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Year 3 > Acute Neurology > Flashcards

Acute Neurology Flashcards

MS, myasthenia, LEMS, MND, PD, dementia

1
Q

What is the scoring for the “eyes” in the GCS?

A

4- spontaneous movement
3- eyes open to vocal
2- eyes open to pain
1- no response

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2
Q

What is the scoring for the “verbal” in the GCS?

A 
5- speaks coherently
4- confused
3- mumbles random words
2- makes random noises
1- no response
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3
Q

What is the scoring for the “motor” in the GCS?

A 
6- normal movement
5- moves towards localised pain
4- extends away from localised pain
3- abnormal flexion
2- abnormal extension
1- no response
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4
Q

What is the definition of a stroke?

A

A sudden onset focal neurological deficit of presumed vascular origin lasting >24 hrs

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5
Q

What is the definition of a transient ischaemic attack?

A

A sudden onset focal neurological deficit of presumed vascular origin which resolves fully within 24 hrs

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6
Q

What are the two types of strokes?

A

Ischaemic (87%)- thrombosis/atherosclerosis/embolism

Haemorrhagic - either SAH/intracerebral haemorrhage

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7
Q

What are the causes of ischaemic stroke?

A

Thrombosis
Embolic (eg. AF)
Hypotension

hypoperfusion → O2 deprivation → ischaemic cascade → cell death → symptoms

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8
Q

What are the causes of haemorrhagic stroke?

A
  • Charcot-Bouchard microaneurysm- associated with chronic hypertension
  • Amyloid angiopathy
  • AV malformations
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9
Q

What are some non-common causes of haemorrhage strokes?

A

Vasculitis
Cocaine use
Trauma
Tumour

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10
Q

What are the risk factors for a stroke? (A-F) + HS

A 
Age
BP- high
Cardiac disease
DM
Exercise
FHx
Hyperlipidaemia
Smoking
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11
Q

What is the epidemiology of a stroke?

A

3rd commonest cause of death
M>F
Age >70
Hx of TIA

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12
Q

What are the clinical features of a cerebrovascular accident (CVA)?

A 
Sudden onset
Weakness
Sensory/visual/speech impairment
Impaired co-ordination
Head/neck pain
Memory often intact
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13
Q

What are the UMN lesion signs?

A 
Spasticity/clonus
Weak arm extensors, leg flexors
Hyper-reflexia
Upgoing plantars
Pronator drift
No fasciculations, muscle wasting
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14
Q

What are the LMN lesion signs?

A 
Hypotonia
General weakness
Hyporeflexia
Normal plantar response
Fasciculations, muscle wasting
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15
Q

What are the signs of an anterior cerebral artery infarct?

A

Contralateral hemiparesis- LOWER>UPPER
Contralateral cortical sensory deficits.

Abulia (absence of willpower to act decisively)
Confusion/altered mental status
Disinhibition and speech perseveration (repeats words)

Primitive reflexes (eg, grasping, sucking reflexes)
Urinary incontinence
Gait apraxia

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16
Q

What are the signs of an MCA stroke?

A

Contralateral hemiparesis- UPPER>LOWER
Contralateral hemisensory loss
Apraxia (parietal is responsible for coordinating movements)
Hemineglect
Receptive/expressive dysphagia (if left sided)
Quadrantanopia (if Meyer’s/Baum’s loop (optic radiations) affected)

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17
Q

What is the presentation if Meyer’s loop is affected?

A

Contralateral homonymous superior quadrantanopia

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18
Q

What is the presentation if Baum’s loop is affected?

A

Contralateral homonymous inferior quadrantanopia

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19
Q

What are the signs of a basilar artery infarct?

A

Cranial nerve pathology (III-XII)
Visual impairments
Cerebellar pathology
Impaired consciousness

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20
Q

What are the signs of a superior cerebellar artery infarct?

A

Dizziness

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21
Q

What are the signs of an anterior inferior cerebellar artery infarct?

A

Dizziness

Deaf

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22
Q

What are the signs of a posterior inferior cerebellar artery infarct?

A

Dizziness
Dysphagic
Dysphonic
(Lateral medullary syndome)

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23
Q

What are the possible signs of a lacunar infarct, depending on where in the brain is affected?

A

Internal capsule- pure motor deficit
Pontine- dizziness/vertigo, bilateral affects
Thalamus- affects consciousness
Basal ganglia- dyskinaesia

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24
Q

What are the signs of an intracerebral haemorrhage?

