teesneuro.org

by Vaasu Bansal (final year medical student) & Neil Archibald (in italics)

Editor’s intro – there aren’t a huge number of true “neurological emergencies”. I heard one Irish registrar introduced a talk on the topic, in front of his Professor, thus:

“There are only 2 neurological emergencies – the MRI machine is broken and the hospital has run out of steroids”.

It is not clear if that registrar ever worked in Ireland again – although he would be welcome in TeesNeuro. Apocryphal jokes aside, you have to admit that Stroke is a proper, card-carrying brain emergency; so much so that in Teesside with have a “Brain Attack Team” on duty each day (who can, obviously, be contacted via the “Bat phone”.

I’m grateful to Vaasu for doing such an amazing job with this section – all the hard work was done by him.

What is Stroke?

Stroke represents one of the most common neurological presentations, with someone suffering an attack every 5 minutes. It is a major cause of death and disability, with 1.3 million stroke survivors in the UK.

Defined simply, stroke is an interruption of blood supply to brain tissue, which leads to ischaemia, neurological dysfunction, and eventual tissue death. This can occur due to either a blockage or a bleed within the vasculature. Consequently, strokes are classified as ischaemic or haemorrhagic respectively. Most strokes – 8 in every 10 – are ischaemic in nature and so the immediate management of stroke is aimed at restoring blood flow to at risk brain tissue.

As a vascular event, stroke is a hyperacute presentation, with symptoms developing within minutes of the vascular injury. The development of tissue ischaemia is progressive and without restoration of perfusion there is irreversible damage and neuronal death. However, restoration of blood flow can reduce and reverse injury to viable tissue.

This can be summarised by the popular phrase, “Time is brain.”

The symptoms of stroke are broad and varied, and none are sensitive or specific in isolation. Instead, there must exist a syndrome which is best explained by loss of neurological function in a vascular territory – be it brain, retina or even spinal cord. Thus, the diagnosis of stroke (which is a clinical one) cannot be made without at least a brief understanding of the relevant neuroanatomy and vascular supply.

At this point, it may be helpful to brush up on the motor and sensory pathways. The Teesneuro lectures on Neurology for Dummies and Neuro-anatomy essentials are great resource to help tie in the concept of anatomy and presentation!

Stroke vs TIA – What’s in a name?

Historically, all cerebrovascular events were divided into stroke and transient ischaemic attacks (TIAs) with a simple distinction – symptoms lasting less than 24 hours were classified as TIA (hence the term transient), and those lasting longer or resulting in death before 24 hours were called stroke.

The 24 hour cut-off was chosen arbitrarily to distinguish patients with and without an infarct, in a time when access to CT was limited and the MRI was not an established technique outside research. The assumption was that patients with a complete resolution of symptoms within 24 hours had a temporary interruption to blood flow, which was rapidly reversed by the body itself, preventing the development of an infarct. In contrast, stroke was assumed to cause sufficient ischaemia to develop an infarct in the brain tissue, leading to irreversible symptoms.

(in practice, most TIAs last minutes only and should really have totally resolved by a maximum of 60 minutes – it is hard to imagine some permanent tissue damage if the ischaemia goes on much longer than this)

When imaging finally caught up, the stroke vs TIA definition was put under scrutiny – around 1 in 3 patients diagnosed with a TIA (using the 24 hour cut-off) actually had an infarct on MRI². This prompted the development of a new, tissue-based definition of TIA: an episode of neurological dysfunction, caused by focal brain ischaemia, without any evidence of acute infarction on imaging.

To summarise the definitions of a TIA:

• time-based: loss of neurological function caused by ischaemia lasting for less than 24 hours

• tissue-based: loss of neurological function caused by ischaemia without evidence of acute infarction

However, the new definition has posed a number of problems as well. The definitions of stroke vs TIA are now ambiguous. It is also inconsistent, as the diagnosis is now dependent on the imaging obtained, and not all centres may have access to MRI. The tissue-based definition also categorises stroke symptoms lasting for more than 24 hours without infarction on MRI as TIA – something that is obviously contradictory to the common understanding of TIA.

It is easy to dismiss this change in definition as a purely academic endeavour, with little clinical consequence. However, the distinction of stroke vs TIA has a profound impact on management for patients. As such, the National Clinical Guidance for Stroke (NCGS) groups “minor and non-disabling strokes” with “TIA”, in contrast with major strokes that cause severe disability to guide management and secondary prevention.

