Anatomy clinical correlates: Anterior blood supply to the brain

Your brain is awake and working hard all day, every day, even when you’re sleeping! So it makes sense that it needs a lot of oxygen and energy, which is why it is well supplied from several major arteries. The circulation of the brain can ultimately be divided into the anterior and posterior circulation, and understanding their anatomy can help us understand the clinical consequences and management of various issues that can arise! So let’s delve into the anterior circulation of the brain!

Remember that the anterior circulation supplies the anterior portion of the brain, and comes from the internal carotid arteries which divide into the anterior and middle cerebral arteries. The anterior circulation then connects to the posterior circulation through the posterior communicating arteries. The posterior circulation comes from the vertebral arteries, which combine to form the basilar artery. Together, the connection between the anterior and posterior circulation form the circle of willis, which is an anastomotic network of arteries at the base of the brain which ensure adequate blood flow to the brain, even in cases where part of this circulation becomes occluded! However, there are still instances where obstruction of these arteries and their branches disrupts blood flow to the brain, causing a stroke, which can lead to irreversible neuronal damage.

Now, a stroke can be classified as either ischemic or hemorrhagic. Ischemic strokes are much more common, and they happen because of an acute blockage of one of the blood vessels supplying the brain. Ischemic strokes can be thrombotic, embolic or hypoxic. A thrombotic stroke occurs when there’s a blood clot in the artery, formed directly at the site of infarction, which typically occurs because of a ruptured atherosclerotic plaque. An embolic stroke, on the other hand, is where an embolus from another part of the body travels to the site of infarction to cause obstruction. For example, with atrial fibrillation, a blood clot can form in the heart, where it then travels through the circulation to eventually obstruct brain vessels.

Then there are hypoxic strokes, where there is not a direct blockage of a vessel but systemic hypoperfusion or hypoxemia of the brain. This can cause inadequate oxygenation of the brain, especially in watershed areas which are supplied by the terminal branches of two large vessels, and are therefore more prone to hypoperfusion injuries.

Hemorrhagic strokes, on the other hand, occur when there is a bleed within the brain tissue called an intracerebral or intraparenchymal bleed, or a bleed in the subarachnoid space called a subarachnoid hemorrhage. This happens most often as a result of chronic untreated hypertension, and associated hypertensive vasculopathy. Other causes include amyloid angiopathy, a ruptured vascular aneurysm and vascular malformations.

Now, we can typically identify which artery of the anterior circulation is affected during a stroke based on clinical symptoms. Let’s start with the middle cerebral artery, or MCA for short, which supplies most of the lateral cerebral cortex of the frontal, parietal and temporal lobes, the insular cortex, as well a large portion of the basal ganglia and internal capsule. Depending on what portion of the MCA is occluded, clinical presentation can vary.

Now, the MCA supplies a large portion of the primary motor and sensory cortex, which can be found along the precentral and postcentral gyrus, respectively. Looking at the motor homunculus, we can see that the MCA supplies the area for the face, trunk and upper extremity. Therefore, lesions of the motor cortex cause weakness or paralysis of the contralateral side of the face and arm and eventual upper motor neuron signs such as hyperreflexia. Looking at the sensory homunculus we can see that the MCA also supplies the face and upper extremity area. Because of this, lesions of the sensory cortex produce loss of sensations in the contralateral side of the face and arm.

The MCA also supplies the posterior part of the inferior frontal gyrus. This area is in the dominant cerebral hemisphere, which is the left hemisphere for right handed people and right hemisphere for left handed people, and is where Broca’s area is located. Lesions of this area cause Broca’s aphasia, where individuals have difficulties planning and executing movements necessary for the production of speech, while their comprehension of speech is not affected. Furthermore, the MCA also supplies the posterior part of the superior temporal gyrus. In the dominant hemisphere this is where Wernicke’s area is located. When injured, it causes Wernicke’s aphasia, where individuals are fluent and may even speak faster than usual, but their comprehension and repetition of spoken and written language is impaired and their speech appears meaningless. So, in a right handed individual presenting with Broca’s or Wernicke’s aphasia, we would suspect a lesion to the left MCA!

An MCA artery stroke can also affect other regions of the brain, such as the frontal lobe which contains the frontal eye field in the middle frontal gyrus. This is the center for voluntary control of eye movements and conjugate gaze to the contralateral side. So when injured, it causes both eyes to deviate towards the ipsilateral side, as if they are looking at the lesion.

The frontal lobe also contains the prefrontal cortex, and its injuries lead to frontal lobe syndrome, where individuals experience personality changes such as problems with planning, initiative, and judgement, while the individual also exhibits socially unacceptable behaviour.

Next, lesions of the angular gyrus of the parietal lobe on the dominant cerebral hemisphere lead to Gerstmann syndrome, which presents with 4 key features: left-right disorientation; finger agnosia, acalculia, and agraphia. Involvement of the parietal cortex on the non-dominant cerebral hemisphere, on the other hand, would cause hemispatial neglect syndrome. This means that individuals have agnosia, or inability to process sensory information, of the contralateral side of the body and the space around it.

Finally, the MCA supplies the subcortical area of the temporoparietal lobe which contains the optic radiation, where depending on which hemisphere is affected a lesion here would result in contralateral homonymous quadrantanopia.

Let’s take a short break and see if you remember the most common clinical syndromes associated with a middle cerebral artery stroke.

Okay, now let’s switch gears and discuss the anterior cerebral artery, or ACA for short, which supplies the medial aspect of the frontal and parietal lobes as well as anterior portions of the basal ganglia and internal capsule.

The ACA supplies specific portions of the primary motor and somatosensory cortex, in particular the anterior and posterior paracentral lobule. When we look at the motor and sensory homunculi, we can see that the ACA mainly supplies the areas for the lower extremities and genitalia.

Therefore, occlusion of the ACA leads to paresis or motor loss of the contralateral leg with eventual upper motor neuron signs such as lower limb hyperreflexia and positive Babinski sign, while lesions of the sensory cortex lead to sensory loss of the contralateral leg. To make matters worse, the left and right ACA can sometimes get occluded at the same time, causing bilateral damage to both hemispheres. Motor control to the urinary sphincters is also located in the anterior paracentral lobule, so bilateral lesions can result in urinary incontinence.

Now, as we recall, the brain is contained within the rigid boney cranium, which provides great protection, but doesn’t allow the intracranial space to expand. Because of this, any mass-occupying lesion, such as a hemorrhagic stroke or a tumor, increases the intracranial pressure and pushes the brain tissue of the frontal, parietal, or temporal lobe away from the lesion.

In a setting like this, the cingulate gyrus of the affected cerebral hemisphere is forced under the falx cerebri which separates the hemispheres, leading to a subfalcine or cingulate herniation. As herniation progresses, the cingulate gyrus pulls the ipsilateral anterior cerebral artery together with it under the falx, where it can be compressed or occluded. This leads to infarction in the regions of the cerebral cortex supplied by the ACA, and its characteristic clinical features, which are hemiplegia and hemisensory loss of the contralateral leg. Subfalcine herniation can also obstruct the foramen of Monro which allows passage of cerebrospinal fluid from the lateral ventricles to the third ventricle, causing obstructive hydrocephalus, or a buildup of cerebrospinal fluid in the brain.