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Map of the Mind: What Each Brain Lobe Is Actually Doing · Understanding the Brain

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  Speaker 1: Right everybody this is a redo again because we have
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  Speaker 1: the better audio now so we're going to combine two
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  Speaker 1: podcasts together this will be discussing the frontal lobes the
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  Speaker 1: original ones I did was part one and two now
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  Speaker 1: we're just going to put them both together so we're
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  Speaker 1: going to be looking at the structure function and psychological
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  Speaker 1: relevance of the neuroanatomy so it's what are the different
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  Speaker 1: lobes do what other what's their structure and what's the
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  Speaker 1: function the structure is actually the different parts of the brain,
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  Speaker 1: the hippocampus, the amygdala, the cortex. The function is how
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  Speaker 1: they communicate and what they do. So we'll be looking
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  Speaker 1: at the frontal lobe, which you know already controls planning, inhibition, decision-making.
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  Speaker 1: Damage here also disrupts executive function like managing, expecting things,
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  Speaker 1: anticipatory function. So how do you anticipate things? The parietal
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  Speaker 1: lobe processes spatial awareness and sensory integration and more. Also,
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  Speaker 1: injury leads to neglect or disorientation. The temporal lobe is
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  Speaker 1: involved in auditory processing, language comprehension, and memory. And damage
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  Speaker 1: to the left temporal lobe impairs verbal comprehension and production.
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  Speaker 1: We'll dive deeper into the Wernicke's area, which is there,
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  Speaker 1: while right temporal lobe damage affects nonverbal memory and facial recognition.
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  Speaker 1: We'll look at the occipital lobe, which handles vision. Lesions
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  Speaker 1: here can cause cortical blindness or visual agnosia. And then
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  Speaker 1: we'll finally wrap up with the limbic system, which is
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  Speaker 1: central to emotion and memory regulation. The amygdala plays a role,
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  Speaker 1: of course, in processing fear, but it also does something
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  Speaker 1: in the emotional salience component. The hippocampus is essential for
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  Speaker 1: memory consolidation, and the hypothalamus governs homeostatic functions. including stress response,
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  Speaker 1: which we looked at HPA, the hypothalamic pituitary adrenal access.
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  Speaker 1: We'll look at basal ganglia, which supports movement and habit learning.
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  Speaker 1: You can think of it being connected to Parkinson's and OCD. Also,
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  Speaker 1: we'll look at a concept called localization and another concept
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  Speaker 1: called lateralization. Lateralization affects language and emotion, especially the left
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  Speaker 1: and right hemispheres of the brain. Localization refers to specific
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  Speaker 1: brain areas that handle specific tasks. So think about plasticity, right?
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  Speaker 1: Neurogenesis refers to the brain's ability to adapt up to
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  Speaker 1: a new injury. You've got to remember, the brain is
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  Speaker 1: pretty complex, and it's a living network that connects to
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  Speaker 1: each other. And understanding how this works means knowing not
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  Speaker 1: just where the things are, what structures, but what they
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  Speaker 1: do and what happens when they break. The EPPP doesn't
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  Speaker 1: just test your ability to label something. It really tests
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  Speaker 1: you how to connect structure to function and function to behavior.
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  Speaker 1: So hopefully we'll be able to get that point across
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  Speaker 1: as we cover today's lecture. You'll need to know what
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  Speaker 1: happens to speech when Broca's area is damaged, which is
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  Speaker 1: in the frontal lobe, or how damage to the prefrontal
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  Speaker 1: cortex can quietly dismantle a person's personality long before it
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  Speaker 1: touches memory or even movement. Prefrontal cortex, again, associated with
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  Speaker 1: a lot of things such as emotional dysregulation, inhibition, controlling compulsiveness, empathy.
