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Neurology and Special Senses > Neurology Conditions > Flashcards

Neurology Conditions Flashcards

1
Q

What is the normal intracranial pressure in adults?

A

<15mmHg

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2
Q

How does raised ICP cause damage?

A

Compression of the brain leads to reduced blood supply to the cells –> Ischaemia –> No ATP –> Failure of NaKATPase –> Raised Na –> water follow –> cytotoxic cellular oedema

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3
Q

What investigations would you request if you suspect raised ICP?

A

CT head
Lumbar Puncture - IF SAFE (no evidence of coning) to get an opening pressure
Glucose, renal function, electrolytes, clotting
Toxicology screen

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4
Q

How does raised ICP present?

A 
Headache
Vomiting
Change in consciousness
Seizures
Cushings reflex
Changes to pupils
Hemiparesis
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5
Q

What are the trio of signs seen in Cushing’s reflex?

A

Hypertension - sympathetic stimulation
Bradycardia - baroreceptors detect raised BP
Bradypnoea/ Cheyne-stokes breathing - Ischaemia to resp centre

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6
Q

What changes are seen to the eyes in raised ICP?

A

Pupils constrict initially then dilate
Peripheral visual field loss
Papilloedema and loss of venous pulsation at the disk
CN 3 and 6 palsy

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7
Q

What are the types of brain herniation?

A

Subfalcine/cingulate
Uncal
Tonsillar

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8
Q

What happens in a subfalcine/cingulate herniation and what does it cause?

A

Cingulate gyrus push under falx cerebri and compress anterior cerebral artery

  • Contralateral weakness - especially leg
  • Gait problems
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9
Q

What happens in an uncal herniation and what does it cause?

A

Uncus herniate through tentorial notch to compress:
CN3 = ipsilateral dilated, down and out
CN6 = diplopia when looking to side of lesion
Reticular formation - reduced GCS
Chemoreceptor trigger zone - N&V
Crus cerebri via kernohan’s notch - Ipsilateral hemiparesis
Ipsilateral PCA - contralateral homonymous hemianopia with macular sparing

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10
Q

What happens in a tonsillar herniation? What symptoms do you get?

A

Cerebellar tonsils herniate through foramen magnum leading to compression of brainstem.
Cardiorespiratory centres compressed - apnoea
Ataxia
CN6 palsy
Headache and neck stiffness
Flaccid paralysis
LOC

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11
Q

How are brain herniations managed?

A 
Raise end of bed to 30 degrees
IV Mannitol
IV Dexamethasone
Fluid restrict
Normothermia
Normoglycaemia 
Analgesia, sedation and anticonvulsants
Decompressive craniectomy
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12
Q

What are the most common types of venous sinus thrombosis?

A

Sagittal sinus

Transverse sinus

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13
Q

How does sagittal sinus thrombosis present?

A 
Headache - often sudden onset
Vomiting
Seizures
Hemiplegia
Decreased visual acuity
Papilloedema
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14
Q

How does transverse sinus thrombosis present?

A 
Headache - often sudden onset
Mastoid pain
Focal CNS signs
Seizures
Papilloedema
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15
Q

How does sigmoid sinus thrombosis present?

A

Cerebellar signs

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16
Q

How does inferior petrosal sinus thrombosis present?

A

CN5&6 palsy

Retro-orbital pain

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17
Q

What commonly causes cavernous sinus thrombosis?

A

Infection - facial pustules, folliculitis, sinusitis

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18
Q

How does cavernous sinus thrombosis present?

A 
Headache
Peri-orbital pain and oedema
Proptosis
Ophthalmoplegia - CN6 first, then 3 and 4
Central retinal vein thrombosis
Hyperaesthesia of upper face (CN5)
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19
Q

What causes venous sinus thrombosis?

A

Hypercoaguable state - pregnancy, COCP, dehydration
Head injury
Tumours
Recent lumbar puncture

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20
Q

What are the differentials for venous sinus thrombosis?

A

Subarachnoid haemorrhage
Arterial infarct
Meningitis
Abscess

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21
Q

How is venous sinus thrombosis managed?

A

Anticoagulate - IV heparin or LMWH then warfarin

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22
Q

What are the complications associated with venous sinus thrombosis?

A

Transtentorial herniation due to mass effect or oedema

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23
Q

How would a venous sinus thrombosis appear on CT with contrast?

