**2. Mind and game theory**

These few examples of technological biomedicine can and must be applied to brain function and neuropsychiatry and not only statistics and few specialists writing "consensus" for everybody. 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**), which are being underestimated nowadays.

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, the brain responds:

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 environmental stimuli is.

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 intervention (**Figure 2**).

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 from a growing tumor.

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 [6–11].

The temporal lobe epilepsy is one of them characterized to behave as a seizure and marking (EEG) to the temporal inferior and superior temporal gyrus [6–9, 11] (**Figure 2**).

Clinically corresponds to nine subtypes obtained through the clinical analysis and combination of temporal and frontal manifestations, considering the following variables:

C = psychotic manifestations.

**2. Mind and game theory**

54 Anxiety Disorders - From Childhood to Adulthood

et al.).

These few examples of technological biomedicine can and must be applied to brain function and neuropsychiatry and not only statistics and few specialists writing "consensus" for everybody.

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

**Figure 5.** Wilder Penfield (public photograph). Mapped the homunculus (Johns Hopkins University).

P = neurodevelopmental antecedents including genetical traits.

A = epileptic behavior, including panic attacks, generalized anxiety and depressive refractory mood that fluctuates within hours.

L = individuals that simulate or plainly lie.

K = sensoperceptual dysfunction. We see what we want to see not corresponding to proper protective neural networks function and memory.

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

• Recommendation:

the pharmaceutical industry [4, 6–11].

poration of such epileptic manifestations.

in the 30s of the past century, using Riemann tensors [2, 13].

life

○ The Neuropsychiatrist recommends consulting your doctor to improve your quality of

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So as in Migraines [12], we should start to deal with an unsolved classification (at least up to now) of anxiety as epileptical equivalent and it starts with: how many days should we support the patient sedated in order to substitute benzodiazepines [4] for a better neuroregulation through anticonvulsive psycho-neuropharmacology with much lesser risks of addictions or nephron-hepatic conditions with sometimes smaller doses than the ones recommended by

The definition of epilepsy is a paroxistic abnormal electrical discharge of any given group of neurons and any group of neurons based on the principle, one neuron, one function: networks develop through vectorial signals that are received at the level of neurofilaments which have quantic sensors in the concept of space, time, and structure that Schrodinger developed

As such if any group of given neuron discharges and recruits a network, ectopically, any given signs and symptoms should or potentially have to manifest themselves and can be registered in cuanti-qualitative analysis of the EEG and or other imaging techniques (**Figure 7**). That is why the International League against epilepsy has not closed the door for future incor-

**Figure 7.** Quantitative analysis mapping of frontotemporal syndromes. (Courtesy of Pando et al., Mexico City).

• This report describes behaviors that can be changed by endogenous factors [2–5].

**Figure 6.** (A) EVPOL logo. Courtesy of Pando et al. research lab in CPALC., Mexico City. (B) MRI of brain with marking of abnormal activity. Courtesy of Pando et.al research lab in CPALC. Mexico City.

The following is described in the opinion that is shown later. The image shows the points in the brain linked to the behaviors.

	- There are antecedents of risk to health, both of a genetic nature and of consequences against environmental interactions, with implications depending on the individual's predisposition to physical or psychological illness over the course of growth and development
	- Due to family history, you cannot perceive the information correctly. You may have obvious or compensated learning disorders.

• Recommendation:

The following is described in the opinion that is shown later. The image shows the points in

**Figure 6.** (A) EVPOL logo. Courtesy of Pando et al. research lab in CPALC., Mexico City. (B) MRI of brain with marking

○ There are antecedents of risk to health, both of a genetic nature and of consequences against environmental interactions, with implications depending on the individual's predisposition to physical or psychological illness over the course of growth and development

○ Due to family history, you cannot perceive the information correctly. You may have

• This opinion is the product of deep scientific and clinical research. Dr. Luis Pando-Orellana endorses and issues this opinion to the best of his knowledge and belief. Dr. Luis Pando-Orellana is a doctor and Doctor of Sciences with a specialty in Neuropsychiatry and Doctor

the brain linked to the behaviors.

