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Year 4 Semester 2 > Neurology > Flashcards

Neurology Flashcards

1
Q

What does the dorsal column pathway include?

A

Proprioception
Vibration
Finetouch

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2
Q

What does the spinothalamic pathway include?

A

Pain

Temperature

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3
Q

What is the parasympathetic NS?

A

Rest and digest

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4
Q

What is the sympathetic NS?

A

Fight or flight

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5
Q

What does the autonomic NS include?

A

Parasympathetic NS

Sympathetic NS

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6
Q

Excitatory neurotransmitters?

A 
Glutamate
Acetylcholine
Noradrenaline
Serotonin
Dopamine
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7
Q

Inhibitory neurotransmitters?

A

GABA

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8
Q

Primary headache syndromes?

A 
Migraine
Tension-type headache
Cluster headache
Medication overuse headache
Benign cough headache
Benign exertion headache
Hypnic headache
'Ice pick' headache
Coital/sex headache
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9
Q

Migraine criteria?

A

> 5 attacks
4-72 hours
≥ 2 of: unilateral, pulsating, moderate/severe pain. avoidance of routine physical activity
Nausea and/or vomiting OR photophobia/phonophobia

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10
Q

Migraine prophylaxis?

A

B-blockers e.g. propanolol
Anti-epileptics e.g. topiramate, sodium valproate
Anti-depressants e.g. amitryptyline

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11
Q

Migraine treatment?

A

Aspirin 900 mg
Anti-emetics e.g. metoclopramide
Triptans

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12
Q

Tension-type criteria?

A

≥ 10 episodes
30 mins-7 days
≥ 2 of: bilateral, non-pulsating, mild/moderate pain, not aggravated by routine physical activity
No nausea/vomiting

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13
Q

Cluster headache criteria?

A 
≥ 5 attacks
Severe/very severe unilateral
15-180 mins
Ipsilateral conjunctival injection, lacrimation, nasal congestion, rhinorrhoea, eyelid oedema, forehead/facial sweating, mitosis/ptosis, sense of restlessness/agitation
Frequency 1-8 per day
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14
Q

Cluster headache treatment?

A

High flow oxygen
SC triptan
Avoid triggers

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15
Q

Cluster headache prophylaxis?

A

Corticosteroids
Verapamil
Lithium

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16
Q

Secondary headache types?

A

Vascular: subarachnoid haemorrhage, intracerebral haemorrhage, subdural haematoma, stroke, intracranial venous thrombosis, carotid/vertebral direction, GCA cerebral venous thrombosis
Infection: meningitis, encephalitis
Pressure: raised ICP, low ICP
Ocular: glaucoma, optic neuritis, eye strain
Facial pain: trigeminal neuralgia
Other: hypercapnia, drugs (e.g. anti-hypertensives)

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17
Q

Red flags for headaches?

A 
Explosive onset/very severe at onset
Recent significant change in pattern
Altered mental status
Onset with exertion, cough, sexual activity
Age > 50 years
Immunosuppression
Neurological abnormalities
Decreased LOC
Meningismus, fever
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18
Q

New, acute headache?

A

Intra-cranial infection
Intra-cranial haemorrhage
First presentation of benign intermittent headache

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19
Q

Recent, subacute headache?

A

Raised ICP
GCA
Transient benign headache

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20
Q

Longer-standing, chronic headache?

A

Primary headache syndrome

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21
Q

Headache alone?

A

Benign cause

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22
Q

Headache and nausea, vomiting, photo/phono-phobia?

A

Serious cause- meningitis, encephalitis

Migraine

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23
Q

Headache and fever, infectious features?

A

Meningitis

Encephalitis

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24
Q

Headache and neurological features?

A

Migraine

Serious cause

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25
Q

Headache examination and investigations?

A 
History
Infection features: temp, rash
Blood pressure
URT examination
Neurological examination
Cervical spine
Bloods: ESR
Lumbar puncture: pressure, white cells (infection, inflammation), bilirubin (subarachnoid haemorrhage), xanthrochromic (subarachnoid haemorrhage)
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26
Q

Causes of blackouts?

A

Syncope
Epileptic seizure
Functional/non-epileptic seizure
Hypoglycaemia

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27
Q

Features of an epileptic seizure?

A 
Long duration
Confusion
Long recovery
Cyanosis
Tongue biting
Jerking
Can have stiffness
May have a warning
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28
Q

Features of syncope

A 
Short duration
Quick recovery
Pallor
Can have some jerking
May/may not have a warning
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29
Q

Blackout investigations?