A

Empty delta sign - superior sagittal sinus should usually fill with contrast but doesn’t when thrombosed

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24
Q

What characteristics of a headache indicate it may be due to a space occupying lesion?

A

Worse on:

  • Waking
  • Lying down
  • Bending forward
  • Coughing
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25
Q

What symptom would mean space occupying lesions must be excluded as a cause?

A

Adult onset seizures - especially if aura (focal or localising) or post ictal weakness

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26
Q

What can cause a space occupying lesion?

A

Metastatic tumours - breast, lung, melanoma
Primary tumour - astrocytoma, glioblastoma, oligodendroglioma, meningioma
Aneurysm
Abscess
Chronic subdural haematoma
Granuloma
Cyst

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27
Q

What are the risk factors for idiopathic intracranial hypertension?

A

Obese
Female
30’s
COCP

Others - steroids, tetracyclines, vit A, lithium

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28
Q

How does idiopathic intracranial hypertension present?

A 
Headache
Narrowed visual fields
Blurred vision and diplopia
CN6 palsy
Enlarged blind spot - papilloedema
No change in cognition and consciousness
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29
Q

How is idiopathic intracranial hypertension managed?

A 
Weight loss
Acetazolamide or topiramate
Prednisolone
Optic nerve sheath fenestration (reduce pressure on optic nerve head)
LP shunt
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30
Q

What is a hydrocephalus?

A

Excess volume of CSF fluid within ventricles due to imbalance of production and absorption

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31
Q

What are the types of hydrocephalus?

A

Obstructive/non communicating

Non-obstructive/communicating: CSF is free to flow but there is an imbalance of production and absorption

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32
Q

What can cause obstructive hydrocephalus?

A

Tumours
Congenital stenosis of the aqueduct
Haemorrhage of ventricles or subarachnoid space

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33
Q

What can be seen in an obstructive hydrocephalus?

A

Dilation of the ventricles superior to site

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34
Q

What can cause a non-obstructive hydrocephalus?

A

Increased production - choroid plexus tumour

Decreased absorption - meningitis, post-haemorrhagic

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35
Q

What investigations would you request for hydrocephalus?

A

CT - rule out differentials

LP - opening pressure and sample CSF

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36
Q

When mustn’t a lumbar puncture be carried out in a patient with a hydrocephalus?

A

If the cause is obstructive as the difference between pressures of the cranium and spine created by the LP will cause brain herniation

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37
Q

How does hydrocephalus present?

A

Signs of RICP i.e. headache worse on waking, lying down and Valsalva

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38
Q

How would hydrocephalus present in infants?

A

Increased head circumference - sutures not closed
Anterior fontanelle bulge
Sun set eye - can’t look up due to superior colliculus (midbrain) compression

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39
Q

What is the triad for normal pressure hydrocephalus?

A

Wet wacky wobbly

Urinary incontinence
Dementia
Disturbed gait - similar to parkinsons

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40
Q

What is a normal pressure hydrocephalus?

What is the appearance of the brain/ventricles?

A

Communicating hydrocephalus thought to be due to poor CSF absorption

Large ventricles (particularly 4th) but normal ICP

No substantial sulcal atrophy

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41
Q

What can cause a subarachnoid haemorrhage?

A

Traumatic or Spontaneous

Berry aneurysm rupture
AV malformation
Pituitary apoplexy
Tumour invading blood vessels
Idiopathic
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42
Q

How does a subarachnoid haemorrhage present?

A 
Sudden onset thunderclap headache - occipital
Vomiting
Collapse, coma, seizure
Meningism
Terson's syndrome - vitreous haemorrhage
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43
Q

What are subarachnoid haemorrhages associated with?

A

Adult polycystic kidney disease
Ehlers danlos
Coarctation of the aorta

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44
Q

What can be seen on CT head in subarachnoid haemorrhages?

A

Hyperdense blood in:
Inter-hemispheric fissure
Sylvian fissues
Basal cistern

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45
Q

What arteries do berry anneurysms most commonly affect?

A

junction of anterior cerebral and anterior communicating

junction of middle cerebral and internal carotid

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46
Q

How are subarachnoid haemorrhages managed?