56 Anxiety Disorders - From Childhood to Adulthood

obvious or compensated learning disorders.

of abnormal activity. Courtesy of Pando et.al research lab in CPALC. Mexico City.

• Opinion:

in Immunology.


So as in Migraines [12], we should start to deal with an unsolved classification (at least up to now) of anxiety as epileptical equivalent and it starts with: how many days should we support the patient sedated in order to substitute benzodiazepines [4] for a better neuroregulation through anticonvulsive psycho-neuropharmacology with much lesser risks of addictions or nephron-hepatic conditions with sometimes smaller doses than the ones recommended by the pharmaceutical industry [4, 6–11].

The definition of epilepsy is a paroxistic abnormal electrical discharge of any given group of neurons and any group of neurons based on the principle, one neuron, one function: networks develop through vectorial signals that are received at the level of neurofilaments which have quantic sensors in the concept of space, time, and structure that Schrodinger developed in the 30s of the past century, using Riemann tensors [2, 13].

As such if any group of given neuron discharges and recruits a network, ectopically, any given signs and symptoms should or potentially have to manifest themselves and can be registered in cuanti-qualitative analysis of the EEG and or other imaging techniques (**Figure 7**).

That is why the International League against epilepsy has not closed the door for future incorporation of such epileptic manifestations.

**Figure 7.** Quantitative analysis mapping of frontotemporal syndromes. (Courtesy of Pando et al., Mexico City).

Signals that are transcribed as semiconductors (neurofilaments) transit through synaptic trees in real time and stock these information for short periods of time between 1 ms up to more than 1 s from one membrane to another through an inter-synaptic space; the first membrane of 50 Å (thickness) initiates the process.

All the way in a tetra-dimensional quanta information traveling through tensors and counter tensors, finding their way through space networks, and respecting the thermodynamical laws with an infinitesimal delay in this essential form of computational quantic central nervous system activity [2, 13] (**Figures 7**–**10**).

We have worked with human models from the cuts taken during anatomic-pathological autopsies of children around 8 years of age who died from accidents (**Figure 2**).

The findings corroborate the convergence/divergence composition from the third, pyramidal neurons of the cerebral cortex. The cortex in the hypocampus shows the same composition, and we think that this is a step for recruiting neurons and to form neural networks provide the structural basis of holograms, as shown in the following sketches [2, 13] (**Figures 8**–**10**).

So if anxiety can be accepted as a most common form of co-morbidity or "aura" in most of structural or functional alterations of the CNS, we must also consider the probable fact that

within the definition of epilepsy, it can and must also be considered as an epileptical equiva-

**Figure 9.** (A) Microphotographs with optical microscopy of cells of the primary visual cortex that were studied morphologically in the present study. Pando-et. al. Pathology Hospital Infantil de México. (Courtesy of Pando, et al.) (B)

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Microphotographs showing the superposed lines of the geometrical relation of the cell bodies.

Mechanisms underlying pathological characteristics have yet to be fully elucidated as stated by Nemeroff et al. (2003), but since then the biochemical research regarding GABA and receptor bioengineering of drugs that block GABA receptors, thus inciting in anxiety response, particularly with gabapentine and derivates working as neuromodulators and compared to the use of benzodiacepines. This must be taken as a proof that anxiety and panic attacks [14]

lent [1, 3, 4, 6–11, 13].

**Figure 8.** (A) Diagram showing the transformation of a photic stimulus and its amplification in the encephalon, generating the formation of an image and an associated memory. (Courtesy Pando et.al). (B) Diagram showing the phenomenon of amplification of information through the convergence/divergence principle in the time domain. (Courtesy Pando et al.).

