Neurological Emergencies Flashcards
1
Q
Describe the clinical features of raised ICP? (9)
A
- Headache
- Altered mental state (lethargy, irritability, slow decision making, abnormal behaviour)
- Papilloedma
- Vomiting (progresses to projectile)
- Pupil changes: irregular or dilated in one eye)
- Cranial nerve palsies (esp unilateral ptosis, III or IV lesions)
- Later changes: hemiparesis, raised BP, bradycardia
- Seizures, syncope if acute rise in ICP
- Cushings reflex
- visual changes: black spots, blurring, enlarged blind spot and reduced peripheral vision (subacute) or reduced central vision and visual acuity (acute advanced)
2
Q
Describe the headache of raised ICP
A
nocturnal, starting on waking, worse on coughing/ moving
3
Q
Describe what papillodema looks like
A
blurring of disc margins, loss of venous pulsations, flame haemorrhages
4
Q
What is the cushings reflex and why does it occur?
A
hypertension + bradycardia + low resp rate due to: Ischaemia at medulla causing sympathetic activation so rise in BP + tachycardia// Baroreceptors detect increase in BP causing Bradycardia// Ischemia @ pons/ medulla resp centers so low resp rate
5
Q
How should raised ICP be investigated?
A
- CT/ MRI for underlying lesions
- blood glucose, renal function and osmolality
- check for signs of CSF leak
- ICP monitoring can be done
6
Q
Give 6 causes of raised ICP
A
- localised mass lesions (eg traumatic haematoma)
- neoplasms (glioma, meningioma, mets)
- abscesses
- focal odema secondary to trauma, infection or infarction
- disturbance of CSF circulation
- major venous sinus thombosis/ obstruction
- diffuse brain odema/ swelling
- idiopathic intracranial hypertension
7
Q
Give 5 causes of diffuse brain odema/ swelling
A
- meningitis
- encephalitis
- diffuse brain injury
- sub arachnoid haemorrhage
- reyes syndrome
- water intoxication
- cerebral venous thrombosis
8
Q
Describe the first line steps to management of raised ICP?
A
- stabilise ABC
- treat seizures with lorazepam +/- phenytoin
- Head CT if meets criteria
- assess C spine, immobilise and order neck CT if not cleared
- involve neurosurgery
- head elevation to 30 degrees
9
Q
When should you intubate someone with a head injury/ raised ICP?
A
If: - sats <92% or - hypoxic on ABG or - GCS <8
10
Q
Describe the further management of someone with raised ICP
A
- Analgesia with morphine and sedation w/ propofol if necessary
- mannitol (risk of hypovolaemia) or hypertonic saline if cerebral odema
- barbiturate coma
- hypothermia
- decompressive craniotomy and shunts
- treat cause (anticoag if venous outflow obstuction, diuretics then shunts if increased CSF, resections/ craniotomys/ steroids for SOLs)
- hyperventilation (causes hypercapnic vasoconstriction so decreases ICP)
11
Q
Describe the clinical features of a subarachnoid haemorrhage?
A
- Sudden onset explosive headache (often occipital) lasting a few seconds or a fraction of a second then a diffuse headache which can last a week or so
- almost always have N+V
- altered mental status
- seizures
- neck stiffness/ meningism signs sometimes present around 6 hrs after
- intraocular haemorrhages seen on fundoscopy in 15%
- other signs of raised ICP
- 10-15% die before getting to hospital
12
Q
What warning symptoms may occur prior to SAH as aneurysm expands and bleeds slightly (sentinel bleeds)?