A

Bed rest, avoid straining, maintain BP
Nimodipine - 21 day to prevent vasospasm - cerebral ischaemia
Surgery - endovascular coiling, craniotomy and surgical clipping

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47
Q

What complications are subarachnoid haemorrhages associated with?

A

Rebleeding - 20%
Cerebral ischaemia - vasospasm
Hydrocephalus - blockage of arachnoid granulations
Hyponatraemia - SIADH

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48
Q

How would you investigate a suspected subarachnoid haemorrhage?

A

CT - very sensitive to timing so if suspicious do LP
LP
CT Angio

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49
Q

When would a lumbar puncture be carried out in suspected subarachnoid haemorrhage? What would the results be?

A

12 hours after headache

RBC start breaking down so sample will be xanthochromic (yellow) due to bilirubin

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50
Q

What causes a subdural haemorrhage? Therefore who do they most commonly affect?

A

Shearing forces on cortical bridging veins

Elderly and alcoholics (brain atrophy = taught bridging veins easier to rupture)

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51
Q

How does a subdural haematoma present?

Who would you see chronic subdurals in? How do they present on CT?

A

Slow onset of symptoms - RICP, upgoing planters etc.

Chronic subdural haematomas can be seen in infants and elderly
They are hypodense on CT

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52
Q

How would a subdural haematoma present on CT?

A

Crescent shaped hyperdense area + midline shift

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53
Q

What is the mechanism of getting an extradural haematoma?

What artery and what vein is commonly lacerated?

A

Acceleration Deceleration or Blow to side of head

Middle meningeal artery
Dural venous sinus

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54
Q

How does an extradural haematoma present?

A

Lucid interval followed by rapid deterioration

RICP
Upgoing plantars
Ipsilateral pupil dilation

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55
Q

How does an extradural haematoma appear on CT?

A

Biconvex hyper dense area

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56
Q

What is the pathophysiology of multiple sclerosis?

A

Chronic cell mediated autoimmune demyelination of the CNS

Attacks are separated in time and space (occur at multiple sites with remission in between)

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57
Q

What is the epidemiology of multiple sclerosis?

A

Mean age of onset = 30
Classically white women
Combination of genetic and environmental factors

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58
Q

How does multiple sclerosis commonly present initially?

A

Just one symptom - e.g. pain on eye movement with blurring of vision

Odd sensations such as wetness, burning or tingling

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59
Q

What systems are affected by multiple sclerosis?

A 
Visual
Mouth
Urinary
Digestive
Sensory
Muscular
Throat - dysphagia
Central
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60
Q

What are the visual manifestations of multiple sclerosis?

A

Nystagmus
Optic neuritis - common first presentation
Diplopia

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61
Q

What are the manifestations of multiple sclerosis seen in the mouth?

A

Difficulty swallowing

Slurring and stuttering of speech

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62
Q

What are the urinary manifestations of multiple sclerosis?

A

Frequency

Incontinence

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63
Q

What are the digestive manifestations of multiple sclerosis?

A

Sudden change in frequency
Constipation
Diarrhoea

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64
Q

What are the sensory manifestations of multiple sclerosis?

A

Increased sensitivity to pain
Tingling
Burning
Pins and needles

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65
Q

What are the muscular manifestations of multiple sclerosis?

A

Weakness
Cramping
Spasm
Lack of co-ordination - cerebellar involvement

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66
Q

What are the central manifestations of multiple sclerosis?

A

Fatigue
Depression
Cognitive impairment
Unstable mood

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67
Q

How can multiple sclerosis progress?

A

3 courses:

  • Relapsing-remitting - complete remission between acute attacks
  • secondary progression - relapsing remitting over time doesn’t fully remit
  • Primary progression - progressive deterioration from onset
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68
Q

How is multiple sclerosis diagnosed?

A

MRI brain - demyelination plaques
MRI spine
CSF Electrophoresis - oligoclonal bands of IgG
Evoked potentials

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69
Q

What signs are seen in multiple sclerosis?

A

Lhermitte - electric shock in trunk and limb when neck flexed

Uhthoff’s - symptoms worse when warm

Pulfrich - Unequal eye latency - straight paths appear curved

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70
Q

How is multiple sclerosis managed?

A

Exercise, stop smoking, avoid stress
Acute relapses - IV methylprednisolone
Disease modifying drugs
Symtom control

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71
Q

What disease modifying drugs are used for multiple sclerosis?

