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Junior Medicine > Neuro > Flashcards

Neuro Flashcards

1
Q

What are the primary headache disorders (3)

A

Tension headache
Migraine
Cluster headache

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2
Q

What are the secondary headache syndromes (8)

A

Raised ICP
Idiopathic intracranial hypertension
Hypertension
Meningeal irritation (SAH/meningitis)
Concussion
Giant cell arteritis
Sinusitis
Drugs

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3
Q

CF of tension headache

A

Continuous severe pressure felt bilaterally over the vertex, occiput and eyes
Variable intensity
Non pulsatile
Occurs daily and can persist for months / years

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4
Q

Management of tension headaches

A

If episodic (15d):
- paracetamol and aspirin (safety net that this can lead to a medication overuse headache)

Preventative treatment:
- low dose amitriptyline 75mg initially

Chronic:
- reassurance
- relaxation techniques
- addressing underlying stressors

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5
Q

CF of cluster headache

A

Short lived episodes of severe unilateral pain typically centred on one eye
Sudden onset
Wakes patient from sleep
- red eye
- nose watering
- ptosis
- vomiting

20% will experience aura

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6
Q

Aetiology for cluster headache

A

Males: females 3:1
Alcohol

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7
Q

Management of cluster headache

A

Exclude secondary causes eg acute angle closure glaucoma
Subcut triptan to take at the start of an attack
Home Oxygen for use during attack

Prophylactic treatment is alcohol avoidance and verapamil

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8
Q

Aetiology of migraine

A

Onset in puberty
Women to men 3:1
Associated with menstruation, OCP use, physical exercise, alcohol, cheese, chocolate, red wine, stress

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9
Q

Pathogenesis of migraine

A

Vasodilation after a period of vasoconstriction correlates with onset

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10
Q

Features of classical migraine with aura

A

Sense of ill health followed by a visual aura in the field of vision opposite to the side of the succeeding headache
Headache is throbbing with anorexia, nausea, vomitting and photophobia
Begins locally and spreads bilaterally
Aggravated by movement
Can last hours - days
Normal neurological exam

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11
Q

Features of a migraine without aura (common migraine)

A

Classical visual / sensory aura is absent but patients may feel non specifically unwell prior to the onset of headache

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12
Q

What is an ophthalmoplegic migraine

A

Migraine with 3rd / 6th nerve palsy

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13
Q

What is a hemiplegic / facioplegic migraine

A

Migraine with temporary limb / facial hemiparesis

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14
Q

How is a hemiplegic migraine different from a TIA

A

In TIAs the maximum deficit is present immediately and headache is unusual whereas in hemiplegic migraine there is slower progression

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15
Q

Long term Migraine management

A

Full neurological exam to rule out focal neurology, raised ICP or meningism
- keep headache diary
- avoid external triggers

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16
Q

Acute migraine management

A

1st line: oral NSAID / paracetamol + anti emetic
Offer oral triptan
- take as soon as symptoms
- can be intranasal if vomitting

No opioids
Follow up if triptan treatment unsuccessful

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17
Q

When are triptans contraindicated

A

IHD
Uncontrolled HTN
Coronary artery spasm

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18
Q

Preventative migraine management

A

Consider if migraine attacks are causing significant disability (>2 mo)
- topiramate / propranolol (1st)
- amitriptyline / anti-convulsants (2nd)

Menstrual related migraines can be treated with mefanamic acid or triptans 2d before menses

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19
Q

Why should the COCP be avoided in migraines with aura

A

Increased stroke risk
Contraceptive methods that prevent menstruation can be tried to try and avoid migraine

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20
Q

What is idiopathic intracranial hypertension

A

Symptoms and signs of raised ICP but no mass lesion on imaging
A disorder of CSF resorption
Causes visual disturbances (Diplopia) and headaches
Associated with pulsatile tinnitus and 6th nerve palsy

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21
Q

Who does idiopathic intracranial hypertension most commonly affect

A

Young obese women

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22
Q

OE of IIH

A

Bilateral papilloedema
Normal CT / MRI
LP will confirm increased CSF pressure

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23
Q

Management of IIH

A

Weight loss may facilitate spontaneous remission
Trial of corticosteroids can be successful
Definitive management is a surgical shunt - prevents optic atrophy

