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Acute Care > Neuro > Flashcards

Neuro Flashcards

1
Q

Define conciousness

A

Consciousness: Wakefulness and awareness

Assessment relies on physical responses at the bedside

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2
Q

Define minimally conscious state

Legal aspects?

A

-May move finger
-Continual (>4weeks) versus permanent (years)
-Could get better
Official solicitor protects people with minimal consciousness

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3
Q

Define persistent vegetative state

A 
Some weeks/months after initial injury
Unawareness of self
Awake but not aware
May open eyes, can breathe and heart will pump
Will not respond to commands, loved ones
Permanent>6 months
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4
Q

Define coma

A

Not awake and not aware
Eyes are closed
No response to environment, voices or pain

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5
Q

Brainstem involvement in consciousness?

A
  • Survival functions
  • Contains ascending reticular activating system (RAS)
  • Determines how awake people are, necessary for consciousness
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6
Q

Define locked in syndrome

A

Patient fully awake and alert but cannot move or speak
Can mimic loss of consciousness
Ocular muscle usually spared (communicate by blinking)
After basilar artery occlusion/pontine injury/ALS/MS

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7
Q

Name 2 confounders of the Glasgow Coma Scale

A

Spinal cord injury

Deafness

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8
Q

When are pupils small and reactive?

A

Opioid use

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9
Q

When are pupils small and unreactive?

A

Pontine haemorrhage

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10
Q

When are pupils unreactive

A

Atropine

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11
Q

When are pupils unreactive and dilated?

A

Brainstem herniation

Seizures

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12
Q

Definition of a stroke

A

Sudden onset loss of CNS functioning lasting >24 hrs due to a vascular cause
Cause of 1/10 deaths in UK

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13
Q

Causes of stroke

A
  • 85% ischaemic

* 15% haemorrhagic

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14
Q

Causes of ischaemic stroke (12)

A
  • Atherothrombosis: 50%, large vessel atheroma causing local narrowing and distal thromboembolism, usually aortic arch, carotid bifurcation, vertebral artery
  • Small vessel disease: 20-25%, lipohyalinosis and fibrinoid degeneration of small intracranial vessels, hypertension. Causes small lacunar infarcts of internal capsule
  • Cardioembolic: 20-25%, emboli secondary to arrhythmia (AF), valvular disease (replacements, vegetations), poor LV function, post MI. Usually left side of heart-> intracranial vessels unless septal defect, then from DVTs
  • Arterial dissection (may present with neck pain and Horner’s syndrome)
  • Hypotension-> watershed infarct after cardiac arrest
  • Vasculitis
  • Hypercoagulability: Antiphospholipid syndrome, malignancy
  • Genetic disorders: mitochondrial, homocysteinuria, CT disorders, sickle cell
  • Illicit drugs (cocaine)
  • Secondary to CNS infection (syphilis, HIV)
  • Trauma to neck vessels
  • Secondary to venous sinus thrombosis
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15
Q

4 types of intracranial haemorrhage

A
  • Intracerebral
  • Subarachnoid
  • Subdural
  • Extradural
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16
Q

Causes of intracerebral haemorrhage

A
  • Hypertension
  • Amyloid angiopathy
  • Trauma
  • Bleeding disorders
  • Illicit drugs (cocaine, amphetamines)
  • Vascular malformations
17
Q

Definition of SAH

A

Subarachnoid haemorrhage
Blood between arachnoid and pia mater
Most often occurs after trauma
If not trauma, usually a spontaneous haemorrhage due to a vascular anomaly

18
Q

Symptoms of SAH

A
  • Vary from delayed presentation of low-grade headache to coma or sudden death
  • Headache (sudden, thunder clap, worst headache ever, occipital
  • Nausea and vomiting
  • Meningism (neck stiffness, photophobia)
  • Seizure and transient loss of consciousness
19
Q

Management of SAH

A
  • Assess GCS and look for focal deficits
  • Plain CT scan (93% sensitivity 24 hrs, 50% at 1 week)
  • If –ve but high clinical suspicion-> LP 12 hrs after onset of symptoms (4 bottles for red cell count, glucose, spectrophotometry and cell counts again)
  • CT angiogram/catheter angiography to find vascular anomaly
20
Q

