clotting

Admit to specialist stroke unit

Discuss with neurosurgical centre to consider surgical treatment

Consider intubation, ventilation and ICU care if they have reduced consciousness

Correct severe hypertension but avoid hypotension
Correct any clotting abnormality

LP 12hrs after onset of symptoms in suspected subarachnoid haemorrhage and normal non contrast CT head

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21
Q

What drug is given to people with subarachnoid haemorrhage which prevents vasospasm?

A

Nimodipine (21 day course - dihydropyridine calcium channel blocker)

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22
Q

What is a common consequence of subarachnoid haemorrhage

A

Syndrome of inappropriate ADH (hyponatremia)

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23
Q

List the risk factors of subarachnoid haemorrhage

A 
HTN
Smoking
Excessive alcohol consumption 
Cocaine use
FH 
Black and female patients 
Age 45-70 
Sickle cell anaemia
Connective tissue disorders - Marfans syndrome or Ehlers Danlos 
Neurofibromatosis 
Autosomal dominant polycystic kidney disease
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24
Q

List the investigations in subarachnoid haemorrhage

A

CT head is first line - blood in subarachnoid space has hyper attenuation

LP is used to collect a sample of CSF if CT head negative - red cell count will be raised and xanthochromia (yellow colour of CSF caused by bilirubin)

Angiography - used to confirm the source of bleeding

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25
Q

Describe the management of subarachnoid haemorrhage

A

Specialist neurosurgical unit
Surgical intervention - coiling, clipping
Nimodipine - prevent vasospasm
Lumbar puncture or insertion of shunt if hydrocephalus
Antiepileptic medications - seziures

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26
Q

Describe the presentation of pituitary apoplexy

A

Sudden onset headache
Visual field defect
Evidence of pituitary insufficiency

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27
Q

What is multiple sclerosis

A

Chronic and progressive demyelination of myelinated neurones in the CNS - autoimmune condition

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28
Q

Who does MS affect

A

More commonly women <50 yo

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29
Q

How does pregnancy and post partum affect MS symptoms

A

Improves them

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30
Q

Name the two types of myelin

A

Schwann cells - PNS

Oligodendrocytes - CNS

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31
Q

Which type of myelin does MS typically affect

A

CNS - oligodendrocytes

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32
Q

What is a characteristic feature of MS lesions?

A

Vary in their location over time - different nerves are affected at different points in time

Disseminated in time and space

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33
Q

What are the causes of MS

A 
Combination of 
Multiple genes
Epstein Barr virus 
Low vit D
Smoking
Obesity
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34
Q

What causes MS symptoms to resolve in early disease?

A

Re-myelination

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35
Q

Describe symptom progression in the first presentation of MS

A

Progress over more than 24hrs and last days to weeks then improve

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36
Q

List some ways MS can present

A

Optic neuritis

Eye movement abnormalities

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37
Q

What occurs in a 6th CN palsy

A

Internuclear ophthalmoplegia - eyes do not move together

Conjugate lateral gaze disorder - when gazing to the direction of the affected eye, the affected eye will not be able to abduct

Double vision

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38
Q

Describe optic neuritis

A 
Loss of vision in one eye 
Central scotoma - enlarged blind spot 
Pain on eye movement 
Impaired colour vision 
Relative afferent pupillary defect
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39
Q

What is Lhermitte’s sign

A

Electric shock sensation that travels down the spine and into the limbs when flexing the neck - indicates disease in the cervical spinal cord and dorsal column
Caused by stretching the demyelinated dorsal column

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40
Q

Give some examples of focal weakness in MS

A

Bells palsy
Horner’s syndrome
Limb paralysis
Incontinence

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41
Q

List some focal sensory symptoms in MS

A

Trigeminal neuralgia
Numbness
Paraesthesia (pins and needles)

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42
Q

Describe ataxia in MS

A

Problem with coordination

Sensory ataxia - loss of proprioceptive sense
Cerebellar ataxia - problem coordinating movement

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43
Q

How do you test for sensory ataxia

A

Romberg’s test

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44
Q

What is psuedoathetosis

A

Writhing movement due to loss of proprioception - sensory ataxia

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45
Q

What is meant by clinically isolated syndrome in MS

A

MS cannot be diagnosed on one episode as the lesions have not be disseminated in time and space

Patients may never have another episode or develop MS - of lesions are seen on MRI then more likely to progress to MS

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46
Q

Describe relapsing-remitting MS

A

Most common pattern at initial diagnosis
Characterised by episodes of disease and neurological symptoms followed by recovery
Active - new symptoms are developing or new lesions are on MRI
Worsening - overall worsening of disability over time

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47
Q

Describe secondary progressive MS

A

Where there was relapsing remitting at first but now there is progressive worsening of symptoms with incomplete remissions

Symptoms have become more and more permanent

Can be classified based on active and/or progressing

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48
Q

Describe primary progressive MS

A

Worsening of disease and symptoms from disease onset without remissions and relapses

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49
Q

How is MS diagnosed

A

MRI scan - typical lesion

Lumbar puncture - oligoclonal bands in CSF

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50
Q

List some conditions which cause optic neuritis

A 
Sarcoidosis
SLE
DM
Syphilis 
Measles
Mumps
Lyme disease
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51
Q

How should optic neuritis be managed

A

Ophthalmology urgent review
2-6 weeks for recovery
Steroids

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52
Q

How is MS managed?

