A 77-year-old woman is brought to the emergency department for evaluation of left-sided numbness and unsteady gait. The patient was having dinner with family one hour ago when she suddenly developed numbness in the left side of her body and could no longer sense the temperature of her food. Past medical history includes diabetes mellitus type II, hypertension, and hyperlipidemia. The patient takes metformin, glipizide, amlodipine, losartan, and atorvastatin. Temperature is 37.0°C (98.6°F), pulse is 102/min, respirations are 15/min, and blood pressure is 190/100 mmHg. Neurological examination demonstrates deficits in touch, two-point discrimination, pain, and temperature on the left side of the body and face. Motor strength and speech are normal. Romberg sign is positive. An ischemic stroke involving which of the following areas of the brain is the most likely cause of her clinical findings?

The cerebral hemispheres are two symmetrical halves of the brain that contain billions of neurons and their connections, forming an amazing network of cells which help govern our everyday actions.

These cerebral hemispheres consist of the cerebral cortex, subcortical white matter, and gray matter masses called the basal ganglia found throughout the subcortical white matter.

Due to the complexity of our brains, the clinical conditions affecting our cerebral hemispheres lead to a variety of abnormal and strange symptoms, so understanding the anatomy of the cerebral hemisphere is crucial in understanding these conditions.

Let’s start with lesions of the cerebral cortex, which is the superficial gray matter of our brains containing billions of neurons responsible for processing information.

Depending on which part of the cortex these lesions occur in, it can cause different clinical manifestations. First, there are lesions of the prefrontal cortex, which is an area responsible for the makeup of a person’s personality and governs social behaviour.

Prefrontal cortex lesions1:04–2:30

So, prefrontal cortex lesions cause frontal lobe syndrome which generally result in personality changes, and can specifically cause problems with planning, initiative, judgment, and social behaviour.

Individuals have difficulty making decisions, and may become impulsive and aggressive. Individuals can also exhibit socially unacceptable behavior, where they no longer restrain from saying or doing inappropriate things, and may also no longer care about their clothing and appearance.Injury to the prefrontal cortex may also contribute to the reemergence of primitive reflexes, such as the grasp reflex, suckling reflex, and groping reflex.

Bilateral damage of the prefrontal cortex may lead to incontinence, gait apraxia, and can even lead to akinetic mutism, where awake individuals lack the will or motivation to move or speak, but will follow you with their eyes in response to noise.

Next up, there are injuries to the frontal eye fields which can be found on the middle frontal gyrus - specifically, in Brodmann's area 8.

Frontal eye field injuries2:30–3:54

Possible causes of lesions to the frontal eye fields include stroke involving the middle cerebral artery, brain tumors, or injury during neurosurgery.This area allows voluntary control of eye movements and conjugate gaze to the contralateral side.

As fibres crossover to the contralateral lateral gaze center which is located in the paramedian pontine reticular formation in order to govern contralateral gaze.Damage to the frontal eye field of one of the cerebral hemispheres will cause both eyes to deviate towards the same side as the lesion, and the inability to voluntarily move the eyes toward the contralateral side.

This is in contrast to a lesion of the paramedian pontine reticular formation, which will cause the eyes to deviate to the contralateral side of the lesion, away from the injury.

So, for example, when eyes are deviated to the right, the lesion can either involve the left paramedian pontine reticular formation or the right frontal eye field.Let’s take a short break and see if you can remember clinical features associated with the prefrontal cortex lesions?

Quiz3:54–4:13

What about the frontal eye field lesion?Continuing with lesions of the cerebral cortex, let’s cover those that can lead to aphasia, which is the inability to understand and produce speech.

Aphasia4:13–8:30

These lesions usually affect the dominant hemisphere, which is the left hemisphere for right handed individuals and the right hemisphere for the left handed individuals.

First let's look at lesions to Broca’s area, or Brodmann’s area 44/45, which is the motor area responsible for controlling the muscles that allow us to produce words and speak.

Located at the inferior frontal gyrus, a lesion to this area results in Broca’s aphasia, also known as motor, non fluent, or expressive aphasia.

In Broca’s aphasia, individuals have difficulties planning and executing movements necessary for the production of speech.

Therefore, they would talk slowly with poor fluency, and there will be increased effort and pauses between words. The individual's comprehension of speech is intact, since Wernicke’s area is preserved, but repetition is usually impaired.

Individuals can have difficulty naming objects and are usually aware of their problem, which can be very frustrating for them.

You can use Broca to remind yourself of the Broken Boca, where Boca means “mouth” in Spanish. When Broca’s area is damaged, the nearby primary motor cortex may also be affected, so patients may also have accompanying symptoms of weakness or paralysis to the contralateral face and upper limb.

Then we can have a lesion to Wernicke’s area, or Brodmann’s area 22/39/40, which is responsible for processing and understanding both written and spoken language, allowing us to understand a sentence and say it back comprehensively.

Wernicke’s area is located in the superior temporal gyrus, so a lesion here results in Wernicke’s aphasia, also known as sensory or receptive aphasia.