A

May not need any
ECG
Some syncope cases: ambulatory ECG, tilt-table testing
Some epilepsy cases: EEG, cerebral imaging

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30
Q

Blackout definition?

A

Episodes of loss of consciousness

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31
Q

Funny turns definition?

A

Discrete episode(s) due to some sort of brain event

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32
Q

Funny turn causes?

A

TIA
Epileptic seizure
Migraine
Other: dissociation/depersonalisation/derealisation, anxiety/panic attacks, hypoglycaemia, sleep-related turns

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33
Q

Coma definition?

A

State of unconsciousness where a person:

  • Cannot be awakened
  • Fails to respond normally to painful stimuli, light, sound
  • Lacks normal sleep-wake cycle
  • Does not initiate voluntary actions
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34
Q

Common causes of coma?

A

Focal brain lesions:

  • Haemorrhagic stroke
  • Intracranial mass lesions- tumour, abscess

Diffuse disorders:

  • Post cardiac/respiratory arrest
  • Overdose
  • Subarachnoid haemorrhage
  • Metabolic disturbances- hypoglycaemia, hepatic failure, renal failure
  • Infection- meningitis, overwhelming sepsis
  • Post-epileptic seizure
  • Non-convulsive status epilepticus
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35
Q

Neurological assessment for coma?

A 
History
General examination
Pupil examination
Eye movements
GCS
CT brain
Drug levels
Lumbar puncture
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36
Q

Immediate coma management?

A

Airways: open, stabilise cervical spine
Breathing: ventilate, intubate
Circulation: pulse, perfusion, BP, correct hypovolaemia, correct arrhythmias, large bore IV access
Treat hypoglycaemia

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37
Q

Ongoing coma supportive care?

A

Monitor
Empty stomach contents
DVT prophylaxis
Maintain blood gas and electrolyte homeostasis
Urinary catheterisation
Regular turning/air mattress to avoid pressure sores

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38
Q

Concussion definition?

A

Traumatic brain injury that alters the way your brain function.
Effects are usually temporary but can include headaches, problems with concentration, balance, co-ordination.
The brain requires time to recover

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39
Q

Mechanisms of brain injury?

A

Contact: coup and centrecoup, causes fractures and contusions
Inertial: acceleration and deceleration
Strain: deformity when mechanical force is applied
Differential movements

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40
Q

Brain hernias?

A 
Uncal herniation
Central transtentorial herniation
Subfalcine herniation
Extracranial herniation
Upwards cerebellar herniation
Tonsillar herniation
https://www.google.com/url?sa=i&rct=j&q=&esrc=s&source=images&cd=&ved=2ahUKEwj4zb2HvOnhAhWD3eAKHfMJC_QQjRx6BAgBEAU&url=https%3A%2F%2Fen.wikipedia.org%2Fwiki%2FBrain_herniation&psig=AOvVaw0O1pUWRy8GBLvxUUHda2Qh&ust=1556220710633814
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41
Q

Delirium definition?

A 
Acute onset
Fluctuating course
Inattention
Disorganised thinking and/or altered LOC
There is a precipitating cause
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42
Q

Dementia definition?

A

Due to disease of the brain
Chronic/progressive
Disturbance of multiple higher comical functions
Conscious not changed
Cognitive functions result in functional impairment
Progressive
Irreversible (in most cases)

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43
Q

Frontal lobe functions?

A 
Executive function
Adaptive behaviour
Personality- especially motivation, inhibition
Impulse control
Planning and initiation
Behaviour sequencing
Social behaviour
Language production- in Broca's area
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44
Q

Temporal lobe functions?

A

Memory

Language comprehension- in Wernicke’s area

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45
Q

Parietal lobe functions?

A

Visuospatial skills

Praxis

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46
Q

Occipital lobe functions?

A

Vision

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47
Q

Alzheimer’s pathogenesis?

A

Beta amyloid plaques and tau tangles

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48
Q

Alzheimer’s features?

A 
Gradual onset
Cognitive impairment
Progressive
Visuospatial function affected early
Defects: short-term memory, language, praxis, visuospatial, executive functioning
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49
Q

Alzheimer’s stages?

A

First 2-3 years post diagnosis
Moderately severe (3-6 years)
Severe (6-10 years)

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50
Q

Alzheimer’s management?

A

Cholinesterase inhibitors for symptoms

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51
Q

Vascular dementia features?

A

After stroke

Step wise deterioration

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52
Q

Vascular dementia management?

