QuestionSBA
QuestionChoice
Vertebrobasilar insufficiency may present in this way, although symptoms are transient, similar to a posterior circulation TIA. They are often triggered by causes of transient reduced cerebral perfusion, such as orthostatic hypotension, which can accentuate previously unknown symptoms
33101
d
Vertebrobasilar insufficiency
QuestionChoice
Pontine infarcts can present with a range of signs from ipsilateral cranial nerve palsy (CN V, VI, VII, and VIII) with contralateral motor/sensory impairment to locked-in syndrome. A similar condition to PICA syndrome - lateral pontine syndrome - would likely produce similar symptoms with the addition of ipsilateral facial nerve palsy due to involvement of the facial nucleus
33100
c
Pontine infarct
QuestionChoice
Weber syndrome presents as ipsilateral oculomotor nerve palsy and contralateral weakness
33099
b
Weber syndrome
QuestionChoice
Lacunary infarcts present with relatively distinct symptoms based on the location within the internal capsule. 1) contralateral hemiparesis with dysarthria and dysphagia 2) ipsilateral cerebellar symptoms 3) hemiparesis with contralateral sensory impairment 4) Pure hemisensory loss. It would unlikely present with Horner's syndrome
33102
e
Lacunar infarct
QuestionChoice
Sudden onset vertigo, nystagmus, and ipsilateral dysphagia, reduced facial sensation, and Horner's syndrome suggests a central cause, particularly dysfunction of the lateral part of the medulla. This is commonly caused by a posterior inferior cerebellar artery or vertebral artery ischaemia. The sensation of vertigo and nystagmus arises from disruption of the lateral vestibular nucleus; dysphagia due to damage to cranial nerves IX & X; reduced facial sensation from the trigeminal nerve root; and Horner's syndrome from the hypothalamospinal fibres where sympathetic fibres run
33098
a
Posterior inferior cerebellar artery syndrome (PICA syndrome)
QuestionComment
Could someone please explain the examination findings?🙏
26762
QuestionComment
You can break Posterior Inferior Cerebellar Artery Syndrome into two sets of symptoms by area since the posterior inferior cerebellar artery supplies the inferior cerebellum and the lateral parts of the medulla (which is why it's also called lateral medullary syndrome)

1 - cerebellum (damage is to the vestibulo-floccular connections)
- dysarthria
- ipsilateral limb ataxia
- vertigo
- Nystagmus

2 - Brain Stem (Medulla)
- ipsilateral Horner's syndrome (descending sympathetic nerve tract in lateral medulla)
- ipsilateral sensory loss (CNV tract in lateral medulla)
- ipsilateral pharyngeal and laryngeal paralysis (CNX exits on the lateral medulla)
- C/L sensory loss (Spinothalmic tract in lateral medulla)

It really helps to look at an axial section of the medulla and go through the structures in the most lateral part and see what will be damaged by infarct.
28270
User
subscriber
Embolism Otitis
User
subscriber
Metabolism Myotonia
Concept
Chapter
# Summary

An ischaemic stroke is a medical emergency characterised by a sudden onset of focal neurological deficit secondary ischaemia. Depending on the affected cerebral area, symptoms can range from contralateral motor and sensory deficits, homonymous hemianopia, to higher cerebral dysfunction (such as aphasia and neglect). Initial management of suspected stroke necessitates urgent neuroimaging, primarily via non-contrast CT scan, to differentiate between ischaemic and haemorrhagic types. Further investigations such as carotid ultrasound, CT/MR angiography, echocardiogram, and various blood tests (e.g., serum glucose and lipids) help define the cause of stroke and quantify vascular risk factors. Acute management of ischaemic stroke involves thrombolysis in selected patients (usually within 4.5 hours of symptom onset), provided there are no contraindications, or mechanical thrombectomy for eligible patients. Long term management usually involves antiplatelet therapy, risk factor optimisation and multidisciplinary rehabilitation.


# Definition

An ischaemic stroke describes a sudden onset focal neurological deficit secondary to focal brain ischaemia, with symptoms lasting >24 hours (or with evidence of infarction on imaging).

# Aetiology

85% of strokes are ischaemic while 15% are haemorrhagic.

Ischaemic stroke occurs when blood supply in a cerebral vascular territory is reduced secondary to stenosis or complete occlusion of a cerebral artery.

The ischaemic penumbra describes the cerebral area surrounding the ischaemic event where there is ischaemia without necrosis. This area is amenable to recovery with thrombolysis.

