(From Dr. Glasser’s Lecture, 14 July 2000, by Brian Buschman)
Return to Semester Two Goodies
Return to The Unofficial Ross Page
The cerebral cortex is divided into the neocortex and the allocortex. The neocortex is the isocortex and is made of 6 layers. The allocortex is 3 layers and is called the paleocortex (for olfaction) and the archiocortex (hippocampus).
The neocortex is six layers with pyramidal cells that are large with long neurons. Pyramidal cells project from one cortical area to another or out of the cortex. Most pyramidal cells are excitatory via glutamate. The neocortex also has Betz cells.
There are also non-pyramidal cells which are small, stellate or granule cells. They have small axons that do not leave the cortex and usually are inhibitory via GABA.
Projection area of the neocortex, like area 4, are mostly pyramidal cells as they tend to send axons long distances. This makes it very hard to see the layers and hence these are called agranular areas.
In granular cortex most of the cells are non-pyramidal cells which are not projection areas. There is a very smooth transition between granular and agranular regions. If the region is an intermediate region, between granular and agranular it’s called homotypical cortex. If it’s one end or the other then it’s heterotypical cortex.
Different layers of the cortex play different roles. Some layers we will need to know and some we can ignore.
Afferent layers come form two sources:
1) Another cortical region via either association fibers on the same side or commissural fibers if from the opposite side.
2) Subcortical inputs. Inputs from the thalamus end in layer 4. Other inputs such as from midbrain raphe end in layers 2 and 3.
Efferent layers go to other cortical areas on layer 3 or leave for subcortical destinations from layers 5 and 6.
(Come in on the lower numbers and go out on the higher ones. From low to high.)
Broadman developed his list of areas based on studying the histology of one human brain but we can see that his system has functional use. We see that:
Language tends to be lateralized to one hemisphere which is referred to the dominant hemisphere. In most people it’s the left brain and it tends to be the side for logical and rational thought. The non-dominant hemisphere is the site of non-verbal expression, pictoralness and creativeness.
Planum temporale is the site in the dominant hemisphere that controls language and is localized into two more specific areas, Broca’s and Wernicke’s areas.
Dysarthria is a speech disorder where the mechanism of speech is damaged. This may include damage to the muscles or nerves (V, VII, IX, X, XII).
Aphasia is a language impediment due to cortical damage.
Broca’s aphasia may be called an anterior, non-fluent or expressive aphasia. Patients cannot speak except for only the most meaningful words. They know what they are talking about but just have trouble getting it out.
Patients with Broca’s aphasia also present with a contralateral hemiplegia because damage to Broca’s area usually also causes damage to part of the motor area. Mote then likely in the part that controls the upper limb. A middle cerebral stroke can cause both Broca’s aphasia and an upper limb hemiplegia.
Wernicke’s aphasia is called posterior, fluent, sensory and receptive aphasias. People have fluent speech but don’t have much mean to what they say. They just babble. They have a difficulty in naming things and may also mix up letters and say something like “wellow” rather then “yellow” which is called a papaphasia.
Patients don’t seem to be aware of the problems and don’t seem to care about life. This can cause a Wernicke’s aphasia to be misdiagnosed as a psychosis.
This is a loss of the arcuate fasciculus connecting the two areas. Patients present with fluency and comprehension but have difficulty with repetition and naming.
If you have a major legion it may encompass both areas and the arcuate fibers. Patients present with all associated losses, inability to name things, loss of repetition, non-fluent and loss of comprehension.
It’s an aphasia affecting the dominant hemisphere’s angular gyrus and is just a fraction of the Wernicke’s aphasia where the patient cannon name things.
Is an inability to write that may be due to a problem with the construction of the letters or of higher cortical function.
A prosody is the rhythm of speech and is a non-dominant hemisphere function. It is carried out in areas similar to Broca’s and Wernicke’s areas on the opposite side. A frontal aprosody causes a motor aprosody. A posterior aprosody is a sensory aprosody that causes the patient to be unable to understand the rhythm of speech.
Alexia is an inability to read. It may be found as:
1) Alexia with agraphia, a legion of the non-dominant angular gyrus.
2) Alexia without agraphia which may be due to selenium damage.
Agnosia is the inability to recognize an object even though the sensation in intact. It’s f a parieto-occipito-temporal accessory legion.
An apraxia is an inability to perform an action despite intact muscle and innervation. An idiomotor apraxia results from an inability to perform an action which can still be done as a reflex action. Such as you will brush your hair in front of a mirror but you can’t do it if you are ask to. It probably involves a legion in Broca’s area, the arcuate fasciculus and the corpus callosum. All the events can be done separately but not as a complete motion.
Unilateral neglect is when a person does not recognize stimulation from ½ of their world. All lower functions are intact in both sides but a legion to the non-dominant cortex can lead to only recognizing the side controlled by the dominant (usually right) side.
Anosognosia is a neglect of a disease which is often associated with a unilateral neglect.
(I expect this to be on the mini)
There are four things associated with a legion to the dominant side angular gyrus:
1) R-L disorientation.
2) Finger agnosia
3) Impaired calculation
4) Impaired writing
Patients may also have an anomic aphasia, difficulty finding the right word and alexia.
Return to Semester Two Goodies
Return to The Unofficial Ross Page