Emergency Neurological Conditions Flashcards

1
Q

Between what layers is a SAH and what is the space called?

A

Pia mater and Arachnoid
Subarachnoid space

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2
Q

What are the two broad causes of SAH? Give some specifics.

A

Traumatic - eg RTA (may be other cranial bleeds as well)

Spontaneous - Rupture of cerebral aneurysm, AV malformation, Vasculitis

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3
Q

Give two modifiable and non modifiable risk factors for Subarachnoid Haemorrhage

A

Modifiable - Hypertension, Smoking, excess alcohol, cocaine use
Non Modifiable - Female, FHx

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4
Q

What are some conditions associated with SAH?

A
  • Cocaine use
  • Sickle cell anaemia
  • Connective tissue disorders such as Marfan syndrome, Ehlers-Danlos
  • Neurofibromatosis
  • ADPKD
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5
Q

What patients are SAH common in?

A

Black patients
Female patients
Age 45-70

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6
Q

Where are Berry Aneurysms normally located?

A

Located at branching points of major blood vessels (points of maximum haemodynamic stress)

30-40% ACA
25% PCA
20% MCA
10% Bifurcation

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7
Q

Name symptoms of Subarachnoid Haemorrhage

A

Thunderclap Headache
Photophobia
Neck Stiffness
Nausea and Vomiting
Vision changes
Neurological symptoms (speech changes, weakness, seizures, LOC)

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8
Q

Name four signs of Subarachnoid Haemorrhage

A

Neck Stiffness
Cranial Nerve Palsy
Reduced Consciousness
Diplopia

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9
Q

What is the first line investigation for SAH and what will be seen?

A

CT Head (if within 6h - 99% sensitivity)

Blood will cause hyperattenuation in sub arach space

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10
Q

When should an LP be done for SAH? What would be a negative LP?

A

After ≥12 hours after symptom onset if CT is non-diagnostic and there is a high index of suspicion

must rule out raised intracranial pressure first

If clear or if Oxyhaemaglobin alone (suggests trauma or traumatic tap)

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11
Q

Name four findings you would expect from a positive Lumbar Puncture for SAH

A
  • Opening Pressure (elevated)
  • Red Cell Count (elevated)
  • Xanthochromia (seen after 12 hours)
  • Bilirubin
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12
Q

Once an SAH has been diagnosed, what further investigation can be done?

A

CT Angiogram (to determine any underlying pathology, can be therapeutic - coil or clip at same time)

Also can locate source of bleeding

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13
Q

Name some medical managements of SAH

A
  • IV fluids and monitoring
  • GCS<8 requires intubation
  • Nimodipine to prevent vasospasm (4 hours for 3 weeks)
  • Analgesia and Antiemetics to prevent ValSalva
  • Antiepileptics to treat seizures
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14
Q

On initial presentation of an SAH you would calculate GCS. What two grading systems can be used?

A
Modified World Federation of Neuro Societies (based on GCS) 
Modified Fisher (risk of vasospasm based on thickness of SAH and any IVH)
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15
Q

Name three possible surgical managements of SAH

A

Coiling
Clipping
External Ventricular Drain (if Hydrocephalus)

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16
Q

Name three complications of SAH

A

Rebleeding
Vasospasm
Hydrocephalus

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17
Q

Define Stroke

A

Clinical syndrome characterised by sudden onset of rapidly developing focal/global neurological disturbance, lasting more than 24h/leading to death (secondary to cerebral bloody supply disruption)

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18
Q

Strokes can be either Ischaemic or Haemorrhagic. How can Ischaemic strokes be classified?

A

By the Bamford/Oxford Classification

TACS, PACS, LAC, POC

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19
Q

Strokes can be either Ischaemic or Haemorrhagic. How can Haemorrhagic strokes be classified?

A

Intracerebral or Subarachnoid

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20
Q

Describe the pathophysiology of an Ischaemic Stroke

A

Either due to Thrombosis, Embolism or Dissection

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21
Q

Describe the pathophysiology of a Haemorrhagic Stroke

A

Usually due to Hypertension (but can also be due to vascular malformations, tumours, or bleeding disorders)

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22
Q

Describe the TAC classification of Ischaemic Stroke

A

Unilateral Sensory/Motor Weakness
Homonymous Hemianopia
Higher Cerebral Dysfunction

Requires 3/3

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23
Q

Describe the PAC classification of Ischaemic Stroke

A

Unilateral Sensory/Motor Weakness
Homonymous Hemianopia
Higher Cerebral Dysfunction

Requires 2/3

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24
Q

Describe the LAC classification of Ischaemic Stroke

A

Can be:
Pure Sensory, Pure Motor, Sensorimotor, Ataxic

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25
Q

Describe the POC classification of Ischaemic Stroke

A

One of the following:
Brainstem Cerebellar Syndrome
Conjugate Eye Movement Disorder
Isolated Homonymous Hemianopia
Bilateral Sensorimotor Loss
Cranial Nerve Palsy and Contralateral Sensory/Motor

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26
Q

Name two Posterior Stroke Syndromes

A

Locked In Syndrome - Basilar Artery

Wallenberg Syndrome - Posteroinferior Cerebellar Artery (Nystagmus, Vertigo, Horners, Diplopia, Dysphagia)

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27
Q

FAST is the tool in the community used to screen for Stroke. What is the Hospital Tool called?

