By Dr. Maddie Swannack

Next Lesson - Raised Intracranial Pressure

Neuroanatomy & Psychiatry


Contents

Abstract

  • A stroke is a life-threatening medical event that occurs when the blood supply to the brain is interrupted. It can be due to ischaemia (caused by a blockage in an artery), haemorrhage (caused by rupture of a blood vessel leading to bleeding within or around the brain), or another cause (rare).

  • A transient ischaemic attack (TIA) involves a temporary interruption to cerebral blood flow. Symptoms are similar to a stroke but resolve completely, usually within minutes to hours and by definition within 24 hours. Some definitions also require that brain imaging shows no acute infarction (tissue death). A TIA is an emergency: NICE advises specialist assessment within 24 hours.

  • Risk factors for ischaemic strokes can be split into modifiable (can be changed, including smoking, high cholesterol, obesity and atrial fibrillation, an irregular heart rhythm) and non-modifiable (including age and family history). Risk factors for haemorrhagic strokes overlap with those for ischaemic stroke, but the most important risk factor is hypertension.

  • Any patient with a suspected stroke needs brain imaging, usually a CT head scan, to show whether the stroke is haemorrhagic in nature. NICE advises scanning straight away in some patients, and otherwise as soon as possible. An ischaemic stroke may not be obvious on an early CT, but aspirin and clot-busting treatment (thrombolysis) are started only once a bleed has been ruled out.

  • The anterior and posterior circulations supply three major cerebral arterial territories: anterior cerebral (ACA), middle cerebral (MCA) and posterior cerebral (PCA). ACA supply is mainly medial frontal and parietal; MCA supply is mainly lateral frontal, parietal and temporal; PCA supply includes occipital and inferior temporal regions.

  • ACA blockage may result in: executive dysfunction (including apraxia, dysarthria, and personality changes), contralateral motor weakness predominantly affecting the leg, contralateral sensory loss predominantly affecting the leg, urinary incontinence and potentially corpus callosum involvement.

  • MCA blockage may result in: contralateral motor weakness in the face, arm and hand, contralateral sensory loss in the face, arm and hand, contralateral homonymous hemianopia (loss of the same half of the visual field in both eyes), aphasia (difficulty producing or understanding language, which may be Broca’s aphasia, Wernicke’s aphasia or global aphasia), and hemispatial neglect (ignoring one side of the world).

  • PCA infarction may cause contralateral homonymous hemianopia, sometimes with macular sparing (the central part of vision is preserved). Thalamic involvement can also cause contralateral sensory loss, whose extent varies with the structures affected.

  • Cerebellar infarctions may cause non-specific symptoms like nausea, headache and dizziness, which can be the only features of a posterior circulation stroke. They may also cause sudden onset vertigo (a spinning sensation) and ipsilateral cerebellar signs, remembered by the mnemonic DANISH: dysdiadochokinesia (cannot make rapid alternating movements), ataxia (poor co-ordination and balance), nystagmus (involuntary rhythmic eye movements), intention tremor (a tremor when reaching for something), slurred speech and hypotonia (reduced muscle tone).

  • Brainstem infarctions may cause contralateral loss of the nerve pathways that carry sensation up and movement down (ascending and descending tracts), and ipsilateral brainstem signs like cranial nerve palsies (paralysis of cranial nerves).

  • Basilar artery infarctions can cause a range of syndromes, including ‘top of the basilar syndrome’ (visual, eye movement and behavioural problems) and ‘locked-in syndrome’ (fully aware but almost entirely paralysed). Severe cases can be life-threatening.

  • The Bamford / Oxford classification groups strokes by their symptoms rather than imaging.

  • Total anterior circulation strokes (TACS) present with all three of the following: unilateral weakness (and/or sensory deficit) of at least two of the face, arm and leg, homonymous hemianopia, and higher cerebral dysfunction (also called higher cortical dysfunction, for example a language problem or neglect).

