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Flashcards in Neuro Deck (33)
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Define conciousness

Consciousness: Wakefulness and awareness
Assessment relies on physical responses at the bedside


Define minimally conscious state
Legal aspects?

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


Define persistent vegetative state

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


Define coma

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


Brainstem involvement in consciousness?

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


Define locked in syndrome

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


Name 2 confounders of the Glasgow Coma Scale

Spinal cord injury


When are pupils small and reactive?

Opioid use


When are pupils small and unreactive?

Pontine haemorrhage


When are pupils unreactive



When are pupils unreactive and dilated?

Brainstem herniation


Definition of a stroke

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


Causes of stroke

• 85% ischaemic
• 15% haemorrhagic


Causes of ischaemic stroke (12)

• 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


4 types of intracranial haemorrhage

• Intracerebral
• Subarachnoid
• Subdural
• Extradural


Causes of intracerebral haemorrhage

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


Definition of SAH

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


Symptoms of SAH

• 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


Management of SAH

• 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


Treatment of SAH

• 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


3 main complications of SAH

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


Factors associated with aneurysm rupture

• 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)


Describe subdural haemorrhage

• 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


Describe extradural haemorrhage

• 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


Describe clinical presentation of TACI and PACI

• 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)


Describe clinical presentation of POCI

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)


LACI clinical presentation

Lacunar, internal capsule
Complete contralateral hemiparesis and/or hemisensory loss


Define amaurosis fugax

• Transient monocular blindness
• Transient retinal artery occlusion (from carotid)


Initial management of stroke

• 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


How do you investigate cause of stroke

Carotid dopplers, ECG, echo, ESR