Neurological emergencies

Question 1

What is status epilepticus? What are its causes?

Answer 1

• Recurrent seizures without recovery in between, or a single seizure lasting more than 30 mins
• Can cause: Cerebral damage: Failure of compensatory mechanisms /autoregulation
• Excitotoxicity , local hypoxia, metabolite accumulation
• Consider a pre-existing diagnosis of Epilepsy: AED withdrawal, Non-compliance, alcohol use and withdrawal; illicit drugs, infection
• Progression of underlying disease - tumour, encephalitis, vasculitis
• NB: Non-epileptic attacks (NEAD) – prolonged seizures, frequency, normal lactate, psych history
• Causes in those with no history of epilepsy: Cerebral Tumour, Intracranial Infection, Hypoglycaemia, Head Injury, Illicit drugs, Drug withdrawal (alcohol), hypoxia, stroke, electrolyte disturbance (Na, Ca, Mg)

Question 2

What signs are important for an A-E in status epilepticus?

Answer 2

• A - Airway – if compromised it needs arrest call and ITU/ anaesthetist
• B – difficult to assess. Sats can be unreliable but Monitor SaO2, give high flow O2
• C – fluids, Bloods: U&E’s, glucose, Ca, Mg, LFT’s, FBC, CRP/ cultures, clotting screen ABG if possible, anticonvulsant levels (if pt was on anti epileptics), toxicology screen, ECG
• ABG - Typical pattern: acidotic, lactate high, glucose OK, 02 can be low
• D – No GCS possible but DEFG: GLUCOSE! BM-10% or 50% glucose if low

Question 3

How is status epilepticus managed?

Answer 3

Begin mx after 5 mins of seizure activity

Question 4

What is idiopathic intracranial hypertension? How does it present?

What are its associations?

Answer 4

• Most commonly seen in obese females in 3rd decade
• Presentation: narrowed visual fields, blurred vision ± diplopia, vith nerve palsy, and an enlarged blind spot, if papilloedema is present
• Consciousness and cognition are preserved.
• Associations - Endocrine abnormalities (Cushing’s syndrome, hypoparathyroidism, ↑↓tsh), sle, ckd, ida, prv, drugs (tetracycline, steroids, nitrofurantoin, and oral contraceptives).

Question 5

How is IIH managed?

Answer 5

• Conservative: Weight loss
• Medical: acetazolamide or topiramate, loop diuretics, and prednisolone (more se than diuretics)
• Surgery: last resort - optic nerve sheath fenestration or lumbar–peritoneal shunt

Question 6

What is normal pressure hydrocephalus and how does it present?

Answer 6

• Wobbly: Apraxic gait the way a person walks “on a boat,” with the body bent forward, legs held wide apart and feet moving as if they’re “glued to the deck.”
• Weird:
  
  • Mild dementia: loss of interest in daily activities, forgetfulness, difficulty completing routine tasks, short-term memory loss.
• Decline in thinking skills that includes overall slowing of thought processes, apathy, impaired planning and decision-making, reduced concentration, and changes in personality and behavior.
• Wet: urinary incontinence (later in disease)

Question 7

How do subdural haemorrhages arise?

Answer 7

• Rupture of the bridging veins in the outermost meningeal layer (between the dura and arachnoid)
• Presentation: raised ICP, shifting midline structures away from the side of the clot and, if untreated, eventual tentorial herniation and coning
• Cause: high impact trauma – sometimes minor or long time ago
• Who: elderly (more atrophy – vessels more likely to rupture) or alcoholic patients

Question 8

How does subdural haemorrhage present? Signs and sx?

Answer 8

• Sx: Fluctuating level of consciousness ± insidious physical or intellectual slowing, sleepiness, headache, personality change, and unsteadiness.
• Signs: raised ICP, seizures. Localizing neurological symptoms (eg unequal pupils, hemiparesis) occur late, often >1 month after the injury.

Question 9

How are subdural haemorrhages investigated and managed?