  • Partial anterior circulation strokes (PACS) present with two of the following three: unilateral weakness (and/or sensory deficit), homonymous hemianopia, and higher cerebral dysfunction. They can also present with higher cerebral dysfunction alone, or with a motor or sensory deficit that is more restricted than in a lacunar stroke.

  • Posterior circulation strokes (POCS) present with one of the following: cranial nerve palsy (paralysis of a cranial nerve) with contralateral motor or sensory deficit, bilateral motor or sensory deficit, conjugate eye movement disorder (cannot move both eyes together in the same direction), cerebellar dysfunction without weakness or sensory loss on the same side, or an isolated homonymous visual field defect.

  • Lacunar strokes (LACS, small strokes deep in the brain) present with one of the following: pure sensory deficit, pure motor deficit, mixed sensory and motor deficit, or ataxic hemiparesis (weakness with clumsiness on the same side of the body).

Core

Introduction

A stroke is a serious, life-threatening medical condition that occurs when the blood supply to a portion of the brain is cut off. It is also known as a cerebrovascular accident. 

 

When the blood supply is cut off, the supply of oxygen and glucose to the brain is cut off. This prevents the production of ATP in this portion of the brain, because respiration needs oxygen and glucose to occur. With limited amounts of ATP, the membrane potentials needed for neuronal transmission stop, and so no neuronal transmission occurs. 

 

Types of Stroke

Given that a stroke is a loss of the blood supply to one portion of the brain, there are two main types of stroke: 

 

Ischaemic Stroke 

Ischaemic strokes are the most common type of stroke, making up around 85% of strokes (source). The arterial supply to a portion of the brain is cut off by a clot in the vessel. The clot may form in the artery itself, often on a fatty plaque (atherosclerosis). It may also form elsewhere, such as in the heart or a larger artery, and travel to the brain. A clot that travels like this is called a thromboembolism. Small deep arteries can also be blocked, which causes lacunar strokes (small strokes deep in the brain, described below).



Haemorrhagic Stroke

Haemorrhagic strokes make up around 15% of strokes. They occur when a vessel in the skull breaks open and causes a bleed in the brain. The bleed can stop blood reaching the area supplied by the end of the artery. It can also raise the pressure within the skull, which compresses the artery and prevents blood flow.

 

Other Types of Stroke 

There are some causes of stroke that do not fit neatly into the ischaemic or haemorrhagic categories. This includes conditions such as carotid artery dissection, where blood flow to the brain is reduced without a typical intravascular clot or intracerebral haemorrhage. 



Transient Ischaemic Attack 

A transient ischaemic attack (or TIA) is often described as a mini-stroke, where stroke-like symptoms come on and then resolve, usually within minutes to hours. In UK clinical guidance, TIA symptoms last less than 24 hours. A newer tissue-based definition also requires that brain imaging shows no acute infarction (tissue death). A TIA is a serious warning sign because a full stroke can follow. NICE advises aspirin 300 mg straight away, unless there is a reason not to give it, and specialist assessment within 24 hours of the symptoms starting.



Risk Factors for Strokes 

Ischaemic Strokes 

There are a number of risk factors for ischaemic strokes, which are very similar to risk factors for other vascular pathologies such as angina (chest pain caused by reduced blood supply to the heart), heart attacks and peripheral vascular disease. (source) 

 

Like with any condition, the risk factors can be split into modifiable and non-modifiable factors. 

 

Modifiable risk factors (ones that can be changed) include: 

  • Smoking 
  • High Cholesterol
  • Diabetes
  • High blood pressure 
  • Obesity 
  • Excessive alcohol intake 
  • Unmanaged atrial fibrillation 

 

Non-modifiable risk factors include: 

  • Increased age 
  • Family History of stroke or TIA 
  • Ethnicity - South Asian, African or Caribbean ethnicities carry higher risk 
  • Personal History of stroke or TIA 
  • Other medical conditions that make the blood more prothrombotic (likely to clot), such as cancer.



Haemorrhagic Strokes

The main risk factor for haemorrhagic strokes is hypertension, a modifiable risk factor. 

The risk is also increased by use of anti-coagulant medication, which increases the risk of all bleeding. 