A

Beta-interferon
Glatiramer
Dimethyl fumerate
Alemtuzimab

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72
Q

What drugs are used in symptom management for multiple sclerosis?

A

Baclofen - spasticity
Gabapentin - Oscillopsia and spasticity
Amantidine, CBT and mindfullness - fatigue
Urinary incontinence - normal meds

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73
Q

What is Parkinson’s disease?

A

Neurodegenerative disorder of the dopaminergic neurones in the pars compacta of the substantia nigra

Lewy bodies can be seen in the brainstem, cortex and basal ganglia

74
Q

What triad of symptoms characterise Parkinson’s disease?

A

Bradykinesia
Hypertonia
Tremor

75
Q

What symptoms are associated with Parkinson’s disease?

A

Asymmetrical symptoms

Bradykinesia - slow to move, shuffling short stepped gait, micrographia, reduced arm swing, microphonia
Hypertonia - leadpipe rigidity - combined with tremor = cogwheel
Resting tremor - 3-5Hz, pill rolling

REM sleep disorder, autonomic dysfunction, stooped posture, dementia/depression

76
Q

What are the main differentials for Parkinson’s?

A 
Benign essential tremor
Huntington's
Wilson's
Lewy body dementia
Psychogenic tremor

Parkinson’s plus - PSP, MSA, CBD

77
Q

How is Parkinson’s diagnosed?

A

Clinical diagnosis based on core triad + response to treatment
Brain bank diagnostic criteria is used

Need to rule out differentials

78
Q

What drug classes can be used to treat Parkinsons?

What important information should patients be given regarding their medication?

A

Don’t stop abruptly and be aware of malabsorption - neuroleptic malignant syndrome

Levodopa
Dopamine agonists - ropinirole
MAO-B Inhibitors - Rasagiline, selegiline
COM-T inhibitors - entacapone

79
Q

What needs to be given alongside Levodopa and why?

What are the side effects of Levodopa?

A

Given with carbidopa to reduce peripheral breakdown

More motor complications and more negatives:

  • Dyskinesia
  • On off effect
  • Dry mouth
  • Palpitations
  • Postural hypo
80
Q

Give an example of a dopamine agonist?

What effect do they have on motor symptoms and motor side effects?

What are their side effects?

A

Ropinirole

Less effect on motor symptoms but fewer motor complications

Hallucinations and impulse control disorders

Ergot derived (bromocriptine) last resort as cause pulmonary, retroperitoneal and cardiac fibrosis

81
Q

Describe the use of MAO-B inhibitors in Parkinson’s: Example and effect on motor symptoms/motor complications

A

Rasagiline

Fewer motor complications but reduced effectiveness

82
Q

What other medications are used for other symptoms of Parkinson’s?

A

Sleepiness - Driving advice, modafinil
REM sleep disorder - melatonin, clonazepam
Postural hypo - fludrocortisone
Hallucinations - quetiapine and lorazepam
Dementia - cholinesterase inhibitor
Saliva drooling - SALT, glycopyronium

83
Q

What is the prognosis of Parkinson’s and what are the main complications?

A

15 years

Aspirational pneumonia, bed sores, infection, poor nutrition, falls, contractures

84
Q

What is Parkinsonism?

A

Other conditions which appear with similar symptoms to Parkinson’s but don’t have same cause

85
Q

What are the main Parkinson’s plus disorders?

What else can cause Parkinsonism?

A

Progressive supranuclear palsy
Multiple system atrophy
Cortico-basal degeneration

Wilson’s, trauma, encephalitis
drugs (metoclopramide, haloperidol, chlorpromazine)

86
Q

What symptoms would make you think a patient has progressive supra nuclear palsy?

A

postural instability - falling backwards
symmetrical
gaze palsies, speech and swallowing problems

87
Q

What symptoms are characteristic of multiple system atrophy?

A

Early autonomic dysfunction - postural hypotension, urge incontinence, erectile dysfunction
cerebellar signs
pyramidal signs - UMN signs

88
Q

What symptoms are associated with corticobasal degeneration?

A

Akinetic rigidity in 1 limb
Cortical sensory loss
Alien limb phenomenon
apraxia: difficulty in motor planning

89
Q

What is motor neurone disease?