A

MDT

Disease modifying drugs

Biologic therapy

Relapses treated with Methylprednisolone - 500mg PO OD for 5 days, 1g IV daily for 3-5days when oral treatments failed previously or where relapses are severe

Exercise
Neuropathic pain - amitriptyline and gabapentin
Depression - SSRIs
Urge incontinence - anticholinergic medications - tolterodine and oxybutynin (worsen cognitive function)
Spasticity - baclofen, gabapentin and physio

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53
Q

What are motor neurone diseases

A

Umbrella term for number of diagnoses
Progressive and ultimately fatal condition where the motor neurones stop functioning

No effect on sensory symptoms and patients should not experience any sensory symptoms

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54
Q

What does progressive bulbar palsy affect

A

Affects the muscles of talking and swallowing

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55
Q

List some MNDs

A

Amyotrophic lateral sclerosis
Progressive bulbar palsy
Progressive muscular atrophy
Primary lateral sclerosis

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56
Q

Describe the neurological signs of MND

A

Bother upper and lower motor neurones affected

Sensory neurones are spared

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57
Q

What causes MND

A

Exact cause is unknown

Genetics (10%) - FH
Smoking
Exposure to heavy metals
Pesticides

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58
Q

List the signs of an upper motor neurone lesion

A

Increased tone
Upgoing plantars
Brisk reflexes

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59
Q

List the signs of a lower motor neurone lesion

A

Muscle wasting
Reduced tone
Fasciculation (twitches in the muscles)
Reduced reflexes

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60
Q

What drugs can be used to slow the progression of MND

A

Riluzole - extends survival by few months

Edaravone - used in US

NIV - support with breathing at night and improves QOL

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61
Q

Give the classic triad of Parkinson’s disease

A

Resting tremor
Rigidity
Bradykinesia

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62
Q

Describe the physiology of Parkinson’s disease

A

Basal ganglia in the middle of the brain are responsible for coordinating habitual movements such as walking, looking around, controlling voluntary movements and learning specific movement patterns

The substantia nigra (part of the basal ganglia) produces dopamine which is essential for the correct functioning of the basal ganglia but in PD there is a gradual and progressive fall in the production of dopamine

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63
Q

Describe the presentation of the tremor in Parkinson’s disease

A

4-6Hz - meaning it occurs 4-6 times a second

Pill-rolling tremor - fingertips and thumb

More pronounced when resting and improves on voluntary

Tremor is worsened if the patient is distracted - ask them to mime painting the fence - exaggerate the tremor

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64
Q

Describe the rigidity in Parkinson’s disease

A

Rigidity is a resistance to passive movement of a joint
If you take their hand and passively flex and extend their arm at the elbow, you will feel a tension in their arms that gives way to movement in small increments.

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65
Q

Describe signs of bradykinesia in Parkinson disease

A

Small handwriting
Shuffling gait
Difficulty initiating movement
Difficulty in turning around when standing, having to take lots of little steps
Reduced facial movements and facial expressions

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66
Q

What other features affect people with Parkinson’s disease

A 
Depression 
Sleep disturbance and insomnia 
Loss of sense of smell (anosmia) 
Postural instability 
Cognitive impairment and memory problems
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67
Q

Describe the difference between benign and essential tremor

A

Parkinson’s tremor - Asymmetrical, 4-6 Hz, worse at rest, improves with intentional movement, other Parkinson’s features, no change with alcohol

Benign essential tremor - Symmetrical, fine tremor, 5-8Hz, improves at rest, worse with intentional movement, worse with caffeine, tiredness and stress, no other Parkinson’s features, improves with alcohol, not present at sleep

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68
Q

What is multiple system atrophy

A

Where neurones of multiple systems in brain degenerates.
Affects the basal ganglia as well as other areas - the degeneration in basal ganglia leads to Parkinson’s presentation. Degeneration in other areas lead to autonomic dysfunction and cerebellar dysfunction (ataxia)

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69
Q

List some of the autonomic dsyfunction

A

Postural hypotension
Constipation
Abnormal sweating
Sexual dysfunction

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70
Q

Describe dementia with Lewy bodies

A

Dementia associated with features of Parkinsonism - visual hallucinations, delusions, disorders of REM sleep and fluctuating consciousness

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71
Q

How is Parkinson’s disease diagnosed?

A

Clinical symptoms and examination

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72
Q

How is Parkinson’s disease treated?

A

On - medication working
Off - medication wear off

Levodopa - synthetic dopamine give PO to boost their own dopamine levels.
Usually combined with a peripheral decarboxylase inhibitors (drug that stops levodopa being broken down in the body before it gets the chance to enter the brain)
Co-careldopa (levodopa and carbidopa)
Co-benyldopa (levodopa and benserazide)

COMT inhibitors - Entacapone - inhibits the COMT enzyme which usually metabolises levodopa in the body and brain. Taken with the levodopa to slow the breakdown of levodopa and extend its effective duration

Dopamine agonists (cabergoline, pergolide, bromocryptine) - mimic dopamine in the basal ganglia and stimulate the dopamine receptors. Less effective than levodopa but used to delay the use of levodopa and the dose of levodopa required.

Monoamine oxidase B inhibitors - enzymes break down neurotransmitters such as dopamine, serotonin and adrenaline. More specific to dopamine and does not act on serotonin or adrenalin. These medications block the enzyme and increase circulating dopamine Used to delay starting levodopa - selegilline and rasagiline

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73
Q

What happens to Levodopa effectiveness over time

A

Becomes less effective

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74
Q

What is the main side effect of levodopa

A

When dopamine levels are too high - this causes dyskinesia (excessive motor activity)

  • dystonia - excessive muscle contraction leads to excessive movement and abnormal posture
  • Chorea - abnormal involuntary movements that can be jerking and random
  • Athetosis - involuntary twisting and writhing movements of the fingers, hands and feet
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75
Q

What is a side effect of the dopamine agonists

A

Pulmonary fibrosis with prolonged use

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76
Q

What is the differential diagnosis for a benign essential tremor

A 
Parkinson's disease
MS
Huntington's chorea
Hyperthyroidism 
Fever
Medication - antipsychotics and salbutamol overuse
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77
Q

Describe the management of benign essential tremor

A

No definitive treatment

Medication can improve symptom - propranolol (non-selective beta blocker) and primidone (barbiturate anti-epileptic)

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78
Q

What is epilepsy

A

An umbrella term for a condition where there is a tendency to have seizures

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79
Q

What are seizures

A

Transient episodes of abnormal electrical activity in the brain

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80
Q

What investigations should be done for epilepsy

A

EEG
MRI brain
ECG

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81
Q

Describe a tonic-clonic seizure

A

Loss of consciousness
Tonic phase before clonic phase
Tonic phase is muscle stiffening
Clonic phase is muscle jerking
May be associated with incontinence, tongue biting, groans and irregular breathing
Post ictal period - confused, drowsy, irritable or depressed

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82
Q

Describe the management of tonic clonic seizures

A

1st line - sodium valproate

2nd line - lamotrigine or carbamazepine

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83
Q

Where do focal seizures originate?