TIA Investigation and Management

“A TIA is an opportunity to prevent a stroke. And prevention is far better than cure.“

TIA clinics typically run 7 days a week and patients are risk-stratified to ensure those at highest risk of going on to have a stroke are seen before they have a chance to do so. Wait too long and there will be gaps in your clinic because the people you are supposed to be seeing will be up on your stroke unit already.

To pick up those at highest risk, most places screen referrals using the ABCD² score. This combines age, blood pressure, clinical features, duration and diabetes into an algorithm for working out who to see soonest. There are lots of sites that offer a calculator but we quite like this one.

In all cases of suspected TIA, immediate treatment with aspirin 300mg is recommended (unless contraindicated). Patients already on low-dose aspirin are not offered an additional dose.

At rapid-access TIA clinics, patients undergo a wide variety of investigations to aggressively reduce the risk of another cerebrovascular event as quickly as possible. Ideally, every patient receives the following investigations on the same day as their specialist appointment:

As discussed, management of TIA is primarily focused on secondary prevention. Risk factors are addressed through the following conservative, medical, and surgical methods:

Lifestyle modification (diet, alcohol, smoking, exercise)

Vascular risk factor modification with:

• antihypertensives
• high intensity statin therapy, e.g. atorvastatin 20-80mg
• antiplatelet therapy – ideally dual antiplatelet therapy (DAPT) unless contraindicated or high risk of bleeding (eg clopidogrel + aspirin for 21 days, followed by clopidogrel monotherapy).
• if DAPT is not suitable, clopidogrel monotherapy is preferred.

Due to the gastrointestinal side-effects of DAPT, it should be prescribed with PPIs for gastroprotection.

If a patient is diagnosed with AF after TIA, anticoagulation should be started immediately once haemorrhage is excluded. Anticoagulation therapy is prioritised over antiplatelet therapy – if a patient is started on or is already on anticoagulation, antiplatelet therapy is not considered.

(There are very few indications for combined antiplatelet and anticoagulation therapy, and are mostly seen in cardiology³.)

Carotid stenosis of 50-99% should be managed surgically (with carotid endarterectomy) or by angioplasty and stenting.

You can find the UK investigation and management guidelines here.

Stroke – Assessment

A typical history of a stroke involves a new and persistent focal neurological deficit. The onset of symptoms is rapid, and may involve subsequent deterioration as ischaemia begins to affect surrounding areas of the brain.

(a good rule of thumb in neurology is that abrupt-onset problems are “vascular” (ischaemic, bleeds), sub-acute (1-2 weeks) are immune-mediated and chronic (months, years) are neurodegenerative. This is quite a nice way of trying to split up and shorten your differential diagnosis in clinical practice)

Common symptoms reported in ischaemic stroke include:

• weakness of the face, arm, or leg
• loss of sensation
• visual deficits
• problems with eye movements and double vision
• inability to communicate – which may be due to damage to the language centres of the brain (Wernicke’s and Broca’s areas) or due to motor weakness of the muscles involved in speaking
• dizziness, nausea, vomiting
• loss of coordination and balance
• loss of consciousness and coma (rare)

Symptoms really depend on the function of the area of brain that has been deprived of blood flow and so presentations can be varied.

It is particularly easy to miss brainstem presentations and, as we shall come to later, this is a vital area with different management (so take a moment to make sure you are clear on the difference between “FAST” presentations and brainstem presentations.

While taking a history, it is also important to establish the following information, as it often helps guide eligibility for treatment, as discussed later.

• time from onset of symptoms (or the time since the patient was last known to be well)
• if the patient woke up from sleep with symptoms
• medical history that might increase the risk of bleeding such as medication, malignancy, recent procedures, and previous episodes of bleeding
• the patient’s pre-stroke functional status, usually assessed using the modified Rankin Scale (mRS)

Haemorrhagic stroke may present with similar loss of function. However, there are some presentations that are more likely to be associated with haemorrhage, which often relate to the increased intracranial pressure.

These include:

• thunderclap headache
• coma and loss of consciousness
• photophobia
• neck stiffness
• nausea and vomiting
• seizures

A thorough examination, along with the presentation, can help give an estimate of the brain territory affected, the amount of disability, and the prognosis.