A
- headache
- dizziness
- orbital pain
- diplopia
- ptosis
- sensory or motor disturbance
- seizures
- dysphagia
- bruits less common
13
Q
Describe the investigation findings consistent with a subarachnoid haemorrhage? (4)
A
- CT scan without contrast: hyperdense blood vessel in basal cisterns (98% sensitive after 2 hrs and 100% after 6, sensitivity drops after 24hrs)
- cerebral panangiography then CT or MR angiography if aneurysm found
- LP if CT scan negative but suspect SAH- spectrophotometry should be able to detect xanthochromia if SAH occured (detected from 12hrs- 2weeks after bleed)
- ECG changes inc prolonged QT, Q waves, ST elevation
14
Q
Describe the urgent and supportive management of a SAH? (4)
A
- stabilise pt and send straight to neurosurgical unit +/- intubation, ventilation, NG tube, analgesia and antiemetics
- endovascular obliteration by platinum spirals (coiling) or direct neurosurgical clipping to prevent rebleeding
- oral nimodipine given to prevent vasospasm which leads to cerebral ischaemia/ stroke
- hydrocephalus can occur as early or late complication, many will resolve on their own but some surgeons drain immediately
15
Q
Describe the further management of an SAH? (3)
A
- secondary prevention (stop smoking etc)
- specialist rehab if lasting impairment
- antifibrinolytics reduce rate of rebleeding but doesnt improve overall outcomes
16
Q
Describe the clinical features of meningitis
A
- Headache
- Fever
- Photophobia
- Neck stiffness
- Vomiting
- Muscle pains
- Non blanching purpuric rash
- seizures
- altered consciousness
- Fatigue, muscle pain
17
Q
What signs require urgent senior review +/- critical care input when managing a meningitis pt? (9)
A
- rapidly progressive rash
- poor peripheral perfusion (cap refill >4/ BP >90mmhg)
- RR <8 or >30
- HR <40 or >140
- acidosis <7.3
- WBC <4
- lactate >4
- GCS <12 or drop of 2
- poor response to initial fluid resus
18
Q
How should suspected meningitis (meningitis without signs of shock, severe sepsis or signs suggesting brain shift) be managed? (7)
A
- blood cultures
- bloods (FBC, renal function, glucose, lactate, clotting, viral PCR, blood gas)
- LP
- dexamethasone 10mg IV
- ceftriaxone IV 2g
- careful fluid resus
- throat swab for meningococal culture
- isolate until abx for 24 hrs, tell microbiology and PH
19
Q
How should suspected meningitis with signs suggestive of brain shift/ raised ICP, severe sepsis or a rapidly evolving rash be managed? (9)
A
- critical care input
- secure airway, give O2
- take bloods, do cultures
- fluid resus (if shock/ sepsis/ rapidly evolving rash)
- ceftriaxone 2g IV
- Dexamethasone 10mg IV (omit if severe sepsis or rapdily evolving rash)
- Neuro imagine such as CT head if signs of raised ICP
- throat swab for meningococcal culture
- DELAY LP
20
Q
What tests should be done on CSF when meningitis suspected? (7)
A
- glucose (w/ concurrent blood glucose)
- protein
- microscopy and culture
- lactate
- meningococcal and pneumococcal PCR
- enteroviral, HSV, VZV PCR
- consider investigations for TB meningitis
21
Q
What are the criteria for delaying LP in meningitis?
A
- signs of severe sepsis
- rapidly evolving rash
- severe cario/ resp compromise
- significant bleeding rik
- signs suggestive of brain compartment shift (do CT first): focal neurosigns, presence of papillodema, continious or uncontrolled seizures, GCS <12
22
Q
State 5 complications of meningitis
A
septic shock, DIC, septic arthiritis, haemolytic anamia, pericadial effusion, subdural effusion, SIADH, seizures, hearing loss, cranial nerve dysfunction
23
Q
Describe the clinical features of encephalitis (5)
A
- bizarre behaviour or confusion
- decreased GCS or coma
- fever
- headache
- seizures
- focal neuro signs (weakness, visual disturbance, aphasia, cerebellar signs)
- history of travel or bite
24
Q
Describe the key differences between meningitis and encephalitis?
A
- Seizures uncommon in meningitis but common in encephalitis
- photophobia, rash and neck stiffness much more common in meningitis
- focal neurological signs are a hallmark feature of encephalitis, but only occur in some and later in meningitis
- mental status is almost always altered in encephalitis, however is common but less so in meningitis
25
How should encephalitis be investigated?
How should encephalitis be investigated?
26
Give 3 common viral and 3 common non viral causes of encephalitis
Viral: HSV, arbovirus, EBV, CMv, VZV, HIB, mumps (paramyxo), measles, rabies, west nile
Non viral: any bacterial meningitis, lyme disease, TB, malaria, legionella, leptospirosis
27
How is encephalitis managed?
