Anatomy clinical correlates: Posterior blood supply to the brain

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Introduction0:00–1:25

Blood supply to the brain can be divided into an anterior and a posterior circulation. The posterior circulation supplies the cerebellum brainstem occipital lobes and inferomedial temporal lobes and comes from the vertebral arteries.
The vertebral arteries combine to form the basilar artery which eventually divides into the posterior cerebral arteries.
The posterior circulation then connects to the anterior circulation through the posterior communicating arteries. Remember that the anterior circulation comes from the internal carotid artery which divides into the anterior and middle cerebral arteries together the connection between the posterior and the anterior circulation form the circle of Willis, which is an anastomotic network of arteries at the base of the brain that ensure adequate blood flow even in cases where part of this circulation becomes occluded.
However, there are still instances where obstruction of these arteries and their branches can disrupt blood flow to the brain.
So, understanding their anatomy and what parts of the brain they nourish can help us better understand the clinical manifestations and management when blood flow to the brain is obstructed, that causes a stroke which can either be ischemic or hemorrhagic ischemic strokes can be caused by thrombi emboli and hypoperfusion injuries with the latter most commonly affecting the watershed areas of the brain hemorrhagic strokes.

STROKE1:25–2:10

On the other hand, occur when there is a bleed within the brain tissue, called an intracerebral or intraparenchymal hemorrhage or a bleed in the subarachnoid space called a subarachnoid hemorrhage.
The posterior circulation of the brain is susceptible to all of these and the clinical signs and symptoms depend on which artery is occluded.
Let's look at the vertebral arteries first, starting with the subclavian steal phenomenon. This is when the vertebral artery on the same side as an occluded or blocked subclavian artery steals blood from the contralateral subclavian artery circulation.

Subclavian steal phenomenon2:10–3:46

This happens when the occlusion is proximal to the vertebral artery. So blood from the contralateral vertebral artery flows to the basilar artery and then continues as retrograde flow through the ipsilateral vertebral artery to the blockage.
This allows blood flow to the area supplied by the occluded subclavian vessel and is often asymptomatic. The most common cause of subclavian stenosis is an atherosclerotic plaque, but other less common causes include takayasu arteritis and complications from cardiovascular surgery like an aortic coarctation repair surgery.
When subclavian steal phenomenon becomes symptomatic, it is considered Subclavian steal syndrome. Clinical features usually occur during an exercise when blood flow to the occluded, arm is not enough to meet demand, causing muscle weakness and claudication, meaning pain or cramping of the muscles.
Individuals can also have neurological symptoms such as lightheadedness, dizziness, and vertigo. Next up.

Medullary syndrome (ASA)3:46–5:45

Let's look at the anterior spinal artery which arises from the vertebral arteries. The anterior spinal artery, together with the vertebral arteries give paramedian branches for the anteromedial parts of the medulla.
This region of the medulla includes many important structures such as the lateral corticospinal tract within the pyramids, medial lemnisci and the hypoglossal nucleus and fibers coming from it.
So when the paramedian branches of the anterior spinal arteries don't provide adequate blood flow. The structures within the anteromedial parts of the medulla are damaged, leading to medial medullary syndrome.
Clinically damage to the lateral corticospinal tracts at this level causes contralateral hemiparesis of the upper and lower extremities.
Damage to the medial lemniscus pathway at this level leads to contralateral hemisensory loss of proprioception, fine touch and vibratory sensations from the trunk and extremities.
And finally damage to the hypoglossal nucleus or nerve fibers leads to ipsilateral flaccid paralysis of the tongue that can be seen as deviation to the paralyzed side when protruded a good way to remember.
The symptoms of medial medullary syndrome is to think of three midline structures. The M in midline stands for medial and all three structures start with an M one motor pathway, cortical spinal tract, two medial lemniscus and three motor fibers of hypoglossal nerve.
Ok. Now, let's look at the posterior inferior cerebellar artery or pika for short, which is a branch of the vertebral artery that supplies the lateral part of the medulla and regions of the cerebellum this region of the medulla.