The NIH Stroke Score (NIHSS) is used to quantify the severity of a stroke based on examination findings such as limb and facial muscle weakness, sensory loss, higher cortical deficits, alertness, etc. Compared to the MRC scale for muscle power, NIHSS is more sensitive for small motor deficits that are otherwise missed.

It is also important to assess the patient for common conditions that may also cause acute neurological changes. Such conditions are commonly known as stroke mimics. The most frequent stroke mimics include:

• hypoglycaemia
• seizures and postictal weakness
• infection – usually systemic infections in older, frail patients who then appear drowsy, slumped and can look like they have had a focal event
• space occupying lesions
• migraine – hemiplegic or vestibular
• peripheral neuropathy, e.g. Bell’s palsy
• functional disorders

Stroke Classification

Stroke can be classified under endless labels (with students often assuming the sole reason to do so being to inflict mental anguish), but consultants promise there is a clinical requirement to help guide management.

(*I think the most important distinction is between anterior and posterior circulation events as these present very differently and have quite different causes, investigation and management)

If you want a quick video on the blood supply to the brain, this 7 minute explainer on YouTube is really excellent.

The most widely taught classification system for stroke is the Oxford-Bamford classification, which divides stroke based on the clinical presentation and likely ischaemic focus:

As ever, the Geeky Medics do it very well.

It is also worth remembering the good old homunculus – remember this guy…?

Well, turns out the middle cerebral artery (MCA) supplies most of the homunculus (dark green) – except the leg (which is mostly supplied by the anterior cerebral artery (ACA); light green). So, after an MCA stroke, the leg can be relatively spared.

In contrast, an anatonimcally “smaller” atroke in an area called the internal capsule – also known as a lacunar stroke – can pick off fibres from almost the entire homunculus, leading to a much more profound hemiparesis that spares very little.

Total Anterior Circulation Stroke (TACS)

TACS is defined by the presence of all 3 of the following:

• unilateral weakness and/or sensory deficit in at least 2 out of 3 of the face, arm, and leg
• homonymous hemianopia
• higher cerebral dysfunction – commonly aphasia and visuospatial disorders

TACS is usually caused by infarction in the middle cerebral artery. The severity reflects a proximal occlusion of the vessel, leading to a large infarct and worse patient outcomes.

Partial Anterior Circulation Stroke (PACS)

PACS is defined by the presence of 2 out of 3 of the same criteria as above OR isolated higher cortical deficit.

The occlusion is more likely to be distal and thus the affected tissue is smaller in size, corresponding to a less severe condition.

Lacunar Stroke (LACS)

LACS affects deep, subcortical structures, often at points where the motor and/or sensory pathways concentrate physically in space, for example the internal capsule or the thalamus. A lacunar infarct (LACI) may present as any of the following:

• pure motor weakness (hemiparesis)
• pure sensory deficit
• mixed sensori-motor stroke
• ataxic hemiparesis
• clumsy-hand dysarthria

Posterior Circulation Stroke (POCS)

POCS affects the posterior circulation, which supplies the posterior cerebrum, cerebellum, and brainstem. The neuroanatomy of this region is complex – tracts often cross over, communicate with various other parts of the nervous system, and are bundled tightly in space. Neighbouring areas often perform drastically different functions.

As a rule of thumb, any presentation involving cranial nerve or cerebellar functions is likely to affect the posterior circulation. Crossed signs, where one side of the face and the other side of the body are affected, are almost exclusively brainstem strokes.

(to put it more succinctly – if the presentation is chaos, and you can’t make any sense of it, then it is probably posterior circulation)

Typical features of a POCS can include:

• cranial nerve palsy with contralateral motor/sensory deficit (crossed signs)
• bilateral motor/sensory deficit
• conjugate eye movement disorders – problems with moving both eyes in tandem, usually in the horizontal direction
• cerebellar dysfunction – e.g. nystagmus, ataxia
• isolated homonymous hemianopia – classically described with macular (central) sparing
• vertigo and hearing loss

To learn more about localisation of brainstem strokes, you can check out the Rule of 4 at Life in the Fast Lane.

Fig 1. Distribution of symptoms referred to as crossed signs. These particular symptoms represent lateral pontine syndrome. Adapted from Gates P. (2011)⁴.