A 
Headache and meningism
Focal neurological signs
N+V
Signs of raised ICP
Seizures
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25
Q

What are the signs/symptoms of a TIA?

A

Usually lasts 10-15 minutes (may be resolved by examination)
Amaurosis fugax (curtain descending)
Global events like syncope/dizziness atypical

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26
Q

What are the initial investigations for a stroke?

A

A-E assessment

URGENT (WITHIN 1HR)
- CT head - rule out haemorrhage

Whilst awaiting CT:

  • BM- hypoglycaemia causing deficit
  • FBC- excludes anaemia/thrombocytopaenia prior to initiation of thrombolytics, anticoagulants, antithrombotics
  • U+Es- exclude electrolyte disturbance as a cause for focal neurological signs + renal failure (contraindication to some interventions)
  • PTT
  • Cardiac enzymes (stroke may be associated with concomitant MI)

ECG- arrhythmias/MI

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27
Q

What is the management of an ischaemic stroke presenting within 4.5hrs?

A
  1. IV alteplase (0.9mg/kg) thrombolysis
    (recombinant tissue plasminogen activator, r-tPA)
  2. aspirin (300 mg, oral)

NB: Endovascular interventions can be beneficial in large vessel occlusions

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28
Q

What are the contraindications for thrombolysis (alteplase)?

A 
Onset of symptoms >4.5 hrs
High INR, APPT, PT
Haemorrhagic stroke
Recent trauma/surgery
Varices/portal hypertension
GI bleeds
Known clotting disorder
BP >180/105
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29
Q

What is the management of a stroke presenting >4.5hrs/where thrombolysis contraindicated?

A

Aspirin (300 mg, oral)

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30
Q

What is the primary prevention for a stroke?

A

Control risk factors

  • stop smoking
  • lower hypertension
  • control diabetes/hyperlipidaemia
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31
Q

What is the secondary prevention for a stroke?

A

IF NO AF:

  • 75mg aspirin for 2 weeks
  • Switch to lifelong 75mg clopidogrel/dipyramidole

IF THEY HAVE AF:
- warfarin prophylaxis

In addition to managing RF (BP, hyperlipidaemia, glycaemic control, smoking, drinking)

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32
Q

What is the surgical prevention for a stroke?

A

Carotid endarterectomy

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33
Q

When would you perform a carotid endarterectomy?

A

If the carotid stenosis is >70% on Doppler scanning

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34
Q

What is the general management of haemorrhagic strokes?

A

Refer to ICU/stroke unit (may require intubation)
Monitor glucose/GCS/BP

Antipyretic- paracetamol
BP monitor- labetalol/nicardipine
Coagulopathy- reverse warfarin/heparin/dabigatran
DVT prophylaxis- heparin/enoxaparin

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35
Q

How is warfarin reversed?

A

Phytomenadione
FFP/prothrombin complex concentrate
Platelet transfusion

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36
Q

How is heparin reversed?

A

Protamine sulphate

Platelet transfusion

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37
Q

How is dabigatran reversed?

A

Idarucizumab

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38
Q

How are thrombolytic agents reversed?

A

FFP/prothrombin complex concentrate
Crypoprecipitate
Platelet transfusion

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39
Q

What are the complications of CVAs?

A 
Aspiration
Cerebral odemea (may lead to brain herniation)
Immobility
Infection
DVT
Seizures
Cardiovascular events
Death
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40
Q

What is the prognosis of a CVA?

A

10% mortality in 1 month
10% recurrence in 1 year
Haemorrhagic has a worse prognosis
TIA 10% chance of stroke in 3 months

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41
Q

What is used to calculate the risk of a TIA progressing into a stroke?

A

ABCD2 score

Age >60
BP >140/90
Clinical presentation- leg weakness, speech impairment
Duration of symptoms - 10-60 mins or >60 mins
Diabetes mellitus

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42
Q

What should you do if the ABCD2 score is >=4?

A

Refer to a stroke specialist

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43
Q

What does an ABCD2 score >=6 indicate?

A
  1. 1% risk of stroke in 2 days

35. 5% risk of stroke in 1 week

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44
Q

What is a seizure?

A

Abnormal paroxysmal excessive or synchronised discharge of cerebral neurons

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45
Q

Define epilepsy

A

Tendency for recurrent UNPROVOKED seizures

>2 seizures to be classed as epilepsy

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46
Q

What is the aetiology of epilepsy?