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24
Q

What is normal ICP

A

0-10mmHg

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25
Q

Causes of increased ICP

A

Vasogenic: increased capillary permeability
- tumour, trauma, ischaemia, infection, haemorrhage

Cytotoxic: cell death leads to oedema

Interstitial: obstructive hydrocephalus- blockage of the normal CSF outflow

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26
Q

Symptoms of raised ICP

A

Headache: dull persistent ache, worse on lying, present on waking, worse by coughing / straining
Vomitting
Seizures

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27
Q

Signs of raised ICP

A

Drowsiness / GCS deterioration
Progressive dilation of pupil on affected side
Cushings reflex is a pre terminal sign of raised ICP indicating imminent brainstem herniation
Bradycardia, hypertension, irregular breathing

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28
Q

Management of raised ICP

A

ABCDE
Elevate head of bed to 30-45 degrees
If intubated hyperventilate to reduce PaCO2
IV mannitol 20%
Corticosteroids if tumour
Fluid restriction

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29
Q

MOA of IV mannitol 20%

A

Osmotic diuretic giving a clinical effect after 20mins
Useful as a temporary measure prior to definitive management
Follow serum osmolality to adjust dosing

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30
Q

What is the best prognostic indicator in the Glasgow coma scale

A

Motor response

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31
Q

What are the categories and scores in the Glasgow coma scale

A

Motor /6
Verbal /5
Eye opening / 4

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32
Q

What is a SAH

A

Bleeding into the subarachnoid space that can occur at any age

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33
Q

Presentation of SAH

A

Thunderclap headache - over seconds, devastating intensity, often occipital
Comes on during times of transient hypertension eg physical activity or sexual intercourse
Vomitting
Photophobia
Increasing drowsiness / coma
Focal neurological signs

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34
Q

OE of SAH

A

Decreased GCS
Neck stiffness and meningism

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35
Q

Aetiology of SAH

A

Berry aneurysm (70%)
Arteriole ours malformations (10%)
No lesion found (20%)

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36
Q

What is a berry aneurysm

A

Developmental rather than congenital
Develops in circle of Willis and adjacent arteries
Most common in anterior communicating artery
Common in those with polycystic kidney disease
RF: smoking, FH, HTN, ehlers-Danlos, Marfans

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37
Q

What is arteriovenous malformation

A

A congenital collection of abnormal arteries / veins

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38
Q

SAH investigations

A

Bloods: FBC, U&E, LFT, ESR, clotting
CT head
Lumbar puncture: CSF will become xanthochromic - yellowish

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39
Q

Management of SAH

A

4 weeks bed rest
BP control
Nimodipine: CCI to prevent vasospasm, reduces mortality
IV fluids
Analgesia, anti emetics
Stool softeners to prevent straining

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40
Q

Complications of SAH

A

Death (30%)
Rebleed
Hydrocephalus - due to fibrosis in the CSF pathways
Cerebral vasospasm

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41
Q

Indications for lumbar puncture

A

Diagnosis of meningitis / encephalitis
Diagnosis of SAH
Measurement of CSF pressure
Therapeutic removal of CSF
Intrathecal drug administration
Diagnosis of miscellaneous neurological conditions

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42
Q

Contraindications to lumbar puncture

A

Suspicion of mass in the brain / spinal cord or raised ICP
Overlying / local infection
Congenital lesions of the lumbar spine
Problems with haemostasis

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43
Q

Lumbar puncture complications

A

Post LP headache - occurs in 30%, onset within 24hrs, with resolution over 2 weeks
- Is classically a constant, bilateral dull ache

Dry tap

Infection

Damage to spinal nerves

Coming of cerebellar tonsils - do not perform if ICP is raised

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44
Q

Describe the procedure of a lumbar puncture

A

Identify L4 space - level with tops of iliac crest
Introduce needle obliquely above L4 parallel to the place of the spine, through the interspinous ligament feeling for a give as the needle enters the subarachnoid space where CSF will begin to flow

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45
Q

Why is a lumbar puncture done at L4 level

A

Because spinal cord ends at L1/2 so it is rare to damage the nerves of the cauda equina