A

Neurodegenerative disease whereby there is selective loss of upper and lower motor neurones in the motor cortex, CN nuclei and anterior horn cells

NO SENSORY LOSS, no sphincter involvement or disturbance to eye movement

90
Q

What are the types of motor neurone disease?

A

Amytophic lateral sclerosis

  • loss in motor cortex and anterior horn cells
  • typically UMN leg and LMN arm

Primary lateral sclerosis
- UMN

Progressive bulbar palsy
- affects brainstem motor nuclei (chewing, swallowing)

Progressive muscular atrophy
- LMN only typically progress from distal to proximal

91
Q

How can motor neurone disease present?

A

Bulbar onset - slurred speech, swallow issues, tongue wasting

UL onset - weak grip, weak abduction, hand cramp, atrophy of hand muscles

LL onset - stumbling spastic gait, foot drop, thigh fasciculations, tibialis ant. wasting

Resp onset - dyspnoea, aspirational pneumonia, overnight hypoventilate

Frontotemporal dementia

92
Q

How is motor neurone disease diagnosed?

A

Clinical diagnosis based on:
- UMN and LMN signs
- Disease progression
No other explanation

93
Q

How would motor neurone disease be investigated?

A

Normal tests to rule out differentials - LP, B12, ACh antibodies
MRI - normal
EMG - large amplitude but long duration (therefore less action potentials)
Nerve conduction - normal motor conduction

94
Q

What is the epidemiology of motor neurone disease?

A

2x more common in men
43-52
10% inherited and may present earlier

95
Q

How is motor neurone disease managed?

A

MDT - palliative and end of life care
Speech - SALT, aids
Diet - modify diet/PEG
Breathing - physio, positive pressure ventilation, BiPAP
Cramps and spasms - baclofen, orthotics, exercises
Drooling - Hyoscine
Choking sensation - opiates

Riluzole can improve survival (only by months)

96
Q

What are the main differentials for motor neurone disease?

A 
!!Cervical spondylosis!! (LMN at level and UMN below)
Benign fasciculations
Myasthenia gravis
Inclusion body myositis
Multifocal motor neuropathy
Lambert-eaton
97
Q

What is the prognosis for motor neurone disease?

A

Median survival - 2-4 years

Most die in sleep - hypercapnia

98
Q

What is bulbar palsy?

A

Result of diseases affecting CN 9-12

LMN lesions of tongue and muscles of articulation and swallowing

99
Q

How does bulbar palsy present?

A

Bag of worms tongue - flaccid + fasciculations
Slurred speech (R is first to go)
Drooling
Raspy nasal voice

100
Q

What is pseudobulbar palsy?

A

Bilateral UMN lesions of corticobulbar tracts (UMN of non-ocular cranial nerves)

101
Q

How does pseudo bulbar palsy present?

A

Slow tongue movements= slow deliberate speech
Exaggerated jaw jerk
Absent palatal movements
Increased reflexes

!!No wasting or fasciculations as UMN

102
Q

What can cause bulbar and pseudo bulbar palsy?

A

MND

Bulbar - polio, diphtheria, syringobulbia, infarct

Pseudobulbar - MS, stroke

103
Q

What is bells palsy?

A

Acute, unilateral, idiopathic facial nerve palsy

104
Q

What are the risk factors for developing Bells palsy?

A

20-40yo
Pregnancy
Diabetes

105
Q

How does bells palsy present?

A 
Forehead not wrinkled
Eyeballs roll up
Eyelid won't close
Flat nasolabial fold
Paralysis of lower face
Ipsilateral post-auricular numbness or pain
Reduced tase
Hypersensitivity to sound
Can't whistle
Food trapped between gum and cheek
Dry eyes
106
Q

What are the main differentials for bells palsy? How would you rule these out/differentiate?

A

Ramsay hunt - ear pain proceded by palsy. Do VSV antibodies

Lyme disease - Can be bilateral. Do Borrelia antibodies

Facial nerve tumour and brainstem lesions - slow onset

Acoustic neuroma

107
Q

How is bells palsy managed?

A

Oral prednisolone

Eye protection and lubricants

108
Q

What complications are associated with bells palsy?

A

Exposure keratopathy and conjunctivitis
Synkinesis - misconnected links lead to unwanted facial movements (eye blink cause upturning of mouth)
Crocodile tears - cry when salivating

109
Q

What are crocodile tears? (in reference to bells palsy)

A

Misconnection of parasympathetics mean unilateral lacrimation not salivation on eating

110
Q

What is the prognosis for bells palsy?