A

70% idiopathic

30% secondary to brain injury, tumour, stroke, infection, head injury, autoimmune

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47
Q

What are the risk factors for epilepsy?

A

FHx
Childhood infections
Neurodevelopmental disorders eg. autism
Metabolic disease eg. storage disorders, PKU

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48
Q

What is the classification of epilepsy?

A

Focal

Generalised

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49
Q

What is the difference between a partial and complex seizure?

A

Partial- no LoC

Complex- LoC

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50
Q

What are the types of generalised seizures?

A 
Tonic-clonic
Absence
Myoclonic
Tonic
Atonic
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51
Q

Describe the common phases of a tonic-clonic seizure? (grand Mal)

A

Prodrome- auras
Tonic phase- stiffening of muscles
Clonic phase- contractions/jerking
Post-ictal- drowsy state

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52
Q

What is the classical presentation of an absence seizure? (petit Mal)

A

Brief staring episodes with behavioural arrest lasting 5-10 seconds
LOC but maintained posture
Children

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53
Q

What is the classical presentation of a myoclonic seizure?

A 
Repetitive myoclonic (fast) jerks of specific muscle groups followed by complete muscle relaxation
Most common in puberty
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54
Q

What is the description of a tonic seizure?

A

Bear hugging posture

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55
Q

What is the description of a atonic seizure?

A

Complete loss of muscle tone

Most common in children

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56
Q

What is the presentation of a temporal focal seizure? (HEAD)

A

Hallucinations
Epigastric discomfort -aura
Automatisms (playing with fingers, lip smacking)
Dysphasia

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57
Q

What is the presentation of a frontal focal seizure?

A

MOTOR signs

  • Muscular spasm spreads from distal part of limb to larger area of the body- JACKSONIAN MARCH
  • Post-ictal flaccid weakness (Todd’s palsy)
  • Involuntary actions (disinhibition)
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58
Q

What is the presentation of a parietal focal seizure?

A

Sensory disturbances (pain, tingling, numbness)

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59
Q

What is the presentation of a occipital focal seizure?

A

Visual phenomena (spots, lines, flashes)

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60
Q

What are the investigations for epilepsy?

A

ELECTROENCEPHALOGRAM (EEG)- indicated in all seizure PTs. post-ictal shows reduced brain activity

BLOODS

  • Blood glucose (hypoglycaemia can cause seizures)
  • FBC (evaluate systemic/CNS infection)
  • Electrolyte panel (electrolyte disturbances can provoke seizures)
  • Serum prolactin (can be transiently elevated following seizures)

BRAIN IMAGING (CT, MRI)- look for structural lesions

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61
Q

What 2 drugs are commonly used in the management of focal seizures?

A

Carabamazepine

Lamotrigine

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62
Q

What is the management for a generalised seizure?

A

1st line: sodium valproate

2nd line: carbamazepine

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63
Q

What is status epilepticus?

A

Either:

  1. A seizure lasting >5 minutes
  2. > 1 seizure within a 5 minute period, without returning to a normal level of consciousness between episodes
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64
Q

What is the management for status epilepticus?

A
  1. Secure airway + high flow O2
  2. IV access + continuous monitoring:
    Monitor: sats, BP, ECG, glucose (w/thiamine if RF)
  3. IV lorazepam (repeat after 10 mins if Rx)
  4. IV phenytoin/phenobarbital
  5. ICU, administer GA eg. midazolam
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65
Q

What are the complications of epilepsy?

A 
SUDEP (sudden unexpected death in epilepsy)
Status epilepticus
Behavioural problems
Fractures
Drug SEs
66
Q

What is a dissociative seizure?

A

Caused by psychological rather than physical issues
Often last much longer than epilepsy
Variable in presentation
Patients most likely able to recall event
Clinical diagnosis

67
Q

Define hydrocephalus

A

Excessive accumulation of CSF in the ventricular

system in the brain.

68
Q

What are the types of hydrocephalus?

A
  1. COMUNICATING/non-obstructive
    - impaired CFS absorption (SAH, meningitis)
    - normal CSF absorption (normal pressure, CSF overproduction)
  2. NON-COMMUNICATING/obstructive
    - obstruction at aqueducts, 4th ventricle or foramina
  3. Hydrocephalus ex vacuo (due to atrophy)
69
Q

What are the causes of communicating hydrocephalus?