In terms of underlying aetiology of ischaemic stroke: 

- 25% are caused by intracranial small vessel atherosclerosis.
- 50% are caused by large vessel atherosclerosis e.g. carotid artery stenosis.
	- Typically results from thrombus formation on the atherosclerotic plaque, and subsequent embolism of the thrombus to a smaller cerebral artery.
- 20% of ischaemic strokes are cardio-embolic 
	- e.g. in atrial fibrillation there is stasis of blood flow in the left atrium, predisposing to thrombus formation in the left atrium, and subsequent embolisation to the brain.
	- Rare causes of ischaemic stroke include primary vascular causes (such as vasculitis and arterial dissection) and haematological causes (prothrombotic states).



# Stroke risk factors

- Age
- Male Sex
- Family History
- Hypertension
- Smoking
- Diabetes 
- Atrial fibrillation
- High cholesterol
- Obesity
- Migraine 

# Stroke classification 

The **Bamford/Oxford Stroke Classification System** is the most common classification system for ischaemic stroke. Although it is not used frequently in clinical practice, it is a helpful aide memoire to remember the localisation of common stroke syndromes.

A total anterior circulation infarct (TACI) is defined by:

- Contralateral hemiplegia or hemiparesis, AND
- Contralateral homonymous hemianopia, AND
- Higher cerebral dysfunction (e.g. aphasia, neglect)
A TACI involves the anterior AND middle cerebral arteries on the affected side.

A partial anterior circulation infarct (PACI) is defined by:

- 2 of the above, OR
- Higher cerebral dysfunction alone.
- A PACI involves the anterior OR middle cerebral artery on the affected side.

A lacunar infarct (LACI) is defined by: a pure motor stroke, pure sensory stroke, sensorimotor stroke, ataxic hemiparesis or dysarthria-clumsy hand syndrome.
A LACI affects small deep perforating arteries, typically supplying internal capsule or thalamus.

A posterior circulation infarct (POCI) is defined by:

- Cerebellar dysfunction, OR
- Conjugate eye movement disorder, OR
- Bilateral motor/sensory deficit, OR
- Ipsilateral cranial nerve palsy with contralateral motor/sensory deficit, OR
- Cortical blindness/isolated hemianopia.

A POCI involves the vertebrobasilar arteries and associated branches (supplying the cerebellum, brainstem, and occipital lobe).

[lightgallery]

# Posterior Stroke Syndromes

There are a number of different posterior stroke syndromes that you should be aware of:

- Basilar artery occlusion is more likely to present with locked in syndrome (quadriparesis with preserved consciousness and ocular movements), loss of consciousness, or sudden death.

- Anterior inferior cerebellar artery results in lateral pontine syndrome, a condition similar to the lateral medullary syndrome but with additional involvement of pontine cranial nerve nuclei. It leads to cerebellar ataxia, vertigo, hearing loss as well as ipsilateral facial weakness
- Wallenberg's syndrome (lateral medullary syndrome) causes ipsilateral Horner's syndrome, ipsilateral loss of pain and temperature sensation on the face, and contralateral loss of pain and temperature sensation over the contralateral body.
- Weber's syndrome/medial midbrain syndrome (paramedian branches of the upper basilar and proximal posterior cerebral arteries): causes an ipsilateral oculomotor nerve palsy and contralateral hemiparesis.

# Acute management of ischaemic stroke


- Patients should be approached in the DR ABCDE manner.
- CT Head should be perfomed on arrival to the emergency department to distinguish ischaemic from haemorrhagic stroke. 
- If no evidence of ischaemic stroke, a CT Angiogram and CT perfusion (in select patients) should be performed to assess for evidence of large vessel occlusion and a salvageable ischaemic penumbra
- Thrombolysis with Alteplase (tissue plasminogen activator) is considered if:
	- The patient presents within 4.5 hours of symptom onset (Up to 9 hours in select patients with good baseline and favourable perfusion imaging) 
	-  No contraindications such as:
		-  Recent head trauma
		-  Recent surgery
		-  Systolic lood Pressure above 185 
		-  Currently taking oral anticoagulation
		-  Raised INR (local guidelines vary)
- Mechanical Thrombectomy is usually considered in patients with:
	- Anterior Circulation Stroke (evidence base is poorer for posterior circulation stroke)
	- Evidence of large vessel occlusion (ideally proximal up to distal M1)
	- Good functional baseline
	- Favourable perfusion criteria indicating salvageable tissue
	- Presenting within 6 hours (Up to 24 hours in select patients with good baseline and favourable perfusion imaging)

If hyper-acute treatments are not offered, patients are started on an antiplatelet agent such as Aspirin or Clopidogrel (local guidelines vary).