Lateral medullary syndrome (PICA)5:45–9:07

It supplies contains many important structures such as the vestibular nuclei, spinal trigeminal nucleus, spinothalamic tract, nucleus, ambiguus, the inferior cerebellar peduncle and sympathetic fibers.
Now, infarction to the PCA can lead to lateral medullary syndrome, also known as Pica or Wallenberg Syndrome. Clinically damage to the vestibular nuclei leads to nystagmus, vertigo, nausea and vomiting damage to the spinal trigeminal nucleus leads to loss of pain and temperature sensation from the ipsilateral side of the face where damage to the spinothalamic tract that is already crossed over at the spinal cord leads to loss of pain and temperature sensation from the contralateral side of the trunk and extremities.
Damage to the nucleus ambiguus which houses the motor nuclei for the cranial nerves. 9, 10 and 11 leads to dysphasia, dysphonia or hoarseness, dysarthria and loss of gag reflex damage to the nucleus ambiguus is actually specific to PCA syndrome, distinguishing this condition from similar ones.
Next up. Damage to the inferior cerebellar peduncle leads to ipsilateral ataxia or lack of muscle control and coordination when performing voluntary movements, dysmetria or inappropriate voluntary action execution such as overreaching for a glass of water and dysdiadochokinesia or an inability to perform rapid alternating muscle movements.
Finally, damage to descending sympathetic fibers can result in Horner syndrome, which includes ptosis and hidrosis and meiosis.
In order to remember the structures damaged in this syndrome, we can remember that the lateral side of the medulla has six SS one, the vestibular nuclei, two, the spinal trigeminal nucleus, three, the spinothalamic tract, four, speech and swallowing representing the nucleus ambiguus, five inferior cerebellar peduncle.
Ok. We know that starts with ac but it sounds like an S and six sympathetics.
Another pneumonic that you can use to recall the most common clinical features of the lateral medullary syndrome is don't pick up, pick a horse hoarseness that can't eat dysphasia.

Lateral pontine syndrome (AICA)9:07–11:44

Ok. Now, after the vertebral arteries combine to form the basilar artery, there is a branch called the anterior inferior cerebellar artery or ICA.
For short, which supplies the lower lateral part of the pons and the inferior and middle cerebellar peduncles. Infarction of the ICA can lead to something called lateral pontine syndrome, also known as the ICA syndrome.
Now, in this region, there are structures like the facial motor nucleus, the vestibular nuclei, the spinothalamic tract, spinal trigeminal nucleus, sympathetic fibers, the middle and inferior cerebellar peduncles and the labyrinthine artery damage to the facial motor nucleus results in ipsilateral facial paralysis due to lower motor neuron damage along with decreased tear and saliva production, loss of taste from the anterior two thirds of the tongue and loss of corneal and stapedial reflexes.
Vestibular nuclei lesions result in nystagmus, vertigo and vomiting, spinothalamic tract. And spinal trigeminal nucleus damage lead to loss of temperature and pain sensations in the ipsilateral side of the face and contralateral side of the trunk and extremities, damage to the inferior and middle cerebellar peduncles result in ipsilateral ataxia, dysmetria, endesa cosa finally, damage to the sympathetic fibers can cause ipsilateral Horner syndrome.
Bear in mind that the ICA typically gives rise to the labyrinthine artery that supplies the inner ear. So, infarction of the ICA also causes ipsilateral sensorineural deafness accompanied with tinotus and vertigo.
Now, when trying to differentiate between all of these syndromes, in particular from lateral medullary syndrome, which shares similar features.
Facial paralysis is specific to ICA territory infarcts. Let's take a short break and see if you can remember the difference between Pica and ICA infarction.

Quiz11:44–11:57

Locked-in syndrome (basilar artery)11:57–14:08

Great. Now let's move on to the basilar artery which supplies the lower midbrain, the anterior medial part of the pons and the anterior parts of the medulla infarction of the basilar artery causes locked in syndrome, which is a scary condition where the individual may have full consciousness but is paralyzed.
More specifically, there is bilateral damage to the descending corticospinal tracts leading to quadriplegia. There is also bilateral damage to the descending cortical bulbar tracts leading to paralysis of the facial mouth and tongue muscles.
There is damage to the paramedian pontine reticular formation, also known as the lateral gaze center, resulting in loss of horizontal gaze.
In addition to damage of the nuclei to cranial nerve four and six, leading to deficits in ocular movement. Now, with locked in syndrome, the reticular activating system or ras for short, which spans across the brainstem can be spared making the individual conscious and aware of their surroundings.
However, they are unable to move and interact with the outside world due to damage of the previously mentioned structures.
The only way of communication is through blinking and vertical eye movements as the oculomotor nucleus in the midbrain is spared.
And the vertical gaze center is located more superiorly in the midbrain respiratory muscles are also paralyzed. So individuals need to be ventilated to easily recall that the locked in syndrome is caused by the basilar artery infarction.
Just remember the pneumonic locked in the basement. OK.