A 
Optimise vascular risk
Stop smoking
Reduce cholesterol
BP control
AF treatment
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53
Q

Dementia with Lewy Bodies features?

A

Fluctuates
Visual hallucinations
Parkinsoniam
Can appear as delirium initially

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54
Q

Dementia with Lewy Bodies management?

A

Avoid antipsychotics

Cholinesterase inhibitors for symptoms

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55
Q

Frontotemporal dementia features?

A

45-65 year old onset
Different types
Overlaps with MND

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56
Q

Frontotempotal dementia management?

A

Non available

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57
Q

Dementia management?

A

Symptoms in Alzheimers and DLB: cholinesterase inhibitors
Treat exacerbating issues: remove sedation, treat depression
Post-diagnostic support for family etc.
Social support
Power of Attorney recommendation
Support for carers

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58
Q

Epilepsy defintion?

A

Manifestation of abnormal paroxysmal neuronal discharges
Recurrent spontaneous seizures
After ≥ 2 seizures

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59
Q

Types of epilepsy?

A

Focal onset
Generalised onset
Unknown onset

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60
Q

Sub-types of focal onset epilepsy?

A

Focal aware
Focal impaired awareness
Focal to bilateral tonic-clonic

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61
Q

What causes focal onset epilepsy?

A

Acquired after damage

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62
Q

What causes generalised onset epilepsy?

A

Usually genetic

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63
Q

Sub-types of generalised onset epilepsy?

A 
Absence
Tonic-clonic
Myoclonic
Atonic
Infantile spasms
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64
Q

Focal seizure management?

A

Carbamazepine

Lamotrigine

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65
Q

Generalised tonic-clonic management?

A

Sodium valproate

Lamotrigine

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66
Q

Absence management?

A

Sodium valproate

Ethosuximide

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67
Q

Myoclonic management?

A

Sodium valporate

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68
Q

Tonic or atonic management?

A

Sodium valporate

Lamotrigine

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69
Q

What is epileptic surgery for?

A

Focal epilepsy

Symptomatic focal- temporal, frontal, occipital lobe

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70
Q

Status epilepticus definition?

A

> 30 minutes of continuous seizure activity or a series of seizures without full resolution between

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71
Q

How to manage status epilepticus?

A 
ABCDE assessment
Benzodiazepine IV
If unable PR/buccal
Repeat benzodiazepine
Phenytoin IV- need cardiac monitoring and notify ICU/anaesthetist
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72
Q

Features of parkinsonism?

A

Bradykinesia
Rigidity
Tremor
Postural instability

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73
Q

Causes of Parkinsonism?

A

Drug-induced
Idiopathic Parkinson’s disease
Other primary degenerative disease
Miscellaneous conditions

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74
Q

Pathogenesis of idiopathic Parkinson’s disease?

A

Lewy bodies
Substantia nigra neuronal death
Related loss of neuromelanin

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75
Q

Can treatment cause disease modification/prophylaxis in Parkinsons?

A

No

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76
Q

Parkinsons medication?

A 
Direct dopamine agonists- ropinorole
Levodopa
Selegeline (alternative to DDAs)
Amantadine (weak dopamine agonist)
Anti-cholinergic drugs
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77
Q

Long term problems with Parkinsons medications?

A 
Treatment is only symptomatic
Drug toxicity
CNS plasticity
Reduced efficacy
Shorter durations of response
Fluctuations in disability
Unpredictable and variable response
Emergence of involuntary movements- chorea, athetosis, dystonia
Confusion, hallucinations, dementia
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78
Q

Difference between stroke and TIA?

A

Stroke > 24 hours
TIA < 24 hours

Stroke due to: cerebral ischaemia or haemorrhage
TIA due to: inadequate cerebral/ocular blood supply

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79
Q

Fixed risk factors for stroke and TIA?

A 
Age
M > F
Race
Previous vascular event
Hereditary
High fibrinogen
Cholesterol- high LDL
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80
Q

Modifiable risk factors for stroke and TIA?

A 
Hypertension
Smoking
High hip to waist ratio
Hyperlipidaemia
Diabetes mellitus
Alcohol
Depression
Heart disease- AF
Oestrogen containing drugs
Polycythae,oa
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81
Q

Stroke causes?

A

80% ischaemic
15% haemorrhage
5% unknown

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82
Q

Presentation of a vascular lesion in stroke?

A 
Sudden onset
No warning
Maximal at onset
Body parts affected simultaneously
Gradual improvements over time
Repeated events
Hemispheric pattern of deficit
LOC is uncommon
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83
Q

How to investigate a stroke/TIA if presentation is ≤ 7 days?