A

Reduced absorption:

  • Meningitis (typically TB)
  • SAH

Increased CSF production:

  • overproduction of CSF
  • Normal pressure hydrocephalus
70
Q

What are the causes of obstructive hydrocephalus?

A
  • Stenosis of the cerebral aqueduct/interventricular foramina
  • Lesions in 3rd, 4th ventricle
  • Posterior fossa lesions (tumour, blood) compressing the 4th ventricle
71
Q

What is hydrocephalus ex vacuo?

A

Compensatory expansion of the ventricles 2/2 parenchymal atrophy

72
Q

What are the clinical features of acute onset hydrocephalus?

A

Features of ↑ ICP:

  • Nausea & vomiting
  • Headache
  • Papilloedema
73
Q

What are the 2 signs of hydrocephalus in neonates?

A

Increased head circumference (fontanelles + sutures not fused)

Sunset sign (upper eyelids become retracted and eyes are turned downwards)

74
Q

What is seen in normal pressure hydrocephalus?

A

Hakim’s triad

  • wet (urinary incontinence)
  • wacky (dementia)
  • wobbly (gait disturbance)

ie features of hydrocephalus WITHOUT excess CSF

75
Q

What are the investigations for hydrocephalus? What would they show?

A

CT/MRI Head – FIRST LINE

  • Ventricular enlargement
  • Might show the cause (eg tumour)

CSF analysis

  • From ventricular drain
  • May show infection

IMPORTANT: LP is contraindicated if HIGH ICP

76
Q

What is the management for hydrocephalus?

A

Interventricular shunts

77
Q

What is spinal cord compression?

A

Injury to the spinal cord with neurological symptoms dependant on the site and extent of injury

78
Q

What are the common causes of spinal cord compression?

A

TRAUMA (young)

Chronic conditions (elderly)

  • Tumours (inc Pott’s)
  • Osteoporosis
  • Corticosteroids
  • Intervertebral disc disease
  • Spinal stenosis -> cauda equina
  • Spinal abscess
79
Q

What are the risk factors of spinal cord compression?

A 
Tumours
Osteoporosis
Corticosteroid Tx
Osteomalacia
Osteomyelitis
Intervertebral disc disease  (disc herniation)
80
Q

What are the motor features of spinal cord compression?

A

Depends on the level and part of spinal cord affected

  • Limb weakness (hemiplegia/paraplegia)
  • UMN symptoms below the level of the lesion
  • LMN symptoms at the level of the lesion
81
Q

What are the clinical features of cauda equina?

A 
LMN symptoms- Flaccid paresis, areflexia
Perianal (saddle) paraesthesia
Bladder retention/incontinence
Leg weakness
Radicular back/leg pain
82
Q

What are the clinical features of Brown-Sequard syndrome?

A

Ipsilateral proprioception loss
Ipsilateral light sensation loss
Ipsilateral paralysis
Contralateral pain + temperature loss

83
Q

What are the investigations for spinal cord compression?

A

Bloods
-FBC, ESR, B12, syphilis serology, U+E, LFT, PSA
Radiology
MRI- definitive

84
Q

What is Guillain-Barre syndrome?

A

Acute autoimmune demyelinating polyneuropathy affecting the PNS

85
Q

What is the pathophysiology of GBS?

A

Autoimmune destruction of myelin sheath/ Schwann cells of peripheral sensory and motor nerves.

TRIGGERS:

  • URTI
  • gastroenteritis (campylobacter jejuni, CMV, HIV)
  • Hodgkin lymphoma
86
Q

Describe the classic disease progression of GBS

A
  1. 2-3 weeks before = URTI/gastroenteritis
  2. peripheral neuropathy- progresses acutely
    - ascending parasthesia + pain
    - symmetrical limb weakness
  3. May progress to affect resp muscles + CN –> paralysis
87
Q

What is the Miller-Fisher variant of GBS?

A

GBS with the following triad:

  • Ophthalmoplegia
  • Ataxia
  • Areflexia

with NO MUSCLE WEAKNESS

88
Q

What are the investigations for GBS?

A

NERVE CONDUCTION STUDIES
- reduced conduction velocity

LUMBAR PUNCTURE
- high protein, normal cell count and glucose

Bloods
- Anti-ganglioside antibodies in MF variant + 25% of GBS

Spirometry
- fixed vital capacity: ventilatory weakness

ECG
-may develop arrhythymia

89
Q

A patient is rushed into hospital having collapsed on the street. After assessing airways, breathing and circulation you now assess their disability. They have not opened their eyes since arriving and only mumble incoherently when told to open their eyes. They do not respond to vocal commands to move however when you squeeze the patient’s trapezius muscle, they move to the appropriate shoulder to slap your hand away and briefly open their eyes.
What is their GCS score?