What to do if we suspect a stroke? 

An acute stroke requires quick action. Outside hospital, the FAST test (Face, Arms, Speech, Time to call 999) is used to spot a stroke or transient ischaemic attack, and an emergency ambulance should be called. In the emergency department, low blood glucose (hypoglycaemia) is excluded as the cause of the symptoms, and a tool such as ROSIER (Recognition of Stroke in the Emergency Room) is used to establish the diagnosis rapidly. The treatments for different types of stroke (ischaemic or haemorrhagic) are very different, and the success in restoring functions that have been lost is time-dependent. This means that in a patient with symptoms that may be consistent with an acute stroke, urgent assessment and rapid brain imaging are crucial.

 

The purpose of the CT head is to rule out a haemorrhagic stroke. NICE advises scanning straight away in some people (for example, if thrombolysis or thrombectomy may be needed, if they take anticoagulants or have a bleeding tendency, or if their level of consciousness is reduced). Everyone else should be scanned as soon as possible and within 24 hours of symptom onset. In the early stages of an ischaemic stroke, CT may appear normal, although subtle early ischaemic changes can sometimes be seen before established tissue death. If there are no signs of haemorrhage on head CT, the stroke is likely to be ischaemic in nature and treatment for that can be considered. This includes aspirin 300 mg, thrombolysis (a clot-busting drug) within 4.5 hours of symptom onset, and thrombectomy (mechanical removal of the clot) in selected people, up to 24 hours after onset in some of them. The choice depends on the time since onset, further imaging and any reasons not to give a treatment.

 

An MRI head would show any areas of ischaemia, making it more definitive in diagnosis of ischaemic stroke. However, MRIs take longer than CTs, and are often not as easily available, making CT scan the initial imaging mechanism of choice. 




Blood Supply to the Brain 

The brain receives blood from the internal carotid and vertebrobasilar (vertebral and basilar arteries) circulations, linked by the arterial ring called the Circle of Willis. The ACA, MCA and PCA are the major cerebral territorial arteries. The MCA arises from the internal carotid artery and is not part of the ring. The anterior and posterior circulations are connected by the posterior communicating arteries.

The Blood Supply to the Brain

Diagram - The Blood Supply to the Brain

SimpleMed original by Dr. Keertana Anne

 

For more information on the Arterial Supply of the Brain, please see our article on the arterial supply to the brain here. 



Territories of Cerebral Arteries 

The anterior cerebral artery (ACA), middle cerebral artery (MCA) and posterior cerebral artery (PCA) supply the three major cerebral cortical territories. They should not collectively be described as terminal branches of the Circle of Willis; the MCA arises from the internal carotid artery outside the ring.

 

Each of these arteries supplies a different portion of the brain. A blockage in the supply of one of them therefore causes symptoms that can be localised to a specific region. This means that the likely location of an infarction can be worked out from the symptoms.

Territories supplied by the major cerebral territorial arteries on the lateral surface of the brain

Diagram - Territories supplied by the major cerebral territorial arteries on the lateral surface of the brain

Licensed under Creative Commons, Source.

 

Territories supplied by the major cerebral territorial arteries on the medial surface of the brain

Diagram - Territories supplied by the major cerebral territorial arteries on the medial surface of the brain

Licensed under Creative Commons, Source.

 

 

Symptoms of a Stroke 

Anterior Cerebral Artery

The ACA supplies the medial and superior portions of the frontal lobe and the anterior parietal lobe, including: 

  • Pre-frontal cortex (executive functions - personality, decision making, planning, organisation), Supplementary motor area (changing between motor behaviours, role in speech production and micturition, which means passing urine) 
  • Paracentral lobule (the part of the primary motor and sensory cortex for the opposite lower limb, shown on the medial part of the homunculus, which is the map of the body across the cortex, and for continence). 
  • Corpus callosum (the band of fibres joining the two halves of the brain; its back part, the splenium, is also supplied by the posterior circulation)



Blockage to the ACA will result in the following symptoms: 

 

Executive Dysfunction 

Executive dysfunction is an umbrella term that describes cognitive, behavioural and emotional difficulties that occur as a symptom of another disorder, in this case a stroke. Examples of executive dysfunction in ACA infarctions are shown below: 

 

Apraxia

Apraxia is the inability to co-ordinate motor planning, meaning that simple motor tasks become very difficult. Patients cannot do tasks such as picking up a drink to take a sip, even though they know how to do it and could do it in the past.