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46
Q

What is a subdural haemorrhage

A

A collection of blood in the subdural space following a rupture of a vein usually following a head injury although can occur spontaneously

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47
Q

What is an acute subdural haematoma

A

Occurs in severe acceleration-deceleration head injury often with co-existing brain damage
These patients are often young and come into hospital with a dilated pupil and no lucid interval before decreased GCS

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48
Q

Management of acute subdural haematoma

A

Craniotomy and early evacuation of the clot is required by neurosurgery
Patients are often seriously ill
ICU admission
ICP monitoring
High incidence of subsequent epilepsy

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49
Q

What is a subacute subdural haematoma

A

May occur spontaneously or after minor trauma
Can be bilateral

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50
Q

Risk factors for subacute subdural haematoma

A

The elderly
Alcohol abuse
Other coagulopathies

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51
Q

Clinical features of subdural haematoma

A

Headache
Drowsiness
Confusion
Focal neurological signs
Stupor and coma occur due to coming as ICP increases

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52
Q

Investigations for suspected subdural haematoma

A

CT scan
Acute subdural haematoma: classic cresenteric shape with increased density conforming to the contour of the skull. May be accompanying midline shift and compression of the ventricles

Chronic subdural haematoma: blood becomes more radiolucent and assumes a Lentiform shape similar to an extradural haematoma

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53
Q

Management of subdural haematoma

A

Chronic may resolve spontaneously
Definitive management may involve burr hole and placement of subdural drain or mini craniotomy and haematoma evacuation

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54
Q

What is meningitis

A

Inflammation of the leptomeninges usually infectious in origin

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55
Q

Aetiology of meningitis

A

Bacterial or viral
70% neisseria meningitidis: classic petechial rash occurs in small epidemics

Streptococcus pneumoniae - more common if skull fractures, ear disease or in those with congenital CNS lesions

Listeria monocytogenes, haemophilus influenza, staph aureus, TB

Viral: enteroviruses, HSV, VZV

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56
Q

Meningitis symptom triad

A

Headache
Neck stiffness
Fever

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57
Q

Symptoms that are unique to acute bacterial meningitis

A

High fever with rigors
Photophobia
Vomiting
Intense malaise coming on over hours

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58
Q

OE for meningitis

A

Kernigs sign positive: hip flexed, extend at the knee to cause pain

Brudzinski’s signs positive: passive flexion of the neck leads to flexion of the knees / hip

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59
Q

What does progressive drowsiness, literalising signs or cranial nerve lesiosn indicate in meningitis

A

Venous sinus thrombosis
Severe cerebral oedema
Hydrocephalus

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60
Q

Investigations for meningitis

A

FBC, U&E, LFT, clotting, glucose, lactate
Serum PCR for pneumococcal and meningococcal antigens
Blood cultures: do not delay abx to wait for blood cultures
LP
Throat swabs

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61
Q

What does yellowish and turbid CSF indicate on LP

A

Pyogenic bacterial meningitis

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62
Q

What does clear CSF indicate on LP

A

Viral meningitis

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63
Q

What does yellowish and viscous CSF indicate on LP

A

Tuberculous meningitis

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64
Q

What is meningococcal meningitis

A

Petechial rash usually Erythematous, non bleaching purpura
Carried in nasopharynx

Immediate IV abx should be given

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65
Q

Clinical features of viral meningitis

A

Almost always a benign self limiting condition which lasts 4-10 days

There may be a headache that follows for some months

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66
Q

Clinical features of TB meningitis

A

May present as per acute bacterial meningitis but more commonly as an insidious illness with fever, weight loss and progressive confusion / cerebral irritation eventually leading to coma

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67
Q

Risk factors for TB meningitis

A

Immunosuppression
Malnourishment
Multiple co-morbidities
TB contact

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68
Q

Treatment for TB meningitis

A

Anti tuberculoid medications for 12 months alongside corticosteroids

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69
Q

Meningitis management

A

LP within 1 hr
Empirical abx

If non blanching rash treat as meningococcal disease : IV benzyl penicillin
If <60 and not immunosuppressed: IV ceftriaxone
If >60 or immunosuppressed: IV ceftriaxone + IV amoxicillin

Notify public health

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70
Q

Meningitis complications (acute)