Answer 9

• Ix: CT/ MRI: banana (crescent shape collection of blood – unilateral) and are not limited by the cranial sutures (they can cross over the sutures).
• Mx: Conservative: address cause
  
  • Medical – urgent reversal of clotting abnormalities
  • Surgery:
    
    • Acute: decompressive craniectomy
    • Chronic: conservative (if no deficit); a surgical decompression if clot size: >10mm or midline shift – depressive – craniotomy or burr hole washout

Question 10

What is an extra dural haemorrhage? Who is it most likely to occur in

Answer 10

• Associations: fracture of temporal bone - typically after trauma to a temple just lateral to the eye
• Presentation: young patient with a traumatic head injury, ongoing headache

Question 11

What are some of the signs and symptoms of extradural haemorrhages?

Answer 11

• Lucid interval: few hours to a few days before a bleed declares itself by ↓GCS from rising ICP
• Increasingly severe headache, vomiting, confusion, and seizures follow, ± hemiparesis with brisk reflexes and an upgoing plantar.
• If bleeding continues, the ipsilateral pupil dilates, coma deepens, bilateral limb weakness develops, and breathing becomes deep and irregular (brainstem compression)

Question 12

What Ix and mx are used for subdural haemorrhages?

Answer 12

• Ix: CT: lemon (bi-convex shape and are limited by the cranial sutures)
• Mx: Surgical: stabilize and transfer neurosurgical unit for clot evacuation ± ligation of the bleeding vessel + craniotomy
  
  • Medical: Care of the airway in an unconscious patient
    
    • Reduce ↓ICP: I+V (+ mannitol ivi)

Question 13

What are the causes of a SAH?

Answer 13

• Pathophysiology: Subarachnoid haemorrhage involves bleeding in to the subarachnoid space, where the cerebrospinal fluid is located, between the pia mater and the arachnoid membrane. This is usually the result of a ruptured cerebral aneurysm.
• Causes: usually cerebral aneurysm

Question 14

What are the signs + sx of SAH?

Answer 14

• Px: sudden onset occipital headache worse from strenuous activity (e.g. sex or exercise), - thunder clap
• Vomiting, collapse, seizures, and coma often follow, Coma/drowsiness may last for days
• Neurological Sx such as speech changes, weakness, seizures and loss of consciousness
• Signs: neck stiffness, kernigs sign (6h to develop), retinal, subhyaloid and vitreous bleeds
• Sentinel headache: pts may earlier have experiences a sentinel headache, perhaps due to small warning leak from offending aneurysm
• Focal neurological deficit: (eg pupil changes indicating a 3rd nerve palsy with a posterior communicating artery aneurysm) or intracerebral haematoma – can help localise
• Signs: neck stiffness, kernigs sign (6h to develop), retinal, subhyaloid and vitreous bleeds

Question 15

What are some of teh causes of spontaneous SAH?

Answer 15

• Intracranial aneurysm* (saccular ‘berry’ aneurysms): this accounts for around 85% of cases. Conditions: PCKD, Ehlers-Danlos syndrome and coarctation of the aorta
• Arteriovenous malformation
• Pituitary apoplexy
• Arterial dissection
• Mycotic (infective) aneurysms
• Perimesencephalic (an idiopathic venous bleed)

Question 16

What ix are used in SAH?

Answer 16

CT brain, MRI brain, CSF, LP, angiograpy

To confirm

• 1st: CT Brain: ASAP. Detect early hydrocephalus
• 2nd: LP: if CT -ve - must wait 12 hours post ictus: raised protein + RCC, Elevated opening pressure,
  
  • Lymphocytic reaction
  • Elevated protein
  • Xanthochromic
  • Gold standard test: spectrophotometry for bilirubin

Following confirmation:

• MRI brain
• Angiography – to locate the source of the bleeding.
  
  • Non-invasive: CTA and MRA
  • Invasive: DSA, Perform endovascular coiling at same time

Question 17

What is the mx of SAH?

Answer 17

ZMx:

• Medical: prevent vasospasm
  
  • Maintain cerebral perfusion,
  • Nimodipine (reduces vasospasm): hypertensive therapy – CCB used to prevent vasospasm
• Surgery: secure aneurysm
  
  • Endovascular coiling vs surgical clipping (requiring craniotomy)
  • Treat hydrocephalus - Ventricular drain/shunt

Question 18

What are some of the complications of SAH?

Answer 18

rebleeding, hydrocephalus, cerebral ischaemia

Question 19

How is a head injury managed?

Answer 19

Question 20

What are the causes of raised ICP?