- start aciclovir within 30 mins or arrival- 10mg/ kg/ 8hrs IV for 14 days as empirical treatment
- specific therapies exist for CMV and toxoplasmosis
- supportive therapy in HDU/ ITU if necessary
- symptomatic treatment with phenytoin if necessary
28
Define status epilepticus
seizure lasting >30 mins or repeated seizures without intervening consciousness - usually in known epilepsy, if 1st presentation then high chance of structural brain lesion
29
How should status epilepticus be investigated/ assesed?
- bedside glucose (dont miss this as cause) early
- pulse oximetry and cardiac monitor while its happening
After treatment started:
- consider anticonvulsant levels, toxicology, LP, blood cultures, urine cultures, EEG, CT and carbon monoxide levels
- CXR to evaluate for possible asipration
- lab glucose, ABG, u&e, ca, fbc, ecg
30
Describe management of status epilepticus (from start of seizure) (inc paeds and adult doses)
0 mins: ABC, high flow O2, check BM, make surroundings safe- (50ml 50% dextrose if hypo)
5 mins: give IV lorazepam 0.1mg/ kg (4mg) slow bolus or rectal diazepam 10-20mg
10-15 mins: (if no response) give 2nd bolus
20-25 mins: phenytoin infusion 20mg/kg (up to 2g) at 50mg/min w/ ECG monitoring AND seek ITU help for general anaesthetic with propofol/ thiopentone if still going at 45 mins
31
Give 5 causes of spinal cord/ cauda equina compression?
- neoplasms (breast, kindey, thyroid, lung, prostate mets, myeloma or primary bone tumours)
- trauma
- infections; abscesses
- spinal stenosis
- transverse myelitis
- disc prolapses (rare but lumbar disc herniations typically cause CES)
- post op haematoma
- spondylolithesis
32
Describe the locations and functions of the 2 main ascending sensory tracts and the main motor tract within the spinal cord
Describe the locations and functions of the 2 main ascending sensory tracts and the main motor tract within the spinal cord
33
What are the upper motor neurone signs?
- Weakness- esp of extensors in arms and flexors in legs
- Hyperreflexia, clonus, upgoing planters
- Hypertonia which is spastic (velocity dependent)- clasp knife
34
What are the lower motor neurone signs
- weakness (pattern consistent with neuronal distribution)
- muscle wasting
- fasiculation
- hypotonia/ flaccidity
- reflexed reduced or absent
- flexor planter reflex
35
Describe the type and distribution of motor and sensory deficit seen with cord lesions
- usually bilateral motor deficit from below level of lesion down- initially LMN signs then UMN over the next hrs.
- LMN signs + loss of reflexes at the level of the lesion
- Presence of a sensory level
- autonomic features may also be present & associated w/ worse prognosis (constipation, retention, incontinence)
36
Describe the MRC grading of muscle weakness
```
0= no contraction
1= flicker of contraction
2= some active movement
3= active movement against gravity
4= active movement against resistance
5= normal power (allowing for age)
```
37
Describe the classifications of head injuries?
- Focal (slit into haematoma (sub, extra or intracerebral) or contusion (coup vs contracoup)
vs
- Diffuse (concussion vs diffuse axonal injury)
AND
- traumatic (split into open/ penetrating vs closed)
vs
- non traumatic (axonia, infection, CVA/ TIA, tumour etc)
38
Describe the pathophysiology of a concussion
- Stretching of axons causes impaired neurotransmission, ion regulation and reduced blood flow causing temporary brain dysfunction
39
Describe the clinical features of post concusion syndrome
Difficulty thinking clearly, slowed down, confusion, headache, N+V, balance problems, tired, light sensitive, irritable, sad, sleep disturbance, trouble falling asleep
40
Describe the pathophys of diffuse axonal injury
- Shearing of grey and white matter interface following traumatic acceleration/ deceleration or rotational forces
- Leads to axonal death so cerebral odema so raised ICP and death
- they get instate LOC with few recovering- v poor prognosis
41
State 5 signs of a basilar skull fracture
racoon eyes, CSF rhinorrhoea, CSF otorrhoea, battle sign, haemotympanum
42
Describe the differences in mechanism between extradural (EDH) and subdural (SDH) haemorrhage?