Fig 2. Homonymous hemianopia (top) compared with hemianopia with macular sparing (bottom). Arrowhead (A) represents the normal blind spot of the left eye. Image via Wikimedia Commons.

(I have never seen this “in the wild” and don’t think my clinical skills are up to finding it. Let yourself off the hook and don’t even try! Much more important to focus on the other posterior symptoms – they are much more common)

Haemorrhagic Stroke

It is not uncommon for patients to present with the clinical features of a “stroke” only to be found to have a bleed once the imaging has been done.

Sometimes, the bleed occurs into an area of acute infarction but, often, it can be a primary haemorrhage. Any bleed into the substance/tissue of the brain is called an intracerebral haemorrhage (to distinguidh it from bleeding into the fluid in/around the brain (subarachnoid haemorrhage).

Intracerebral haemorrhage (ICH) is usually spontaneous, due to age-related small vessel disease or in patients with poorly controlled hypertension. Secondary macrovascular causes can include vascular malformations such as arteriovenous malformations (AVM), dural fistulas (dAVF), and cavernomas.

Subarachnoid haemorrhage (SAH) can be due to ruptured aneurysms or direct from blood vessels (non-aneurysmal). Aneurysms are actually very common, with 1 in 50 people having an unruptured aneurysm. However, only a small fraction of these ever lead to haemorrhage. Another common cause is trauma, although this should be fairly obvious from the history or presentation.

Fig 3. Intracerebral Haemorrhage. Image via Wikimedia Commons. Note the fact that acute blood is pretty obvious on CT scans and this is a quick and easy way to investigate. MRI, on the right, has a number of differebt sequences you can request if haemorrhage is on the cards. Most come as standard now but SWI and gradient ECHO sequences are particularly good at picking up even very small bleeds.

Fig 4. Subarachnoid Haemorrhage. Image via University Department of Neurosurgery, Inselspital Bern ©. Note the CT image showing focal SAH following trauma and the CT angiography demonstrating a small aneursym as the underlykng cause of SAH in the patient on the right.

Investigations

As stroke is a clinical diagnosis, investigations are primarily helpful in excluding differentials and searching for the underlying cause for the vascular event.

I like to think of it as either a problem with the pump (heart), the large vessels (carotid and vertebral) and the small vessels (affected by all the usual vascular risk factors)

Common investigations therfore include:

• Bloods – look for glucose, cholesterol, clotting, renal impairment, FBC etc. Some of these speak to risk factors and some to what treatments you should or should not be using

• ECG – identifies atrial fibrillation, which is a frequent cause for emboli formation in the left atrium. It may also show LV hypertrophy from hypertension or other potential structural changes

• CXR – quite a simple test that is often overlooked

• Carotid imaging – more useful for TIA, as carotid intervention is avoided during acute stroke. Please note this is only relevant for ANTERIOR circulation events in any case. These days, you get some excellent images of the vessels by CT or MR angiography and vascular imaging is often part of the initial scan at presentation

In younger populations, that may not have a high risk of vascular comorbidity, it is important to consider rarer causes of vascular insults. These can include conditions such as vasculitis, haematological abnormalities (such as sickle cell disease, polycythaemia, leukaemia) and infections such as syphilis, HIV and endocarditis.

Haemorrhagic causes such as aneurysms and sinus venous thromboses are also more common in younger populations.

Imaging

Imaging is a core aspect of stroke, largely due to the various reasons stroke can occur and the wide range of management available depending on classification. The National Optimal Stroke Imaging Pathway (NOSIP) recommends that patients receive a CT brain, CT angiography, and CT perfusion in the same sitting, ideally within 20 minutes of presentation.

CT Brain

Non-contrast CT is the first-line modality in stroke imaging, and is primarily used to rule out haemorrhagic stroke, which is managed in dramatically different ways compared to ischaemic stroke. A normal CT does not rule out ischaemic stroke, as the early signs of ischaemia are subtle and may not have time to develop before the patient is imaged.

Haemorrhagic Findings

In the acute phase, blood appears hyperdense (white) on CT. It may be present within the tissue of the brain itself (ICH) or within the subarachnoid space (SAH).

Intracranial haemorrhage is an absolute contraindication for most drugs given in the treatment of ischaemic stroke, and usually requires neurosurgical involvement.