A

CT scan

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84
Q

How to investigate a stroke/TIA if presentation is ≥ 7 days?

A

MRI scan

85
Q

Mimics of stroke/TIA?

A 
Sepsis
Syncope
Seizure
Spreading migraine aura
Functional
86
Q

How to diagnose a stroke/TIA?

A

Localise the lesion- symptoms, neurological signs, imaging confirmation

87
Q

Types of stroke?

A

Total anterior circulation stroke
Partial anterior circulation stroke
Lacunar stroke
Posterior circulation stroke

88
Q

How does a total anterior circulation stroke present?

A

All of:
Unilateral weakness of face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction

89
Q

How does a partial anterior circulation stroke present?

A

2 of:
Unilateral weakness of face, arm and leg
Homonymous hemianopia
Higher cerebral dysfunction

90
Q

How does a posterior circulation stroke present?

A

1 of:
Cranial nerve palsy and a contralateral motor/sensory deficit
Bilateral motor/sensory deficit
Conjugate eye movement disorder
Cerebellar dysfunction
Isolated homonymous hemianopia or cortical blindness

91
Q

How does a lacunar stroke present?

A 
1 of:
Pure sensory stroke
Pure motor stroke
Sensori-motor stroke
Ataxic hemiparesis
92
Q

Which stroke types are usually caused by carotid disease?

A

Total anterior and partial anterior

93
Q

Which stroke types have higher recurrence?

A

Partial anterior and posterior circulation

94
Q

Which stroke type has the highest chance of death?

A

Total anterior

95
Q

What increases risk of stroke following a TIA/minor stroke?

A 
Older age
Hypertension
Clinical features- weakness, speech
Longer duration
Diabetes mellitus
Positive imaging
96
Q

Ischaemic stroke management?

A

Hyperacute:
Thrombolysis
CLOT retrieval
Neurosurgical decompression

Acute:
Stroke unit
Supportive care- fluids, feeding
Prevention and management of complications e.g. DVT prevention if immobile
Manage co-morbidities

Rehabilitation

Secondary prevention:
Exercise
Smoking cessation
Healthy weight
Diet
BP control
Antiplatelets
Statin
Anticoagulation if in AF
PFO closure if needed
Carotid endarterectomy
97
Q

Haemorrhagic stroke management?

A

Hyper-acute:
Sometimes BP lowering

Acute treatment:
Stroke unit
Supportive care- fluids, feeding
Prevention and management of complications e.g. DVT prevention if immobile
Manage co-morbidities
Secondary prevention:
Exercise
Smoking cessation
Healthy weight
Diet
BP control
Avoid antiplatelets
Avoid anticoagulation
98
Q

What is the thrombolytic drug used?

A

Alteplase 1 mg/kg

99
Q

Contraindications to thrombolysis after stroke?

A

Minor surgery in last 14 days
GI/urinary tract bleeding in last 21 days
History of ICH, intracranial malignancy or intracranial AVM
Symptoms suggestive of subarachnoid haemorrhage
BP > 185 systolic or > 110 diastolic
INR > 1.7
Hyperglycaemia > 20
Hypoglycaemia < 3

100
Q

What is MS?

A

Inflammatory disease affecting all of the CNS

101
Q

Types of MS?

A

Relapse-remitting (+ secondary progressive)
Fulimant
Primary progressive

102
Q

Common nerves affected in MS?

A

Optic nerve -> optic neuritis
Medial longitudinal fascicularis -> internuclear ophthalmoplegia
Corpus callous -> often asymptomatic
Spinal cord

103
Q

MS presentation?

A

Visual:: optic neuritis, optic atrophy, Uhthoff’s phenomenon, internuclear ophthalmoplegia
Sensory: pins and needles, numbness, trigeminal neuralgia, Lhermitte’s syndrome
Motor: spastic weakness (legs), transverse myelitis
Cerebellar: ataxia, tremor
Other: urinary incontinence, sexual dysfunction, intellectual deterioration

104
Q

Features contraindicatory to MS?

A 
Diminished/lost reflexes
Patterns of weakness that fit a single root/nerve/very variable
Lots of pain
Seizures
Reduced consciousness
Respiratory compromise
105
Q

Investigations in suspected MS?

A

Exclude other diagnoses
Routine bloods
MRI brain and spine
Consider LP if brain scan is normal

106
Q

How to diagnose MS?

