Week 1: Acute neurological emergencies (3) Flashcards

1
Q

patient with unilateral weakness differential

A

stroke
TIA
bells palsy

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2
Q

General presentation of stroke and TIA

A
  • Sudden onset of focal neurological symptoms, which cannot be explained by other conditions e.g. hypoglycaemia
    • Numbness
    • Weakness
    • Slurred speech
    • Visual disturbance
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3
Q

define stroke

A
  • is a clinical syndrome of presumed vascular origin characterized by rapidly developing signs of focal or global disturbance of cerebral functions which lasts longer than 24 hours or leads to death.
    • 85% ischaemia 15% haemorrhagic
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4
Q

define transient ischaemic attack

A

is a transient (less than 24 hours) neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without evidence of acute infarction.

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5
Q

define bells palsy

A
  • Bell’s palsy is an acute, unilateral facial nerve weakness or paralysis of rapid onset (less than 72 hours) and unknown cause.
    • Herpes simplex virus, varicella zoster virus, and autoimmunity may contribute to the development of Bell’s palsy, but the significance of these factors remains unclear.
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6
Q

presentation of bells palsy

A

A diagnosis of Bell’s palsy can be made when no other medical condition is found to be causing facial weakness or paralysis

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7
Q

symptoms of bells palsy include

A
  • Rapid onset (less than 72 hours).
  • Facial muscle weakness (almost always unilateral) involving the upper and lower parts of the face. This causes a reduction in movement on the affected side, often with drooping of the eyebrow and corner of the mouth and loss of the nasolabial fold.
  • Ear and postauricular region pain on the affected side.
  • Difficulty chewing, dry mouth, and changes in taste.
  • Incomplete eye closure, dry eye, eye pain, or excessive tearing.
  • Numbness or tingling of the cheek and/or mouth.
  • Speech articulation problems, drooling.
  • Hyperacusis.
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8
Q

management of bells palsy

A
  • The person should be advised to keep the affected eye lubricated by using lubricating eye drops during the day and ointment at night. The eye should be taped closed at bedtime using microporous tape, if the ability to close the eye at night is impaired.
  • For people presenting within 72 hours of the onset of symptoms, prescription of prednisolone should be considered.
  • Antiviral treatment alone is not recommended, but it may have a small benefit in combination with a corticosteroid; specialist advice is recommended if this is being considered.
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9
Q

urgent referall for bells palsy is required when..

A
  • Worsening of existing neurologic findings, or new neurologic findings.
  • Features suggestive of an upper motor neurone cause.
  • Features suggestive of cancer.
  • Systemic or severe local infection.
  • Trauma.
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10
Q

assessment of patient with unilateral weakness: history

A
  • Clinical feature e.g. neurological deficits, headache, vomiting, decreased LoC
  • Onset
    • Time (is there pt eligible for tPA)
    • Speed, duration, intensity
  • Risk factors for stroke and TIA
  • PMH e.g. stroke, liver disease, cancer, dementia, miscarriage, recent surgery or trauma
  • Family history
    • Stroke
    • Hyperlipidaemia
  • Medication history
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11
Q

assessment of patient with unilateral weakness: examination

A
  • Level of consciousness (LoC)
  • ABCDE
  • Neurological system examination
    • Face Arm Speech Tests (FAST)- validated tool for rapid assessment
  • Cardiovascular look for arrhythmia .e.g AF, murmurs or pulmonary oedema
  • General health
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12
Q

assessment of patient with unilateral weakness: investigations

A
  • Blood tests
    • Check blood glucose to rule out hypoglycaemia
    • FBC, LFTs, U and E, clotting times, blood culture
  • CT scan
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13
Q

TIA presentation (suspect TIA instead of stroke fi

A

Most TIAs are thought to resolve within 1 hour but can persist for up to 24 hours. Focal neurological deficits may include:

  • Unilateral weakness or sensory loss.
  • Dysphasia.
  • Ataxia, vertigo, or loss of balance.
  • Syncope.
  • Sudden transient loss of vision in one eye (amaurosis fugax), diplopia, or homonymous hemianopia.
  • Cranial nerve defects.
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14
Q

management of TIA

A
  • For people who have had a suspected TIA within the last week
    • Offer aspirin 300mg immediately (+PPI for those with GORD)
    • Refer to specialist assessment and investigation team
  • For people who have had a suspected TIA more than a week ago
    • Refer for specialist appointment with 7 days
  • Give people with suspected TIA and their family/carers info for recognising a stroke
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15
Q

causes of stroke in the young

A
  • Vasculitis
  • Thrombophilia
  • Subarachnoid haemorrhage
  • Venous sinus thrombosis
  • Carotid artery dissection e.g. via near strangling or fibromuscular dysplasia
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16
Q

causes of stroke in the old

A
  • Thrombosis in situ
  • Athero-thromboembolism e.g. from carotid arteries
  • Heart emboli (e.g. atrial fibrillation, infective endocarditis or MI)
  • CNS bleed associated with hypertension, head injury, aneurysm rupture)
  • Sudden blood pressure drop by more than 40 mmHg
  • Vasculitis e.g. giant cell arteritis
  • Venous sinus thrombosis
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17
Q

risk factors for stroke

A
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18
Q

suspect stroke insread of TIA if

A
  • The person presents with sudden onset, focal neurological deficit which is ongoing or has persisted for longer than 24 hours and cannot be explained by another condition such as hypoglycaemia. The clinical features of stroke vary depending on causative mechanism and the area of the brain affected and may include:
    • Confusion, altered level of consciousness, and coma.
    • Headache — usually of insidious onset and gradually increasing intensity in intracranial haemorrhage, and sudden, severe headache in subarachnoid haemorrhage which may be associated with neck stiffness. Sentinel headache(s) may occur in the preceding weeks.
    • Unilateral weakness or paralysis in the face, arm, or leg.
    • Sensory loss — paraesthesia or numbness.
    • Ataxia.
    • Dysphasia.
    • Dysarthria.
    • Visual disturbance — homonymous hemianopia, diplopia.
    • Gaze paresis — this is often horizontal and unidirectional.
    • Photophobia.
    • Dizziness, vertigo, or loss of balance — isolated dizziness is not usually a symptom of TIA.
    • Nausea and/or vomiting.
    • Specific cranial nerve deficits such as unilateral tongue weakness or Horner’s syndrome (miosis, ptosis, and facial anhidrosis).
    • Difficulty with fine motor coordination and gait.
    • Neck or facial pain (associated with arterial dissection).
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19
Q

management of stroke

A
  • Arrange immediate emergency admission to an acute stroke facility
  • Ensure hospital receives advanced notification of arrival
    • Details inc: time of onset, symptom evolution, current condition, and medications
  • Do not start anticoagulation or antiplatelet treatment in people following ischaemic stroke until intracerebral haemorrhage has been excluded
  • While awaiting transfer: ABDE and give supplemental oxygen if sats are less than 95%
  • If ischaemic clot (identified by CT) can give tPA if meets guideline
    • Potentially emergency endovascular procedures
    • Other procedures
      • Carotid endarterectomy
      • Angioplasty and stents
  • If haemorrhagic
    • Emergency measures- stop blood thinners
      • Surgical clipping
      • Coiling
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20
Q

types of stroke

A

anterior cerebral artery

middle cerebral artery

  • proximal
  • lenticulostriate artery occlusion
  • distal

posterior cerebral artery

  • cerebellar
  • basilar
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21
Q

which classification is used with stroke

A

Bamford/oxford classification

22
Q

TACS

A

(total anterior circulation stroke)

  • All 3 of
    • Unilateral weakness (+/- sensory deficit) of the face, arm and leg
    • Homonymous hemianopia
    • Higher cerebral dysfunction
      • Dysphasia/aphasia
      • Visuospatial disorder
23
Q