Praxis (the ability to plan and carry out purposeful movements) depends on motor-planning networks, usually centred in the dominant hemisphere. ACA infarction involving medial frontal regions or the corpus callosum can impair purposeful movement. Callosal disconnection (the two halves of the brain can no longer communicate) may cause left-hand apraxia, including after a right ACA infarct. Apraxia is not restricted to dominant-hemisphere ACA lesions (areas of damage).

 

Dysarthria 

Slurred speech is also common in ACA infarcts.

 

Personality Changes 

Personality changes are also common in ACA infarctions due to damage to the frontal lobe. These changes are often noticed only in the long term, because in the acute phase the stress of the situation can mask a lot of personality changes. 



Unilateral, Contralateral Motor Weakness Mainly Affecting the Leg

The ACA supplies the medial portion of the brain, which includes the regions of the motor cortex that predominantly supply the contralateral leg and trunk (according to the motor homunculus). 

The weakness will be contralateral to the side of the ischaemia as the motor impulses decussate (cross the midline) on their path from brain to muscle. 

 

Unilateral, Contralateral Sensory Loss Mainly Affecting the Leg

The ACA supplies the medial portion of the brain, which includes the regions of the sensory cortex that predominantly supply the contralateral leg and trunk (according to the sensory homunculus). 

The sensory loss will be contralateral to the side of the ischaemia as the sensory impulses decussate (cross the midline) on their path from skin to brain.

 

Urinary Incontinence

The paracentral lobules are key for the control of micturition. They are made up of portions of the frontal and parietal lobes in the great longitudinal fissure (the gap between the two hemispheres of the brain). This midline portion of the brain is supplied by the ACA, so ischaemia in this region can lead to incontinence. 

 

Corpus Callosum Involvement 

The corpus callosum is mainly supplied by the ACA, although its back part (the splenium) also receives blood from the posterior circulation. An ACA infarction can therefore damage the corpus callosum. This can cause rare callosal disconnection syndromes, such as Alien Hand Syndrome (a hand that seems to act on its own). These result from the loss of the pathways through the corpus callosum, so the connections between the two hemispheres of the brain are significantly reduced or lost. Split Brain Syndrome is the name given to the effects seen in people who have had the corpus callosum cut surgically (callosotomy).



Middle Cerebral Artery

The MCA supplies part of the frontal lobe, and the lateral parts of the temporal and parietal lobes. 

 

The MCA is usually described in four segments, M1 to M4 (the horizontal, insular, opercular and cortical segments). Its branches include the lenticulostriate arteries (small branches to deep structures) and the superior and inferior divisions. They supply different portions of the MCA territory. A main trunk blockage of the MCA will take out all of them, while a small infarct may spare some regions. It is not important at this level to know which branches of the MCA supply which exact function. 

 

The MCA supplies: 

  • Basal ganglia (motor control)
  • Internal capsule (descending motor tracts)
  • Lateral parts of the primary motor and sensory cortex (face,  hand and arm)
  • Broca’s area in the dominant hemisphere - responsible for the production of speech
  • Wernicke’s area in the dominant hemisphere - responsible for the comprehension of speech
  • The optic radiations (the visual pathway from the thalamus to the occipital lobe)



The MCA supplies a large area of the brain. A main trunk blockage (occlusion) results in the loss of a massive portion of the brain and is therefore associated with a high mortality.

Main trunk MCA infarctions are also prone to haemorrhagic transformation. This is when an initially ischaemic injury, caused by a blocked main trunk of the MCA, develops a bleed as the tissue dies.



