Anatomy clinical correlates: Cerebral hemispheres
AssessmentsAnatomy clinical correlates: Cerebral hemispheres
USMLE® Step 1 style questions USMLE
USMLE® Step 2 style questions USMLE
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?
Content Reviewers:Viviana Popa, MD, Scott Caterine, BSc (Hons.), MSc, MB, BCh, BAO (Hons.)
Contributors:Elizabeth Nixon-Shapiro, MSMI, CMI, Cassidy Dermott, Jake Ryan
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. 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. 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? 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. 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? What about Wernicke’s aphasia?