Treatment of SAH

A
  • Resuscitation, airway protection if GCS<8
  • Analgesia and anti-emetics
  • IV hydration to maintain cerebral blood flow and avoid ischaemia
  • NIMODIPINE 50mg 4hrly for 21 days from onset of symptoms
  • BP control (hypertension-> rebleed, hypotension-> ischaemia)
  • VTE prophylaxis
  • Neuro obs
  • Hydrocephalus treatment (shunt?, head up)
  • Aneurysm? Embolisation via coiling or craniotomy and clipping
21
Q

3 main complications of SAH

A
  • Vasospasm (leads to delayed ischaemic neurological deifcits)
  • Hydropcephalus (communicating/obstructive, may require LP or shunt)
  • Hyponatraemia (cerebral salt wasting and SIADH, risk of seizures)
22
Q

Factors associated with aneurysm rupture

A
  • Previous rupture of same aneurysm (30% rebleed within 1 month)
  • Previous rupture of a contemporaneous aneurysm
  • Size
  • Posterior circulation
  • Smoking
  • Evidence of growth/compression (IIIrd nerve palsy)
23
Q

Describe subdural haemorrhage

A
  • Collection of blood in the potential space between dura and arachnoid mater
  • Seen in extremes of age, esp after trauma (eg falls in the elderly)
  • May present with cerebral contusions and depressed GCS
  • Due to stretching and tearing of the bridging veins as they cross to drain into a dural sinus when shearing force is applied
  • Crescent shaped
24
Q

Describe extradural haemorrhage

A
  • Collection of blood between the inner surface of the skull and the outer layer of dura
  • Commonly associated with trauma and associated skull fracture, seen in the young. On-going severe headache, gradually lose consciousness over next few hours.
  • Usually the bleeding is associated with a torn middle meningeal artery
  • Lens/lemon shaped
  • Can cause midline shift/herniation
25
Q

Describe clinical presentation of TACI and PACI

A

• TACI = total so all 3, PACI is partial to 2/3

  • Contralateral hemiparesis (relative leg sparing) and/or hemisensory loss
  • Contralateral homonymous hemianopia
  • Dysphasia (if dominant hemisphere, receptive W if more posterior, expressive B if more anterior) or sensory neglect and apraxia (non-dominant hemisphere, gaze towards side of lesion)
26
Q

Describe clinical presentation of POCI

A

Posterior circulation infarct
• Vertebrobasilar territory
• Ipsilateral cerebellar signs (cerebellum)
• Contralateral homonymous hemianopia (occipital lobe)
• Diplopia, quadrantparesis, cerebellar features, crossed sensory symptoms, Horner’s syndrome (brainstem)

27
Q

LACI clinical presentation

A

Lacunar, internal capsule

Complete contralateral hemiparesis and/or hemisensory loss

28
Q

Define amaurosis fugax

A
  • Transient monocular blindness

* Transient retinal artery occlusion (from carotid)

29
Q

Initial management of stroke

A
  • Acute stroke unit
  • Supportive measures (O2, IV fluid, glucose and electrolyte monitoring)
  • CT within 1 hr
  • Thrombolysis with IV rTPA if ischaemic (or clot retrieval!?)
  • Aspirin if ischaemic, 300mg for 2 weeks then 75mg for life
30
Q

How do you investigate cause of stroke

A

Carotid dopplers, ECG, echo, ESR

31
Q

Prognosis of stroke

A
  • 20% mortality in first month (pneumonia, PE)
  • 50% survivors are dependent at 1 yr
  • Large MCA stroke- >90% dead or dependent at 1 yr
32
Q

Prognosis after TIA

A
  • Risk of recurrence 5% at 2 days, 12% at 1 month, 5% per year after
  • Esp risk if carotid stenosis/cardioembolism
33
Q

Differential for TIA

A
  • Hypoglycaemia
  • Migraine with aura (spreading symptoms, photophobia, phonophobia, headache, lasts hours, visual scintillations)
  • Focal epilepsy (then Todd’s paresis?)
  • Hyperventilation
  • Retinal bleeds
  • Chronic pain/severe anxiety/depression

Acute Care (11 decks)

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