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  Speaker 1: There's a lot of components of the prefrontal cortex that
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  Speaker 1: if it's damaged can cause problems, and we'll look at
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  Speaker 1: that a little bit later. So the frontal lobe, especially
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  Speaker 1: the prefrontal cortex, this one is responsible for executive functions
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  Speaker 1: like planning, decision-making, making judgments, moral decisions, inhibition control, inhibitory
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  Speaker 1: controls here. working memory, emotional regulation. And it also houses
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  Speaker 1: what they call Broca's area in the left hemisphere, which
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  Speaker 1: coordinates speech production. When the frontal lobe is injured, the
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  Speaker 1: person doesn't necessarily lose IQ. They actually lose control. They
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  Speaker 1: might know the right thing to do, but fail to
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  Speaker 1: act on it. So let's take a look. Sorry for
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  Speaker 1: the long delay there. When the frontal lobe is injured,
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  Speaker 1: the person, again, loses control. They might become impulsive, apathetic,
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  Speaker 1: or socially inappropriate. Think of a client with a traumatic
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  Speaker 1: brain injury who starts gambling excessively or becomes sexually disinhibited.
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  Speaker 1: We've also seen individuals in the prison systems, like serial
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  Speaker 1: rapists and things of that nature, that actually have either
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  Speaker 1: delayed maturation or reduced volume in the prefrontal cortex. So
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  Speaker 1: it's not just a behavior problem. That's a prefrontal cortex dysfunction.
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  Speaker 1: A famous case you probably remember from undergrad is Phineas Gage,
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  Speaker 1: the railroad worker who survived a metal rod passing through
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  Speaker 1: his frontal lobe. He may have survived it, but it
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  Speaker 1: affected his personality considerably, and I even believe he got
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  Speaker 1: divorced because of it. He went from reliable and polite
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  Speaker 1: to erratic and vulgar and sexually promiscuous. His intellect was intact,
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  Speaker 1: but his personality was completely altered and pretty much destroyed
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  Speaker 1: his life. Damage here often mimics mood or personality disorders.
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  Speaker 1: So someone with new impulsivity or poor planning shows no
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  Speaker 1: mood symptoms and a history of head trauma, consider a
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  Speaker 1: neurological cause. So antisocial personality behavior, we see a lot
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  Speaker 1: of issues with the frontal lobe, just like borderline personality
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  Speaker 1: disorder as well. Depression, I think, I believe is in
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  Speaker 1: the right dorsolateral part of the prefrontal cortex. Not relevant
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  Speaker 1: to the EPPP, but just thought I'd throw it in there.
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  Speaker 1: We head over to the parietal lobe. The parietal lobe
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  Speaker 1: integrates sensory information, especially spatial processing, body awareness, and tactile perception.
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  Speaker 1: Think of this lobe when you see questions about hemispatial neglect,
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  Speaker 1: particularly in right parietal damage. The client might eat food
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  Speaker 1: only on one side of the plate or fail to
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  Speaker 1: groom one side of the body. So again, you have
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  Speaker 1: hemisphere damage here, lateralization we talked about earlier. Left parietal
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  Speaker 1: damage can cause agraphia, writing impairment, or Finger agnosia, trouble
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  Speaker 1: identifying fingers, collectively known as Gerstmann syndrome, G-E-R-S-T-M-A-N-N. So again,
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  Speaker 1: if it's on the right side, you're going to have
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  Speaker 1: a client who might eat food only on one side
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  Speaker 1: of the plate or fail to groom. Left parietal damage
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  Speaker 1: associated with possibly agraphia, alcuculia, mouth difficulty, and finger agnosia,
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  Speaker 1: trouble identifying fingers. Clients might deny ownership of a limb
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  Speaker 1: or misinterpret their spatial position in a room. This isn't
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  Speaker 1: them hallucinating. It's that the brain's map is going offline. Remember,
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  Speaker 1: the parietal lobe is important for spatial processing, body awareness,
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  Speaker 1: and tactile perception like touch, pain, temperature. Now we head
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  Speaker 1: over to the temporal lobe located near the ears. The
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  Speaker 1: temporal lobe processes auditory input, language comprehension, and memory formation.