A

≥ 2 attacks with ≥ 2 objective clinical lesions

if there is lower clinical presentation you need MRI, SCF evidence

107
Q

Types of treatment for MS?

A

Symptomatic
Acute relapse treatment
Disease modifiers

108
Q

Symptomatic treatment for MS?

A 
Physiotherapy
Ani-spasmodics
Neuropathic pain treatment
Aids
Fatigue
Spasticity: baclofen, danrolene, tizanide, physiotherapy, botox
Bladder dysfunction: unstable bladder (oxybutynin, tolterodine), uncoordinated bladder (self catheterisation)
Erectile dysfunction: sildenafil
109
Q

Acute relapse treatment for MS?

A

Oral steroids- 500 mg methylprednisolone

110
Q

Disease modifying treatment for MS?

A

Beta-interferon: avonex, rebid, betaferon, extavia
Glatiramer acetate
Natalizumab

111
Q

Is there any treatment for progressive MS?

A

No licensed treatment

Potential neuroprotective treatment- lamotrigine/phenytoid

112
Q

What is myasthenia gravis?

A

Disorder of neuromuscular junction

113
Q

Myasthenia gravis presentation?

A 
Fatiguable weakness
Diurnal variation
Diplopia (double vision)
Dysarthria
Ptosis
Dysphagia
Dyspnoea
Neck weakness
114
Q

What exacerbates the features of myasthenia gravis?

A 
Pregnancy
Hypokalaemia
Infection
Over-treatment
Change of climate
Emotion
Exercise
Gentamicin
Opiates
Tetracycline
Quinine
Beta blockers
115
Q

Investigations in suspected myasthenia gravis?

A

Neuroimmunology- anti-AChR antibody, anti-MUSK antibody
Bloods: TFTs, B12
CT mediastinum
Electromyography

116
Q

What types of treatment options are there for myasthenia gravis?

A

Symptomatic
Surgical
Immunosuppression

117
Q

Symptomatic treatment for myasthenia gravis?

A

Anti-cholinesterase

118
Q

Surgical treatment for myasthenia gravis?

A

Thymectomy

119
Q

When to consider surgery for myasthenia gravis?

A

Generalised myasthenia gravis
< 50 years
AChR antibody positive

120
Q

Immunosuppression treatment for myasthenia gravis?

A

Corticosteroids
Azathioprine
Alternatives: methotrexate
IV immunoglobulin or plasmapheresis

121
Q

What medications to avoid in myasthenia gravis?

A 
Gentamicin
Clarithromycin
Beta blockers
Sedative drugs
Calcium channel blockers
Aminoglycoside antibiotics and erythromycin
Benzodiazepines
Curare-type muscle relaxants
122
Q

Presentation of Lambert-Eaton myasthenia syndrome?

A

Subacute proximal weakness
Gait difficulty
Sensory and autonomic disturbances, especially dry mouth
Bulbar and ocular muscles are rarely affected

123
Q

Treatment of Lamber-Eaton myasthenia syndrome?

A

Symptomatic: 3,4-diaminopyridine
Immunosuppression and plasmapheresis
Treat underlying tumour

124
Q

What is a myopathy?

A

Primary disorder of muscle with gradual onset symmetrical weakness

125
Q

Acquired causes of myopathy?

A 
Inflammatory
Endocrine
Associated with systemic illness
Drug induced
Toxic
126
Q

Hereditary causes of myopathy?

A 
Muscular dystrophies
Myotonias
Channelopathies
Metabolic myopathies
Mitochondrial myopathies
127
Q

Signs in favour of a myopathy?

A 
Gradual onset of symmetrical proximal weakness
Specific muscle groups affected
Preserved tendon reflexes
No paraesthesia or bladder problems
No fasciculation
128
Q

Myopathy symptoms?

A

Cramp
Contractures
Myotonias- impaired muscle relaxation after forceful voluntary contraction

129
Q

Investigations if suspect a myopathy?

A

Bloods- ESR, CK, AST, LDH
EMG
Muscle biopsy
Genetic testing

130
Q

What is muscular dystrophy?

A

A group of genetic diseases with progressive degeneration and weakness of specific muscle groups

131
Q

How do muscular dystrophies present?

A

Unusually firm muscles (infiltration by fat/connective tissue)
Marked variation in size of individual muscle fibres on histology

132
Q

Types of muscular dystrophy?

A

Duchenne’s muscular dystrophy
Becker’s muscular dystrophy
Fascioscapulohumeral muscular dystrophy

133
Q

What is a myotonic disorder?