A

Temporal lobe

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84
Q

Describe the presentation of focal seizures

A 
These affect hearing, speech, memory and emotion Hallucinations
Memory flashbacks
Deja vu 
Doing strange things on autopilot 
Post-ictal weakness
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85
Q

How do you treat focal seizures

A

1st line - carbamazepine or lamotrigine

2nd line - sodium valproate or levetiracetam

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86
Q

Describe absence seizures

A

Happen in children
Patient becomes blank, stares into space and then abruptly returns to normal
These last 10-20seconds and the patient will not respond in this time

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87
Q

What is the management of absence seizures

A

Sodium valproate or ethosuximide

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88
Q

Describe atonic seizures

A 
Drop attacks 
Brief lapses in muscle tone 
Don't usually last more than 3 mins 
Begin in childhood 
Indicative of lennox-gastaut syndrome
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89
Q

Describe the management of atonic seizures

A

1st line - sodium valproate

2nd line - lamotrigine

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90
Q

Describe myoclonic seizures

A

Sudden brief muscle contractions - sudden jump
Patient remains awake during the episode
Most often occur in juvenile myoclonic epilepsy

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91
Q

How are myoclonic seizures treated

A

1st line - sodium valproate

2nd line - lamotrigine, levetiracetam, topiramate

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92
Q

Describe infantile spasms (West syndrome)

A

Rare disorder - full body spasms
starting in infancy at around 6 months - poor prognosis where 1/3 die before 25 and the rest are seizure free
Treated with prednisolone and vigabatrin

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93
Q

How does sodium valproate work

A

Increases the activity of GABA

Relaxing effect on the brain

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94
Q

List some side effects of sodium valproate

A

Teratogenic
Liver damage and hepatitis
Hair loss
Tremor

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95
Q

List some notable side effects of carbamazepine

A

Agranulocytosis
Aplastic anaemia
Induces P450 enzyme system - drug interactions

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96
Q

List some notable effects of phenytoin

A

Megaloblastic anaemia
Vit D and folate deficiency
Osteomalacia

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97
Q

List some notable side effects of ethosuximide

A

Night terrors

Rashes

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98
Q

List some notable side effects of lamotrigine

A

Stevens - Johnson syndrome or DRESS syndrome

Leukopenia

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99
Q

Define status epilepticus

A

A seizure lasting >5 mins or >3 seizures in 1 hour

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100
Q

How do you treat status epilepticus

A 
ABCDE approach 
Secure the airway - NP tube
Give high flow O2 
Assess cardiac and respiratory function 
Check blood glucose 
Gain IV access - cannulate 
IV lorazepam 4mg, repeat after 5 mins 
If seizure persists try IV phenytoin and call anaesthetists with view to intubate and ventilate
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101
Q

What is the name of the post-ictal weakness focal epileptic patients get

A

Todd’s paresis

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102
Q

What type of symptoms do frontal lobe seizures cause

A

Motor - jerking of the limb

Jacksonian march

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103
Q

What types of symptoms would occur with an occipital lobe seizure

A

Visual hallucinations

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104
Q

What symptoms would a parietal lobe seizure present with

A

Paraesthesia

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105
Q

What symptoms do temporal lobe focal seizures present with

A 
Hallucinations
Epigastric rising
Emotional 
Automatisms - lip smacking, grabbing and plucking
Deja vu 
Dysphasia
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106
Q

Describe a Jacksonian March

A

Seizure begins in one part of the body and then spreads over larger area of the brain causing a tonic clonic seizure

Secondary generalisation

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107
Q

When and how can anti-epileptic drugs be stopped

A

If seizure free for >2yrs and stopped over 2-3months

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108
Q

How can epileptic seizures be differentiated from vasovagal syncope

A

Vasovagal syncope - no post ictal period and rapid recovery

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109
Q

What is neuropathic pain, give examples of the causes

A

Abnormal functioning of the sensory nerves delivering abnormal and painful signals to the brain

Burning, tingling, pins and needles, electric shocks, loss of sensation to touch over the affected area

Post herpetic neuralgia from shingles in the distribution of a dermatome usually on the trunk

Nerve damage from surgery

MS

Diabetic neuralgia

Trigeminal neuralgia

Complex regional pain syndrome (CRPS)

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110
Q

What is the DN4 questionnaire

A

Used to assess the characteristics of neuropathic pain and the examination of the area
Scored out of 10 and a score >4 indicates neuropathic pain

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111
Q

Which drugs can be tried to relieve neuropathic pain

A

Amitriptyline
Duloxetine
Pregabalin
Gabapentin

Tramadol - short term flares
Capsaicin cream

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112
Q

Which drug is first line when treating trigeminal neuralgia

A

Carbamazepine

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113
Q

Describe complex regional pain syndrome

A

Abnormal nerve functioning - abnormal sensations and neuropathic pain

Often triggered by an injury to that area

Intermittent swelling, change in colour, temperature, flush and abnormal sweating

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114
Q

Describe the path of the facial nerve

A

Exits the brainstem at the cerebellopontine angle
Passes through the temporal bone and parotid gland
Divides into 5 branches that supply different areas of the face - temporal, zygomatic, buccal, marginal mandibular and cervical

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115
Q

Describe the functions of the facial nerve

A

Motor - facial expression, stapedius in inner ear and the posterior digastric, stylohyoid and platysma muscles of the neck

Sensory - taste of anterior 2/3 tongue

Parasympathetic - submandibular and sublingual salivary glands and the lacrimal gland

116
Q

Describe the nerve innervation of the forehead

A

Each side of the forehead has upper motor neuron innervation by both sides of the brain