A

Sepsis
Hydrocephalus
Adrenal haemorrhage: Waterhouse friedrichsen syndrome

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71
Q

Meningitis complications (long term)

A

Brain abscess
Seizure disorders
Cranial nerve palsies: sensorineural hearing loss or gaze palsies
Ataxia / muscular hypotonia

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72
Q

What is a brain abscess

A

Generally very rare
Most usually a complication of otitis media / paranasal sinus infection or bacterial endocarditis
Can be a history of head trauma / neurosurgery
Presents with expanding mass lesion, fever and systemic illness

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73
Q

Treatment of brain abscess

A

Surgical drainage
Broad spectrum abx
High dose corticosteroids

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74
Q

Complications of brain abscess

A

Mortality is high
Those who do survive often develop epilepsy

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75
Q

What is encephalitis

A

Inflammation of the brain parenchyma
Usually viral origin
Most commonly HSV

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76
Q

CF of encephalitis

A

Headache
Drowsiness
Fever
Malaise
Confusion
Occasional seizures
Rarely mood changes

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77
Q

Encephalitis investigations

A

CT head / MRI : shows diffuse oedema in temporal lobes
LP: raised opening pressure, raised lymphocytes, raised protein, positive viral PCR
Viral serology: blood and CSF samples to confirm pathogen

78
Q

Encephalitis management

A

IV Aciclovir for >10 days

79
Q

What is epilepsy

A

Continuing tendency to have seizures
A seizure is a transient abnormal neurological event resulting from paroxysmal discharge of cerebral neurones
Can be partial or generalised

80
Q

Describe the stages of a tonic clonic seizure

A

Aura: vague warning phase
Loss of consciousness
Tonic phase: rigidity, tongue biting, incontinence, cyanosis
Clonic phase: convulsions, frothing, jerking
Post ictal: drowsy, confusion, coma

81
Q

What are the 3 types of generalised seizures

A

Tonic clonic
Absence
Tonic

82
Q

What is an absence seizure

A

Typically less than 10s in 4-10yr olds
Stimulated by hyperventilation and flashing lights
Remit by puberty but pre dispose to adult epilepsy

83
Q

What is a tonic seizure

A

Extended or flexed trunk

84
Q

What is a clonic seizure

A

Jerking

85
Q

Wha is a Myoclonic seizure

A

Brief shock like movements

86
Q

what is an atonic seizure

A

Drop to the ground

87
Q

What is a partial seizure

A

No impairment of consciousness
Associated with sensory aura

Temporal lobe involvement: lip smacking / chewing
Frontal lobe involvement: Motor movements, speech arrest, Jacksonian march
Parietal lobe involvement: sensory disturbances, tingling, numbness
Occipital lobe involvement: visual disturbances

88
Q

What is a complex partial seizure

A

Where consciousness is impaired at some stage

89
Q

What is temporal lobe epilepsy

A

Classical aura with sense of fear / deja vu and hallucinations
Confusion, anxiety and automatisms eg lip smacking, chewing

90
Q

Secondary causes of seizures

A

Structural abnormalities: trauma, space occupying lesion, stroke

Developmental: cerebral palsy

Metabolic: hypo / hyper glycaemia, calcaemia, natraemia

Drugs: withdrawal, cocaine, TCAs, SSRIs, ciprofloxacin

Infection: encephalitis, HIV, syphilis

91
Q

Immediate seizure management

A

Recovery position
Removing harmful objects

92
Q

What is status epilepticus

A

When a seizure lasts over 3 mins or starts outside hospital and is still ongoing once in hospital

But is typically a seizure >30mins

93
Q

Management of status epilepticus

A

ABCDE: 100% oxygen
IV/PR/SL lorazepam
Finger prick glucose
If alcohol suspicion: IV pabrinex
Females: preg test
Then initiate 2nd anti convulsant: IV levetiracetam / phenytoin
If >20 mins - ICU - intubate under GA
CT head, LP, cultures

94
Q

Causes of status epilepticus

A

Epilepsy
Hypoxia
Stroke
Brain injury
Metabolic derangements
Infections
Eclampsia
Drug withdrawal
Toxicity