A. 2
B. 5
C. 8
D. 9
E. 13
A

C. 8

E- 3
V- 2
M- 5

90
Q

An 85-year-old woman presents to A+E struggling to talk. Her husband brought her in 30 minutes ago after she was unsteady on her feet and fell over. You assess her consciousness and find she has a GCS of 15. On examination you find she has right-sided hemiparesis with positive Babinski sign. You assess her blood pressure and find it to be 170/100.
What is the most appropriate next step?

A. ACEi IV
B. Alteplase IV
C. Urgent CT head scan
D. Aspirin 300mg oral
E. Urgent carotid doppler
A

C. Urgent CT head scan

91
Q

A 65-year-old man presents with sudden onset left sided weakness. He is obese, type II diabetic and has high cholesterol. On examination you find a left-sided hemiparesis with his arm more affected than the leg. There is also an equal hemisensory loss. He is unable to see anything at the bottom of his vision on his left-hand side.
Which vascular territory has likely been affected?

A. Right middle cerebral artery
B. Right anterior cerebral artery
C. Left middle cerebral artery
D. Right carotid artery
E. Right posterior cerebral artery
A

A. Right middle cerebral artery

92
Q

A 25 year old woman has an episode of altered consciousness lasting a few minutes. She has no memory of the event but just beforehand she developed a sense of déjà vu and had a rising feeling in her stomach.
What is the most likely cause?

A. Absence seizure
B. Vasovagal episode
C. Complex partial seizure
D. Simple partial seizure
E. Cardiac arrhythmia
A

A. Absence seizure

93
Q

A 15 year old girl who is a known epileptic has arrived at hospital having a seizure. The seizure started over 30 minutes ago while she was having dinner and has not regained consciousness since. Her mother says she has had 3 seizures over the past 3 months before being diagnosed with and treated for epilepsy, but none were as bad as this. Life support examination reveals that the airways are open, patient is breathing and pulse is 110 bpm. Her GCS is 8/15. You set up two IV lines ready for the patient to be managed.
What is the most appropriate next step?

A. Perform an EEG
B. Check glucose
C. Perform CT scan
D. Give IV lorazepam
E. Give IV thiopentone
A

D. Give IV lorazepam

94
Q

A 26-year-old man was admitted for severe food poisoning and put on antibiotics, a week later in his hospital bed he’s started to notice pins and needles across his lower limb, and he’s been feeling weak in that region also. What’s the most likely diagnosis?

A. Guillain Barre Syndrome
B. Meningism
C. Antibiotic allergy
D. B-12 deficiency
E. Stokes-Adams attack
A

A: Guillain Barre Syndrome

95
Q

3 leading causes of death worldwide

A
  1. IHD
  2. Stroke
  3. COPD
96
Q

How can thrombosis lead to ischaemic stroke?

A

In the elderly arises from atherosclerosis
Affecting mainly small vessels (lacunar infarcts) and less commonly large vessels (eg MCA)

Can also arise from pro-thrombotic states (dehydration, thrombophilia)

97
Q

How can embolisms form and lead to ischaemic stroke?

A
  • intimal flap of carotid dissection
  • atheromatous plaques in the carotid arteries
  • LHS heart (AF)
  • Rarely- venous circulation and pass through a right-left heart defect (VSD)
98
Q

How can hypotension lead to ischaemic stroke?

A

Reduced blood supply to the entire brain 2/2 systemic hypotension (e.g. cardiac arrest)

Most commonly affects WATERSHED AREAS-brain ischaemiathat is localized to border zones between the tissues supplied by ACA, PCA and MCA

99
Q

How are ischaemic strokes classified?

A

Bamford (Oxford) Classification System

Uses clinical findings alone to diagnose type of stroke

100
Q

What are the classic signs of an anterior circulation stroke?

(AC-HUH!)

A
  • Homonymous hemianopia
  • Unilateral weakness (and/or sensory deficit) of the face, arm and leg
  • Higher cerebral dysfunction (dysphasia, visuospatial disorder)
101
Q

What are the classic signs of a posterior circulation stroke?