In Wernicke’s aphasia, individuals are fluent, well articulated, and may even speak faster than usual, but their comprehension and repetition of spoken and written language is impaired.

Because of this, they don't find the right words to use and their speech appears meaningless, which has been described as “word salad”.

Quick tip, you can use Wernicke to remember Word salad. Unlike Broca’s aphasia, individuals with Wernicke’s aphasia are unaware of their deficits, so they will speak as if nothing is wrong.

On a quick note, the optic radiation is in close proximity to Wernicke’s area, so individuals can also have accompanying symptoms of contralateral superior quadrant visual field defects.

Both Broca’s and Wernicke’s areas are connected by a bundle of white matter tracts called the arcuate fasciculus, which is located beneath the supramarginal gyrus and the frontoparietal operculum.

Lesions of the arCuate fasciculus cause Conduction aphasia. In conduction aphasia, individuals have preserved fluency and comprehension of speech, but the repetition of spoken language is severely impaired.

They can also have difficulty naming objects and they are aware of their deficits. And finally, when lesions are so extensive that they affect both Broca’s and Wernicke’s areas, that causes global aphasia.

With global aphasia, there’s a loss of speech production, and loss of understanding of both written and spoken words. Individuals are not able to formulate, comprehend, or repeat both spoken and written language.Let’s take another break and see if you can remember the common symptoms of Broca’s aphasia?

Quiz8:30–8:48

What about Wernicke’s aphasia?Okay, now let’s switch gears and look at lesions of the medial aspect of the precentral gyrus, also known as the anterior paracentral lobule.

Paracentral lobule lesions8:48–9:51

This area is responsible for motor control of the lower limbs. Damage to the paracentral lobule causes contralateral lower limb weakness and upper motor neuron lesion signs, such as hyperreflexia and positive Babinski sign.

Because the falx cerebri extends between the hemispheres to the corpus callosum, a common and usually benign type of tumor called a parasagittal meningioma can compress and affect the paracentral lobules of 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, let’s switch gears and cover Gerstmann syndrome, which is caused by a lesion of the angular gyrus, located in the inferior parietal lobe of the dominant hemisphere.

Gerstmann syndrome9:51–11:08

The angular gyrus is an area that integrates visual, acoustic and somatosensory information in order to understand and solve problems, particularly in regards to speech and number processing.

The angular gyrus is supplied by the angular and posterior parietal arteries, which are branches of the middle cerebral artery, and occlusion of these arteries can result in Gerstmann Syndrome.

Gerstmann syndrome typically has 4 key features, which are left-right disorientation which is confusion differentiating the left and right side of the body; finger agnosia which is the inability to recognize individual fingers on your hand; acalculia which is the inability to perform mathematical calculations, and agraphia which is the inability to write.

Furthermore, some lesions may also result in aphasia, as well as alexia which is the inability to read. Now a similar lesion in the inferior parietal lobe of the non dominant hemisphere typically results in hemispatial neglect syndrome.

Hemispatial neglect syndrome11:08–12:19

This area also receives its blood supply from angular and posterior parietal arteries of the middle cerebral artery. Clinical features associated with this syndrome is spatial neglect of the contralateral side of the body.

Simply put, if the non-dominant hemisphere is the right one, as is the case for right handed individuals, a lesion in the inferior parietal lobe results in a lack of awareness of the left half of the body and the space around it.

An example of this is construction apraxia, where when asked to draw a clock, the individual only draws the right half of the clock but is unaware they have not drawn the whole thing, or dressing apraxia where they only dress half of their body.

The individual also suffers from anosognosia, which is an indifference or lack of ability to recognize their condition. And just briefly, let’s cover the hippocampus, which is part of the limbic system and is involved in memory formation.

Hippocampal damage12:19–13:34

Individuals with bilateral hippocampal damage develop anterograde amnesia, which means they are unable to make new memories, but they can still recall old ones.

Neurons of the hippocampal cortex are extremely vulnerable to ischemic damage, and injury begins just 5 minutes after the onset of hypoxia.

The hippocampus is so vulnerable to ischemia because it constitutes a watershed area, which means it receives its blood supply from the terminal branches of two different arteries, the anterior choroidal artery and the posterior cerebral artery, with limited collateral blood supply.

Therefore, there is a high risk for hippocampus injury in clinical situations which are more likely to damage these vessels, such as hypertension, smoking, dyslipidemia and diabetes and situations with excessive metabolic demand, like during an epileptic seizure, Let’s take another short break and see if you can remember what are the syndromes and clinical features of a dominant parietal cortex lesion?

Quiz13:34–13:58

And what about non-dominant?Ok, let's take a look at a lesion that affects the function of the basal ganglia, particularly a lesion of the subthalamic nucleus.

Subthalamic nucleus lesions13:58–15:34

Normally, the subthalamic nucleus assists the basal ganglia in the regulation of movements by exciting the globus pallidus internus, which inhibits the thalamus.

Once the subthalamic nucleus gets damaged, the globus pallidus internus stops inhibiting the thalamus, which overstimulates the motor cortex, causing a condition called hemiballismus.