A

Causes stiffness, limitation of movement, sometimes weakness and tonic muscle spasm
Contractions usually provoked by cold and direct muscle stimulation

134
Q

What is radiculopathy?

A

Nerve root compression

135
Q

What is myelopathy?

A

Compression of the spinal cord

136
Q

Causes of radiculopathy?

A

Acute disc
Spondylosis
Tumours
Inflammatory conditions e.g. shingles

137
Q

Presentation of radiculopathy?

A

Pain- in nerve root distribution, disc prolapse, mechanical causes e.g. coughing, spinal tenderness
Weakness and reflex changes- in nerve root distribution
Sensory loss- in nerve root distribution

138
Q

What is myeloradiculopathy?

A

Presence of UMN signs or sensory signs below the level of the radiculopathy in cervical spine

139
Q

What is polyradiculopathy?

A

Compression of more than one nerve root

140
Q

Causes of polyradiculopathy?

A

Lumbar canal stenosis

Inflammatory e.g. Guillain-Barré syndrome, inflammatory meningitis, sarcoidosis, neoplastic process in the spinal fluid

141
Q

Presentation of C5 radiculopathy?

A

Weak deltoid and supraspinatus
Reduced supinator jerks
Numb elbow
Pain in neck/shoulder and radiating down front of arm the elbo

142
Q

Presentation of C6 radiculopathy?

A

Weak biceps and brachioradialis
Reduced biceps jerk
Numb them and index finger
Pain in shoulder radiating down arm below elbow

143
Q

Presentation of C7 radiculopathy?

A

Weak triceps and finger extension
Reduced triceps jerk
Numb middle finger
Pain in upper arm and dorsal forearm

144
Q

Presentation of T1 radiculopathy?

A

Was in all intrinsic hand muscles
Horner’s syndrome
Pain in upper anterior and medial arm

145
Q

Presentation of L2 radiculopathy?

A

Weak hip flexion and adduction

Pain across upper thigh

146
Q

Presentation of L3 radiculopathy?

A 
Weak knee extension and hip abduction
Reduced knee jerk
Numb from mid thigh to just below knee
Positive femoral stretch test
Pain across lower thigh
147
Q

Presentation of L4 radiculopathy?

A 
Weak knee extension
Reduced knee jerk
Numb on medial portion of lower leg
Positive femoral stretch test
Pain across lower thigh
148
Q

Presentation of L5 radiculopathy?

A

Weak toe dorsiflexion and eversion
Numb anterior lower leg down to foot and lateral lower leg
Positive sciatic stretch test
Pain across lateral shin to dorm of foot and great toe

149
Q

Presentation fo S1 radiculopathy?

A

Was ankle plantarflexion, toe inversion, knee flexion
Reduced ankle jerk
Positive sciatic stretch test
Pain across posterior calf to lateral foot (sole) and little toe

150
Q

Investigations in suspected radiculopathy?

A

MRI of relevant spinal level
EMG
CSF examination- in multiple radiculopathy or if evidence of systemic illness

151
Q

Treatment of lumbar disk disease (radiculopathy)?

A

Rest then mobilise
Education to avoid injury
Consider surgery if: radicular pain continues, neurological deficit

152
Q

Treatment of cervical disk protrusions (radiculopathy)?

A

Often improves spontaneously or with conservative treatment
Conservative treatment: physiotherapy, soft collar, traction
Consider surgery if: pain persists or marked radicular weakness

153
Q

Treatment of benign compressive tumours (radiculopathy)?

A

Surgical decompression

154
Q

Presentation of acute cauda equina compression?

A 
Altering/bilateral root pain in legs
Saddle anaesthesia
Loss of anal tone
Bladder/bowel/sexual changes
Distal sensory loss in feet
155
Q

Treatment of cauda equina syndrome?

A

Disk prolapse -> MRI and neurosurgeons
Malignancy -> high dose steroids, radiotherapy, oncologists
Treatment: urgent surgical decompression

156
Q

Treatment of lumbar canal stenosis (polyradiculopathy)?

A

Surgical decompression

157
Q

Red flags for back pain?

A 
< 20 years
> 55 years
Acute onset in elderly people
Constant/progressive pain
Nocturnal pain
Worse pain on being supine
Fever, night sweats, weight loss
PMH of malignancy
Abdominal mass
Thoracic back pain
Morning stiffness
Bilateral or alternating leg pain
Neurological disturbance
Sphincter disturbance
Current/recent infection
Immunosuppression
Leg claudication or exercise related leg weakness/numbness
158
Q

What nerve roots contribute to the median nerve?