A blockage in the MCA may result in: 

 

Unilateral, Contralateral Motor Weakness in the Face / Hand / Arm 

The MCA supplies the lateral portion of the brain, which includes the regions of the motor cortex that supply the face, hand, and arm (according to the motor homunculus). 

The weakness will be contralateral to the side of the ischaemia as the motor impulses decussate (cross the midline) on their path from brain to muscle. 

 

However, in some MCA infarctions a full hemiparesis (weakness of one whole side of the body) may be seen, including the leg, which is supplied by the ACA, not the MCA. Whether this happens depends on where along the path of the MCA the infarction occurs. It is due to the loss of the internal capsule, which is the common path for all motor impulses leaving the primary motor cortex. 



Unilateral, Contralateral Sensory Loss in the Face / Hand / Arm

The MCA supplies the lateral portion of the brain, which includes the regions of the sensory cortex that supply the face, hand and arm (according to the sensory homunculus). 

The sensory loss will be contralateral to the side of the ischaemia as the sensory impulses decussate (cross the midline) on their path from skin to brain.

Contralateral Homonymous Hemianopia 

Loss of the blood supply to the optic radiations can result in a homonymous hemianopia. This is a loss of the same half of the visual field in both eyes. The side of the visual field lost will be contralateral to the side of the lesion.

The optic radiations have an upper part, which runs through the parietal lobe and carries the lower half of the visual field, and a lower part, which runs through the temporal lobe and carries the upper half. Damage to only one of these parts can therefore cause loss of a quarter of the visual field rather than a whole half.

For more information explaining the presentations and pathophysiology of visual lesions, see our article on the visual system here. 

 

Aphasia

MCA infarction can lead to three different types of aphasia depending on which areas are damaged. However, aphasia only occurs if the dominant hemisphere is damaged, as both speech and language centres are found in the dominant hemisphere. 

 

Broca’s Aphasia occurs when the Broca’s area of the dominant hemisphere of the brain is damaged. Broca’s area is located in the frontal lobe, and loss of function results in reduced speech fluency with preserved comprehension of the speech of others. Producing speech takes a lot of effort, and the speech consists of a few short words without sentence structure. Broca’s aphasia is also known as expressive aphasia. 

 

Wernicke’s Aphasia occurs when the Wernicke’s area of the dominant hemisphere of the brain is damaged. Wernicke’s area is located in the temporo-parietal region, and loss of function results in fluid sentences composed of muddled words. Wernicke’s aphasia is often described as ‘word salad’ because the patient uses many words in sentences that are unrelated to the question, and so can also be called fluent aphasia. 

 

Global Aphasia occurs when both Broca’s and Wernicke’s areas are damaged. This is a severe disorder that affects all language abilities. The patient has great difficulty understanding speech, speaking, naming objects, reading and writing.



Hemispatial Neglect 

Hemispatial neglect occurs with a non-dominant hemisphere infarction of the MCA. It is a condition in which the patient is not able to acknowledge one entire half of their world despite the fact that they are physically able to see it. It is a loss of attention and awareness to one side of their world, and usually occurs on the contralateral side to the infarction.

In the examples below, the patient can follow instructions but is only aware of one half of the task.

Examples of Left Sided Hemispatial Neglect

Diagram - Examples of Left Sided Hemispatial Neglect

Licensed under Creative Commons, Source.

 

Posterior Cerebral Artery

The PCA supplies the occipital visual cortex, inferior temporal regions, parts of the parietal lobe and parts of the thalamus. The optic radiations are not supplied exclusively by the PCA: their vascular supply also includes MCA branches and the anterior choroidal artery (a small branch of the internal carotid artery), with variation along their course.

 

A blockage in the PCA may result in: 

 

Contralateral Homonymous Hemianopia with Macula Sparing 

Infarction of the visual cortex in PCA territory can cause contralateral homonymous hemianopia: loss of the same half of the visual field in both eyes. The pattern depends on the site and extent of the infarct.

Macular sparing means that central vision is preserved because its cortical representation near the occipital pole escapes injury. Blood reaching the area by a back-up route (collateral perfusion) from MCA branches can contribute to this sparing after PCA occlusion. This is a cortical phenomenon, not a dual MCA/PCA blood supply to the retinal macula.