95
Q

Investigations for seizures

A

Bloods: FBC, U&E, LFT, Ca, Mg, glucose

Head CT / MRI

EEG

96
Q

Management of epilepsy

A

After 2 seizures start treatment

Generalised: 1st line: valproate (Lamotrigine in females child bearing)
Adjuncts may be clobazam, carbamazepine, levetiracetam

Partial seizures: 1st line carbamazepine, (Lamotrigine female)

97
Q

What are the triggers that are important to avoid in epilepsy

A

Infection
Lack of sleep
Alcohol
Drugs
Hypoglycaemia
Caffeine
Stress
Flashing lights

98
Q

MOA of valproate

A

Potentiate GABA and causes Na channel blockage

99
Q

Side effects of valproate

A

Rash
Sedation
Weight gain
Hair loss
Tremor
Birth defects
Thrombocytopenia
Liver damage

100
Q

Side effects of levetiracetam

A

Benign side effect profile
Rarely causes severe skin reactions (SJS)

101
Q

MOA of Lamotrigine

A

Blocks Na channels and reduces glutamate release

102
Q

Side effects of Lamotrigine

A

Not highly sedating but risk of bone marrow toxicity
Withdraw if patient develops rash or flu like symptoms

103
Q

MOA of carbamazepine

A

Na channel blocker

104
Q

Side effects of carbamazepine

A

Rashes
Dizziness
Double vision
Agranulocytosis
Birth defects
Liver damage

105
Q

Side effects of phenytoin

A

Increased gum growth
Nystagmus
Failure of combined OC pill

106
Q

Metabolism of phenytoin

A

Displays zero order kinetics thus requires therapeutic drug monitoring
Metabolism saturates at a variable level leading to disproportionate increases in plasma concentrations after this point

107
Q

When can withdrawal of seizure medication be considered

A

If the patient is seizure free for 2-4yrs
Drug should be reduced in dose every 4 weeks
Patient should stop driving during withdrawal

108
Q

What should epileptic drugs be combined with in pregnancy

A

5mg folic acid daily in 1st trimester
Vitamin K in 3rd trimester as there is a tendency for neonatal bleeding

109
Q

What are the rules surrounding epilepsy and driving

A

Tell DVLA immediately and stop driving if had a seizure
If the attack was while awake and involved LOC - licence revoked

If after 1 seizure can reapply after 6 months
If multiple seizures can reapply after 1yr

110
Q

What are the role of upper motor neurones

A

Originate in motor cortex and travel down to the brain stem or spinal cord
Fibres decussate at the level of the medulla oblongata and travel down the lateral corticospinal tract to innnervate interneurons / LMN

111
Q

What are the role of lower motor neurons

A

Originate in the ventral horn of the spinal cord, receive innervation from upper motor neurones and then travel to innervate ipsilateral muscles or glands

112
Q

Signs of LMN pathology

A

Weakness
Wasting
Fasciculation
Hypotonia
Hyporeflexia

113
Q

Signs of UMN pathology

A

Weakness (extensor in upper limb, flexor in lower limb)
No wasting
Hypertonia, spasticity
Hypereflexia
Loss of fine motor movements
Pronator drift
Extensor plantar response
Clonus

114
Q

LMN lesion differential diagnoses

A

Ventral horn pathology: MND
Peripheral nerve pathology
Muscular pathology
NMJ pathology

115
Q

UMN lesion differential diagnoses

A

Vascular: stroke
Inflammatory: MS, MND
Neoplastic: tumour
Degenerative: Parkinson’s
Infective: post meningitis
Extra: drugs

116
Q

Pathophysiology of MND

A

Degenerative disease of the upper and lower motor neurones in the spinal cord, cranial nerve motor nuclei and motor cortex leading to progressive loss of motor function
Mean onset 50-70
Sensory exam always normal

117
Q

What is the amyotrophic lateral sclerosis pattern of MND

A

Most common
Loss of spinal and brainstem lower motor neurones and also cortical upper motor neurones
Mixed signs
There is a progressive spastic tetraparesis and added lower motor neuron signs : wasting and fasciculation
Brisk reflexes
Up going plantars

118
Q

What is the progressive muscular atrophy pattern of MND

A

Neuronal loss restricted to spinal lower motor neurons, giving purely LMN signs
Painless wasting begins in the small muscles of the hands and spreads