A

C6-T1

159
Q

What is median nerve compression associated with?

A 
Pregnancy
Rheumatoid arthritis
Hypothyroidism
Diabetes
Acromegaly
Myeloma
Idiopathic
160
Q

Presentation of median nerve compression at the wrist?

A

Carpel tunnel syndrome
Weakness of abductor policies brevis
Sensory loss over radial 3.5 fingers

161
Q

Presentation of median nerve compression due to anterior interosseous nerve lesions?

A

Weakness of flexion of distal phalanx of the thumb and middle finger

162
Q

Treatment for carpel tunnel syndrome?

A

Splinting
Local steroid injection
Consider decompression surgery

163
Q

Two causes of mononeuropathy?

A

Axonal injury

Focal demyelination/conduction block

164
Q

Causes of axonal injury mononeuropathies?

A 
Vasculitis
Diabetes mellitus
Sarcoidosis
Leprosy
HIV
CMV
Lyme
Hepatitis C
165
Q

Causes of focal demyelination/conduction block mononeuropathies?

A

Chronic inflammatory demyelinating polyradiculopathy- MADSAM, MMN
Multiple compression neuropathies- hypothyroidism, diabetes mellitus
Hereditary neuropathy with liability to pressure palsy (HNPP)
Lymphoma
Severe burns
Sickle cell disease

166
Q

What nerve roots contribute to the ulnar nerve?

A

C7-T1

167
Q

Presentation of ulnar nerve compression

A

Weakness/wasting of medial wrist flexors, interossei, medial lumbricals
Hypothenar eminence wasting
Weak 5th digit abduction and 4th and 5th DIP flexion
Sensory loss over medial 1.5 fingers and ulnar side of hand
Froment’s sign

168
Q

Treatment of ulnar nerve compression?

A

Rest
Avoid pressure
Soft elbow splinting (if symptoms continue)
Hand splint- to prevent clawing
Surgery- if chronic associated with weakness/failure of splinting

169
Q

Which nerve roots contribute to the radial nerve?

A

C5-T1

170
Q

Presentation of radial nerve compression?

A

Wrist and finger drop with elbow fixed and arm pronated

Sensory loss is variable

171
Q

Treatment of radial nerve compression?

A

Most resolve spontaneously

Lively splint may help to improve hand function during recovery

172
Q

Which nerve roots contribute to the phrenic nerve?

A

C3-C5

173
Q

Presentation of phrenic nerve compression?

A

Orthopnoea

Raised hemidiaphragm on CXR

174
Q

Which nerve roots contribute to the common peroneal nerve?

A

L4-S1

175
Q

Presentation of common perineal nerve compression?

A

Foot drop
Weak ankle dorsiflexion/eversion
Sensory loss over dorsal foot

176
Q

Which nerve roots contribute to the tibial nerve?

A

L4-S3

177
Q

Presentation of tibial nerve compression?

A

Inability to stand on tiptoe (loss of plantar flexion)
Inability to invert the foot or flex the toes
Sensory loss over sole

178
Q

What is mononeuritis multiplex?

A

Involvement of ≥ 2 peripheral nerves in a mononeuropathy

179
Q

Causes of mono neuritis multiplex?

A

Diabetes mellitus
Connective tissue disorders e.g. RA, SLE
Vasculitis
Rare: sarcoidosis, amyloid, leprosy

180
Q

What is polyneuropathy?

A

Motor and/or sensory disorder of multiple peripheral or cranial nerves, usually symmetrical and widespread. Often worse distally

181
Q

Broad causes of polyneuropathy?

A

Acquired
Hereditary
Demyelinating
Axonal

182
Q

Acquired causes of polyneuropathy?

A 
Dysmetabolic- diabetes
Drugs- amiodarone, antibiotics, anti-retrovirals, chemotherapy, phenytoin
Mechanical or compressive
Cancer
Immune related
Toxins- alcohol, NO
Infectious
183
Q

Hereditary causes of polyneuropathy?

A 
Hereditary motor and sensory neuropathy
Hereditary neuropathy with liability to pressure palsies
Familial brachial plexopathy
Familial amyloidosis
Prophyria
MND
184
Q

Demyelinating causes of polyneuropathy

A 
Immune related- Guillain Barré syndrome
Multiple compression neuropathies
Drugs
Lymphoma
Severe burns
Hereditary e.g.Charcot Marie Tooth 1, HNPP
Sickle cell disease
185
Q

Axonal causes of polyneuropathy?