 

Contralateral Sensory Loss

The PCA supplies the thalamus, which is involved in the transmission of sensory impulses from the body to the cortex. A PCA infarction can therefore cause contralateral sensory loss, which is often partial rather than complete and depends on the specific thalamic nuclei affected. 



Cerebellar Infarctions

There are many different arteries that supply the cerebellum, so any cerebellar infarction may involve the superior cerebellar artery, anterior inferior cerebellar artery or posterior inferior cerebellar artery. 

 

An infarction in the cerebellum may result in:

 

Non-Specific Symptoms

Nausea, vomiting, headache and dizziness can all be signs of cerebellar infarction. They are non-specific and have many other causes, but a posterior circulation stroke (one affecting the cerebellum or brainstem) can present with these symptoms alone and is easily missed. In a patient with stroke risk factors they should therefore still prompt consideration of a stroke. Bedside eye-movement tests such as HINTS (Head Impulse, Nystagmus, Test of Skew) can help, and an early CT scan can look normal.

 

Sudden Onset Vertigo

Any patient with risk factors for a stroke who has sudden onset vertigo (a spinning sensation) that does not change with position should be considered for a stroke. Other conditions can cause sudden, long-lasting vertigo too. Vestibular neuritis (inflammation of the nerve that carries balance signals from the inner ear to the brain) and labyrinthitis (inflammation of the inner ear) both cause symptoms that can start suddenly and ease over a few days. The key is a good history and examination to tell a stroke from other causes of vertigo, such as Meniere’s Disease or these inner-ear conditions.

 

Ipsilateral Cerebellar Signs - DANISH

There are six symptoms that together represent the ‘cerebellar signs’ and suggest pathology in the cerebellum. Together they spell the mnemonic DANISH. 

 

Dysdiadochokinesia - the inability to perform rapidly alternating movements. One test is rapid pronation and supination (turning the palm down and up) of one hand onto the other hand. Another is sliding the heel of one foot up and down the front of the other shin (called the heel-shin test).

 

Ataxia - a symptom characterised by a reduction in co-ordination and balance. It often results in a wide-based stance of walking, and can be confused with intoxication as the patient is unsteady and may stumble often on walking. 

 

Nystagmus - an involuntary movement of one or both eyes with a rhythmic and repetitive pattern. The rhythmic movement has two phases. The slow phase is the pathological deviation of the eye from where it is supposed to be. The quick phase is the snap back to where it should be to maintain vision. The eye or eyes can deviate in any direction (vertical, horizontal, rotational). Not all nystagmus is abnormal. For example, healthy people can show end-point nystagmus when the eyes are held as far to the side as they will go. Nystagmus that is not a normal variation should be assessed for an underlying cause, such as a cerebellar stroke.  

 

Intention Tremor - a tremor that is only present when trying to perform a task, and not at rest. It is examined most often with the ‘finger-nose’ test. The patient is asked to move their finger from their own nose to the examiner’s finger, which is held in front of them. The tremor will be most prominent when the patient is concentrating to tap either their nose or the finger. 

 

Slurred Speech - slurring of the speech is a sign of a cerebellar pathology. If a patient has slurred speech, check for other cerebellar signs or signs of cerebral ischaemia. Slurred speech can also be caused by facial muscle paralysis, as seen in an MCA blockage.

 

Hypotonia - reduced muscle tone in the limbs (less resistance when a relaxed limb is moved passively) is a sign of cerebellar pathology. It is not present in every cerebellar disorder. 




Brainstem Infarctions 

Contralateral Ascending and Descending Tract Loss

All sensory and motor tracts travel through the brainstem on their way between brain and spinal cord. This means that a brainstem stroke will involve the loss of the sensory and motor impulses. These signs are often contralateral because many major sensory and motor pathways cross the midline at some point between the spinal cord and brainstem. 