A

By 6 months everyone have degree of recovery - if not consider alternate diagnosis

Incomplete paralysis without axonal degeneration - recover within weeks

Complete paralysis - 80% recover, 20 % start recovery later

111
Q

What is myasthenia gravis?

A

Autoimmune disease where nicotinic acetylcholine receptors on the post-synaptic NMJ are blocked by antibodies

112
Q

How does muscle fatigue progress in myasthenia gravis?

A 
Extraocular
Bulbar - swallow and chew
Face
Neck
Limbs
Trunk
113
Q

How does myasthenia gravis present?

A 
Ptosis - at night
Diplopia
Drooped mouth and snarl - when smiling
Peek sign - eyelids separate on manual closure
Voice fade on counting to 50
Unable to whistle
114
Q

At what age do people commonly present with myasthenia gravis?

A

Women - child bearing

Men - 70’s

115
Q

What investigations are requested for Myasthenia Gravis? What are the results?

A

Anti-ACh antibodies
Repetitive nerve stimulation shows reduced AP
CT thorax - thymoma

116
Q

What can exacerbate myasthenia gravis?

A

Hypokalaemia
Infection
Change in climate, emotion or exercise
Drugs - Abx, Opiates, Beta blockers, lithium, phenytoin

117
Q

What is myasthenia gravis associated with?

A

RA and SLE
Thymic hyperplasia
Thymic tumours

118
Q

How is myasthenia gravis managed?

A

AChE inhibitors - pyridostigmine
Immunosuppression - prednisolone
Thymectomy
Trigger avoidance

119
Q

What are the ADR’s associated with AChE inhibitors?

A 
Lacrimation
Salivation
Sweating
Vomiting
Miosis
120
Q

What is a myasthenic crisis?

A

Life threatening weakness of resp muscles

121
Q

How can myasthenic crises be managed?

A

Intubate and ventilate
Plasma exchange
Immunosuppression and immunoglobulins

122
Q

How could you differentiate between a myasthenic crisis and a cholinergic crisis?

A

Myasthenic: history of poor compliance. Good response to endrophonium challenge

Cholinergic (over medicated): Other cholinergic symptoms. Endrophonium challenge leads to fasciculations, miosis and worsening respiratory function

123
Q

What is temporal arteritis?

A

Granulomatous vasculitis of medium and large sized vessels

Also known as giant cell arteritis

124
Q

Who is commonly affected by temporal arteritis?

A

Women

>50

125
Q

How does temporal arteritis present?

A

Rapid onset within <1 months
Headache - temporal/occipital
Jaw claudication

Vision changes (ant. ischaemic optic neuropathy)
- amourosis fugax and visual disturbance
Scalp tenderness
Polymyalgia rheumatica symptoms
- aching
- morning stiffness (NOT WEAK) in proximal limbs
Systemic symptoms
- lethargic, depression, low grade fever
126
Q

How would you investigate suspected temporal arteritis?

A

ESR - raised
CRP
Temporal artery biopsy - can get skip lesions so don’t ignore -ve biopsy
Temporal artery USS - halo sign, thickening and occlusion

127
Q

How is temporal artery managed?

A 
DONT DELAY 
High dose oral prednisolone - 4 weeks then taper
\+ PPI, bisphosphonate and calcium
Urgent ophthalm review
Tocilizumab

If vision loss - IV methylprednisolone

128
Q

What are the complications associated with temporal arteritis?

A

Irreversible bilateral vision loss - optic nerve ischaemia

Glucocorticoid related issues - diabetes, bone loss, infections

129
Q

What are the types of neurofibromatosis?

A

Type 1 - von recklinghausen
Type 2

Both autosomal dominant

130
Q

How does neurofibromatosis type 1 present?

A 
Cafe-au-lait spots (within 1st year of life and increase)
Freckling
Neurofibromas - dermal, nodular
Lisch nodules
Short
Macrocephaly
Mild learning disability
Optic gliomas
131
Q

How does neurofibromatosis type 2 present?

A

Cafe-au-lait spots (fewer)

Bilateral vestibular schwannoma - sensorineural hearing loss, tinnitus, vertigo, compress local structures, RICP

Form of cataract

Meningiomas and gliomas

132
Q

How are neurofibromatosis type 1 and 2 managed?