Hemiballismus usually presents as the sudden, involuntary and large amplitude flailing of one or both extremities on the side of the body that is contralateral to the side of the lesion.

To remember this, you can use the word hemi-ball-ismus to recall that “half of the body goes ballistic”. The subthalamic nuclei mainly receives blood from the small penetrating arteries of the middle cerebral arteries called the lenticulostriate arteries and small branches from the posterior circulation.

Due to the small size of these arteries they are prone to blockage, especially in the setting of hypertension or diabetes.

Strokes occurring from these small arteries are called lacunar strokes.Okay, now let’s discuss another condition called Kluver-Bucy syndrome, which can be caused by bilateral lesions of each amygdala and surrounding cortex of the temporal lobe.

Kluver-Bucy syndrome15:34–16:58

These lesions usually develop as a complication of viral encephalitis typically caused by herpes simplex virus type 1, which usually affects the temporal lobe.

Some other possible causes include temporal lobe surgery that aims to treat epilepsy, head trauma that leads to temporal lobe contusions, or hypoperfusion of the bilateral anterior choroidal arteries supplying the amygdala.

Kluver-Bucy syndrome usually presents with three types of disinhibited behavior: hypersexuality, or increased sexual drive; hyperphagia, or uncontrollable desire to eat; and hyperorality, which is an urge for exploring objects by mouth.

Other symptoms that can develop are visual agnosia, or psychic blindness, where individuals can not recognize objects that they see, in addition to personality changes, like passivity or docility.Speaking about hunger, the hypothalamus contains two more nuclei that regulate hunger, which are the lateral hypothalamic nucleus and the ventromedial nucleus.

Hunger16:58–18:07

The lateral nucleus stimulates hunger and represents the hunger or feeding center. Lesions of the lateral nucleus therefore cause loss of appetite, and anorexia and starvation.

The ventromedial nucleus, on the other hand, monitors blood glucose and mediates satiety, and stimulation of this area reduces hunger.

Injury or a lesion to this area can lead to hyperphagia and obesity. In order to easily differentiate between these lesions, just remember that Lateral Lesion makes you Lean, while the VentroMedial injury makes you Very Massive.

Injuries which can affect these nuclei include tumors, like a craniopharyngioma, infection, trauma, and vascular disorders.

Finally, let's finish off by taking a look at the thalamus and its role in relaying somatosensory information. The ventral posterolateral nucleus of the thalamus receives input from the spinothalamic tract and dorsal columns of the contralateral side of the trunk and extremities, while the ventral posteromedial nucleus receives input from the trigeminal pathway of the contralateral side of the face, and projects this information to the cortex via the thalamocortical fibers in order to be processed.

Thalamic nuclei lesions18:07–19:18

Therefore damage to these two nuclei may result in complete contralateral sensory loss. This means that the individual loses the sense of touch, tactile discrimination, vibration, proprioception, pain and temperature from the contralateral side of the body, and may even lead to unsteady gait.

Damage to these thalamic nuclei can be due to vascular compromise or local compression from things such as tumours. Quiz time!

What happens when there is an injury to the subthalamic nucleus? Also, can you recall, injury to which hypothalamic nuclei can cause anorexia and hyperphagia?

Alright, as a quick recap… Lesions of the prefrontal cortex can lead to personality changes, often causing issues in decision making, socially unacceptable behaviour, and apathy towards appearance.

Quiz19:18–19:41

A lesion of the frontal eye field leads to deviation of the eyes to the ipsilateral side, while lesion of the paramedian pontine reticular formation leads to deviation of the eyes to the contralateral side.

Review19:41–21:57

Lesions to Broca’s area can cause motor or expressive aphasia resulting in difficulty producing words and word repetition.

Wernicke’s area lesions can cause sensory or receptive aphasia, where individuals have fluent speech but have difficulty with language comprehension.

Damage to the arcuate fasciculus leads to conduction aphasia leading to difficulties in repetition of spoken language, while damage to all these areas leads to global aphasia.

Damage to the paracentral lobule causes contralateral lower limb upper motor neuron signs, with bilateral damage also causing incontinence.

Lesions of the dominant parietal cortex cause Gerstmann syndrome which presents with left-right disorientation, finger agnosia, acalculia and agraphia, while lesions of the non-dominant parietal cortex cause hemispatial neglect.

Bilateral damage to the hippocampus causes anterograde amnesia. Injury to the subthalamic nucleus results in hemiballismus.

Kluver-Bucy syndrome is caused by bilateral damage to both of the amygdala. Lesions of the lateral hypothalamic nucleus lead to anorexia while lesions of the ventromedial nucleus lead to obesity.

Damage to the ventral posterolateral and posteromedial nuclei of the thalamus leads to the total contralateral sensory deficit.

to both of the amygdala. Lesions of the lateral hypothalamic nucleus lead to anorexia while lesions of the ventromedial nucleus lead to obesity.

Damage to the ventral posterolateral and postural, medial nuclei of the salamis leads to the total contralateral