Signals that are transcribed as semiconductors (neurofilaments) transit through synaptic trees in real time and stock these information for short periods of time between 1 ms up to more than 1 s from one membrane to another through an inter-synaptic space; the first membrane

All the way in a tetra-dimensional quanta information traveling through tensors and counter tensors, finding their way through space networks, and respecting the thermodynamical laws with an infinitesimal delay in this essential form of computational quantic central nervous

We have worked with human models from the cuts taken during anatomic-pathological

The findings corroborate the convergence/divergence composition from the third, pyramidal neurons of the cerebral cortex. The cortex in the hypocampus shows the same composition, and we think that this is a step for recruiting neurons and to form neural networks provide the structural basis of holograms, as shown in the following sketches

So if anxiety can be accepted as a most common form of co-morbidity or "aura" in most of structural or functional alterations of the CNS, we must also consider the probable fact that

**Figure 8.** (A) Diagram showing the transformation of a photic stimulus and its amplification in the encephalon, generating the formation of an image and an associated memory. (Courtesy Pando et.al). (B) Diagram showing the phenomenon of amplification of information through the convergence/divergence principle in the time domain. (Courtesy Pando et al.).

autopsies of children around 8 years of age who died from accidents (**Figure 2**).

of 50 Å (thickness) initiates the process.

58 Anxiety Disorders - From Childhood to Adulthood

system activity [2, 13] (**Figures 7**–**10**).

[2, 13] (**Figures 8**–**10**).

**Figure 9.** (A) Microphotographs with optical microscopy of cells of the primary visual cortex that were studied morphologically in the present study. Pando-et. al. Pathology Hospital Infantil de México. (Courtesy of Pando, et al.) (B) Microphotographs showing the superposed lines of the geometrical relation of the cell bodies.

within the definition of epilepsy, it can and must also be considered as an epileptical equivalent [1, 3, 4, 6–11, 13].

Mechanisms underlying pathological characteristics have yet to be fully elucidated as stated by Nemeroff et al. (2003), but since then the biochemical research regarding GABA and receptor bioengineering of drugs that block GABA receptors, thus inciting in anxiety response, particularly with gabapentine and derivates working as neuromodulators and compared to the use of benzodiacepines. This must be taken as a proof that anxiety and panic attacks [14]

**Figure 11.** GABA synapsis diagram. Courtesy from Neurochemistry by Laguna et al. Biochemistry 2013, Unam, Mexico.

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Lehninger 6th edition and Nihon Yukirigaku, The life cycle of GABA. Faculty of Dental Science, Japan.

**Figure 12.** Drugs Associated to Gaba: Gaba receptors. Ubication of Gaba Receptors. (public scheme).

**Figure 10.** From bidimensional formations through fractal mathematics, we obtain images as "holograms" that are the perception of each individual during the process of each individual's perception and networks from the outside or inside world (A–C). Courtesy from Neuroradiology authored book by Stoopen M, García R. Advances in Diagnosis through Images. 2010. Journal ed. Arg. (Spanish).

as well as post-traumatic stress [1, 15–17] respond to drugs that act within the context of neuromodulation of epileptical phenomena [18] (**Figures 11**–**13**).

So GABA deals with phosphorylation, highly reactive for activation of mRNA and process of transcription to produce antioxidative products, regulating these proceedings through NADPH and also regulates succinate and glutamate to stabilize neurons (includes Astroglía) (Shatsberg et al. 2008; Pando et al. 2017; Doctoral thesis National Politechnical Institute, National School of Biological Science) [18].

So which drugs interact with GABA if associated to anxiety?

The answer to this question goes rapidly to anticonvulsive drugs. More than inhibitors of the recapture of serotonine, and particularly at the subcortical level in the basic ganglia [18].

Anxiety as an Epileptical Equivalent (Temporal Lobe Epilepsy) http://dx.doi.org/10.5772/intechopen.78241 61

**Figure 11.** GABA synapsis diagram. Courtesy from Neurochemistry by Laguna et al. Biochemistry 2013, Unam, Mexico. Lehninger 6th edition and Nihon Yukirigaku, The life cycle of GABA. Faculty of Dental Science, Japan.