 

Ipsilateral Brainstem Signs

Brainstem signs are very complex, and you do not need to learn them in detail at this point. The brainstem shares a blood supply with the cerebellum, so some cerebellar strokes can cause brainstem signs. 

The easiest signs to explain are the paralysis of cranial nerves. Cranial nerves have nuclei (clusters of nerve cells) in the brainstem, so losing the blood supply to a nucleus paralyses its nerve. This will usually occur on the same side, as most cranial nerves and nuclei do not cross the midline. The trochlear nerve is an exception: its fibres cross in the midbrain (the top part of the brainstem), so it supplies the superior oblique eye muscle on the opposite side.



Basilar Artery Infarctions 

Basilar artery occlusion can cause a range of posterior-circulation syndromes, including life-threatening brainstem injury. The presentation depends on the branches involved and the extent of infarction; top-of-the-basilar syndrome and locked-in syndrome are two well-known patterns, but other patterns occur.

 

Distal basilar occlusion can cause top-of-the-basilar syndrome, involving the rostral (upper) brainstem and posterior cerebral territories. Possible features include:

  • Visual and oculomotor (eye movement) defects
  • Altered behaviour or alertness, including dreamlike behaviour
  • Hallucinations 

 

Injury to the ventral pons (the front surface of the pons, part of the brainstem), including from basilar artery disease, can cause classic locked-in syndrome. Its features include:

  • Severe paralysis of the limbs and loss of speech, with some eye movements or blinking preserved
  • Preservation of consciousness 
  • Preservation of vertical eye movements due to sparing of rostral midbrain structures above the level of the lesion

In classic locked-in syndrome, awareness is preserved despite severe impairment of motor output. Vertical eye movements or blinking may allow purposeful communication; the available movements depend on lesion extent.



Bamford / Oxford Classification 

The most commonly used classification system for ischaemic strokes is the Bamford or Oxford classification. It categorises ischaemic strokes based on their initial presenting symptoms, without the need for imaging.

 

Total Anterior Circulation Stroke (TACS)

A TACS is a large stroke affecting a large proportion of the cortex supplied by the anterior circulation.  

 

It needs all three of the following symptoms:

  1. Unilateral weakness (and / or sensory deficit) of at least two of the face, arm and leg
  2. Homonymous hemianopia (loss of the same half of the visual field in both eyes)
  3. Higher cerebral dysfunction (such as dysphasia, a language problem, or neglect)



Partial Anterior Circulation Stroke (PACS)

A PACS is a less severe form of a TACS where only a portion of the area supplied by the anterior circulation is affected. 

 

It requires either two of the following symptoms, isolated higher cerebral dysfunction, or a motor or sensory deficit that is more restricted than in a lacunar stroke:

  1. Unilateral weakness (and / or sensory deficit) of at least two of the face, arm and leg
  2. Homonymous hemianopia (loss of the same half of the visual field in both eyes)
  3. Higher cerebral dysfunction (such as dysphasia, a language problem, or neglect)



Posterior Circulation Stroke (POCS)

A POCS is a stroke involving a portion of the posterior circulation. It includes areas of the cortex supplied by the posterior cerebral arteries and infarctions of the brainstem and cerebellum. 

 

It needs only one of the following features:

  1. Cranial nerve palsy and contralateral motor or sensory deficit 
  2. Bilateral motor or sensory deficit 
  3. Conjugate eye movement disorder (inability to move both eyes together in the vertical or horizontal plane). 
  4. Cerebellar dysfunction without ipsilateral long-tract deficit (weakness or sensory loss on the same side)
  5. Isolated homonymous visual field defect (for example, a homonymous hemianopia)

 

Lacunar Stroke (LACS)

A LACS is a subcortical stroke (deep, below the cortex), a blockage in one of the small branches known as the perforating arteries. 

 

It needs only one of the following:

  1. Pure sensory deficit 
  2. Pure motor deficit 
  3. Mixed sensory and motor deficit 
  4. Ataxic hemiparesis (weakness and ataxia present on the same side of the body).

 

 

Edited by: Dr. Marcus Judge

Reviewed by: Adrian Judge

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