A

NIHSS

  • Good Score is <4
  • Score>22 high risk of haemorrhagic transformation with thrombolysis
  • Score>26 means thrombolysis is contraindicated
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28
Q

Name 5 investigations for a suspected stroke

A

CT head
ECG
Echo
Bloods
Carotid Doppler

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29
Q

How is a Haemorrhagic Stroke Managed?

A

Depends on the extent of the bleed and suitability for intervention

Large bleeds - decompressive hemicraniotomy or suboccipital craniotomy

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30
Q

How is an Ischaemic Stroke managed ideally?

A

Thrombolysis with Alteplase (synthetic tPA)

If within 4.5 hours and NIHSS is between 5 and 26

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31
Q

Name three contraindications to Thrombolysis

A

Ischaemic stroke within the past 3 months
Active Bleeding
Intracranial Neoplasm
Previous Haemorrhagic Stroke

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32
Q

If Thrombolysis is contraindicated in terms of Ischaemic Stroke management, what is the next line?

A

300mg Asparin for 2w followed by 75mg Clopidogrel lifelong

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33
Q

What is a Thrombectomy?

A

Removal of the thrombus done in specialist centres by interventional neuroradiology
Can be combined with Thrombolysis

Location specific and depends on brain tissue viability

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34
Q

Name two early and two late complications of Stroke

A

Early - Haemorrhagic transformation, Cerebral Oedema (eg Malignant MCA)
Late - Mobility and Sensory Issues, Fatigue

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35
Q

What are the DVLA rules surrounding driving after a stroke?

A

Cars and Motocycles - stop for a month and inform if further symptoms after this time

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36
Q

Other than the medical team, name three professions involved in Post Stroke care

A

SALT
Phsyiotherapists
Palliative care

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37
Q

What are some causes of Raised Intracranial Pressure?

A
  • Neoplasms
  • Abscess
  • Haemorrhage
  • CSF disturbance - hydrocephalus
  • IIH
  • Meningitis
  • Cerebral oedema
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38
Q

What are the normal ranges for intracranial pressure

A
  • Adults - 1-15mmHg
  • Children - 5-7mmHg
  • Term infants - 1.5-6mmHg
  • general rule = >20mmHg is raised
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39
Q

What is Cushing’s triad/reflex/response?

A

HYPERTENSION - increased MAP to maintain cerebral perfusion pressure

BRADYCARDIA - increased MAP detected by baroreceptors which stimulate bradycardia via increased vagal activity

APNEA - compression of brainstem damages respiratory centres

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40
Q

Raised ICP is initially compensated by shunting blood and CSF out. When it begins to decompensate, what are the symptoms?

A

Classic Triad - Headache, Papilloedema, Vomiting (projectile)

Pupillary changes, third nerve palsies, hypertension, bradycardia,

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41
Q

What features of a headache are suspicious of raised intracranial pressure?

A
  • Constant
  • Worse in morning
  • Worse on bending/straining
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42
Q

Name three investigations for raised ICP

A
CT/MRI 
Bloods (renal function, electrolytes, osmolality) 
ICP monitoring (only if abnormal scan or low GCS)
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43
Q

First line managements for raised ICP

A
  • Airway and breathing
    • maintain sats
  • Circulation
    • maintain MAP and therefore CPP
  • Sedation, analgesia, paralysis
    • decreases metabolic demand
    • prevents cough, shivering (may increase ICP)
  • Head tilt
    • improves cerebral venous drainage
  • Temperature
    • prevent hyperthermia
    • may by therapeutic hypothermia
  • Anticonvulsants
    • prevent seizures, reduce metabolic demand
  • Nutrition and PPI
    • improve healing and prevent stomach ulcer from increased vagal activity
  • Mannitol or hypertonic saline - osmotic diuresis
44
Q

Name three second line managements of raised ICP

A

Barbiturate Coma
Hypothermia
Decompressive Hemicraniectomy

45
Q

What is the ‘Traditional’ definition of Status Epilepticus?

A

Single Seizure lasting over 30 minutes, or two seizures in succession without recovery in between

46
Q

What is the ‘Practical’ definition of Status Epilepticus?

A

Single Seizure lasting over 5 minutes or recurrent seizures without recovery

47
Q

What are the three broad classifications of Seizures?