Each side of the forehead only has lower motor neuron innervation from one side of the brain

117
Q

What can be seen in an UMN facial palsy

A

Forehead sparing

118
Q

Describe the symptoms of Bells palsy

A

Forehead affected
Drooping of the eyelid
Exposure of the eye
Loss of the nasolabial fold

119
Q

List some causes of an UMN facial palsy

A

Cerebrovascular accident
Tumour
Bilateral - pseudobulbar palsy and MND

120
Q

List some causes of LMN facial palsy

A 
Bells palsy
Ramsay Hunt syndrome 
Otitis media
Malignant otitis externa 
HIV
Lyme disease
Diabetes
Sarcoidosis
Leukaemia
MS
Guillian Barre syndrome 
Acoustic neuroma 
Parotid tumours 
Cholesteatoma 
Direct nerve injury
Injury during surgery 
Base of skull fracture
121
Q

How long does recovery from Bells palsy take?

A

several weeks - 12 months however some never recover completely (1/3 left with residual weakness)

122
Q

How is Bells palsy treated

A

Prednisolone
50mg for 10days
60mg for 5 days followed by a 5 day reducing regime of 10mg a day

Lubricating eye drops

123
Q

What may happen as a result of Bells palsy

A

Exposure keratopathy

124
Q

Describe Ramsay Hunt syndrome

A

Varicella zoster virus (VZV)
Unilateral LMN facial palsy
Tender vesicular rash in ear canal, pinna, around ear on affected side
The rash can extend to the anterior 2/3 of the tongue and hard palate

125
Q

How is Ramsay Hunt syndrome treated

A

Prednisolone
Aciclovir
Lubricating eye drops

126
Q

What happens to perception of sound in an UMN facial nerve palsy

A

Hyperacusis - hypersensitivity to sound

Paralysis of stapedius

127
Q

When should facial nerve palsies be referred to ENT or neurology

A

Worsening or new neurological findings
Red flag features of cancer
No signs of improvement after 3 weeks of treatment
Symptoms of aberrant reinnervation 5 months or more after original onset
Unclear diagnosis

128
Q

Describe the symptoms of a brain tumour

A

Focal neurological lesion
Signs of raised ICP
Often asymptomatic at the beginning

129
Q

List some causes of raised intracranial pressure

A

Brain tumour
Intracranial haemorrhage
Idiopathic intracranial hypertension
Abscesses or infection

130
Q

Describe the presentation of raised intracranial pressure

A

Headache - constant, nocturnal, worse on waking, coughing, straining or bending forward, vomiting

Altered mental state
Visual field defects 
Seizures - focal 
Unilateral ptosis
Third and sixth nerve palsy 
Papilloedema
131
Q

What is Papilloedema

A

Swelling of the optic disc secondary to raised intracranial pressure

The sheath around the optic nerve is connected with the subarachnoid space - possible for CSF under high pressure to flow into the optic nerve sheath and causes swelling

132
Q

Describe the fundoscopic changes of Papilloedema

A

Blurring of the optic disc margin
Elevated optic disc - curve in retinal vessels
Loss of the venous pulsation
Engorged retinal veins
Haemorrhages around optic disc
Paton’s lines - creases in the retina around the optic disc

133
Q

Which cancers commonly metastasise to the brain

A

Breast
Lung
Renal cell carcinoma
Melanoma

134
Q

Describe gliomas

A

Tumours of glial cells

  • Astrocytoma - glioblastoma multiforme
  • oligodendroglioma
  • Ependymoma

Graded from 1-4 - grade 1 is most benign and grade 4 is most malignant

135
Q

Describe a meningioma

A

Tumour of the meninges in the brain and lead to raised ICP and neurological symptoms

136
Q

Describe pituitary tumours

A

Benign but if they become large can press on the optic chiasm causing bitemporal hemianopia (loss of the outer half of vision in both eyes

Hypo or hyperpituitarism

  • Acromegaly
  • Cushing’s syndrome
  • Hyperprolactinaemia
  • Thyrotoxicosis
137
Q

Describe acoustic neuroma

A

Tumour of Schwann cells surrounding the auditory nerve that innervates the inner ear

Occur at the cerebellopontine angle

Usually unilateral, bilateral ones associated with neurofibromatosis type 2

Slow growing but eventually grow large enough to cause symptoms and become dangerous

  • Tinnitus
  • Hearing loss
  • Balance problems

Associated with facial nerve palsy

138
Q

Describe the treatment of pituitary tumours

A

Trans-sphenoidal surgery
Radiotherapy
Bromocriptine - block prolactin secreting tumour
Somatostatin analogues - octreotide - block growth hormone secreting tumour

139
Q

What is Huntington’s chorea

A

Autosomal dominant progressive deterioration of nervous system

Asymptomatic until symptoms begin age 30-50

140
Q

Describe the genetic abnormality in Huntington’s chorea

A

Trinucleotide repeat disorder of HTT gene on chromosome 4

141
Q

Describe what is meant by anticipation in Huntington’s chorea

A

Each successive generation, more trinucleotide repeats resulting in earlier onset and increased severity of disease

142
Q

Describe the presentation of Huntington’s chorea

A

Begins with cognitive, psychiatric or mood problems

  • Chorea - involuntary, abnormal movements
  • Eye movement disorders
  • Speech difficulties - dysarthria
  • Swallowing difficulties
143
Q

Describe the prognosis of Huntington’s chorea

A

15-20yrs life expectancy following diagnosis

Death is often due to respiratory disease or suicide

144
Q

Describe myasthenia gravis

A

Autoimmune condition

Weakness gets progressively worse with activity and improves with rest

145
Q

At what age does myasthenia gravis tend to present

A

<40yo women

>60 men

146
Q

What type of tumour is linked to myasthenia gravis

A

Thyoma (tumour of thymus gland)

147
Q

Describe normal conduction across the neuromuscular junction

A

Pre-synaptic neurone secretes acetylcholine across the synapse which then binds to post synaptic receptors and stimulates a signal in the muscle and muscle contraction occurs

