Session 10

Question 1

What is a transient ischaemic attack (TIA)?

Answer 1

A stroke that recovers within 24 hours of the onset of symptoms

Question 2

How will a patient with a left anteriorcerebral artery stroke present?

Answer 2

Motor - contralateral lower limb more than upper limb. Initially flaccid paralysis followed by spasticity
Sensory - contralateral sensory loss of all modalities of the lower limb
Incontinence
Split brain syndrome/ alien hand syndrome

Question 3

How will a patient with a left middle cerebral artery stroke present?

Answer 3

Main trunk occlusion - considerable cerebral oedema, raises intracranial pressure and can lead to malignant MCA. Treated by decompressive hemicraniectomy.
Motor - contralateral upper limb and face, sometimes lower limb. Initially flaccid paralysis followed by spasticity
Sensory - contralateral sensory loss of all modalities of the upper limb and face
Visual disturbance
Speech disturbance

Question 4

Why can some MCA strokes lead to paralysis of the legs?

Answer 4

Proximal occlusions affect the blood supply to the internal capsule (via the lenticulostriate arteries) which carries descending motor fibres from all of the motor cortex.

Question 5

What visual disturbances may result from a MCA stroke?

Answer 5

Proximal occlusion - contralateral homonymous hemianopia (both optic radiations affected)
Distal - just one optic radiation can be affected so can lead to contralateral homonymous superior/inferior quadrantanopia

Question 6

What speech disturbances may result from a MCA stroke?

Answer 6

Depends on dominant hemisphere (usuallyleft) and which branch is occluded.
Global aphasia, brocas or wernickes aphasia can result

Question 7

What can resulat from an MCA stroke in the non-dominant hemisphere?

Answer 7

Hemispacial neglect, tactile/visual extinction (touch/visual field both sides at some time and only notice one side) and anosognosia (severe lack of insight)

Question 8

How will a patient with a left posterior cerebral artery stroke present?

Answer 8

Contralateral homonymous hemianopia with macular sparing (which is supplied by MCA). More likely to present without other symptoms than in an MCA stroke

Question 9

How will a patient with a left cerebellar artery stroke present?

Answer 9

DANISH - dysdiadochokinesia, ataxia, nystagmus, intention tremor, slurred speech, hypotonia
If proximal occlusion - also brainstem signs - damage to tracts affecting contralateral side of body and damage to ipsilateral cranial nerve nuclei

Question 10

How will a patient with a basillar artery stroke present?

Answer 10

Proximal - locked in syndrome (pontine arteries)

Distal - BILATERAL occipital lobe infarction, bilateral thalamic infarction, bilateral midbrain involvement

Question 11

How will a patient with a left lenticulostriate artery stroke present?

Answer 11

Isolated contralateral paralysis involving face, upper limb and lower limb. Pure motor stroke.

Question 12

How will a patient with a left thalamoperforator artery (branch of PCA) stroke present?

Answer 12

Isolated contralateral sensory loss in all modalities involving face, upper limb and lower limb. Pure sensory stroke.

Question 13

What are common stroke mimics?

Answer 13

Hypoglycaemia, epilepsy, migraine, intracranial tumors/infections

Question 14

What are the general features of management of a stroke?

Answer 14

CT head to rule out haemorrhage. If within 4.5 hours and no contraindications thrombolysis is initiated. After 48 hours aspirin is started for 14 days. Statins are initiated.

Question 15

What is a cerebral contusion?

Answer 15

Bruising of the brain whereby blood mixes with cortical tissue due to microhaemorrhages and small blood vessel leaks

Question 16

What is concussion?

Answer 16

Head injury with temporary loss of function due to stretching and injury to axons

Question 17

What are the symptoms of post-concussion syndrome?

Answer 17

Cognition/memory - reduced concentration, slower thinking, difficulty remembering new information
Physical - headache, nausea/vomiting, dizziness, blurred vision, fatigue, light sensitivity
Mood - irritability, sadness, anxiety
Sleep - more/less than normal

Question 18

What is a diffuse axonal injury?

Answer 18

Shearing of the interface between grey and white matter following traumatic acceleration/deceleration damaging the intracerebral axons

Question 19

After what time does the loss of consciousness become severe?

Answer 19

24 hours (moderate after 30 mins)

Question 20

After what time does post traumatic amnesia become severe?

Answer 20

7 days (moderate after 1 day)

Question 21

What is the criteria for an urgent head CT?

Answer 21

GCS <13 or <14 after 2 hours of injury
Focal neurological deficit
Seizure
LOC plus age >65 or coagulopathy or amnesia >30 mins
>1 episode of vomiting
Suspected basilar skull fracture

Question 22

What is an extradural haemorrhage?

Answer 22

Collection of blood between inner surface of skull and periosteal dura mater, mostly due to trauma
Most commonly MMA (branch of maxillary artery), sometimes due to a torn venous sinus
Looks like a lemon on CT!

