Now for a new topic- the brain! Unlike the other topics covered in this course so far, I haven't actually written very much on the brain (in fact pretty much all I've written is in one other post, and it doesn't say very much).
Cerebral Blood Supply
One of the few things that I did mention in my other post (albeit only briefly) is the cerebral blood supply. I've also touched on this in a Cardiovascular System post for PHYL2001. The brain is pretty dependent on good blood flow, as it requires oxygen and glucose for metabolism, accepting no other substitutes. Blood vessels supplying the brain do not have receptors for adrenaline or noradrenaline (as these would cause the blood vessels to constrict, which you never want happening to the brain), but instead respond to local cues such as autoregulation and local mediators (see here for more details). The base of the brain has a circular formation of arteries called the Circle of Willis. This circular formation provides anastomoses, which provide alternate pathways in the case of blockages.
Blood vessels supplying the brain have very tight endothelial junctions that prevent nasty stuff from getting through. Astrocytes help out with this too, forming a structure called the Blood Brain Barrier (BBB). While lipid-soluble molecules such as alcohol and some anaesthetics can cross easily, larger and/or charged molecules cannot.
The BBB is not fully formed at birth, which can cause some issues with regards to giving the right dosages of medications and so forth. Also, a condition called kernicterus can occur when bilirubin crosses the BBB. This is a problem shortly after birth when the baby gets rid of their old foetal haemoglobin in order to get new haemoglobin- red blood cells are destroyed, causing an increase in bilirubin that may cross the BBB.
The BBB can also be breached due to other causes, such as hypertension, infection and trauma. One significant effect of BBB damage is the entry of white blood cells. The brain normally has its own supply of immune cells, separate to immune cells of the rest of the body. Hence, immune cells from the rest of the body may be unable to recognise antigens in the brain, and essentially begin to wage war on the brain.
Cerebrospinal Fluid
Another important fluid in the brain is cerebrospinal fluid (CSF). It is formed in the choroid plexus, which is located in the third and fourth ventricles. CSF circulates through the ventricles and subarachnoid space. Arachnoid villi, which "poke into" venous sinuses, are the point at which CSF can enter the blood and essentially get washed out of the brain. CSF flow is always one-way: CSF flows into the blood, but not back. In contrast to blood, CSF contains hardly any protein- protein in the CSF is generally a marker of some kind of disease.
So what does CSF do? CSF helps to protect the brain. It also helps it to float around a bit so that it's not smashed up against the top of the spine. As I just alluded to, CSF gets washed out in the blood, so CSF is also a medium through which waste products can be removed. If CSF cannot be drained for whatever reason, hydrocephalus, or "water brain," can result. This causes increased intracranial pressure (ICP), which I'm going to talk about now.
Increased Intracranial Pressure (ICP)
Increased intracranial pressure, as the name suggests, is basically increased pressure within the skull. This can be caused by increased CSF (as mentioned earlier), tumours, trauma, haemorrhage, infection and so on. As there is only so much room within the skull, the pressure presses against the blood vessels, meaning that there is less blood flow. Build-up of CO2 causes vasodilation (for more information about this, see here), which increases volume, which increases pressure, and the vicious cycle continues. Signs of ICP include lethargy, headache, vomiting and papilledema (a "fuzzy" kind of area at the back of the eye as pressure pushes against the nerves).
ICP can affect eye movement, as the pressure can press on cranial nerve III (the oculomotor nerve). This causes ptosis, which is a half-closed eyelid, and an unresponsive, dilated pupil on the same side (ipsilateral) to the pressure. (Side note: "ipsilateral" = same side, "contralateral" = opposite side.) This latter effect is due to impairment of the parasympathetic nervous system, which generally constricts pupils when you want to rest.
Another effect of ICP is that parts of the brain can herniate, or push into one another. In cingulate hernias, one part of the brain pushes into the hemisphere at the level of the cingulate gyrus. Uncal hernias occur where the cerebrum meets the cerebellum, and cerebellar/tonsillar hernias occur in the cerebellum. Uncal and cerebellar hernias are particularly dangerous as they can compress the brainstem, which deals with a lot of vital functions such as respiration and heart rate.