Ischaemic Findings

Hyperacute changes (typically 0-6 hours) on CT that support a diagnosis of ischaemic stroke include direct visualisation of clot in situ (hyperdense MCA sign; below left) and a loss of grey-white matter differentiation (insular ribbon sign; below right).

These are followed by acute changes (24 hours – 1 week) including cortical hypodensity and parenchymal swelling. These are often hard to identify (and definitely not something you are expected to do!), especially if the area affected is small. Again, this is why a normal CT head cannot rule out stroke!

As time goes on, changes in brain tissue may cause the initially visible signs to be masked over, resulting in a falsely reassuring CT (1-3 weeks).

In the longer term, tissue death leads to loss of brain tissue and replacement by the surrounding CSF – showing what we refer to as encephalomalacia.

CT Angiography

CT angiography is rapidly becoming a widely offered investigation and is necessary for the endovascular retrieval of clots, known as thrombectomy. It is also used to assess large-vessel disease such as atherosclerosis and dissection.

In haemorrhagic stroke, CT angiography can be used to identify aneurysms and other sources of bleeding within the brain.

Certain findings on CTA may lead to the decision of performing intra-arterial angiography. Also known as digital subtraction angiography (DSA), it is an invasive radiological intervention where a catheter is passed through the femoral or radial arteries into the carotids to better visualise the vasculature. It is often used to distinguish between micro and macrovascular causes of ICH.

CT Perfusion

CT perfusion is a fancy extension of angiography, where the flow of contrast through tissue is used to identify the core and penumbra of the infarct.

The core of an infarct represents the area of tissue that is irreversibly damaged. The penumbra surrounds the core and represents a region which is not receiving the required blood flow, but can potentially be salvaged with timely intervention. CT perfusion has allowed for the extension of thrombolysis and thrombectomy windows through the identification of the mismatch between the core and the penumbra.

MRI

MRI is exceptionally sensitive for stroke, but is more time consuming and may not be relevant in all cases, e.g. clear infarct on CT. The appearance of stroke on MRI is complex, and varies with time since onset and the different sequences.

It is however important to know that MRI sequences such as diffusion-weighted imaging (DWI) can be used in cases where there is diagnostic uncertainty or mild symptoms. Susceptibility-weighted imaging (SWI) is another sequence that is especially sensitive for haemorrhage.

Acute Management

The management of stroke depends on whether it is classified as ischaemic or haemorrhagic.

Ischaemic

Once haemorrhagic stroke has been excluded, all patients should receive aspirin 300mg within 24 hours.

All patients with ischaemic stroke should also be considered for thrombolysis and thrombectomy.

Thrombolysis is a medical treatment involving the use of fibrinolytic drugs, most commonly alteplase, to break down clots in circulation. However, the mechanism of action also means that thrombolytics can lead to severe bleeding. Thus, thrombolytic treatment has several contraindications, which must be considered before administration. Most of these relate to the risk of causing a bleed that could cause significant harm, e.g. previous intracranial haemorrhage, recent GI haemorrhage, oesophageal varices etc.

Initially, thrombolysis was only proven to be effective when administered before 4.5 hours from onset of symptoms. Not only is this a highly restrictive window, but it also excluded patients who had strokes in their sleep or had strokes with an unknown onset time.

However, with the use of CT perfusion and MRI DWI studies, thrombolysis can now be administered up to 9 hours later – if there is sufficient salvageable tissue, as evidenced on specialised imaging.

Thrombectomy is the endovascular removal of a clot, usually performed by interventional radiologists. It can be offered to patients presenting with thrombi in large vessels, such as the carotid artery and initial branches of the MCA.

In recent years, some centres have begun to offer basilar artery thrombectomy.

(this intervention is nothing short of miraculous, particularly for devestating strokes. Clot retrieval is particularly important for brainstem events as these can be treated later than you might think and still do well.)

To be eligible for thrombectomy, patients must have large clinical deficits (usually NIHSS > 6) and a good pre-stroke functional status (usually mRS 0-2). Ideally, it should be carried out within 6 hours from the onset of stroke. This window can be extended up to 24 hours using CT perfusion and MRI studies, similar to thrombolysis.

Thrombectomy is often performed in combination with thrombolysis. In the absence of any contraindications, thrombolysis should be administered as soon as possible after excluding haemorrhage, without delaying intra-arterial clot retrieval.