119
Q

What is the primary lateral sclerosis pattern of MND

A

Rare, disease confined to cortical UMN giving purely UMN signs
Progressive spastic tetraparesis

120
Q

What is the bulbar presentation pattern of MND

A

Bulbar symptoms with preservation of limb function in early stages
Poor prognosis due to early resp involvement

121
Q

How to diagnose MND

A

Clinical in the presence of progressive, mixed upper / lower motor neurone signs in multiple limbs

Bloods: rule out differentials
Spinal cord MIR: rule out myelopathy / radiculopathy
Nerve conduction studies / EMG for evidence of denervation

122
Q

Management of MND

A

Educate about disease
Social and carer assessments important
Riluzole: inc pre synaptic glutamate release can increase survival in ALS patient by an average of 3-4mo
Nutritional support
Overnight NIV if resp weakness
Pneumococcal / influenza vaccines

123
Q

Complications of MND

A

Fatigue
Spasticity
Pain
Mobility issues
Mental health

124
Q

Prognosis of MND

A

Remission is not known
Patients diagnosed with ALS pattern MND die within 3-5yr

125
Q

What is a muscular dystrophy

A

Genetically determined diseases that result in progressive deterioration

126
Q

What are myopathies

A

Diverse group of conditions that are grouped due to their predominant effect on muscle

127
Q

What is neurogenic disease

A

Disease of peripheral nerves or motor neurones that cause secondary skeletal muscle atrophy

128
Q

Investigations for suspected myopathy

A

Serum muscle enzymes: creatine kinase - raised in muscular dystrophies and inflammatory muscle disorders

Electromyography

Muscle biopsy - can differentiate between denervation and muscular disease

129
Q

What is duchenne muscular dystrophy

A

Most common muscular dystrophy
X linked recessive
30% are spontaneous mutations
Caused by mutation in the dystrophin gene making muscle fibres liable to break down with repeated contraction

130
Q

Signs of duchenne muscular dystrophy

A

Onset in early childhood

  • global muscle weakness
  • calf psuedohypertrophy: due to fatty replacement of muscle
  • gowers sign: use of hands to climb up to standing
131
Q

Investigations for duchenne muscular dystrophy

A

Investigations will show raised CK
Genetic testing / muscle biopsy can confirm the diagnosis

132
Q

Prognosis of duchenne muscular dystrophy

A

Poor
Patients die in late teens due to resp failure and cardiomyopathy

133
Q

What is Becker muscular dystrophy

A

Less common
Produces partially functioning dystrophin
Symptoms are milder
Patients generally live until mid 40s

134
Q

What is myotonic dystrophy

A

Autosomal dominant condition causes by a CI- channelopathy
Symptoms more severe with each generation due to expansion of CTG repeat

CF: muscle weakness and myotonia
Inabiltuy to relax muscles

Comes on in adolescence with facial and lower limb weakness

135
Q

What is myotonic dystrophy associated with

A

Cataracts
Frontal baldness
Mental impairment
Cardiac abnormalities

136
Q

What is polymyositosis

A

Inflammation of striated muscle causing proximal muscle weakness
- no pain
- wasting
- insidious or acute onset
- malaise, weight loss, fever
- difficulty squatting and climbing stairs
- can lead to resp failure

137
Q

What is dermatomyositosis

A

Polymyositosis with associated skin involvement
Classic heliotrophic rash
Associated periorbital oedema
Vasculitic patches over the knuckles

138
Q

Investigations for polymyositosis / dermatomyosis

A

Bloods:
- serum CK : raised
- ESR: rarely raised
- ANA: most positive
- RF: 50% are RF positive
Myositis specific antibodies

EMG

MRI

Needle muscle biopsy

139
Q

Management of polymyositis / dermatomyositis

A

Prednisolone / DMARDS until clinically inactive
IVIG therapy in some cases

140
Q

What is inclusion body myositis

A

Insidious onset of proximal and distal muscle wasting
Can be asymmetrical
Affects white males >50

141
Q

Investigations for inclusion body myositis

A

ANA not positive
Myositis specific antigens negative
Muscle biopsy shows inflammatory infiltrate and vacuoles containing beta amyloid

142
Q

What is myasthenia gravis

A

Autoimmune disorder resulting in insufficient functioning acetylcholine receptors