A

Focal
Generalised (both hemispheres)
Unknown

48
Q

What are the subclassifications of Focal Seizures?

A

Can be aware or impaired awareness

Sensory or motor depending on first presenting symptom

49
Q

What are the subclassifications of General Seizures?

A

Tonic Clonic
Tonic
Myoclonic
Atonic
Absence

50
Q

Name four prehospital managments for Status Epilepticus

A

Note Time
Turn on side and cushion head
Don’t restrain
Buccal Midazolam/Rectal Diazepam if available

51
Q

Describe the hospital management of Status Epilepticus in terms of stages

A

Stage 1 - A to E, O2, IV access and bloods

Stage 2 - AED therapy, Pabrinex/Glucose where relevant

Stage 3 - Determine aetiology, further AEDs, ITU

52
Q

Describe the Anti-Epileptic Drug Choice for Status Epilepticus

A

1) Lorazepam IV/Diazepam PR/Midazolam Buccal
2) Second Dose
3) IV Phenytoin and ECG monitoring

53
Q

How is refractory Status Epilepticus managed?

A

ITU for General Anaesthesia with Thiopentone

54
Q

Name three complications of Status Epilepticus

A

Hyperthermia
Arrhythmia
Long term Neuro Damage

55
Q

How should suspected Meningococcal Sepsis be managed in the community?

A

IM Benzyl Penicillin

56
Q

What is the first line management for Meningitis at UHL?

A

IV Ceftriaxone (Meropenem if PA) and Dexamethasone (unless immunosupressed)

Notify PHE

57
Q

What is the first line management for Meningitis at UHL if over 60/immunocompromised?

A

Ceftriaxone + Amoxicillin + Dexamethasone

58
Q

Who requires PEP for Meningitis?

A

If prolonged contact with affected in the last 7 days

Single dose Ciprofloxacin

59
Q

What is GCA?

A

Sight threatening vasculitis characterised by inflammation of medium and large sized arteries

Preferential involvement of temporal/opthalmic/occipital

60
Q

Describe the pathophysiology of GCA

A

Granulomatous inflammation, vessel wall damage and release of angiogenic factors leads to narrowing and ischaemia

61
Q

Name four symptoms of GCA

A

Unilateral Temporal Headache
Scalp Pain
Jaw Claudication
Visual Blurring

62
Q

Name four signs of GCA

A

Abnormal Temporal Artery (thickened, tender)
Scalp Tenderness
Transient/Permanent Visual Loss
Optic Disc Changes (pale and swollen)

63
Q

How is GCA diagnosed?

A

3/5 of

Age>50
New Headache
Temporal Artery Abnormality
Elevated ESR
Abnormal Biopsy

64
Q

Name four investigations for GCA

A

ESR/CRP
Temporal Artery Biopsy
Duplex USS (halo occlusions and stenosis)
Opthalmological assessment

65
Q

How is GCA managed?

A

Prompt high dose steroids (before investigations if clinical suspicion is high)
With visual symptoms requires 3d IV Methylpred before switching to oral

Vit D, PPI, Bisphosphonate

66
Q

Name three complications of GCA

A

Visual Loss
Arterial Aneurysm
Arterial DIssection

67
Q

Name 5 causes of Spinal Cord Injury

A

Trauma
Tumours
Prolapsed Disc
Haematoma
Inflammatory DIsease

68
Q

Other than insiduous progression, name five red flags for spinal cord injury

A

Gait Disturbance
Loss of Bladder/Bowel Function
L’hermitte’s sign
UMN signs in lower limbs
LMN signs in upper limbs

69
Q

How does a Spinal Cord Injury present?

A

Cervical Spine - Quadraplegia
Thoracic Spine - Paraplegia
Root pain in legs
May have loss of autonomic activity

70
Q

What is Spinal Shock?

A

Physiological loss/depression of function lasting hours to weeks

Flaccid areflexia and paralysis before becoming hypertonic

71
Q

What is Neurogenic Shock?

A

Damage to descending motor pathways resulting in loss of vasomotor tone and cardiac innervation

72
Q

What is Brown Sequard Syndrome?

A

Complete cord hemisection results in:

  • Ipsilateral dermatomal loss
  • Ipsilateral loss of DCML
  • Contralateral loss of spinothalamic below level (may be a few below due to Lissauers)
73
Q

Name five signs of a LMN lesion

A

Weakness
Wasting
Hypotonia
Areflexia
Fasciculations

74
Q

Name four signs of an UMN lesion

A

Weakness
Hypertonia
Hyperreflexia
Upgoing plantars

75
Q

What is Central Cord Syndrome?

A

Central Cord Compression and oedema resulting in more upper limb weakness than lower

76
Q

What is Anterior Cord Syndrome?