EDH: almost always traumatic
SDH: usually traumatic but less major trauma, can be spontaneous also
43
Describe the difference in presentation between EDH and SDH
EDH: young pt, LOC followed by lucid interval then rapid decline in consciousness, signs of raised ICP etc
SDH: acute bleeds can be any age, chronic bleeds seen in elderly, reduced GCS, neuro signs, or chronic bleeds= insidious neurological decline
44
Where is the bleed for EDH and SDH? What is the radiological appearance?
EDH: middle meningeal artery, lentiform shape, limited by suture lines
SDH: bridging veins, cresent shaped, not bound by suture lines but unable to cross midline due to falx cerebri, chronic bleeds appear hypodense- can have acute on chronic
45
What is the definitive management for EDH and SDH?
EDH: urgent craniotomy to relieve raised ICP, if small can just observe
SDH: acute- surgery to relieve raised ICP, if chronic and not causing symptoms then many are left alone
46
What are the criteria for a head CT within 1 hr of head injury?
- GCS <13 or <15 after 2 hrs
- focal neuro deficit
- suspected skull or C spine fracture
- seizure or vomiting >1 time
47
What are the criteria for head CT within 8 hrs of head injury?
```
- LOC or amnesia
AND
- age >65 (or)
- coagulopathy (or)
- high impact injury (or)
- retrograde amnesia of > 30 mins
```
48
When is a CT neck NOT required to clear the neck and allow mobilisation?
- no posterior midline cervical tenderness
- no evidence of intoxication
- pt altert and orientated to person, place, time and event
- no focal neuro deficit
- no painful distracting injuries
49
How do acute bulbar and pseudobulbar palsies present differently?
- A bulbar palsy is one of the nuclei of CN IX- XII (medulla)
- A true bulbar palsy= LMN lesion (, flacid fassiculating tongue, normal or decreased jaw jerk and reduced gag reflex, quiet nasal speech)
- corticobulbar palsy/ pseudobulbar palsy is UMN (hot potato speech, increased jaw and palatine reflexes, mood incontinent giggling/ weeping, spastic tongue)
50
List causes of bulbar and a pseudobular palsies?
Bulbar: MND, guillian barre, polio, MG, syringobulbia, brainstem tumours or central pontine demyelinolysis
Pseudobulbar: MS, MND, BILATERAL stroke or centralpontine demyelinolysis
51
Subarachnoid Haemorrhage is bleeding between the arachnoid and pia mater. What are the two broad causes? Give some specifics.
Traumatic - eg RTA (may be other cranial bleeds as well)
Spontaneous - Rupture of cerebral aneurysm, AV malformation, Vasculitis
52
Give two modifiable and non modifiable risk factors for Subarachnoid Haemorrhage
Modifiable - Hypertension, Smoking
| Non Modifiable - Female, ADPCKD
53
Where are Berry Aneurysms normally located?
Located at branching points of major blood vessels (points of maximum haemodynamic stress)
30-40% ACA
25% PCA
20% MCA
10% Bifurcation
54
Name four signs of Subarachnoid Haemorrhage
Neck Stiffness
Cranial Nerve Palsy
Reduced Consciousness
Diplopia
55
When is a Lumbar Puncture for Subarachnoid Haemorrhage required?
If more than 6 hours from onset
If strong clinical suspicion but no findings on CT
56
When should an LP be done for SAH? What would be a negative LP?
After 12 hours
If clear or if Oxyhaemaglobin alone (suggests trauma or traumatic tap)
57
Name four findings you would expect from a positive Lumbar Puncture for SAH
Opening Pressure (elevated)
Red Cell Count (elevated)
Xanthochromia
Bilirubin
58
Once an SAH has been diagnosed, what further investigation can be done?
CT Angiogram (to determine any underlying pathology, can be therapeutic - coil or clip at same time)
59
Name four medical managements of SAH
- IV fluids and monitoring
- GCS<8 requires intubation
- Nimodipine every 4h for 3w
- Analgesia and Antiemetics to prevent ValSalva
60
Name three possible surgical managements of SAH
Coiling
Clipping
External Ventricular Drain (if Hydrocephalus)
61
Name three complications of SAH
Rebleeding
Vasospasm
Hydrocephalus
62
Define Stroke
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)
63
Strokes can be either Ischaemic or Haemorrhagic. How can Ischaemic strokes be classified?