If hyper-acute treatments are offered, antiplatelets are usually started 24 hours after the treatment following a repeat CT Head that excludes any haemorrhagic transformation.

# Stroke investigations (Post-acute)

MRI Head with Diffusion Weighted Imaging (DWI) is the gold standard test to confirm the presence of an acute ischaemic stroke, which can be present within a few minutes of stroke onset. Due to logistical challenges of acute MRI scanning, this is normally performed within 24 hours following initial hyperacute treatment.

Investigations in the post-hyperacute phase aim to further define the cause of the stroke and to quantify vascular risk factors.

These include:

- Carotid ultrasound (to identify critical carotid artery stenosis)
- 24 to 72 hour cardiac monitoring to assess for evidence of atrial fibrillation
- CT/MR angiography (to identify intracranial and extracranial stenosis)
- Echocardiogram (if a cardio-embolic source is suspected). 
- In young patients further investigation e.g. a vasculitis screen or thrombophilia screen may be necessary.
- HbA1c and Serum Lipids to optimise other cardiovascular risk factors 


# Stroke management (Chronic)

Rehabilitation and supportive management will include an **MDT approach** with involvement of physiotherapy, occupational therapy, speech and language therapy, and neurorehabiliation.


The key steps in secondary stroke prevention can be remembered by the mnemonic HALTSS:

- Hypertension: 
	- Studies show there is no benefit in lowering the blood pressure acutely (as this may impair cerebral perfusion) unless there is malignant hypertension (systolic blood pressure >180 mmHg). Anti-hypertensive therapy should, however, be initiated 2 weeks post-stroke.
- Antiplatelet therapy:
	- Patients should be administered Clopidogrel 75 mg once daily for long-term antiplatelet therapy. In patients with ischaemic stroke secondary to atrial fibrillation, however, warfarin (target INR 2-3. or a direct oral anticoagulant (such as Rivaroxaban or Apixiban) is initiated 2 weeks post-stroke.
- Lipid-lowering therapy:
	- Patients should be prescribed high dose atorvastatin 20-80 mg once nightly (irrespective of cholesterol level this lowers the risk of repeat stroke).
- Tobacco
	- Offer smoking cessation support.
- Sugar:
	- Patients should be screened for diabetes and managed appropriately.
- Surgery:
	- Patients with ipsilateral carotid artery stenosis more than 50% should be referred for carotid endarterectomy. Patients with over 70% stenosis have the most benefit from endarterectomy



# References

[Click here for NICE Clinical Knowledge Summaries](https://cks.nice.org.uk/topics/stroke-tia/)

[Click here for Radiopedia](https://radiopaedia.org/articles/lacunar-stroke-syndrome?lang=gb)
185
Picture
3247
Bamford Image.png
images/8zv7r9rp1728310518503.jpg
images/8zv7r9rp1728310518503_256.jpg
images/8zv7r9rp1728310518503_512.jpg
+PcFDIL6RZeHeXiOoooQagZbuA==
186
Ischaemic Stroke
Topic
34
Neurology
Video
Concept
186
Ischaemic Stroke
165
ncKMYZA
images/videos/neurology.png
Haemorrhagic stroke
Video
Concept
186
Ischaemic Stroke
247
Dy6PDaW
images/videos/neurology.png
Quesmed Tutorial: Neurology
Video
Concept
186
Ischaemic Stroke
205
kLytkNr
images/videos/neurology.png
Ischaemic Stroke
6620
Posterior inferior cerebellar artery syndrome presents with vertigo, nystagmus, dysphagia, facial sensory loss, and Horner's syndrome due to medullary ischaemia.
A 68-year-old man has presented to accident and emergency with sudden onset vertigo, unchanged on position, with no hearing impairment or tinnitus. He has new hoarseness and dysphagia, struggling to swallow his saliva.

On examination head impulse test is negative; he has right-sided unilateral vertical nystagmus and right-sided skew deviation. He has reduced sensation on the right side of his face with right-sided ptosis and miosis.

Which of the following is the most likely diagnosis?
a