Fig 9. Mechanical thrombectomy with a stent retriever device. Adapted from Samaniego, E. A. et al. (2018).⁸

Blood pressure is not routinely controlled during ischaemic stroke, as high blood pressure is usually a physiological response to ischaemia and is a compensatory mechanism to increase cerebral blood flow.

Reducing blood pressure can impact the blood flow to the infarcted area through collateral blood supply and worsen symptoms.

However, as BP over 185/110 mmHg is a contraindication for thrombolysis, control may be required for treatment when patients are otherwise eligible.

Clinicians may also decide to lower BP in situations where it is causing significant harm, such as in hypertensive encephalopathy, hypertensive nephropathy, pre-eclampsia etc.

Haemorrhagic

Subarachnoid Haemorrhage

Subarachnoid haemorrhages are some of the deadliest and most disabling acute neurological events. Most are caused by the rupture of an aneurysm. Around 10-15% of patients die before reaching the hospital, with an overall mortality of around 44%.⁹

Mortality is largely attributed to complications following haemorrhage.

General management includes reversal of anticoagulation and adequate analgesia. Common complications and their management are discussed below:

Rebleeding

Prevented by interventions such as endovascular coiling and surgical clipping. Coiling is preferred over clipping, however not all aneurysms may be candidates for endovascular intervention.

Vasospasm

Also known as delayed cerebral ischaemia. Sustained smooth muscle contraction of the blood vessels leading to reduced flow, worsening neurological deficit and reduction in consciousness. Managed with nimodipine, a calcium channel blocker.

If vasospasm develops, it is treated with volume expansion and vasopressors to raise blood flow through the vessel

Hydrocephalus

Due to problems with reabsorption of CSF, the ventricles of the brain may enlarge and apply pressure to the brain. Managed by lumbar or extraventricular drain.

Fig 10. Endovascular coiling (left) vs Neurosurgical clipping (right). Adapted from Pierot, L. et al. (2013)10 and Goodney, P. R. et al. (2015).¹¹

Fig 11. Intra-arterial angiography demonstrating vasospasm. A) Arrowhead indicates aneurysm of right AICA. B) Arrowhead indicates vasospasm of the right PCA, 12 days after SAH. Adapted from Sehy, J. V. et al. (2010).¹²

Intracerebral Haemorrhage

As with SAH, the aim of management of ICH is the prevention of further bleeding and other complications.

To prevent expansion of the haematoma, anticoagulation should be reversed as appropriate and blood pressure should be controlled urgently in most cases.

Complications such as hydrocephalus should be managed with the appropriate interventions.

Patients with features suggesting a diagnosis other than spontaneous ICH, e.g. sinus venous thrombosis, vascular malformation should undergo further investigations such as CT/MR venogram and DSA.

Ward Care

All stroke patients should be admitted to a stroke unit to maintain normal physiological status and optimal care. Evidence shows that patients receiving care in a dedicated stroke ward have lower rates of death and dependency.¹³

Simple considerations in patient care include prompt swallowing assessments, maintenance of blood glucose, hydration and nutrition.

Patients should be checked for a safe swallow within 4 hours of arrival, and definitely before being given food, fluids, or medication. This is usually done by Speech and Language Therapists – although other members of the stroke team may also be trained to early swallow assessments. In cases of impaired swallow or delayed assessment, patients may require IV fluids, nasogastric feeding and suctioning, and changes to oral medication.

Ensure that patients maintain a blood glucose between 5-15 mmol/L, with close monitoring to avoid hypoglycaemia.

Patients should also be optimised to prevent and treat deep vein thrombosis and pulmonary embolism. These are especially common in patients suffering from stroke, as they are often completely immobilised due to paralysis.

It is also important to assist patients with early mobilisation where possible and safe with the help of physical and occupational therapists.

Secondary Prevention of Ischaemic Stroke

The secondary prevention of ischaemic stroke is largely similar to the management of TIA. Long-term medication aims to reduce the risk of further stroke and optimise vascular risk factors. Interventions include:

• Lifestyle modification, e.g. alcohol, smoking, diet, exercise

• Vascular risk factor modification

• Antihypertensives

• High intensity statin therapy, e.g. atorvastatin 20-80mg

• Antiplatelet therapy

Antiplatelet therapy can be started 24 hours after the administration of thrombolysis. For major/disabling stroke, monotherapy with clopidogrel is preferred. Aspirin may be given if clopidogrel is not tolerated

DAPT is avoided in major strokes due to the increased risk of bleeding into the infarct. It may be used based on clinical judgement for other indications, such as ACS/recent coronary stenting
DAPT (clopidogrel + aspirin) may be used in non-disabling, minor strokes (same as TIA)

Always consider gastroprotection with PPI

In stroke patients with atrial fibrillation, anticoagulation is preferred over antiplatelet therapy for secondary prevention.