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  Speaker 1: On the left side, it houses what we mentioned earlier,
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  Speaker 1: Wernicke's area, and it's responsible for understanding speech. So when
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  Speaker 1: this area is damaged, it can lead to something called
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  Speaker 1: Wernicke's aphasia, fluent but meaningless speech and poor comprehension. The
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  Speaker 1: hippocampus tucked deep into the temporal lobe forms new declarative memories, right?
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  Speaker 1: So the temporal lobe is where you're going to have
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  Speaker 1: the hippocampus tucked into, and if that's damaged bilaterally on
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  Speaker 1: both sides of the hemispheres, As in Korsakoff syndrome, which
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  Speaker 1: was originally called Korsakoff syndrome, which is usually caused by
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  Speaker 1: chronic alcohol use that leads to thiamine deficiency, a vitamin,
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  Speaker 1: patients develop what they call anterograde amnesia. Anterograde amnesia, they
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  Speaker 1: can't form new memories. They can't encode. So even though
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  Speaker 1: long-term memories remain, they're unable, they can retrieve a lot
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  Speaker 1: of these memories, but they can't encode new ones. A
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  Speaker 1: lot of times when you see individuals like this, If
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  Speaker 1: they have anterograde amnesia, you'll see this also in dementia.
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  Speaker 1: What ends up happening when you ask them, hey, did
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  Speaker 1: you see what happened last month? They'll actually go back
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  Speaker 1: a couple of years. If you try to get them
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  Speaker 1: to talk about anything recent within the last few months
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  Speaker 1: or weeks, what they'll usually do if they're trying to
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  Speaker 1: hide it is talk about something that happened a few
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  Speaker 1: years back, maybe even 20 years back. So at first,
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  Speaker 1: if you're encountering this person at a party or something,
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  Speaker 1: you may not notice it. You just may think, oh,
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  Speaker 1: they're kind of reminiscing or they're stuck in the past.
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  Speaker 1: But as a clinician, if you keep asking questions, you
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  Speaker 1: keep noticing this pattern, then you know you might have
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  Speaker 1: something there. Temporal lobe epilepsy often comes with emotional auras
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  Speaker 1: like strange smells, deja vu, and sudden fear. This shows
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  Speaker 1: how closely the limbic or the emotional system and temporal
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  Speaker 1: structures are tied to affect. Finally, we go to the
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  Speaker 1: occipital lobe, and that sits at the back of the
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  Speaker 1: brain and processes visual information. Lesions can cause cortical blindness.
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  Speaker 1: Visual signals arrive but aren't interpreted. Also, it can lead
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  Speaker 1: to visual agnosia, inability to recognize objects, or prosopagnosia, face blindness.
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  Speaker 1: And this is located in the area called the fusiform gyrus.
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  Speaker 1: Fusiform gyrus is affected. Visual hallucinations, whether simple like flashes
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  Speaker 1: of light or complex like faces or figures, often originate
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  Speaker 1: here as well. The client describing seeing people without delusions
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  Speaker 1: might not be psychotic. They may have occipital seizures or
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  Speaker 1: what they call Charles Bonnet syndrome, which is common in
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  Speaker 1: older adults with vision loss. In addition, when you have
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  Speaker 1: occipital lobe damage, it can also lead to blurry vision
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  Speaker 1: or seeing double. We've seen that in the cartoons or
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  Speaker 1: in the movies, right? If you get hit in the
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  Speaker 1: back of the head, you could have loss of vision
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  Speaker 1: in half your visual field as well. So this could
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  Speaker 1: be an issue that could happen to individuals. Double vision
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  Speaker 1: is diplopia, D-I-P-L-O-P-I-A. Again, it could be damage to the occiput. lobe,
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  Speaker 1: cranial nerve damage, or brain stem or cerebellar lesions. Now
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  Speaker 1: we move on to the limbic system. The limbic system
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  Speaker 1: is the brain's emotional center, right? This includes the amygdala,
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  Speaker 1: which tags emotional significance like fear, Onto stimuli, damage leads
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  Speaker 1: to flat affect and poor threat recognition. So when you're
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  Speaker 1: thinking of flat affect, of course, schizophrenia tends to come
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  Speaker 1: to mind. Individuals who are diagnosed with antisocial personality disorder,
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  Speaker 1: but in particular psychopaths, psychopaths tend to have poor threat
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  Speaker 1: recognition and hypoactive amygdala. So they're not operating at a
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  Speaker 1: normal function. They're actually below baseline. So they have a
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  Speaker 1: lower responding amygdala. Hippocampus, that's where it codes new memories.