148
Q

What happens to neuromuscular junction transmission in myasthenia gravis

A

Antibodies to the acetylcholine receptor are produced. These bind to the post synaptic membrane and block the receptor. Acetylcholine is prevented from stimulating the post synaptic membrane and prevent muscle contraction
As more receptors are used up during more muscle activity, more become blocked
There is more muscle weakness the more the muscles are used This improves with rest when more receptors are free for use again

Complement system is also activated and this damages the postsynaptic membrane

Antibodies against Muscle specific kinase (MuSK) and antibodies against low density lipoprotein receptor related protein 4 (LRP4) - used to create the ACH receptor. Destruction of these by antibodies leads to inadequate receptors

149
Q

Describe the presentation of myasthenia

A 
Proximal muscles 
Diplopia - weak extraocular muscles 
Ptosis
Weak facial muscles 
Difficulty swallowing
Fatigue in the jaw when chewing 
Slurred speech 
Progressive weakness with repetitive movement

Symptoms are worse at night time

150
Q

Describe the examination and investigations for myasthenia gravis

A

Upward gazing - diplopia on further eye movement test

Repeated blinking will exacerbate ptosis

Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides

FVC

Check for thymectomy scar

151
Q

How is a diagnosis of myasthenia gravis made

A

Test for antibodies - AchR, MuSK, LRP4

CT/MRI thymus

Edrophonium test - IV dose of edrophonium chloride (neostigmine) - block acetylcholinesterase enzyme in NMJ - relieves the weakness temporally

152
Q

Describe the treatment of myasthenia gravis

A

Reversible anticholinesterase inhibitors - pyridostigmine and neostigmine
Immunosuppression - prednisolone and azathioprine
Thymectomy
Rituximab
Eculizumab

153
Q

Describe a myasthenic crisis and its treatment

A

Severe complication of MG
Life threatening
Caused by other illness such as respiratory illness
Patients may require NIV or full intubation and ventilation
IVIG and plasma exchange may help

154
Q

Which drug should be avoided in people with myasthenia

A

Beta blockers

155
Q

Which anaesthetic drug are patients with myasthenia gravis often resistant to?

A

Suxamethonium

156
Q

What is Lambert-Eaton Myasthenia

A

Slow progression
Proximal muscles more
Damage to the neuromuscular junction - antibodies produced by the immune system against voltage gated calcium channels in the presynaptic terminals of the NMJ
Tends to occur more in patients with small cell lung cancer

157
Q

How is Lambert-eaton myasthenia treated?

A

Immunosuppressants - prednisolone or azathioprine
IV immunoglobulins
Plasmaphoresis

158
Q

What is charcot marie tooth disease

A

Inherited disease that affects the peripheral motor and sensory nerves
Dysfunction in the myelin or the axons
Autosomal dominant pattern
Symptoms usually start to appear before the age of 10 but onset can be after 40

159
Q

Name some classical features of Charcot Marie tooth disease

A

High foot arches
Distal muscle wasting causing inferted champagne bottle legs
Weakness in lower legs - ankle dorsiflexion
Weakness in the hands
Reduced tendon reflexes
Reduced muscle tone
Peripheral sensory loss

160
Q

List the causes of peripheral neuropathy

A 
Alcohol
B12 deficiency 
Cancer and Chronic kidney disease
Diabetes 
Drugs - isoniazid, amiodarone and cisplatin
Vasculitides
161
Q

Describe Guilian-Barre syndrome

A

Acute paralytic polyneuropathy - affects the PNS

Causes acute, symmetrical, ascending weakness and sensory symptoms

162
Q

Which infections is Guillian Barre most associated with?

A

Campylobacter jejuni
Cytomegalovirus
Epstein Barr virus

163
Q

Describe the pathophysiology of Guillian Barre syndrome

A

Molecular mimicry - B cells of the immune system create antibodies against antigens on the pathogen that causes the preceding infection
These antibodies also match the proteins on the nerve cells
They may have target proteins on the myelin sheath of the motor nerve cell or the nerve axon

164
Q

Describe the presentation of Guillian Barre syndrome

A

Symmetrical ascending weakness
Reduced reflexes
Peripheral loss of sensation or neuropathic pain
Progress to affect the cranial nerves

165
Q

Describe the clinical course of Guillian Barre syndrome

A

Symptoms start within 4 weeks of the preceding infection

Start in the feet and progress upwards
Symptoms peak within 2-4 weeks then a recover period can last moths to years

166
Q

Describe how Guillian Barre is diagnosed

A

The Brighton criteria is used

Nerve conduction studies - reduced signal through nerves

LP for CSF - raised protein with a normal cell count and a normal glucose

167
Q

How is Guillian Barre syndrome treated?

A 
IV IG 
Plasma exchange 
Supportive care
VTE prophylaxis 
Resp failure may require intubation, ventilation and admission
168
Q

Describe the prognosis of Guillian Barre syndrome

A

80% fully recover
15% left with some neurological disability
5% will die

169
Q

Describe neurofibromatosis

A

Nerve tumours throughout the nervous system
Benign - do cause neurological and structural problems

Two types - type 1 is more common than type 2

170
Q

Describe neurofibromatosis type 1

A

NF1 gene mutations on chromosome 17 - neurofibromin (tumour suppressor gene). Inheritance is autosomal dominant
2 of the 7 features:
Cafe au lait spots
Relative with NF1
Axillary or inguinal freckles
Bony dysplasia - bowing of the long bone or sphenoid wing dysplasia
Iris haematomas - Lisch nodules (yellow brown spots on the iris)
Neurofibromas or plexiform neurofibroma
Glioma of the optic nerve

171
Q

How do you investigate Neurofibromatosis

A

Genetic testing
X-ray - investigate bone pain and bone lesions #CT and MRI - investigate lesions in the brain, spinal cord and elsewhere in the body

172
Q

Describe neurofibromatosis type 2

A

Chromosome 22 protein merlin (tumour suppressor protein) important in Schwann cells and mutations lead to development of schwannomas

173
Q

What is neurofibromatosis most associated with?