Finally, ICP can also affect blood pressure. Cerebral ischaemia signals to vasomotor centres, in what is called "Cushing's reflex" (which has nothing to do with Cushing's syndrome, aside from that they were both discovered by the same guy). This causes systemic vasoconstriction, increasing the blood pressure. The increased blood pressure is picked up by baroreceptors, which slow the heart rate. At the same time, the increased blood pressure causes CO2 to reach the lungs faster, and when this is detected, respiration slows. Despite all of this, the increased blood pressure does help ischaemia to improve, to the point where signals to the vasomotor centres cease and the blood pressure drops again. This causes ischaemia to recur, causing the cycle to start all over again. The overall effect is a rise in blood pressure. This rise is greater in systolic than in diastolic blood pressure, so pulse pressure also increases.
Neurological Dysfunction
Aside from the more general problems that I've spoken about earlier, such as increased ICP, some types of neurological dysfunction have more local (focal) effects depending on the part that is damaged.
Lesion locations
This is going to be a bit all over the place, but bear with me.
The first little anatomy tidbit that I'm going to tell you about is the tentorium cerebelli. It's like an extension of the dura mater that separates the cerebrum and cerebellum. Lesions above the tentorium cerebelli are said to be supratentorial, and tend to cause a specific problem in a discrete area of the body. Infratentorial lesions (below the tentorium cerebelli), however, tend to cause more widespread impairment. Respiratory and circulatory function may be affected, as the brainstem lies in this area.
Next up, the hemisphere that is affected may cause different issues. I'm sure you've heard the whole "left brain" vs. "right brain" thing before, so I won't go into it any more (especially since the professor didn't say any more about it).
The area of the brain that gets affected may also affect whether consciousness is retained or not. If the cortex is affected, consciousness won't be lost unless an extensive area is affected. However, if the Reticular Activating System (RAS) in the medulla is affected, even if the lesion is small, you could get knocked out right away.
Motor dysfunction
More vague-ish anatomy lessons!
Upper motor neurons of the brain can be divided into two groups: pyramidal and extrapyramidal. Pyramidal tracts, such as lateral corticospinal neurons, cross to the other side of the body at the medulla, and are responsible for voluntary actions. Extrapyramidal tracts, such as ventral corticospinal neurons, cross to the other side of the body at the exit level from the spinal cord, and are generally responsible for postural reflexes. As both types of tracts cross from one side to the other, effects in these neurons cause contralateral (i.e. on the other side to the injury) spastic paralysis. (Spastic paralysis is basically when your muscles can't relax.)
Lower motor neurons are the last neurons in the "chain" that deliver a message to the muscle cell. Hence, not all of them are really "low down"- cranial nerves that communicate directly to muscle cells are also called lower motor neurons. These do not cross over, and thus they cause ipsilateral flaccid paralysis (flaccid paralysis being when your muscles can't contract).
Sensory deficits
Just like with upper motor neurons, sensory nerves also cross over. Spinothalamic nerves (that run from the spine to the thalamus) are responsible for crude touch, pain and temperature, and they cross over pretty much as soon as they enter the spinal cord. Hence, damage to the spinothalamic nerves tend to affect the side contralateral to the injury. Dorsal column nerves deal with fine touch, pressure and stretch and don't cross over until they get to the medulla, so damage to these nerves causes problems on the ipsilateral side.
Visual defects
Vision, which is mainly controlled by cranial nerve II, is kinda funky. Essentially, each eye has two nerves coming out of it. Nerves of the inner retinas, which deal with peripheral vision, cross over at the optic chiasm, so a lesion in the middle of the optic chiasm will get rid of your peripheral vision. Nerves of the outer retinas do not cross over. If there is a lesion past the optic chiasm, hemaniopia, or loss of vision of half of the visual field, will result. This is because you've essentially cut the nerve for the ipsilateral outer retina and the contralateral inner retina.
Aphasias
Aphasias are the inability to express or understand language. They come in three main types. Expressive (motor) aphasia is caused by a problem in Broca's area, receptive aphasia is caused by a problem in Wernicke's area, and global aphasia is caused by a problem in both Broca's and Wernicke's area, as well as the connecting fibres between them.
There are, of course, many other language problems that a person can develop. This isn't a speech pathology course, so I'm not going to go into all of them- in fact, I'm only really going to touch the very tip of the iceberg. Dysarthria is a problem with verbal articulation caused by motor injury (the person can't control the muscles required for speech). Agnosia is a loss of verbal recognition, where a patient can recognise an object but can't tell you what it is (i.e. they can't match the name with the object, just like how sometimes people have trouble matching names to faces).
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