A

No cure
Remove symptomatic schwannoma
Annual hearing tests for type 2

133
Q

What organisms commonly cause meningitis in adults?

A

Neisseria meningitidis
Strep pneumoniae

Listeria monocytogenes if immunocompromised

134
Q

What investigations should be done if you suspect meningitis?

A

DONT DELAY TREATMENT

Lumbar puncture
Blood culture
PCR - neisseria
Blood gases

135
Q

How would a lumbar puncture vary with the different causes for meningitis?

A

Bacterial - cloudy, low glucose, high protein, polymorphs

Viral - clear, normal glucose and protein, lymphocytes

Tuberculous - clear, low glucose, high protein, lymphocytes

136
Q

How is meningitis managed in primary care?

A

Single dose benpen (ideally IV, likely IM) if non-blanching rash. If pen allergic no alternative

No rash - urgent hospital transfer, no empirical abx

137
Q

How is viral meningitis managed?

A

Supportive

Present same as bacterial so usually follow that guidance

138
Q

What is the general management for meningitis?

A

Blood cultures
IV ceftriaxone - empirical
Dexamethasone

Meningococci - ceftriaxone
Pneumococci - vancomycin + ceftriaxone
HiB - ceftriaxone

139
Q

What are the main complications associated with meningitis?

A

Deafness - most common
Other neurological signs - epilepsy, paralysis
Infections - sepsis, intracerebral abscess
Pressure - brain herniation, hydrocephalus

140
Q

What is prophylaxis is recommended for close contacts of those with meningitis?

A

Seek advice from regional health protection unit

Usually give prophylactic abx

141
Q

What would indicate a CT head within an hour of arrival?

A 
GCS <13
GCS<15 2hrs after injury
Suspected open or depressed skull fracture
Signs of basal skull fracture
Post-traumatic seizure
Focal neurological deficit
More than 1 episode of vomiting
142
Q

What would indicate the C spine needs immobilisation?

A 
GCS <15
Neck pain or tenderness
Focal neurological deficit
Paraesthesia in extremities
Any clinical suspicion of cervical spine injury
143
Q

What should be done is GCS <8?

A

Call anaesthetist

144
Q

Why is pain management important in head injury management?

A

Can lead to raised ICP

145
Q

What would indicate a CT head within 8 hours?

A

Patient on warfarin
Some LOC or amnesia +
- Age 65 years or older
- Any history of bleeding or clotting disorders
- Dangerous mechanism of injury
- More than 30 mins retrograde amnesia of events immediately before injury

146
Q

What is an epileptic seizure?

A

Transient occurrence of signs or symptoms due to abnormal electrical activity in the brain

Manifest as disturbance of consciousness, behaviour, emotion, motor function or sensation

147
Q

What is epilepsy?

A

Disease of brain defined by:

  • At least 2 unprovoked seizures more than 24hrs apart
  • One unprovoked seizure with risk of 2nd within 10 years similar to those who have had 2
  • Diagnosis of epilepsy syndrome
148
Q

What are the risk factors for epilepsy?

A

Family history
Genetic condition associated - tuberous sclerosis or neurofibromatosis
Febrile seizures
Previous intracranial infections, brain trauma, surgery
Co-morbid conditions such as CVS disease or cerebral tumours

149
Q

How is epilepsy assessed?

A 
Check for risk factors
Before, during, after event
EEG
Imaging
Bloods

Urgently refer all people suspected of 1st seizure

150
Q

What general advice would you give to people with epilepsy?

A 
Try and record episodes
Avoid driving, swimming and bathing
Protect from injury
Don't restrain seizing person
Place in recovery position post seizure
151
Q

What is the immediate management for epilepsy?

A 
>5 mins - buccal midazolam or rectal diazepam
IV lorazepam if access
2 doses of drug (5 mins apart)
IV phenytoin if seizures continue
Intubation and Rapid sequence induction
152
Q

What is the general management for epilepsy?

A

Monotherapy
Different monotherapy
Dual therapy
Surgery or deep brain stimulation

153
Q

When can anti-epileptic drug withdrawal be considered?

A

2-4 year seizure free

Gradually withdrawn over 2-3 months

154
Q

What is the management for generalised seizures?

