Epidural Hematoma

Recall that dura is tightly attached to the skull so to get blood above dura, you need to rupture a high
pressure circuit so that it can separate dura from skull.

 When you get a fracture, rupturing the middle meningeal artery this results in a collection of
blood between the skull & the dura. Hence when you get a collection of blood, & because the
dura is tightly attached to the skull, points at the edge of blood will remain tightly attached,
then you’ll have this separation of dura from skull creating the classic lens-shaped lesion.

 Over time blood will build up, the patient could be completely asymptomatic, but all of a
sudden the blood will keep putting pressure until it ruptures either attached points, which
would expand the hematoma, this would result in herniation “talk & die syndrome”, because
the patient can be asymptomatic for hours then all of a sudden they would pass away.
 Alzheimer’s disease

This is a cell membrane of a neuron, & on this cell there’s a receptor derived from amyloid precursor
protein, we don’t know what this receptor does but we know, when this receptor is being broken
down, & recycled “recall it’s a receptor made of proteins” by an alpha secretase enzyme, which
results in an alpha by-product which can be turned over without any problem, however sometimes it
can be broken down by a beta secretase enzyme, resulting in a beta by-product, & the problem with
beta product is that it can’t be turned over, & instead it deposits as an amyloid “AB amyloid”, so start
depositing in brain, & it’s the deposition of AB amyloid which results in Alzheimer’s disease.
 Parkinson’s disease

 Cortex communicates with the basal ganglia, then it sends its input back into the cortex, &
the purpose of this loop is to help regulate the movement. The key processing center of the
ganglia is the striatum, which can send either stimulatory signals to cortex or inhibitory
signals to cortex. In addition it can receive input from the substania nigra, from the
dopaminergic neurons of pars compacta releasing dopamine. When they release
dopamine, binding of D1 receptors on the striatum will result in extra stimulation of the
cortex, & binding of D2 would result in decreased inhibition of the cortex, hence the overall
effects of dopamine are increased stimulation, & decreased inhibition to cortex, thus both
will work to increase cortical function so you can increase movement.
 Huntington’s chorea

 Cortex signals basal ganglia (striatum), which is going to send a signal back to cortex,
which is going to help regulate the movement. What’s important to know is that the
striatum is composed of two important gray matter structures, the first is the caudate, &
the second is the putamen. Imagine if you knock out the GABAergic neurons of caudate,
you’ll lose an important structure of straitum resulting in a movement disorder; because
you damaged the basal ganglia.

 GABA is an inhibitory neurotransmitter, so that the GABAergic neurons of the caudate

nucleus, actually providing an inhibitory signal to cortex. The idea here is that the cortex is
designed to move, & fire muscle very quickly, however you don’t want random firing, hence
you have GABAergic neurons, thus when you’ll lose them, you’ll lose the inhibitory hold on
the cortex so random firing, random purposeless movement.