A

Affects cerebellum + brainstem:

  • Cranial nerve palsy and a contralateral motor/sensory deficit
  • Bilateral motor/sensory deficit
  • Conjugate eye movement disorder (e.g. horizontal gaze palsy)
  • Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
  • Isolated homonymous hemianopia
102
Q

What signs may be present in lacunar infarct? which signs will not be present?

A

There is NO LOSS OF HIGHER CEREBRAL FUNCTION (e.g. dysphasia).

THERE MAY BE:

  • Pure sensory stroke
  • Pure motor stroke
  • Sensori-motor stroke
  • Ataxic hemiparesis
103
Q

How may haemorrhagic stroke cause symptoms?

A
  • mass effect
  • raised ICP
  • cerebral hypoperfusion
  • secondary ischaemic injury
  • cerebral herniation
  • due to the toxic effects of the accumulating blood on the brain
104
Q

What are the ischaemic and haemorrhage stroke pointers?

A

Ischaemic pointers: carotid bruit, AF, past TIA, IHD

Haemorrhagic pointers: meningism, severe headache

105
Q

What are some of the general features of stroke?

A

SUDDEN onset
Weakness/numbness in the face, arm or leg
Change in vision
Dizziness, loss of coordination/balance
Problems with speech
Specific presentation depends on the area of the brain that is affecting

106
Q

What is the scoring system used to assess the risk of stroke in AF patients?

A

CHADS-Vasc score

CHF
Hypertension
Age >75
Diabetes Mellitus
Stroke/TIA
Vascular disease
Sex- F
107
Q

What scoring system is used to discern the risk of bleeding in AF patients?

A

HAS-BLED score

Hypertension
Abnormal renal/liver function
Stroke
Bleeding
Labile INR
Elderly (>65)
Drugs/alcohol
108
Q

posterior cerebral artery arises from which artery? What does is supply?

A

BASILAR

supplies the occipital lobe and the inferomedial part of the temporal lobe.

109
Q

Which 2 arteries form the anterior circulation of the brain? Which arteries do they arise from?

A

ACA- arises from internal carotid branches

MCA- arises from vertebra-basilar branches

110
Q

Why does ACA stroke cause contralateral hemiparesis affecting legs>arms?

A

The ACA supplies the more medial part of the hemispheres and in the primary motor cortex, the leg is represented more medially.

111
Q

Why does ACA stroke cause contralateral hemiparesis affecting legs>arms?

A

The ACA supplies the more medial part of the hemispheres

In the primary motor cortex, the leg is represented more medially.

112
Q

Why does MCA stroke cause contralateral hemiparesis affecting arms/face>legs?

A

MCA supplies the more lateral parts of the hemispheres

In the primary motor cortex, the upper limbs are represented more laterally.

113
Q

Damage to which 2 areas may causes receptive and expressive aphasia, respectively?

A

Broca’s area: responsible for speech production (expressive aphasia)- ‘broken speech’

Wernicke’s area: responsible for language comprehension (receptive aphasia)

114
Q

What are the optic radiations? What are they comprised of?

A

Tracts that carry information from lateral geniculate nucleus to the primary visual cortex in 2 loops:

  • Meyer’s = inferior optic radiation (temporal lobe)
  • Baum’s = superior optic radiation (parietal lobe)
115
Q

Which 2 ways might a PCA stroke affect vision?

A
  1. Macular sparing contralateral homonymous hemianopia

2. Visual aphasia (if visual association cortex affected)

116
Q

State the key signs of cerebellar damage (DANISH)

A 
Dysdiadochokinesia
Ataxia (gait and posture)
Nystagmus
Intention tremor
Slurred, staccato speech
Hypotonia/heel-shin test

NOTE: cerebellar lesions lead to IPSILATERAL signs

117
Q

signs of brainstem damage?

A
  • CN pathology

- decreased consciousness

118
Q

What causes Amaurosis fugax?

A

Occlusion of the retinal artery (branch of ophthalmic artery which is a branch of the ICA)

Patients will often describe a unilateral progressive vision loss “like a curtain descending”.

119
Q

What are lacuna infarcts?

A

Small infarcts (2–20 mm in diameter) in the deep cerebral white matter, basal ganglia, or pons, presumed to result from the occlusion of a single small perforating artery supplying the subcortical areas of the brain

120
Q

A 70-year-old right-handed man is discovered by a family member to have difficulty speaking and comprehending spoken language, and an inability to raise his right arm. On examination, power is 2/5 in his right arm, 4/5 in his right leg and 5/5 in his left arm and leg. A CT head scan is performed and an ischaemic stroke is diagnosed.
What type of stroke is it?