143
Q

Pathophysiology of myasthenia gravis

A

Generation of IgG autoantibodies to the ACh receptor located on the post synaptic membrane of the motor end plates

Blocks synaptic transmission at the NMJ

Is associated with other autoimmune pathology

144
Q

One main cause of myasthenia gravis

A

Thymoma
- tumour of thymus epithelial cells

145
Q

CF of myasthenia gravis

A

Muscle fatigability progressively with exercise
Diplopia and ptosis
Dysphagia
Speech difficulties
Face, neck, limb girdle weakness

146
Q

Associated factors for myasthenia gravis

A

Thymomas in 15%
Autoimmune disorders: pernicious anaemia, autoimmune thyroid disorders, rheumatoid, SLE
Thymic hyperplasia

147
Q

Investigations for suspected myasthenia gravis

A

Single fibre electromyography
TFT and CT for thymoma
Serum anti AChR antibody titre: raised in 90%
Tensilon test: injection of edrophonium will produce rapid improvements in features - not commonly used due to risk of cardiac arrhythmia

148
Q

Management of myasthenia gravis

A

Long acting acetylcholinesterase inhibitors: pyridostigmine

Immunosuppression: prednisolone, azathioprine

Thyectomy

149
Q

Prognosis for myasthenia gravis

A

May never progress past ophthalmoplegia and long periods of remission can occur
Outlook is poor if there is resp muscle involvement

150
Q

What is radiculopathy

A

Pathological process affecting nerve roots emerging from the spinal cord

  • produces a classic radicular syndrome with pain, sensory changes and weakness in the specific dermatomes / myotomes supplied by the particular nerve root
151
Q

What is neuropathy

A

Pathological process affecting a peripheral nerve

152
Q

What is peripheral neuropathy

A

Diffuse, symmetrical disease, usually beginning peripherally
Can be motor, autonomic or both

153
Q

What is demyelinating neuropathy

A

Damage spares axons but affects Schwann cells
- more common in immune mediated disease such as GBS
Inferred by decreased conduction velocity

Schwann cells can regrow so will improve with treatment

154
Q

What is axonal neuropathy

A

Nerve cell bodies are unable to maintain long axonal processes leading to degeneration that starts at the periphery progressing up towards nuroenal cell

Axons cannot regrow so outcomes are poor

155
Q

Metabolic causes of peripheral neuropathy

A

Diabetes mellitus
B12 / folate / thiamine deficiency
Uraemia (CKD)

156
Q

Toxic causes of peripheral neuropathy

A

Alcohol
Chronic liver disease
Radiation

157
Q

Autoimmune causes of peripheral neuropathy

A

RA
Connective tissue disorder
Hypothyroidism

158
Q

Inflammatory causes of peripheral neuropathy

A

Guillain-Barré syndrome
Chronic inflammatory demyelinating polyneuropathy

159
Q

Drugs that can cause peripheral neuropathy

A

Amiodarone
Statins
Hydralazine
Phenytoin
Abx

160
Q

Infective causes of peripheral neuropathy

A

Syphilis
HIV

161
Q

Vascular causes of peripheral neuropathy

A

Vasculitis

162
Q

Neoplastic causes of peripheral neuropathy

A

Myeloma
Paraneoplastic syndromes

163
Q

Inherited causes of peripheral neuropathy

A

Charcot-Marie tooth - present before the age of 20 with progressive neuropathy

Friedrich’s ataxia - cerebellar ataxia noted in the first decade combined with UMN limb signs and peripheral neuropathy

164
Q

What can long standing peripheral neuropathy lead to

A

Claw deformities of the foot (pes cavus)

Joint arthropathies (Charcot foot)

Ulceration

165
Q

Investigations for suspected peripheral neuropathy

A

Bloods: FBC, U&E, LFT, HbA1c, B12, ANCA, VDRL, autoantibodies

Nerve conduction studies

LP

Peripheral nerve biopsy

166
Q

What is guillain barre syndrome

A

An immune mediated demyelination of the peripheral nervous system often triggered by an infection (campylobacter)

167
Q

Initial symptoms of guillain barre syndrome

A

Back / leg pain
Paralysis 1-3 weeks after an infection - infection can be trivial and unidentified