As anticoagulation poses a larger bleeding risk than antiplatelets, anticoagulation is not started in the acute phase of stroke.

Anticoagulation can be started 5-14 days after onset of moderate to severe stroke based on clinical judgement. Antiplatelet therapy with aspirin is used until anticoagulation is started.

For minor stroke, anticoagulation may be started as soon as bleeding has been excluded (similarly to TIA)

Long Term Care

Patients with stroke often require extensive support despite optimum treatment within target times. Neurological deficits often do not correlate with the size of the infarct, and can lead to ongoing issues with disability.

Patients continue to require support from other members of the MDT after discharge.

References

Stroke Unit Trialists’ Collaboration. Organised inpatient (stroke unit) care for stroke. Cochrane Database Syst Rev. 2013 Sep 11;2013(9):CD000197. doi: 10.1002/14651858.CD000197.pub3. Update in: Cochrane Database Syst Rev. 2020 Apr 23;4:CD000197. PMID: 24026639; PMCID: PMC6474318.

Shah, S., Saver, J., Kidwell, C., Albers, G., Rothwell, P., Ay, H., Koroshetz, W., Inatomi, Y., Uchino, M., Demchuk, A., Coutts, S., Purroy, F., Alvarez-Sabin, J., Sander, K., Sander, D., Restrepo, L., Wityk, R., Marx, J., Easton, J., & Grp, M. (2007). A multicenter pooled, patient-level data analysis of diffusion-weighted MRI in TIA patients. 38(2), 463–463.

Floyd C N, Ferro A. Indications for anticoagulant and antiplatelet combined therapy BMJ 2017; 359 :j3782 doi:10.1136/bmj.j3782

Gates P. (2011). Work out where the problem is in the brainstem using ‘the rule of 4’. Practical neurology, 11(3), 167–172. https://doi.org/10.1136/practneurol-2011-000014
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Dorfman K, Convexal subarachnoid haemorrhage in ischaemic stroke. Case study, Radiopaedia.org (Accessed on 19 Oct 2024) https://doi.org/10.53347/rID-85107

Gaillard F, Sharma R, Abed Al Aal A, et al. Stroke. Reference article, Radiopaedia.org (Accessed on 19 Oct 2024) https://doi.org/10.53347/rID-7975

Samaniego, E. A., Roa, J. A., Limaye, K., & Adams, H. P., Jr (2018). Mechanical Thrombectomy: Emerging Technologies and Techniques. Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association, 27(10), 2555–2571. https://doi.org/10.1016/j.jstrokecerebrovasdis.2018.05.025

Pobereskin L. H. (2001). Incidence and outcome of subarachnoid haemorrhage: a retrospective population based study. Journal of neurology, neurosurgery, and psychiatry, 70(3), 340–343. https://doi.org/10.1136/jnnp.70.3.340

Pierot, L., & Wakhloo, A. K. (2013). Endovascular treatment of intracranial aneurysms: current status. Stroke, 44(7), 2046–2054. https://doi.org/10.1161/STROKEAHA.113.000733

Goodney, P. R., Dzebisashvili, N., Goodman, D. C., & Bronner, K. K. (2015). Variation in the Care of Surgical Conditions: A Dartmouth Atlas of Health Care Series. The Dartmouth Institute for Health Policy and Clinical Practice.

Sehy, J. V., Holloway, W. E., Lin, S. P., Cross, D. T., 3rd, Derdeyn, C. P., & Moran, C. J. (2010). Improvement in angiographic cerebral vasospasm after intra-arterial verapamil administration. AJNR. American journal of neuroradiology, 31(10), 1923–1928. https://doi.org/10.3174/ajnr.A2215

Stroke Unit Trialists’ Collaboration (2013). Organised inpatient (stroke unit) care for stroke. The Cochrane database of systematic reviews, 2013(9), CD000197. https://doi.org/10.1002/14651858.CD000197.pub3