PCA infarct14:08–16:45

And last but not least, there's the posterior cerebral artery or PCA for short, which is the terminal branch of the basilar artery and supplies areas such as the occipital lobe, inferomedial temporal lobe splenium of the corpus callosum thalamus, as well as the hippocampal formation and amygdala located within the temporal lobe during a PCA infarct.
One commonly affected area is the primary visual cortex found in the occipital lobe. And lesions here cause contralateral hemianopia where individuals lose vision in the contralateral halves of the visual fields of both eyes.
However, the central part of the visual field is usually preserved a phenomenon known as macular sparing. This is thanks to the collateral branches of the middle cerebral artery, supplying the part of the visual cortex that receives input from the macula of the eye.
Bilateral damage to the occipital lobes results in cortical blindness. However, the pupils are still reactive to light since the light reflex does not involve the visual cortex.
Furthermore, a PCA territory infarct can also affect the splenium of the corpus callosum which connects the occipital lobes.
And also allows visual input to reach the parietal language centers of the dominant hemisphere. Damage to the dominant hemisphere can result in dyslexia as well as alexia without agraphia.
Meaning that they lose the ability to read but can still write. Non-dominant hemisphere.
Lesions include visual agnosia which is the inability to recognize objects and prosopagnosia, which is the inability to recognize faces.
If the thalamus is affected during a PCA territory, infarct, the individual may experience numbness and paresthesia of the contralateral face, trunk and limbs.
Finally, lesions of the dominant or bilateral temporal lobes, hippocampal formations and amygdalas lead to the development of amnesia where individuals can't form new long term memories.

Quiz16:45–16:56

Ok. Final quiz.
Can you name all the arteries of the posterior circulation? All right.
As a quick recap, the brain is supplied by the posterior and anterior circulation where the posterior circulation comes from the vertebral arteries, which combine to form the basilar artery and eventually branch as the posterior cerebral arteries, all which are susceptible to stroke or infarct, stenosis of the subclavian artery can cause subclavian steal phenomenon where we get retrograde flow through the vertebral artery on the affected side.

Review16:56–20:05

In order to maintain perfusion of the affected subclavian anterior spinal artery infarction leads to medial medullary syndrome, damaging the lateral corticospinal tract, the medial lemnisci and the hypoglossal nucleus or fibers coming from it.
Infarction of the posterior inferior cerebellar artery or PCA leads to lateral medullary syndrome or Wallenberg syndrome causing damage to the vestibular nuclei, spinal trigeminal nucleus, spinothalamic tract, nucleus, ambiguus, the inferior cerebellar peduncle and sympathetics damage to the nucleus ambiguus is specific for this syndrome.
And symptoms include dysphagia, hoarseness, dysarthria, and loss of gag reflex infarction of the anterior inferior cerebellar artery or ICA causes lateral pontine syndrome, which is when there's damage to the facial motor nucleus, which is specific to this syndrome.
The vestibular nuclei, the spinothalamic tract, spinal trigeminal nucleus, sympathetic fibers, the middle and inferior cerebellar peduncles and the labyrinthine artery infarction of the basilar artery leads to locked in syndrome that includes quadriplegia, paralysis of the facial mouth and tongue muscles and loss of horizontal gaze.
But the individual may still retain consciousness and can only communicate through blinking and limited eye movements. The PC supplies the occipital lobe, medial temporal lobe, splenium of the corpus callosum and hippocampal formation.
A PCA stroke can lead to the contralateral hemianopia with macular sparing PCA territory. Infarct can also lead to dyslexia, alexia without agraphia, visual agnosia, prosopagnosia and numbness of the contralateral face, trunk and limbs.