Answer 20

• Primary or metastatic tumours
• Head injury
• Haemorrhage (subdural, extradural, subarachnoid, intracerebral, intraventricular)
• Infection: meningitis, encephalitis, brain abscess
• Hydrocephalus
• Cerebral oedema
• Status epilepticus.

Question 21

What are some of the signs and sx of raised ICP?

Answer 21

• Headache (worse on coughing, leaning forwards), vomiting.
• Altered GCS: drowsiness, listlessness, irritability, coma.
• Hx of trauma.
• ↓HR and Widening PP/ ↑BP, irregular breathing (Cushing’s response)
• Eyes:
  
  • Pupil changes
  • ↓Visual acuity; peripheral visual field loss
  • Papilloedema: unreliable sign

Question 22

What is a normal ICP in adults

Answer 22

7-15 mmHg

Question 23

What are the investigations used to look at raised ICP?

Answer 23

• Bloods: u&e, fbc, lft, glucose, serum osmolality, clotting, blood culture, toxicology screen.
• Imaging: CT head + MRI
• Specialist: Then consider LP if safe. Measure the opening pressure!
• Invasive ICP monitoring
  
  • catheter placed into the lateral ventricles of the brain to monitor the pressure (>20 - further treatment)

Question 24

How is raised ICP managed?

Answer 24

• Conservative: correct hypotension and treat seizures. Elevate the head of the bed (30 to 40)
  
  • If intubated: controlled hyperventilation: to reduce pCO2 (causes cerebral vasoconstriction and reduces ICP rapidly
    
    • Caution: reduce blood flow to already ischaemic parts of the brain
• Medical: IV mannitol
  
  • Corticosteroids: dexamethasone 10mg IV – only for oedema surrounding tumours
• Specialist removal of CSF:
  
  • Drain from intraventricular monitor (see above)
  • Repeated LP
  • Ventriculoperitoneal shunt (hydrocephalus)

Question 25

How is meningitis ix and mx

Answer 25

• Bloods: FBC, U&E, glucose, LFT, CRP, clotting, lactate and HIV serology, cultures, MCS
• LP – usually within 1h of hospital arrival CI: meningococcal septicaemia with purpuric rash, or if there is infection at the site of LP
• Urgent CT Head: required before LP if clinical signs of raised ICP
• Mx: If a non-blanching rash is present, give benzylpenicillin 1.2g IM/IV before admitting.
  
  • Abx: IV ceftriaxone 2g immediately and continue every 12-hours initially
  • >60 years or older, or pregnant, or immunocompromised - iv ceftriaxone 2 g every 12 hours+ IV amoxicillin 2 g (Listeria cover)
  • Dexamethasone 10 mg IV every 6 hours - in all cases of suspected bacterial meningitis:

Question 26

What are the signs of bulbar and corticobulbar palsies?

Answer 26

Bulbar Palsy: Signs: LMN lesion of the tongue and muscles of talking and swallowing: flaccid, fasciculating tongue (like a sack of worms); jaw jerk is normal or absent, speech is quiet, hoarse, or nasal.

Corticobulbar palsy: UMN lesion of muscles of swallowing and talking due to bilateral lesions above the mid-pons, eg corticobulbar tracts (MS, MND, stroke, central pontine myelinolysis).

Question 27

How does temporal arteritis present?

Answer 27

• Sx: Headache, temporal artery and scalp tenderness (eg when combing hair), tongue/jaw claudication, amaurosis fugax, or sudden unliateral blindness.
  
  • Extracranial symptoms: malaise, dyspnoea, weight loss, morning stiffness, and unequal or weak pulses.The risk is irreversible bilateral visual loss, which can occur suddenly if not treated—ask an ophthalmologist.

Question 28

How is temporal arteritis ix and mx?

Answer 28

• Ix: ESR & CRP are ↑↑, ↑platelets, ↑alp, ↓Hb.
  
  • Temporal artery biopsy: within 14 days of starting steroids, or fdg-pet - Skip lesions
• Mx: Start prednisolone 60mg/d PO immediately or IV methylprednisolone if evolving visual loss or history of amaurosis fugax.
  
  • Reduce prednisolone once symptoms have resolved and ↓ESR; ↑dose if symptoms recur

Answer 29

• Broca’s: Expressive aphasia: Left posterior inferior frontal gyrus
• Wernicke’s: Receptive aphasia: Posterior part of the superior temporal gyrus