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  Speaker 1: So bilateral damage leads to anterograde amnesia. So bilateral damage
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  Speaker 1: meaning both to the left and the right side of
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  Speaker 1: that hippocampus. Because when you look at each brain structure,
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  Speaker 1: they actually have different functions when you look to the
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  Speaker 1: left and the right. It's too much for the EPPP,
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  Speaker 1: so we won't do it here. I might expand it
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  Speaker 1: once we're done covering part one and part two and
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  Speaker 1: go further into these topics maybe to help you in
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  Speaker 1: the future just in general. Hypothalamus manages hunger, thirst, and
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  Speaker 1: body temperature and controls the HPA axis for stress response.
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  Speaker 1: A lot of times you'll get questions that are connected
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  Speaker 1: to trauma, addiction, or regulatory disorders. So if a client
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  Speaker 1: with PTSD shows hypervigilance and poor memory for the trauma,
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  Speaker 1: you're seeing here what? An overactive amygdala, that's hypervigilance. The
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  Speaker 1: sympathetic nervous system kicks in. And impaired hippocampus integration. So
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  Speaker 1: encoding memories could be a problem here. The HPA axis,
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  Speaker 1: which we've talked about before, regulated by the hypothalamus, also
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  Speaker 1: connects stress to illness. So chronic overactivation floods the body
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  Speaker 1: with cortisol, increasing vulnerability to anxiety, depression, and metabolic disease,
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  Speaker 1: and we covered this in another episode. Subcortical structures, subcortical
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  Speaker 1: meaning underneath the cortex, deep in the brain lie the
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  Speaker 1: brazil ganglia, the thalamus, and the brainstem. These are structures
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  Speaker 1: that coordinate movement, attention, that's where you're focusing, arousal, and
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  Speaker 1: habit formation. So when I said attention, you should be
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  Speaker 1: thinking about things like maybe ADHD and things of that nature. Also,
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  Speaker 1: when it comes about movement, you should be thinking about Parkinson's.
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  Speaker 1: And that leads us to our first area, the basal ganglia,
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  Speaker 1: which is critical for motor control and procedural learning. Procedural
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  Speaker 1: learning could be things like riding a bike. Damage is
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  Speaker 1: linked to Parkinson's disease. One of the reasons is dopamine
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  Speaker 1: depletion in a part of the brain called the substantia nigra.
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  Speaker 1: So there's low levels of dopamine. This is why they'll
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  Speaker 1: recommend sometimes L-DOPA to increase the dopamine levels. And if
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  Speaker 1: it goes too high, the levels, that could lead to psychosis.
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  Speaker 1: Back to this. In the basal ganglia, we also see
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  Speaker 1: associations with Huntington's disease and OCD. Clients may show repetitive behaviors, tics,
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  Speaker 1: or motor rigidity. So when you think about ADHD or autism,
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  Speaker 1: the caudate and the putamen, caudate is C-A-U-D-A-T-E, and then
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  Speaker 1: putamen is P-U-T-A-M-E-N. Hopefully I'm pronouncing that right. Those are
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  Speaker 1: associated with autism, and they're within the basal ganglia. And
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  Speaker 1: reduced volume in those two brain structures are linked to impulsivity, inattention,
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  Speaker 1: and hyperactivity. You can see it's also linked to ADHD. Actually,
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  Speaker 1: my apologies. So in that area, the reduced volume in
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  Speaker 1: the caudate, putamen, are linked to impulsivity, inattention, hyperactivity for ADHD.