A

Bilateral acoustic neuromas (hearing loss, balance problems, tinitus)

174
Q

How is neurofibromatosis managed

A

Supportive - monitor the disease and treat any complications such as surgical resection

175
Q

List some complications of neurofibromatosis type 1

A

Migraines
Epilepsy
Renal artery stenosis - causing hypertension
Learning and behavioural problems
Scoliosis of the spine
Vision loss
Malignant peripheral nerve sheath tumours
Gastrointestinal stromal tumour (sarcoma)
Brain tumours
Spinal cord tumour with associated neurology
Increased risk of breast cancer and leukaemia

176
Q

List some red flags of headaches

A

Fever, photophobia, neck stiffness (meningitis, encephalitis)
New neurological symptoms (haemorrhage, malignancy, stroke)
Dizziness (stroke)

Visual disturbance (temporal arteritis or glaucoma)

Sudden onset occipital headache (SAH)

Worse on coughing or straining (raised ICP)

Postural, worse on standing, lying or bending over (raised ICP)

Severe enough to wake person up from sleep

Vomiting - raised ICP or CO poisoning

History of trauma (ICH)

Pregnancy (pre-eclampsia)

177
Q

Describe a tension headache, the triggers and its management

A

Mild ache across the forehead in a band like pattern around the head

Due to muscle ache in frontalis, temporalis and occipitalis muscles

Come on and resolve gradually and do not produce any visual changes

Triggers - stress, depression, alcohol, skipping meals, dehydration

Treatment - reassurance, hot towels, relaxation techniques, basic analgesia

178
Q

Describe what is meant by a secondary headache

A

Similar presentation to tension headache but with a clear cause

Non specific headache secondary to underlying medical conditions, alcohol, head injury and carbon monocide poisoning

179
Q

Describe sinusitis and its course and treatment

A

Inflammation in the ethmoidal, maxillary, frontal or sphenoidal sinuses

Facial pain behind the nose, forehead, eyes

Tenderness over sinus

Resolves within 2-3 weeks

Most is viral

Nasal irrigation with saline can be helpful

Prolonged symptoms (>10 days) treated with steroid nasal spray and antibiotics are occasionally required

180
Q

Describe what an analgesia overuse headache is and how it is treated

A

Long term analgesia use
Non specific features to a tension headache
Secondary to continous or excessive use of analgesia
Withdrawal of the analgesia is important in treating these headaches

181
Q

Describe a hormonal headache

A

Related to low oestrogen
Non specific, generic, tension type headache
2 days before and first 3 days of period, around menopause and during pregnancy (2nd half pregnancy should raise suspicion of pre-eclampsia)

COCP can help treat this

182
Q

Describe cervical spondylosis

A

Degenerative changes in the cervical spine
Causes neck pain made worse by movement
Presents with a headache
Exclude other causes of neck pain - inflammation, malignancy, infection

183
Q

Describe trigeminal neuralgia

A

Trigeminal nerve has 3 branches - ophthalmic, maxillary, mandibular

Compression of the nerve
Occurs in patients with MS
Intense facial pain that comes on spontaneously and lasts for few seconds to hours
Often described as electrical shock pain
Attacks often worsen over time
Triggers - spicy food, cold weather, caffeine, citrus fruits

Carbamazepine or surgical decompression

184
Q

List some types of migraine

A

Migraine without aura
Migraine with aura
Silent migraine
Hemiplegic migraine

185
Q

Describe the headache in migraine

A 
Lasts between 4 and 72hrs 
Moderate to severe in frequency 
Uusally unilateral but can be bilateral 
Photophobia and phonophobia 
With or without aura
Nausea and vomiting
186
Q

Describe the aura in migraine

A

Visual changes associated with migraine

  • sparks in vision
  • Blurring vision
  • Lines across vision
  • Loss of different visual fields
187
Q

Describe a hemiplegic migraine

A 
Mimics a stroke
Typical migraine symptoms 
Sudden or gradual onset
Hemiplegia - unilateral weakness of the limbs 
Ataxia 
Change in consciousness
188
Q

List some triggers of migraines

A 
Stress
Bright lights
Strong smells
Certain food 
Dehydration 
Menstruation
Abnormal sleep patterns
Trauma
189
Q

List the 5 stages of migraine

A 
Prodromal stage (3 days before) 
Aura (60 mins)
Headache (4 to 72hrs) 
Resolution stage - headache fades away or is relieved by vomiting or sleeping 
Postdromal/recovery
190
Q

Describe the acute management of migraine

A

Paracetamol

Triptans - 5HT receptor agonists - smooth muscle contraction in arteries to cause vasoconstriction, peripheral pain receptors inhibited activation of pain, reduce neuronal activity in the CNS

NSAIDs

Antiemetics

191
Q

Describe migraine prophylaxis

A 
Propranolol
Topiramate 
Amitriptyline 
Acupuncture
Supplementation with B2 (riboflavin) 
Avoid triggers
192
Q

What is a contraindication to topirmate

A

Pregnancy

193
Q

Describe cluster headaches

A

Cluster of attacks and then disappear for a while

Typical patient is 30-50yo, smoker, triggered by alcohol, strong smell and exercise

194
Q

Describe the symptoms of a cluster headache

A 
Red, swollen and watering eye 
Pupil constriction (miosis) 
Eyelid drooping (ptosis) 
Nasal discharge 
Facial sweating
195
Q

What is the treatment of cluster headache

A

Triptans - Sumatriptan 6mg SC

High flow O2 100% for 15-20mins

196
Q

What prophylaxis of cluster headaches can be given

A

Verapamil
Lithium
Prednisolone - short course for 2-3 weeks to break the cycle

197
Q

When is carotid endarterectomy performed

A

Symptomatic stenosis >75%

198
Q

List some causes of myasthenic crisis

A 
Pregnancy 
Emotion
Exercise
Chest sepsis 
Hypokalaemia 
Beta blockers
Antibiotics -tetracyclines 
Opiates 
Acetylcholinesterase inhibitors
199
Q

Problems with which structures can cause ptosis?