168
Q

CF of guillain barre syndrome

A

Ascending weakness starts in lower limbs
Reduced / absent reflexes
Distal paraesthesia
Few sensory signs

169
Q

Investigations for suspected GBS

A

Clinical
Nerve conduction studies
Raised CSF protein on LP

170
Q

Management of GBS

A

Severe cases progress rapidly
Prevent pressure sores, infections, DVT
Decreased FVC may indicate ventilatory failure - intubation
SC heparin + stockings
High dose IVIG within 2 weeks

171
Q

Prognosis of GBS

A

Little disability before spontaneous recovery
Complete recovery over months
Left with residual weakness
10% mortality in acute phase

Poor prognosis: old age, rapid onset of symptoms, axonal patterns of damage

172
Q

Define stroke

A

An acute focal neurological deficit of cerebrovascular origin that persists >24hrs

173
Q

Types of ischaemic stroke

A

Thrombotic : thrombosis from large vessels eg carotid

Embolic: blood clot but fat, air or clumps of bacteria can act as embolus - usually caused by AF

174
Q

Types of haemorrhagic stroke

A

Intracerebral haemorrhage: bleeding within brain

Subarachnoid haemorrhage: bleeding on the surface of the brain

175
Q

Risk factors for haemorrhagic stroke

A

Age
HTN
Arteriovenous malformation
Anticoagulants
Heavy recent alcohol intake

176
Q

Risk factors for ischaemic stroke

A

Age
HTN
Smoking
Hyperlipidaemia
AF
DM
Use of oestrogen OC

177
Q

What is a lacunar infarction

A

Microinfarcts caused by small vessel disease : arteriosclerosis
Usually affecting sub cortical areas eg basal ganglia
Can be asymptomatic eventually leading to vascular pseudo-Parkinsonism or vascualr dementia

178
Q

What is global ischaemia

A

Infarcts at arterial boundary zones due to a global reduction in blood flow due to severe hypotension

Can cause death of the majority of neurons 24hrs after the insult with the patient remaining in vegetative state

179
Q

What are the 3 zones of cerebral ischaemic damage

A

Infarct core: tissue certain to die
Oligaemic periphery: tissue that will survive due to collateral supply
Ischaemic penumbra: tissue in between can have either outcome

180
Q

CF of stroke

A

Contralateral limb weakness
Facial weakness
Visual disturbances
Higher dysfunction
Rare epilepsy

181
Q

Examples of higher dysfunction

A

Expressive aphasia
Receptive aphasia
Apraxia
Asteregnosis
Agnosia
Inattention

182
Q

Why should serum prolactin be tested after a seizure

A

Elevated serum prolactin is indicative of a true seizure as oppose to a pseudo seizure

183
Q

What should be ruled out on the presence of a third nerve palsy associated with pain

A

Posterior communicating artery aneurysm

184
Q

What are the features of a third nerve palsy

A

Eye is deviated down and out
Ptosis
Pupil may be dilated

185
Q

Characteristics of Webers syndrome

A

Ipsilateral CN III palsy
Contralateral hemiparesis

186
Q

Which cranial nerves are affected in vestibular Schwannomas

A

V, VII and VIII

187
Q

Presentation of pontine haemorrhage

A

Reduced GCS
Paralysis
Bilateral pin point pupils

188
Q

Features of juvenile Myoclonic epilepsy

A

Teenage girls
Exacerbated by sleep deprivation
Daydreaming (absence seizure)
Arm jerking sharply (tonic clonic + Myoclonic)

189
Q

Characteristics of infantile spasms

A

Brief spasms of sudden uncontrolled movements including flexion of the head, trunk, limbs and extension of the arms

Hypsarrhythmia on EEG

190
Q

Differentiating feature between meningitis and encephalitis

A

Abnormalities in brain function are present in encephalitis but in meningitis cerebral function remains normal

191
Q

Who should receive IV dexamethasone after meningitis

A

Anyone who does not have meningococcal septicaemia (a non blanching purpuric rash), septic shock, recently out of surgery or immunocompromised

192
Q

Prophylaxis for people in contact with patients with meningitis

A

Oral ciprofloxacin or rifampicin

Junior Medicine (6 decks)

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