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  Speaker 1: And for autism, the basal ganglia, the enlarged caudate nucleus,
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  Speaker 1: especially in early development, we'll see there. It's implicated in
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  Speaker 1: motor control, reward processing, and routine behaviors. So just to
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  Speaker 1: make sure you got a little bit of clarity there.
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  Speaker 1: We head over to the thalamus. That's the brain's relay station.
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  Speaker 1: It routes sensory information to the cortex. Thalamic strokes often
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  Speaker 1: present with mixed sensory loss and cognitive changes. The brainstem,
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  Speaker 1: this keeps you alive. A lot of involuntary muscle control,
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  Speaker 1: like breathing, heart rate, and consciousness. Damage here is extremely dangerous.
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  Speaker 1: But milder dysfunction can explain sleep issues, vertigo, or cranial
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  Speaker 1: nerve symptoms. There's 12 cranial nerves. The one that usually
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  Speaker 1: relates to us, one of the ones, the major ones
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  Speaker 1: for our world, is the vagus nerve. And lastly today,
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  Speaker 1: we're going to talk about lateralization, localization, plasticity, and neurogenesis.
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  Speaker 1: The left hemisphere is usually dominant for what? Language, logic,
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  Speaker 1: and linear thinking really kicks in around two years of age.
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  Speaker 1: The right governs spatial awareness, emotional tone, and facial recognition,
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  Speaker 1: and some even argue are unconscious memories. Language problems after
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  Speaker 1: left hemisphere stroke are more common. Emotion recognition and prosody
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  Speaker 1: loss occur more often after right damage. If you're interested
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  Speaker 1: in lateralization, there's a great book by Ian McGilchrist that
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  Speaker 1: you can read. It's a big book. He's got a
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  Speaker 1: couple of them, but they're dealing a lot with the
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  Speaker 1: differences between the right and left hemisphere of the brain,
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  Speaker 1: separate again from the EPPP. Localization means function is specific,
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  Speaker 1: like Broca's area is specific for speech production. The occipital
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  Speaker 1: lobe equals vision. Plasticity refers to its ability to rewire
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  Speaker 1: after injury, especially in younger people. If one area is damaged,
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  Speaker 1: another may adapt over time. Neurogenesis is the formation of
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  Speaker 1: new neurons. It occurs primarily in the hippocampus. It makes sense.
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  Speaker 1: Every time you have a new memory, memories can evolve,
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  Speaker 1: even in adulthood, especially with enriched environments, exercise, and learning.
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  Speaker 1: We saw taxi drivers, when they used to have maps
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  Speaker 1: before GPS, they had huge hippocampuses, I think 400% bigger
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  Speaker 1: than the average person. Oddly enough, when they retired from
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  Speaker 1: that job, it came back to a baseline. Here's a
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  Speaker 1: question for you. If a nine-year-old suffers a left hemisphere
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  Speaker 1: stroke and loses expressive language over time, speech returns via
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  Speaker 1: the right hemisphere. That's not magic. What's happening there is
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  Speaker 1: plasticity in motion. So again, behavior, a lot of it
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  Speaker 1: is mapped to biology. Every lobe and every little groove
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  Speaker 1: and every connection helps explain why people feel and act
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  Speaker 1: and struggle the way they do. Our next presentation is
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  Speaker 1: both two podcasts combined. Again, we're going to be dealing
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  Speaker 1: with neurotransmitters. We'll go deep into those as well. We'll
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  Speaker 1: revisit the substantia nigra with dopamine and others. Thanks for listening.