A

Damage to spinal artery, lower limbs affected more than upper

77
Q

How is Spinal Cord Injury Investigated?

A

Spine MRI
U and Es
Hb and Haematocrit

78
Q

How is Spinal Cord Injury managed?

A

Referral to neurosurgeons (if metastatic see Onc notes)
Steroids
DVT and PE prophylaxis

Can consider Vasopressors such as dopamine to maintain perfusion

79
Q

Define Cauda Equina

A

Compression of nerve roots caudal to the level of spinal cord termination, causing one or more of: Bladder/Bowel Dysfunction, Saddle Anaesthesia, Sexual Dysfunction, Lower Limb Neuro Deficit

80
Q

How can Cauda Equina be investigated?

A

Normally diagnosed from a good examination and history
MRI (40% show no abnormalities)
Urodynamic Studies (post surgery)

81
Q

Name two differentials for Cauda Equina

A

Conus Medullaris Syndrome (less prominent pain, more urinary retention and constipation)

Mechanical Back Pain

82
Q

How is Cauda Equina managed?

A

Urgent Surgical Decompression

Treat underlying cause

83
Q

What is Cerebral Perfusion Pressure?

A

The available blood for brain tissue

CPP = MAP - ICP

Aim for >90

84
Q

Describe a Subfalcine Herniation

A

Cingulate gyrus pushed under the free edge of the falx on the same side as mass
Can cause compression of the ACA

85
Q

Describe a Tentorial Herniation

A

Uncus herniates through Tentorial Notch

Damages ipsilateral CNIII

Occludes blood flow in Posterior Cerebral and Superior Cerebellar

Can cause secondary brain stem haemorrhage (Duret)

86
Q

Describe a Tonsilar Herniation

A

Cerebral Tonsils pushed through Foramen Magnum, compressing brainstem

87
Q

Name 5 worrying features following a Head Injury

A

Vomiting
Reduced GCS
Confusion
Signs of a Basal Skull Fracture
Cushings triad

88
Q

What are the three branches of GCS?

A

Eye Opening
Verbal Response
Motor

Best response out of each side is used

89
Q

Describe the scoring of Eye Opening with GCS

A

4 - Spontaneously
3 - To Voice
2 - To Pain
1 - None

90
Q

Describe the scoring of Verbal Response with GCS

A

5 - Conversation
4 - Confused
3 - Words
2 - Sounds
1 - None

91
Q

Describe the scoring of Motor Response with GCS

A

6 - Obeys Commands
5 - Localises
4 - Withdraws
3 - Flexes
2 - Extends
1 - None

92
Q

Name four indicaions for Head CT post Head Injury according to NICE

A

GCS<13 initially
Suspected Skull #
Focal Neurological Signs
>1 episode of vomiting

93
Q

Describe the severity of Head Injury in terms of GCS

A

Mild (13-15)
Mod (9-12)
Severe (3-8)

94
Q

How is secondary brain injury prevented after Head Trauma

A

Intubate if low GCS
Avoid Hypoxia and Maintain pO2 >13
Use Vasopressors if required
30 degree head tilt

95
Q

What is a Bulbar Palsy

A

Features as a result of diseases affecting the lower cranial nerves (VII - XII)

96
Q

Name four broad classifications of Bulbar Palsies

A

Muscle Disorders
Diseases of Motor Nuclei in Medulla and Lower Pons
Diseases of Intramedullary Nerves of Spinal Cord
Diseases of Peripheral Nerves supplying muscles

97
Q

Name four presenting features of Bulbar Palsies

A

Weak and wasted tongue
Drooling
Absent palatal movements
Dysphonia

98
Q

Name five causes of Bulbar Palsy

A

Diptheria
Poliomyelitis
MND
Syringobulbia
Guillaine Barre Syndrome

99
Q

What is Pseudobulbar Palsy?

A

Disease of the corticobulbar tracts causing an UMN lesion
May have UMN signs in limbs

100
Q

Name three causes of Pseudobulbar Palsy

A

MS
Internal Capsule Infarcts
Neurosyhphilis

101
Q

How is Bulbar Palsy investigated?

A

Speech Assessment (Electromagnetic Articulography)
Routine Bloods
CT/MRI

102
Q

How is Bulbar Palsy Managed?

A

Admission if dysphagia
Treat underling cause
Anticholinergics for drooling
Baclofen for Spasticity

103
Q

Name four diseases affecting the NMJ and causing Respiratory Distress

A

Lambert Eaton
Myasthenia Gravis
Clostrodium Botulinim
Organophosphates

104
Q

Name four diseases affecting the Muscle and causing Respiratory Distress

A

MND
Acid Maltase Deficiency
Electrolyte Disturbance (hypokalaemia)
Polymyositits

105
Q

Name one diseases affecting the nerves and causing Respiratory Distress

A

Guillaine Barre Syndrome