A

Midbrain
Cervical sympathetic chain
Oculomotor nerve

200
Q

Describe pronator drift and what it signifies

A

Patient holds out arms with palms upwards
Observe for signs of pronation for 20-30 seconds
Ask patient to close eyes
Pronation with or without downward movement of the forearm suggests an UMN pyramidal tract lesion in the contralateral side as supinator’s are weaker than pronator muscles in this context

201
Q

Describe spasticity

A

Associated with pyramidal tract lesions
Velocity dependent - the faster you move the limb, the worse it is - typically increased tone in intial part of movement which then suddenly reduces past a certain point - clasp knife spasticity - also accompanied by weakness

202
Q

Describe rigidity

A

Velocity independent - feels the same no matter how fast you move the limb

203
Q

What are the two types of rigidity

A

Cogwheel rigidity - involves a tremor superimposed on hypertonia resulting in intermittent increases in tone during movement of the limb - Parkinson’s disease

Lead pipe rigidity - uniformly increased tone throughout the movement of muscle - subtype of rigidity is typically associated with neuroleptic malignant syndrome

204
Q

Describe the MRC power scale

A

0 - no contraction
1 - Flicker or trace of contraction
2- active movement, with gravity eliminated
3 - active movement against gravity
4 - active movement against gravity and resistance
5 - normal power

205
Q

Which myotome and muscles are tested when assessing shoulder abduction

A

C5 (axillary nerve)

Deltoids

206
Q

Which myotome and muscles are tested when assessing shoulder adduction

A

C6/7 (thoracodorsal nerve)

Latissimus dorsi, teres major, pectoralis major

207
Q

Which myotome and muscles are tested when assessing elbow flexion

A

C5/6 (musculocutaneous and radial nerve)

Coracobrachialis, biceps brachii and brachialis

208
Q

Which myotome and muscles are tested when assessing elbow extension

A

C7 (radial nerve)

Triceps brachii

209
Q

Which myotome and muscles are tested when assessing the wrist extension

A

C6 (radial nerves)

Extensors of the wrist

210
Q

Which myotome and muscles are tested when assessing wrist flexion

A

C6/7 (median nerve)

Flexors of the wrist

211
Q

Which myotome and muscles are tested when assessing finger extension

A

C7 (radial nerve)

Extensor digitorium

212
Q

Which myotome and muscles are tested when assessing finger abduction

A 
T 1 (ulnar nerve) 
Abductor digiti minimi 
First dorsal interosseous
213
Q

Which myotome and muscles are tested when assessing thumb abduction

A

T1 (median nerve)

Abductor pollicis brevis

214
Q

Describe the pattern of weakness in an upper motor neuron lesion

A

Pyramidal weakness
Extensors in the upper limb are weaker than the flexors
Flexors in the lower limb are weaker than the extensors

215
Q

Describe a reinforcement manoeuvre you can do to ensure the reflexes are absent

A

Ask patient to clench their teeth - relaxes the arms

216
Q

Which myotome supplies the biceps reflex

A

C5/6

217
Q

Where do you hit to elicit the biceps reflex

A

Medial aspect of the antecubital fossa

218
Q

Which myotome is the supinator reflex

A

C5/6

219
Q

Where do you hit to elicit the supinator (Brachioradialis) reflex

A

Brachioradialis tendon - 4 inches proximal to the base of the thumb on the posterolateral aspect of the wrist

220
Q

Which myotome is the triceps reflex

A

C7

221
Q

Where do you hit to elicit the triceps reflex

A

Triceps tendon - Superior to the olecranon process of the ulnar

222
Q

Describe hyperreflexia

A

Associated with UMN lesion - loss of inhibition from higher brain centres which normally exert a degree of suppression over the lower motor neuron reflex arc

223
Q

Describe hyporeflexia

A

LMN lesion - loss of efferent and afferent branches of the normal reflex arc

224
Q

Describe the reflexes in cerebellar disease

A

Often normal

Can be pendular - less brisk and slower in their rise and fall

225
Q

Describe where you would test each of the dermatomes

A

C5 - lateral aspect of the lower edge of the deltoid muscle

C6 - palmar side of the thumb

C7- palmar side of middle finger

C8 - palmar side of little finger

T1 - medial aspect of antecubital fossa,, proximal to medial epicondyle of Humerus

226
Q

What does light touch sensation involve

A

Dorsal columns

Spinothalamic tract

227
Q

What does pin-prick sensation involve

A

Spinothalamic tracts

228
Q

What does vibration sense involve

A

Dorsal columns

229
Q

What does proprioception involve

A

Dorsal columns

230
Q

What causes peripheral neuropathy

A

Chronic alcohol excess

Diabetes mellitus

231
Q

What is a radiculopathy

A

Nerve root damage

232
Q

What is mononeuropathy

A

Nerve damage

233
Q

What type of sensory disturbance is caused by a thalamic lesion

A

Contralateral sesnory loss

234
Q

What type of weakness results from myopathy

A

Symmetrical proximal muscle weakness

235
Q

Describe an intention tremor

A

Broad, coarse, low frequency tremor that develops as a limb reaches the endpoint of a deliberate movement

236
Q

What does dysmetria and intention tremor suggest

A

Ipsilateral cerebellar pathology

237
Q

What does dysdiadochokinesia suggest

A

Inability to perform rapid, alternating rapid movement - suggest ipsilateral cerebellar pathology

238
Q

What is a broad based ataxic gait associated with?

A

Midline cerebellar pathology - lesion in MS or degeneration of the cerebellar vermis secondary to chronic alcohol excess

239
Q

In unilateral cerebellar disease in which direction will patients veer to?