A

Left middle cerebral artery stroke

121
Q

What investigations are done for stroke in a sub-acute setting?

A
  • MRI
  • CT angio/MRA (if suspect large vessel occlusion- candidates for endovascular thrombectomy)
  • Carotid doppler (CAS)
122
Q

How are patients rehabilitated/monitored in the stroke unit?

A 
MDT approach:
Swallowing assessment
VTE prophylaxis
GCS monitoring
Early mobilization
123
Q

Differentiate different causes of collapse based on the ‘before’ history

A

REFLEX: precipitating factor, pre-syncopal symptoms- eg nausea, pallor, sweating, and narrowing of visual fields

CARDIAC: chest pain, palpitations, pallor

ORTHOSTATIC: standing up, dehydration, drugs (antihypertensives)

EPILEPSY: aura/no warning

NON-EPILEPSY: PMH depression, missed meals (hypoglycaemia)

124
Q

Differentiate different causes of collapse based on the ‘during and after’ history

A

REFLEX: seconds-mins. Brief clonic jerking of the limbs may occur (no tonic/clonic sequence). Rapid recovery.

CARDIAC: seconds, rapid spontaneous recovery

EPILEPSY: < 3 minutes, TONGUE BITING, twitching, incontinence. Postictal state

125
Q

What is a Strokes-Adams attack?

A

Transient arrhythmias (eg bradycardia due to complete heart block) drop CO –> LOC.

Attacks may happen several times a day and in any posture.

126
Q

Differentiate different causes of collapse based on the ‘before’ history

A

REFLEX: precipitating factor, sweating, pale (vasovagal). tight collar, head turning (carotid sinus hypersensitivity)

CARDIAC: chest pain, palpitations, pallor

ORTHOSTATIC: standing up, dehydration, drugs (antihypertensives)

EPILEPSY: aura/no warning

NON-EPILEPSY: PMH depression, missed meals (hypoglycaemia)

127
Q

What conditions may trigger secondary seizures?

A 
Tumours
Infection
Inflammation
Trauma
Fever (febrile seizure)
128
Q

What conditions may trigger secondary seizures?

A

Tumours
Infection
Inflammation
Trauma

129
Q

if you take a collapse Hx - what must you first establish?

A

was there a witness

130
Q

State some triggers for epileptic seizures

A
  • lack of sleep
  • flickering lights
  • alcohol
  • stress
    there may not be a trigger
131
Q

What is Todd’s Paresis?

A

A syndrome associated with weakness/paralysis after a focal-onset seizure.

Most commonly affects one limb/one half of the body

132
Q

What is Todd’s Paresis?

A

a syndrome associated with weakness or paralysis of part or all of the body after a focal-onset seizure. It most commonly affects one limb or one half of the body

133
Q

How might a patient present after an epileptic seizure?

A 
Slow recovery
Post-ictal headache
Confusion
Myalgia
Todd’s paresis
134
Q

How do you make the diagnosis of epilepsy?

A

CLINICAL

2 or more unprovoked seizures occurring > 24 hours apart

135
Q

What are the side effects/risks of carbamazepine?

A

neutropenia
osteoporosis
depression, weight gain

136
Q

What are the side effects/risks of lamotrigine?

A

Stevens-Johnson syndrome (severe skin reaction –look at derm)
depression, weight gain

137
Q

What are the side effects/risks of sodium valproate?

A

teratogenic- avoid in pregnancy
(lamotrigine usually preferred)
depression, weight gain

138
Q

What are some triggers for status epileptics?

A

non-adherence to medication
alcohol abuse
OD & toxicity

139
Q

A 16-year-old boy presents to A & E after collapsing on a cricket game. According to his cricket coach, the boy was unconscious for about one minute during which time, he was moving his arms and legs around. Further review revealed that he had experienced a similar episode a month before. What is the most appropriate drug for this patient?

A

suggests generalised epileptic seizure –> give sodium valproate

140
Q

signs of GBS

A

Hypotonia
Flaccid paralysis ( = weakness/paralysis & ↓ muscle tone)
Altered sensation/numbness
↓ /absent weakness
Fasciculations
Can also have autonomic symptoms (urinary retention, ileus)

141
Q

What is a hallmark CSF feature of demyelinating polyneuropathies?