Question 23

How will a patient with an extradural haemorrhage usually present?

Answer 23

LOC due to impact of initial injury. In 40% of patients there is a transient recovery with ongoing headache (lucid interval). ICP increases leading to rapidly deteriorating level of consciousness.
Cranial nerve palsies as brain structures herniate

Question 24

Briefly explain the treatment for an extradural haemorrhage

Answer 24

ABCDE
Small EDH - conservative management and neurological follow up
Large EDH - craniotomy and clot evacuation

Question 25

What are the complications of an extradural haemorrhage?

Answer 25

Brain damage, coma, seizures, weakness, pseudoaneurysm, AV fistula

Question 26

What is an subdural haemorrhage?

Answer 26

Collection of blood between meningeal dura mater and arachnoid mater that can be acute (<3 days), subactue or chronic (>3 weeks) Bleeding occurs due to shearing forces on cortical bridging veins - mostly trauma but can be spontaneous Poorer prognosis than EDH Looks like banana on CT!

Question 27

How do subdural haemorrhages present?

Answer 27

Acute - trauma, most have neurological abnormalities. Hyperdense on CT Subacute/chronic - more common in elderly, can present with gradual confusion and general cognitive decline. Hypodense on CT

Question 28

What is an subarachnoid haemorrhage?

Answer 28

Collection of blood between arachnoid mater and pia mater. Usually in middle aged <60s spontaneously secondary to berry aneurysm rupture, also traumatic

Question 29

How does a subarachnoid haemorrhage present?

Answer 29

Thunderclap headache, meningism, N&V, fever, LOC, focal neurological deficits

Question 30

Briefly explain the treatment for a subarachnoid heamorrhage

Answer 30

Lumbar puncture to aid diagnosis - presence of RBCs, xanthochromia (yellow CSF - bilirubin) Stabilise, prevent rebleeding, correct hyponatraemia, if large bleed neurosurgical intervention

Question 31

What are the complications of a subarachnoid heamorrhage?

Answer 31

Hydrocephalus, focal neurological deficits, coma, seizures, cognitive decline, headaches

Question 32

What components of the intracranial space can compensate for an expanding mass?

Answer 32

Venous volume and CSF

Question 33

What are signs ans symptoms of raised intracranial pressure?

Answer 33

Headache - generalised, worse in morning, aggravated by bending, coughing Vomiting - can progress to projectile Visual disturbance - blurring, transient blinding on posture change, papilloedema, retinal haemorrhage if rapid rise in ICP Depression of conscious level In infants - slowly increasing head size

Question 34

Describe Cushing's reflex in untreated ICP

Answer 34

Herniation through foramen magnum | Last effort to perfuse brain - high BP, bradycardia and low respiratory rate. Poor prognostic sign

Question 35

What are causes of raised intracranial pressure?

Answer 35

Increased cerebral blood volume - venous sinus thrombosis, venous outflow obstruction Cerebral oedema - meningitis, encephalitis, diffuse head injury, infarction Increased CSF - hydrocephalus, choroid plexus adenoma SOL - abscess, tumour, heamorrhage

Question 36

How does CSF leave the ventricles to the subarachnoid space?

Answer 36

Through two lateral and one medial foramen of the 4th ventricles (exits at venous sinuses)

Question 37

What is hydrocephalus?

Answer 37

Accumulation of CSF due to an imbalance between production and absorption of CSF with subsequent enlargement of brain ventricles

Question 38

What are the two subtypes of hydrocephalus?

Answer 38

Non communicating/obstructive - CSF is obstructed in the ventricles, usually aqueduct blockage, can be congenital or aquired (e.g. meningioma) Communicating - there is a connection between ventricles and subarachnoid. Due to reduced absorption or blockage of the venous drainage system or increased production - mostly post meningitis, also subarachnoid haemorrhage,, trauma, neoplasia

Question 39

What is idiopathic intracranial hypertension and how is it treated?

Answer 39

Raised ICP without evidence of hydrocephalus or mass lesion. Usually obese women after weight gain. Treatment - weight loss, carbonic anhydrase inhibitors, CSF drainage, shunts

Question 40

What are the principles of management of raised CSF?

Answer 40

Reduce CSF - shunts, diuretics whilst waiting intervention Reduce expanding mass - surgical resection, steroids for brain tumour Reduce cerebral oedema - treat cause, mannitol, hypertonic saline (draws water into vessels) Reduce cerebral blood volume - anticoagulation, stenting venous sinus

Question 41

What is the acute managemnt of raised ICP?

Answer 41

30 degree head elevation, oxygen, measure glucose, treat any shock, hypertonic saline, call anaesthesist, CT scan, ventilate, catheter NOT LUMBAR PUNCTURE (could herniate brain)