A

The side of the pathology

240
Q

What does a high stepping gait possibly indicate

A

Foot drop

241
Q

What does tandem gait show

A

Dysfunction of cerebellar vermis (alcohol induced cerebellar degeneration)
Weak flexors or sensory ataxia

242
Q

Describe hemiparetic gait

A

One leg held stiffly and swings round in an arc with each stride (circumduction) - associated with stroke

243
Q

Describe spastic paraparesis gait

A

Bilateral hemiparetic gait with both legs stiff and circumduction
Inverted and scissor feet
Hereditary spastic paraplegia

244
Q

Describe Romberg’s test

A

Ask patient to put feet together and arms by their side

Close eyes - if patient has proprioceptive or vestibular dysfunction then will struggle to remain standing

245
Q

What is a positive Romberg’s and what does it suggest

A

Falling without correction

Sensory ataxia - proprioceptive dysfunction (Ehlers Danlos), B12 deficiency, Parkinson’s disease and ageing

Vestibular dysfunction - vestibular neuronitis and Menieres disease

246
Q

What does swaying with correction during rombergs test suggest

A

Rombergs negative

Cerebellar disease due to truncal ataxia

247
Q

Describe what may be observed with increased tone in the leg

A

When lifting knee off the bed, the ankle will come up too

248
Q

Describe ankle clonus

A

Involuntary rhythmic muscular contractions and relaxations that is associated with UMN lesions of the descending motor pathways (stroke, MS, cerebral palsy)

Position patients legs so the knee and ankle are slightly flexed, supporting the leg with your hand under their knee so they can relax
Rapidly dorsiflex and partially evert the foot to stretch gastrocnemius muscle
Keep the foot in this position and observe for clonus (>5 rhythmic beats of dorsiflexion and plantarflexion)

249
Q

Which myotomes and muscles are assessed when testing hip flexion

A

L1/2 (iliofemoral nerve)

Iliopsoas

250
Q

Which myotomes and muscles are assessed when testing hip extension

A

L5/S1/S2

Gluteus maximus

251
Q

Which myotomes and muscles are assessed when testing knee flexion

A

S1 (Sciatic nerve)

Hamstrings

252
Q

Which myotomes and muscles are assessed when testing knee extension

A

L3/4 (femoral nerve

Quadriceps

253
Q

Which myotomes and muscles are assessed when testing ankle dorsiflexion

A

L4/5 (deep peroneal nerve)

Tibialis anterior

254
Q

Which myotomes and muscles are assessed when testing ankle plantarflexion

A

S1/2
Tibial nerve
Gastrocnemius and soleus

255
Q

Which myotome and muscles are assessed when testing big toe extension

A

L5 (deep peroneal nerve)

Extensor hallucis longus

256
Q

Which myotome is associated with the patella reflex

A

L3/4

257
Q

Which myotome is associated with the ankle jerk reflex

A

S1

258
Q

Which myotome is associated with the plantar reflex

A

L5 and S1

259
Q

Describe babinskis sign

A

Extension of the big toe and spreading of the other toes - UMN lesion

260
Q

What is L1 dermatome

A

Inguinal region and very top of medial thigh

261
Q

What is the L2 dermatome

A

Middle and lateral aspect of anterior thigh

262
Q

What is the L3 dermatome

A

MEDIAL ASPECT OF KNEE

263
Q

What is the L4 dermatome

A

Medial aspect of lower leg and ankle

264
Q

What is the L5 dermatome

A

Dorsum and medial aspect of big toe

265
Q

What is the S1 dermatome

A

Dorsum and lateral aspect of the little toe

266
Q

What does inability to perform heel to shin test show

A

Incoordination - Dysmetria - ipsilateral cerebellar pathology

267
Q

What is a relative afferent pupillary defect and what does it show

A

Constriction less so in the affected pupil
Swinging light test shows relative pupillary dilation when light shone from healthy eye to damaged eye

Retinal damage - central retinal artery occlusion, vitreous
detachment , compression due to tumour or abscess
Optic neuritis

268
Q

What is an unilateral efferent defect and what does it show

A

Compression caused by the extrinsic pathway

Ipsilateral pupil dilates and is non-responsive but consensual response the unaffected pupil is normal

269
Q

What is visual neglect and what does it show?

A

Deficiet in awareness of one side of the visual field

Stroke in contralateral parietal region

270
Q

What is the function of the inferior oblique

A

Elevates, abducts and laterally rotates the eyeball

271
Q

What is the function of the superior oblique

A

Depresses, abducts and medially rotates the eyeballs

272
Q

Describe the function of the medial rectus

A

Adducts the eyeball

273
Q

Describe the function of the lateral rectus

A

Abduct the eyeball

274
Q

Describe the function of the superior rectus

A

Elevation, adduction, medial rotation of the eyeball

275
Q

Describe the function of the inferior rectus

A

Depression, adduction and lateral rotation of the eyeball

276
Q

What are the features of an oculomotor nerve palsy

A

Down and out pupil
Ptosis
Mydriasis

277
Q

What are the features of a trochlear nerve palsy

A

Vertical diplopia when looking inferiorly

278
Q

Which muscle is supplied by the trochlea nerve

A

Superior oblique

279
Q

Which muscle is supplied by the abducens nerve

A

Lateral rectus muscle

280
Q

What does abducens nerve palsy cause

A

Convergent squint

Horizontal diplopia

281
Q

What is a normal rinnes test

A

Air conduction > Bone conduction

282
Q

What would be the Rinnes test for sensorineural deafness

A

Air conduction >Bone conduction

Rinnes positive

283
Q

What would be the Rinnes test for conductive deafness

A

Bone conduction > Air conduction

Rinnes negative

284
Q

Describe normal Weber’s

A

Sound heard equally in both ears

285
Q

Describe Weber’s in sensorineural deafness

A

Sound head louder in the normal ear

286
Q

Describe Weber’s in conductive deafness

A

Sound heard louder on the side of the affected ear

287
Q

Describe the head thrust test/vestibular ocular reflex

A

Ask pt if they have any neck problems

Tell pt to focus on your nose at all times

Turn their head rapidly to left and then to right

Normal - eyes fix on your nose
Vesibular pathology - eyes move in direction of head movement before a corrective refixation saccade towards your nose

Finals (18 decks)

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