A 
Dysmetabolic- diabetes
Immune/infectious- HIV, CMV, Lyme, Hepatitis C, leprosy
Hereditary- Charcot Marie Tooth
Post infectious- Guillain Barré syndrome
Sarcoidosis
Drugs and toxins e.g. alcohol
Cancer
Vasculitis
186
Q

Which type of polyneuropathy can you treat?

A

Demyelinating ones

187
Q

Which type of polyneuropathy can you not treat?

A

Axonal damage ones

188
Q

Investigations into polyneuropathies?

A 
Bloods: glucose, ESR, CRP, U&amp;Es, LFTs, vitamin B12, folate
Serum protein electrophoresis
ANA, ANCA
Chest X-ray
HIV serology
Others: vitamin E, vitamin A, genetic testing, lyme serology, serum ACE, serum amyloid
Nerve conduction studies
Electromyography
189
Q

Causes of sensory polyneuropathy?

A

Diabetes mellitus
CKD
Leprosy
Alcohol

190
Q

Presentation of sensory polyneuropathy?

A 
Numbness
Pins and needles
Paraesthesia
Glove and stocking distribution
Difficulty handling small object
Signs of trauma e.g. finger burns
Joint deformation
Diabetic and alcohol are painful
191
Q

Cause of diabetic neuropathy?

A

Axonal degeneration

192
Q

Patterns of diabetic neuropathy?

A

Distal symmetrical neuropathy
Asymmetrical proximal neuropathy
Autonomic neuropathy
Mononeuropathies and radiculopathies

193
Q

Causes of motor polyneuropathy?

A

Guillain Barré syndrome
Lead poisoning
Charcot-Marie Tooth syndrome
Alcohol

194
Q

Presentation of motor polyneuropathy?

A 
Often progressive
Weak or clumsy hands
Difficulty walking- stumbling, falls
Difficulty breathing
Signs of LMN lesion
195
Q

Guillain Barré syndrome mechanism for motor neuropathy?

A

Acute inflammatory demyelinating polyneuropathy

196
Q

Presentation of motor neuropathy due to Guillain Barré syndrome?

A 
Acute
Varying severity
A few weeks after infection a symmetrical ascending muscle weakness starts
Sensory symptoms in legs and arms at onset
Examination findings minimal
May have pain in back, buttock, thigh
Muscle weakness affects legs > arms
Arreflexia
197
Q

Treatment for motor neuropathy due to Guillain Barré syndrome?

A

Monitor vital capacity, if < 1 -> ventilation
Monitor for evidence of autonomic dysfunction
Monitor: pressure areas
Venous thrombosis prophylaxis
Chest and limb physiotherapy
Supportive care for paralysed patients
Shortening the disease course- plasma exchange, IV immunoglobulin

198
Q

Causes of autonomic polyneuropathy?

A 
Diabetes mellitus
Guillain Barré syndrome
Sjögren's syndrome
HIV
Leprosy
SLE
Toxic
Genetic
Paraneoplastic
199
Q

Presentation of autonomic polyneuropathies?

A

Sympathetic: postural hypotension, decreased sweating, ejaculatory failure, Horner’s syndrome
Parasympathetic: constipation, nocturnal diarrhoea, urine retention, erectile dysfunction, Holmes-Adie pupil

200
Q

Effects of alcohol and drugs?

A 
Intoxication
Dependence
Withdrawal/DTs
Seizures
ARBD
Wernicke's encephalopathyKorsakoff's
Pellagra
Blackouts
Central pointine and extrapontine myelinolysis
Marchiafava-Bignami disease
Hepatic encephalopathy
Neuropathy
Ataxia
201
Q

Treatment of alcohol dependence?

A

Antabuse
Acamproate
Naltrexone
Baclofen

202
Q

What two systems are within the UMN?

A

Cortico-spinal system

Cortico-bulbar system

203
Q

Function of the cortico-bulbar system?

A

Controls the cranial LMNs

204
Q

Function of the cortico-spinal system?

A

Control the spinal LMNs

205
Q

What is the portico-spinal system also called?

A

The pyramidal system

206
Q

Third nerve palsy presentation?

A

Eye down and out
Ptosis
Mydiasis (pupil dilated)

207
Q

Sixth nerve palsy presentation?

A

Esotropia (one/both eyes turn in)

Diplopia (double vision)

208
Q

Seventh nerve palsy (Bell’s palsy) presentation?

A

One sided facial droop

Year 4 Semester 2 (3 decks)

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