PACS

A

(partial anterior circulation stroke)

  • Only 2 of
    • Unilateral weakness (+/- sensory deficit) of the face, arm and leg
    • Homonymous hemianopia
    • Higher cerebral dysfunction
      • Dysphasia/aphasia
      • Visuospatial disorder
24
Q

POCS

A

(posterior circulation stroke)

  • One of the following
    • Cranial nerve palsy and contralateral motor/sensory deficit
    • Bilateral motor/sensory deficit
    • Conjugate eye movement disorder
    • Cerebellar dysfunction
    • Isolated homonymous hemianopia (with macular sparing)
25
Q

LACS

A

(lacunar strokes 15ml lesions)

  • One of the following:
    • Pure sensory deficit
    • Pure motor deficit
    • Senori-motor deficit
    • Ataxic hemiparesis
26
Q

where does the anterior cerebral artery supply

A
  • Arises as one of the branches of the internal carotid
  • Doesn’t supply many anterior structures
  • Supplies medial areas of the brain
    • Grey matter distribution: ACA loops back all over the superior surface of the corpus callosum and sends multiple branches to the medial aspect of the cerebral hemisphere (mostly frontal and parietal lobes)
    • White matter distribution: as the ACA loops around the CC it will send lots of branches into the white matter of the CC
27
Q

example of areas of the brain affected during ACA strpke

A
  • medial areas of the sensory and motor homunculus
    • contralateral lower limb more affected
  • paracentral lobules
    • incontinence
  • corpus coallosum
    • split brain syndrome- both hemispheres cannot work together
  • frontal lobe
    • personality changes
    • apraxia
28
Q

where does the middle cerebral artery supply

A
  • Arise as continuations of the internal carotids
  • Run laterally and go over the insular cortex and energy through sylvian fissure onto the surface of the cerebral hemisphere
    • Branches of the MCA = lenticular striate arteries which supplies the basal ganglia
  • Lateral areas of the brain supplies more lateral aspects of the cerebral hemispheres
    • Frontal
    • Parietal
    • Temporal
29
Q

proximal artery occlusion

A
  • Will affect everything downstream too e.g. lenticulate striate arteries, inferior and superior arteries of the MCA
  • Common à internal carotid directly supplies the MCA
30
Q

presentation of proximal MCA occlusion

A
  • contralateral hemiparesis
  • contralateral snesory deficit (soley face and arms)
  • contralateral homoymous heianopia

if left sides- aphases

more commonly right sided i.ei left sided heispatial neglect

31
Q

why is right sided MCA stroke more common

A
  • Usually more common on right side because left parietal region has dual bilateral blood supply
32
Q

Examples of affected areas with proximal MCA occlusion : Problems with the lateral motor homunculus

A
  • Contralateral upper limb and face motor problems
  • Actually clinically we usually see a complete hemiparesis → flaccid → spastic hemiparesis
    • Why? Because the MCA also supplies the internal capsule (lenticulate striate arteries) which carries fibres from the face, arm and leg
33
Q

Examples of affected areas with proximal MCA occlusion: Problems with the lateral sensory homunculus

A
  • Upper limbs and face sensory problems
  • Like likely to be full body sensory problems
  • Because the posterior parts of the internal capsule are supplies by the PCA- therefore mismatch between sensory and motor deficits
34
Q

Examples of affected areas with proximal MCA occlusion: problems with vision

A
  • Contralateral homonomous hemianopia
  • Destruction of both superior and inferior optic radiations as they run through the temporal and parietal lobes
35
Q

Examples of affected areas with proximal MCA occlusion: problems with speech

A
    • Broca’s aphasia (frontal)
      * Reduction in speech fluidity
      • Wernicke’s aphasia (temporal/parietal)
        • Problems with understanding language
      • If proximal occlusion= both Broca’s and Wernicke’s
36
Q

Examples of affected areas with proximal MCA occlusion : neglect like symptoms

A
  • Lesions which affect the right parietal lobe
  • Pt has issue with acknowledging what is going on, on the LHS
    • E.g. may only eat half of the meal
37
Q