A

1st line - Valproate

2nd line - lamotrigine or carbemazepine

155
Q

What is the management for focal seizures?

A

1st - carbemazepine (or lamotrigine)

2nd - Levetiracetam or valproate

156
Q

What are the general ADR’s associated with anti-epileptic drugs?

A 
Drowsiness
Suicidal thoughts and behaviours
Aggresion
Hadaches
Tremor
Ataxia
Gum hypertrophy
Menstrual disturbance
157
Q

What are the side effects of valproate and how is it monitored?

A

Osteoporosis, weight gain

LFT for months
FBC before starting

158
Q

What are the side effects of carbamazepine and how is it monitored?

A

Rash, osteoporosis, SIADH, hyponatraemia, diplopia, enzyme inducer

Drug conc levels, FBC, LFT, U&E, GFT monitored

159
Q

What are the side effects of phenytoin and how is it monitored?

A

Rash, osteoporosis, arrhythmia, raised ALP, low Ca and folic acid, BM affected, enzyme inducer

Drug conc levels and blood count monitored

160
Q

What are the side effects of lamotrigine and how is it monitored?

A

Rash - inc. stephen johnsons, arrhythmia

Drug conc levels

161
Q

What are the side effects of levetiracetam and how is it monitored?

A

Behaviour and mood changes

Risk of infection

162
Q

What is subacute combined degeneration of the cord?

A

Dorsal and lateral columns affected by vitamin B12 deficiency

163
Q

How does subacute combined degeneration of the cord present?

A

Joint position and vibration sense lost
Distal paraesthesia
UMN signs - typically legs - extensor plantars, brisk knee reflex, absent ankle reflex

164
Q

How is subacute combined degeneration of the cord managed and what are the complications?

A

Vit B12

Stiffness and weakness persist

165
Q

What are most cerebellopontine angle tumours?

A

Vestibular schwannomas

166
Q

What is a classical history of a vestibular schwannoma?

A

Progressive changes

Vertigo
Hearing loss
Tinnitus
Absent corneal reflex

CNV, VII and VIII affected

167
Q

How are cerebellopontine angle tumours investigated and managed?

A

MRI
Urgent ENT referral
Audiometry
Observe, give radio or do surgery

168
Q

What is the prognosis of a cerebellopontine angle tumour?

A

Slow growing and benign

169
Q

What are the borders of the cavernous sinus?

A

Roof - meningeal layer of dura
Medial - body of sphenoid
Floor - endosteal layer of dura
Lateral - meningeal layer of dura

170
Q

What runs through the cavernous sinus?

A 
CNIII
CNIV
CNV - 1 and 2
CNVI
Internal carotid artery
171
Q

Describe the epidemiology of a pituitary adenoma

A

Common - 10% of all people
Often never found or found incidentally
10% of all adult brain tumours

172
Q

How can pituitary adenomas be classified?

A

Size - micro <1cm macro >1cm

Hormonal status

173
Q

What investigations are done for pituitary adenomas?

A

Pituitary blood profile
Visual field test
MRI brain with contrast

Symptoms will depend on the hormones secreted and what it compresses

174
Q

What are some differentials for pituitary adenomas?

A 
Pituitary hyperplasia
Craniopharyngioma
Meningioma
Brain mets
Lymphoma
Hypophysitis
Vascular malformation
175
Q

How are pituitary adenomas managed?

A

Hormone therapy
Surgery - transsphenoidal transnasal hypophysectomy
Radio

176
Q

What pupil/eye changes would you see in a central herniation

A

fixed dilated pupils

sunset eyes - paralysed upward eye movement with pupil covered by lower lid

177
Q

What is the contents of the cavernous sinus

A

Internal carotid artery
CN 3,4,6
Trigeminal nerve: ophthalmic and maxillary divisions

178
Q

What is the first line investigation for ?venous thrombosis

A

MRI with venography

179
Q

Describe the passage of CSF

A 
Lateral ventricle
foramen of monroe
3rd ventricle
cerebral aqueduct 
4th ventricle 
foramen of luschka/magendie
180
Q

How does someone with myasthenic react to different types of neuromuscular blocking anaesthetic agents?

A

Increased sensitivity to non-depolarising (Rocuronium)

Reduced sensitivity to depolarising (Suxamethonium)

Neurology and Special Senses (28 decks)

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