A

Albuminocytological dissociation:

  • ↑ protein (reflects inflammation)
  • normal/low glucose & WCC (no infection)
142
Q

who antibodies may be present in GBS?

A

Anti-ganglioside antibodies

  • very common in Miller-Fisher variant
  • 25% GBS cases
143
Q

30% of cases of GBS are cases occur after what type of infection?

A

gastroenteritis infection caused by Campylobacter jejuni

144
Q

What is the epidemiology of hydrocephalus?

A 
Bimodal distribution (affects the young & 
elderly)
145
Q

Explain 2 ways in which the signs and symptoms of hydrocephalus manifest

A
  1. excess CSF –> raised ICP

2. CSF permeates through the ependymal lining into the periventricular white matter–> damage and gliotic scarring.

146
Q

How can hydrocephalus be classified according to cause?

A

NON-COMMUNICATING/OBSTRUCTIVE
CSF flow obstruction

COMMUNICATING
↓ absorption, ↑production of CSF (issue outside ventricular system)

147
Q

What are the clinical features of gradual onset hydrocephalus?

A

Cognitive impairment
Unsteady gait
Double vision
CN palsies (pressure on nerves)

148
Q

Differentiate between:

  • spinal cord compression
  • cauda equina
  • radiculopathy
A

SC COMPRESSION

  • issue is with spinal cord
  • UMN signs
  • trauma, conditions affecting vertebrae

CAUDA EQUINA

  • issue is with caudal equina (L2-S5)
  • LMN signs
  • disc compression/spinal canal stenosis

RADICULOPATHY

  • issue is in the nerve route ie as it exits spinal cord
  • LMN signs
149
Q

What are the sensory features of spinal cord compression?

A

Sensory loss below a specific level

Back pain

150
Q

What are the autonomic features of spinal cord compression?

A

Constipation
Urinary retention
Erectile dysfunction

151
Q

What investigations would you do for cord compression?

A

RADIOGRAPHY- MRI or CT (MRI is Definitive)
- Lateral radiographs of spine to look for loss of alignment, fractures etc.

BLOODS

  • FBC, CRP, U&Es, calcium, ESR
  • Immunoglobulin electrophoresis (multiple myeloma)

URINE
- look for Bence Jones proteins (multiple myeloma)

152
Q

What causes cauda equina syndrome?

A

Lumbosacral nerve roots that form the cauda
equina in the spinal canal become compressed

Often by disc compression & stenosis of the spinal canal

153
Q

Define radiculopathy

A

Range of symptoms occurring due to the
compression of a nerve at or near the ROOT as it exits the spinal cord.

eg sciatica

154
Q

What are the sensory features of radiculopathy?

A

DERMATOMAL pattern

Pain, numbness

155
Q

What are the motor features of radiculopathy?

A

LMN symptoms for the muscles innervated by this spinal root:

  • muscle atrophy
  • fasciculations (muscle twitching)
  • hypotonia/hyporeflexia
  • negative Babinski sign
  • flaccid paralysis
156
Q

Causes of radiculopathy?

A 
Degenerative disc disease
Osteoarthritis
Spondylolisthesis (forward displacement of vertebra)
Tumours
Infection
157
Q

Investigations for radiculopathy

A

Pain that has not responded to Tx for 6-8 weeks should be imaged.
CT/MRI can help visualize a lumbar disc herniation

158
Q

How does sciatica present?

A

Lumbosacral nerve root impingement causes:

  • Pain & tingling radiating from the lower back to ipsilateral leg
  • Weakness in calf muscles
159
Q

How is sciatica diagnosed?

A

Clinical diagnosis- straight leg raise test:

Pain in the distribution of the sciatic nerve is reproduced on passive hip flexion (30-70o)
= positive Lasegue’s sign

Sensitive but not specific (CT/MRI may be indicated)

160
Q

A 62-year-old woman presents with back pain and difficulty walking. On examination there is increased tone and hyper-reflexia in both legs. She has not opened her bowels or passed urine for the previous day. She has a past medical history of breast cancer, diagnosed two years earlier. Which is the most likely diagnosis?

A

Spinal cord compression

GBS not autonomic features
cauda equina/radiculopathy not UMN signs

161
Q

What is a dissociative seizure?

A

Involuntary episodes of movement, sensation, or behaviours that have no biological correlate

(management is psychotherapy)

162
Q

When would you suspect dissociative seizures?

A

Prolonged duration

Hx of abuse, psychological or emotional precipitants

Year 3 (38 decks)

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