Lenticulostriate arteries occlusion

A
  • Due to small emboli coming up from the internal carotid
  • Cause lacunar stroke cause destruction of small areas in the internal capsule and basal ganglia
38
Q

Examples of affected areas with lenticulate artery occlusion

A
  • Usually smaller deficits
  • Deficits depends where the lacunar stroke occurs
  • In the thalamus= sensory deficits
  • In the internal capsule
    • E.g. could occur on the posterior arm of the internal capsule and cause motor problems with the leg, trunk or arm
    • E.g. At the genu= face motor problems
  • If in both thalamus and internal capsule= mixed sensory and motor deficits
39
Q

distal MCA occlusions can be split into

A

superior and inferior division problems

40
Q

superior division problems

A
  • Supplies the lateral frontal lobe e.g. primary motor cortex and the Broca’s area
  • Examples of superior division problems
    • Contralateral face and arm weakness
    • Broca’s (Expressive) aphasia
      • Only if occurs on the LHS
41
Q

Inferior division problems

A
  • Supplies the lateral parietal lobe and the superior temporal
  • Examples of inferior division problems e.g. primary sensory cortex and Wernicke’s area
    • Contralateral face and arm loss of sensation
    • Wernicke’s aphasia
    • Homonomous hemianopia if both optic radiations are damaged or a quadrantanopia if just one radiation is affect
      • Without macula sparing
42
Q

posterior cerebral artery supplies

A
  • Posterior areas of the brain, thalamus and midbrain supply
43
Q

examples of affected areas with PCA occlusions

A
  • Contralateral Homonomous hemianopia with macula sparing
  • Contralateral sensory loss due to thalamic involvement
44
Q
  • Contralateral sensory loss due to thalamic involvement
A
  • More likely to be PCA which supplies the oxygen to the thalamus where the sensory (and motor) pathways go through
45
Q

Contralateral Homonomous hemianopia with macula sparing

A
  • If MCA damaged- everything will be destroyed (doesn’t matter if we have a contralateral supply by the PCA to the macula)- the damage is done
  • If PCA occlusion causes damage to the optic radiations, you still have contralateral supply to macula from the MCA therefore macula sparing
46
Q

cerebellary artery occlusions presentations

A
  • DANISh symptoms- ipislateral
    • cerebllar tract supply ipsilateral side of the body
    • ipsilateral horners syndrome
      • superior and infeiror cerebeal arteries wrap around the brainstem (can also affect sympathertics running laterally)
    • contralateral sensory signs
      • sensory pathways run laterally in the brainstem- pre-decussation
47
Q

DANISH symptoms

A
48
Q

basilar artery occlusion

A
  • Supply the brainstem- can lead to sudden death
  • Issues with superior aspect of brainstem
    • Visual and oculomotor defects
49
Q

Occlusion which spans both side of basilar artery (inc pontine arteries)

A
  • Circle of Willis is a circular therefore can supply most of the cerebral area and the vertebral arteries can supply the some of the brainstem and cerebellar
  • Therefore will be a small lesion but can have a large clinical effect e.g. Locked in syndrome
    • Complete bilateral motor response
    • Can only do oculomotor movements because ewe are below the oculomotor nuclei
    • Preserved consciousness
50
Q

extradural haemorrhage

A
  • trauma
  • LOC and lucid intervals
  • middle meningeal artery
  • biconvex shape on CT
51
Q

subdural haemorrhage

A
  • trauma
  • torn bridging veins
    • older patients due to tension of bridging veins → atrophy
  • concave shape on CT
52
Q

subarachnoid haemorrhage

A

Presents with

  • Headache(48%) - thunderclap
  • Dizziness
  • Orbital pain
  • Diplopia
  • Visual loss (anterior communicating artery aneurysm)

Causes

  • Arteriovenous malformation (AVM)(10%)
  • Saccular aneurysms (berry aneurysms)