**Figure 12.** Drugs Associated to Gaba: Gaba receptors. Ubication of Gaba Receptors. (public scheme).

as well as post-traumatic stress [1, 15–17] respond to drugs that act within the context of

**Figure 10.** From bidimensional formations through fractal mathematics, we obtain images as "holograms" that are the perception of each individual during the process of each individual's perception and networks from the outside or inside world (A–C). Courtesy from Neuroradiology authored book by Stoopen M, García R. Advances in Diagnosis

So GABA deals with phosphorylation, highly reactive for activation of mRNA and process of transcription to produce antioxidative products, regulating these proceedings through NADPH and also regulates succinate and glutamate to stabilize neurons (includes Astroglía) (Shatsberg et al. 2008; Pando et al. 2017; Doctoral thesis National Politechnical Institute,

The answer to this question goes rapidly to anticonvulsive drugs. More than inhibitors of the recapture of serotonine, and particularly at the subcortical level in the basic ganglia

neuromodulation of epileptical phenomena [18] (**Figures 11**–**13**).

So which drugs interact with GABA if associated to anxiety?

National School of Biological Science) [18].

through Images. 2010. Journal ed. Arg. (Spanish).

60 Anxiety Disorders - From Childhood to Adulthood

[18].


As seen, the proposition to treat anxiety with other neuromodulators, including fitopharmacology different from antidepressives or benzodiacepines, is a serious and documented stand

Anxiety as an Epileptical Equivalent (Temporal Lobe Epilepsy)

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63

Most literatures talk about anxiety, but a very few intend to define it, because it is a subjective feeling and even the DSM in any version talks about it as a comorbidity of many pathologies, but does not define it as such; the proposal is to promote anxiety as an epileptic entity; its definition as another variety of epilepsy when related to temporal lobe epilepsy or diencephalic

There are no conflict of interests in this manuscript. The funding comes from CPALC Mexico

[2] Pando-orellana LA, Cabrera ML, Diaz Cintra S, et al. Modelo matemático de la relación functional neural, basado en microestructura. Revista Mexicana de Neurociencia.

[3] Vera F, Pando-Orellana LA, et al. EEG in patients with anxiety disorder. Revista Mexicana

[4] Pando LA. etal. Medical addictions. Revista Mexicana de Neurociencia. 2014;**15**(3):179-182 [5] Pando-Orellana LA et al. EVPOL questionnaire confiability and validity of the instrument in a sample of Mexican patients. Revista Mexicana de Neurociencia. 2009;**10**(6):443-445

[6] Johnson EK, Jones JE, Seidenberg M, Hermann BP. The relative impact of anxiety, depression, and clinical seizure features on health-related quality of life in epilepsy.

[7] Reuber M, Andersen B, Elger CE, Helmstaedter C. Depression and anxiety before and

after temporal lobe epilepsy surgery. Seizure. 2004;**13**:129-135

in anxiety therapeutics [18].

**Conflict of interest**

**Author details**

**References**

Luis A. Pando-Orellana

2016;**17**(3):3-1

CPALC/INCIch., Mexico City, Mexico

de Neurociencia. 2013;**14**(6):335-340

Epilepsia. 2004;**45**:544-550

alterations belonging to the limbic system [19–22].

city (Centro Para la Atención de Lesiones Cerebrales).

Address all correspondence to: drpando@hotmail.com

[1] Torta R, Keller R, et al. Epilepsia. 1999;**40**(Suppl. 10):s2-s20

**Figure 13.** Functions of neuromodulators. From Hospital Fray Bernardino Alvarez resident's internal operating manual, Mexico.

Antiepileptic drugs can be grouped according to their major mechanism of action. Some antiepileptic drugs work by acting on combination of channels or through some unknown mechanism of action (**Figure 14**).


**Figure 14.** Drugs and site of action. (Courtesy of Fray Bernardino Alvarez Hospital).

As seen, the proposition to treat anxiety with other neuromodulators, including fitopharmacology different from antidepressives or benzodiacepines, is a serious and documented stand in anxiety therapeutics [18].

Most literatures talk about anxiety, but a very few intend to define it, because it is a subjective feeling and even the DSM in any version talks about it as a comorbidity of many pathologies, but does not define it as such; the proposal is to promote anxiety as an epileptic entity; its definition as another variety of epilepsy when related to temporal lobe epilepsy or diencephalic alterations belonging to the limbic system [19–22].