By the Bamford/Oxford Classification
TACS, PACS, LAC, POC
64
Strokes can be either Ischaemic or Haemorrhagic. How can Haemorrhagic strokes be classified?
Intracerebral or Subarachnoid
65
Describe the pathophysiology of an Ischaemic Stroke
Either due to Thrombosis, Embolism or Dissection
66
Describe the pathophysiology of a Haemorrhagic Stroke
Usually due to Hypertension (but can also be due to vascular malformations, tumours, or bleeding disorders)
67
Describe the TAC classification of Ischaemic Stroke
Unilateral Sensory/Motor Weakness
Homonymous Hemianopia
Higher Cerebral Dysfunction
Requires 3/3
68
Describe the PAC classification of Ischaemic Stroke
Unilateral Sensory/Motor Weakness
Homonymous Hemianopia
Higher Cerebral Dysfunction
Requires 2/3
69
Describe the LAC classification of Ischaemic Stroke
Can be:
| Pure Sensory, Pure Motor, Sensorimotor, Ataxic
70
Describe the POC classification of Ischaemic Stroke
```
One of the following:
Brainstem Cerebellar Syndrome
Conjugate Eye Movement Disorder
Isolated Homonymous Hemianopia
Bilateral Sensorimotor Loss
Cranial Nerve Palsy and Contralateral Sensory/Motor
```
71
Name two Posterior Stroke Syndromes
Locked In Syndrome - Basilar Artery
Wallenberg Syndrome - Posteroinferior Cerebellar Artery (Nystagmus, Vertigo, Horners, Diplopia, Dysphagia)
72
FAST is the tool in the community used to screen for Stroke. What is the Hospital Tool called?
NIH Stroke Scale
- Good Score is <4
- Score>22 high risk of haemorrhagic transformation with thrombolysis
- Score>26 means thrombolysis is contraindicated
73
Name 5 investigations for a suspected stroke
```
CT head
ECG
Echo
Bloods
Carotid Doppler
```
74
How is a Haemorrhagic Stroke Managed?
Depends on the extent of the bleed and suitability for intervention
Large bleeds - decompressive hemicraniotomy or suboccipital craniotomy
75
How is an Ischaemic Stroke managed ideally?
Thrombolysis with Alteplase (synthetic tPA)
If within 4.5 hours and NIHSS is between 5 and 26
76
Name three contraindications to Thrombolysis
Ischaemic stroke within the past 3 months
Active Bleeding
Intracranial Neoplasm
Previous Haemorrhagic Stroke
77
If Thrombolysis is contraindicated in terms of Ischaemic Stroke management, what is the next line?
300mg Asparin for 2w followed by 75mg Clopidogrel lifelong
78
What is a Thrombectomy?
Removal of the thrombus done in specialist centres by interventional neuroradiology
Can be combined with Thrombolysis
Location specific and depends on brain tissue viability
79
Name two early and two late complications of Stroke
Early - Haemorrhagic transformation, Cerebral Oedema (eg Malignant MCA)
Late - Mobility and Sensory Issues, Fatigue
80
Raised ICP is initially compensated by shunting blood and CSF out. When it begins to decompensate, what are the symptoms?
Classic Triad - Headache (worse on waking), Papilloedema, Vomiting (projectile)
Pupillary changes, third nerve palsies, hypertension, bradycardia
81
Name 5 first line managements for raised ICP
```
Avoid Pyrexia
Head Elevation at 30 degrees
Sedation
Mannitol (not if hyperosmotic or hypovolaemic)
Analgesia
```
82
Name three second line managements of raised ICP
Barbiturate Coma
Hypothermia
Decompressive Hemicraniectomy
83
Name three complications of Status Epilepticus
Hyperthermia
Arrhythmia
Long term Neuro Damage
84
What is the first line management for Meningitis at UHL?
IV Ceftriaxone (Meropenem if PA) and Dexamethasone (unless immunosupressed)
Notify PHE
85
What is the first line management for Meningitis at UHL if over 60/immunocompromised?
