**1. Introduction**

Examples of these are headaches, even though we have classic definitions and descriptions of such "disease" in Oliver Sacks in his book Migraine [1], in which, by the way, he makes a central point and establishes serious questioning toward cultural aspects of photopsias: a kind of environment influence and memory in its manifestations.

Once upon a time, during my practice in the Lacandon jungle during the late 1970s, a patient came in talking and complaining using the indigenous Mayan Tzéltal language; said to my interpreter: I feel **Kuúch, which means pain:** But what kind of pain?

The usual semiology did not work within this context. He had a **heart ache** which at the end of this consultation meant, he was depressed and the anxiety made his heart "ache."

> © 2016 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2018 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

I asked myself if this heart could really "ache" though it came from emotional impact. The answer (to my best clinical knowledge) was YES, it aches. What else could drive this man to search for help, in a context of magical thoughts, shamanes and syncretic ideas?

The models involve blood-brain barrier (BBB) studies of markers like S100B protein (Pando et al. in print); choline/creatine ratio visualizes through spectroscopy the affective disorders or PET/CT as marker for dementia and epilepsy particularly temporal lobe, then it has to

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**Figure 2.** Frontotemporal views of one of our specimens. (courtesy of Pando et al. National institute of Cardiology

**Figure 3.** PET/CT with temporal lobe asymmetry (FDG marking). Courtesy of Pando et al., images from CT scanner,

"Ignacio Chavez").

Mexico City.

mean something correlating it with clinical manifestations (**Figures 1**–**5**).

Years later as a specialist, I became very interested in the temporal lobe, with a very big question: is the temporal lobe and its connections with ventral-lateral thalamus responsible of such symptoms?

Again the answer was YES. And if so, how to prove it?

Again if so: can we consider the temporal lobe and its connections the real rhythm **pacer** of the brain, instead of the occipital? Again the answer is YES [2].

The quest started about 20 years ago: Prove it!

So here are the facts that were gradually published in my native language: Spanish [2–4].

www.evpol.com.mx

Reviewing antecedents and history, we owe a great deal to three persons: Paul Broca, Wilder Penfield, and Isaac Costero. We are talking a century later about the Cajal legacy from Spain.

Paul Broca a century ago talked and supported the internal brain or Limbic system, Wilder Penfield mapped the homunculus 1930s, and Costero (1980s) established the neurovegetative connections of carotid sensors with CNS and thalamic connections.

There we have our "new" platform to understand, directly and indirectly, the role of temporal lobe syndromes, which by the way we all "have" but need to be discerned, as we can appreciate in EEG quantitative analysis (**Figure 1**): as to why temporal lobe is always marking for increased activity?

So up to now, we have more data to correlate symptoms with changes in the EEG and sophisticated imaging and biological markers that do not contradict other models of Mind Brain Analysis (like the Game theory originated in the nineteenth century).

**Figure 1.** Geometrical power frontotemporal syndrome (courtesy of Pando et al.).

The models involve blood-brain barrier (BBB) studies of markers like S100B protein (Pando et al. in print); choline/creatine ratio visualizes through spectroscopy the affective disorders or PET/CT as marker for dementia and epilepsy particularly temporal lobe, then it has to mean something correlating it with clinical manifestations (**Figures 1**–**5**).

I asked myself if this heart could really "ache" though it came from emotional impact. The answer (to my best clinical knowledge) was YES, it aches. What else could drive this man to

Years later as a specialist, I became very interested in the temporal lobe, with a very big question: is the temporal lobe and its connections with ventral-lateral thalamus responsible of such symptoms?

Again if so: can we consider the temporal lobe and its connections the real rhythm **pacer** of the

So here are the facts that were gradually published in my native language: Spanish [2–4].

Reviewing antecedents and history, we owe a great deal to three persons: Paul Broca, Wilder Penfield, and Isaac Costero. We are talking a century later about the Cajal legacy from Spain. Paul Broca a century ago talked and supported the internal brain or Limbic system, Wilder Penfield mapped the homunculus 1930s, and Costero (1980s) established the neurovegetative

There we have our "new" platform to understand, directly and indirectly, the role of temporal lobe syndromes, which by the way we all "have" but need to be discerned, as we can appreciate in EEG quantitative analysis (**Figure 1**): as to why temporal lobe is always marking for increased activity? So up to now, we have more data to correlate symptoms with changes in the EEG and sophisticated imaging and biological markers that do not contradict other models of Mind Brain

search for help, in a context of magical thoughts, shamanes and syncretic ideas?

Again the answer was YES. And if so, how to prove it?

The quest started about 20 years ago: Prove it!

52 Anxiety Disorders - From Childhood to Adulthood

www.evpol.com.mx

brain, instead of the occipital? Again the answer is YES [2].

connections of carotid sensors with CNS and thalamic connections.

Analysis (like the Game theory originated in the nineteenth century).

**Figure 1.** Geometrical power frontotemporal syndrome (courtesy of Pando et al.).

**Figure 2.** Frontotemporal views of one of our specimens. (courtesy of Pando et al. National institute of Cardiology "Ignacio Chavez").

**Figure 3.** PET/CT with temporal lobe asymmetry (FDG marking). Courtesy of Pando et al., images from CT scanner, Mexico City.

We all experience clinical variations of the very same frontotemporal syndrome, and these instruments are allowing us to understand how to aboard them (including autopsies) (**Figure 2**),

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So if anxiety means a constant or increasing FEELING of emotional discomfort, with an urgent necessity of relief by searching just about any means available; like in the game theory,

If you have a certain set of cards and it is the upper hand to the "house," you pass through to the reward that is transmitting the message that your senses are sending whatever the

There are times though in which the message does not go through, with a barrier of an overwhelmed house (brain) with demand of reward, and central temporal lobe like in medial sclerosis discharges (**Figures 1**–**3**), that is, with an alarm manifestation but abnormally with persistent anxiety, no matter the prefrontal cortex. So the frontal is freed from emotional filters and thought containment is surpassed within the balance that the frontal and temporal lobe must have. A psychosis is established at least for the duration of the ictus, perpetuating itself until either by internal homeorrexic mechanisms or external inter-

The intensity of the phenomena varies from mild to panic attacks and the process can be triggered by any disrupting affective loss up to discharges that come from altered networks

Everybody "has" a frontotemporal syndrome, in any time given; [2–5] because that is how we respond emotionally; but it is to the clinician to determine the underlying pathology if so

The temporal lobe epilepsy is one of them characterized to behave as a seizure and marking

Clinically corresponds to nine subtypes obtained through the clinical analysis and combina-

A = epileptic behavior, including panic attacks, generalized anxiety and depressive refractory

K = sensoperceptual dysfunction. We see what we want to see not corresponding to proper

Attached a report from the EVPOL (Virtual EEG, Pando et al.) SYSTEM that correlates the geometric power of the cerebral map with a 100 question inventory of frontotemporal mani-

(EEG) to the temporal inferior and superior temporal gyrus [6–9, 11] (**Figure 2**).

tion of temporal and frontal manifestations, considering the following variables:

P = neurodevelopmental antecedents including genetical traits.

festations related as well to anxiety and panic attacks [2–5] (**Figure 6**).

which are being underestimated nowadays.

the brain responds:

vention (**Figure 2**).

from a growing tumor.

C = psychotic manifestations.

mood that fluctuates within hours.

L = individuals that simulate or plainly lie.

protective neural networks function and memory.

[6–11].

environmental stimuli is.

**Figure 4.** Single positron emitted tomography with cortical hypo-perfusion post hypovolemic shock. (Courtesy of Pando et al.).