Ceftriaxone + Amoxicillin + Dexamethasone
86
Name 5 causes of Spinal Cord Injury
```
Trauma
Tumours
Prolapsed Disc
Haematoma
Inflammatory DIsease
```
87
Other than insiduous progression, name five red flags for spinal cord injury
```
Gait Disturbance
Loss of Bladder/Bowel Function
L'hermitte's sign
UMN signs in lower limbs
LMN signs in upper limbs
```
88
How does a Spinal Cord Injury present?
Cervical Spine - Quadraplegia
Thoracic Spine - Paraplegia
Root pain in legs
May have loss of autonomic activity
89
Define Cauda Equina
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
90
How can Cauda Equina be investigated?
Normally diagnosed from a good examination and history
MRI (40% show no abnormalities)
Urodynamic Studies (post surgery)
91
Name two differentials for Cauda Equina
Conus Medullaris Syndrome (less prominent pain, more urinary retention and constipation)
Mechanical Back Pain
92
How is Cauda Equina managed?
Urgent Surgical Decompression
Treat underlying cause
93
What is Cerebral Perfusion Pressure?
The available blood for brain tissue
CPP = MAP - ICP
Aim for >90
94
Describe a Subfalcine Herniation
Cingulate gyrus pushed under the free edge of the falx on the same side as mass
Can cause compression of the ACA
95
Describe a Tentorial Herniation
Uncus herniates through Tentorial Notch
Damages ipsilateral CNIII
Occludes blood flow in Posterior Cerebral and Superior Cerebellar
Can cause secondary brain stem haemorrhage (Duret)
96
Describe a Tonsilar Herniation
Cerebral Tonsils pushed through Foramen Magnum, compressing brainstem
97
Name 5 worrying features following a Head Injury
```
Vomiting
Reduced GCS
Confusion
Signs of a Basal Skull Fracture
Cushings triad
```
98
What are the three branches of GCS?
Eye Opening
Verbal Response
Motor
Best response out of each side is used
99
Describe the scoring of Eye Opening with GCS
4 - Spontaneously
3 - To Voice
2 - To Pain
1 - None
100
Describe the scoring of Verbal Response with GCS
```
5 - Conversation
4 - Confused
3 - Words
2 - Sounds
1 - None
```
101
Describe the scoring of Motor Response with GCS
```
6 - Obeys Commands
5 - Localises
4 - Withdraws
3 - Flexes
2 - Extends
1 - None
```
102
Name four indicaions for Head CT post Head Injury according to NICE
GCS<13 initially
Suspected Skull #
Focal Neurological Signs
>1 episode of vomiting
103
Describe the severity of Head Injury in terms of GCS
Mild (13-15)
Mod (9-12)
Severe (3-8)
104
Name four broad classifications of Bulbar Palsies
Muscle Disorders
Diseases of Motor Nuclei in Medulla and Lower Pons
Diseases of Intramedullary Nerves of Spinal Cord
Diseases of Peripheral Nerves supplying muscles
105
Name four presenting features of Bulbar Palsies
Weak and wasted tongue
Drooling
Absent palatal movements
Dysphonia
106
Name five causes of Bulbar Palsy
```
Diptheria
Poliomyelitis
MND
Syringobulbia
Guillaine Barre Syndrome
```
107
What is Pseudobulbar Palsy?
Disease of the corticobulbar tracts causing an UMN lesion
| May have UMN signs in limbs
108
Name three causes of Pseudobulbar Palsy
MS
Internal Capsule Infarcts
Neurosyhphilis
109
How is Bulbar Palsy investigated?
Speech Assessment (Electromagnetic Articulography)
Routine Bloods
CT/MRI
110
How is Bulbar Palsy Managed?
Admission if dysphagia
Treat underling cause
Anticholinergics for drooling
Baclofen for Spasticity
111
Name four diseases affecting the NMJ and causing Respiratory Distress
Lambert Eaton
Myasthenia Gravis
Clostrodium Botulinim
Organophosphates
112
Name four diseases affecting the Muscle and causing Respiratory Distress
MND
Acid Maltase Deficiency
Electrolyte Disturbance (hypokalaemia)
Polymyositits
113
Name one diseases affecting the nerves and causing Respiratory Distress
Guillaine Barre Syndrome
