.

1. BOOK
TITLE :
MINDSET KINETICS AND CRIME BEHAVIOR- QUANTITATIVE METHODS? A NEW FORENSIC QUANTITATIVE
APPROACH . HOW BIOCHEMISTRY , TOXICOLOGY , IMAGING PRINCIPLE CAN HELP IN JURISDICTIONAL SETTINGS .
AUTHORS
1)luisetto m applied pharmacologist, independent researcher Italy 29121 maurolu65@gmail.com
2) Naseer Almukhtar, professor Dr., physiology, college of medicine, University of Babylon, Hilla, Iraq. E mail:
Naseer2012.Almukhtar@gmail.com
3) Farhan Ahmad Khan Associate Professor and Head, Department of Pharmacology
Government Medical College, Shahdol, M.P, India.
4) Khaled Edbey , Professor, department of chemistry University of Benghazi libia
5) Ahmed Yesvi Rafa Founder and President, Yugen Research Organization (YRO), Independent
ResearcherBangladesh
6) Oleg Yurevich Latyshev Harvard university Cambridge, United States Department
John F. Kennedy School of Government in Cambridge, MA.
KEYWORDS: CRIME, MINDSET KINETICS, QUANTITATIVE METHODS, PHYSIO-PATHOLOGY , JURISDICTIONAL
CHAPTER 1 ABSTRACT

2. In some non voluntary crimeis crucial verify the amygdala and limbic systemphysio-pathology of human responsible
of the facts under a
Jurisdictional contest.
But is relevantto verify this condition in really objective and instrumental way .
Many other human physio-pathological condition aredeeply investigated using biochemical or imagingtechnique :
today many organ and system are currently evaluated with high number of biomedical ,instrumental or imagingtest
also In basal or stressingcondition.
The objective setting of amygdala and limbic systemmust be added in jurisdictional procedurenotas a prove but an
additional information to be correctly evaluated.
In this work after a literatureevaluation some global conclusion areproduced .
CHAPTER 2 INTRODUCTION
Often is possibleto say : One second after often is too much.
In many crime situation mindsetkinetics of amygdala , limbic system, thalamus is a crucial aspectto be adequately
considered in jurisdictional settings.
This neuronal system are involved in manage of anger , impulsivity ,aggressiveness,fear and other emotional
response to various kind of stimulous.
In article“Amygdala Hijack and the Fight or FlightResponse”By Arlin Cuncic 2018 : “The term "amygdala hijack"was
introduced by the psychologistD.Goleman .He used the term to recognize that although we have evolved as
humans, we retain an ancient structurein our brain that is designed to respond swiftly to a threat.
FIGURE N. 1 lymbic system – thalamus

3. Figure n . 2
Figure n.3 amygdala activation
FIG. 4 amygdal activation

4. Figure n.5 18 FDG glucose amygdala activation
Figure n 7 amygdala hypoperfusion MRI and SPECT
Whileat one time this was designed to protect us, itcan interfere with our functioning in the modern world where
threats are often more subtlein nature. The amygdala is involved in the brain fear circuit,responsiblefor the fight-or-
flightresponsethat causes to respond to threats.

5. The amygdala is responsiblefor decidingwhatmemories arestored and where they arestored. The level of emotion
that is attached to a memory determines where itis stored in the CNS.
When faced with a threatening situation, thalamus,which receives incomingstimuli,sends signals to the amygdala
and the cortex.
If amygdala senses danger, it makes a splitsecond decision and begins the fight-or-flightresponsebefore the cortex
has time to over-rule it.
This cascadeof events triggers the release of adrenaline,which leads to increased heartrate, blood pressure,and
breathing. racingheart,shaking,sweating, and nausea as this happens.
the amygdala triggers a sudden and intense unconscious emotional responsethatshuts off the cortex, making ithard
for you to think clearly aboutthe situation.The brain triggers the release of stress hormones likecortisol,you find it
increasingly hard to problem solveand concentrate. This whole process takes a toll,and is possiblenotrecover to
original level of functioningfor several hours.
Chronic stress also playsa rolein the functioningof fear circuitry in thebrain.People with post-traumatic stress
disorder (PTSD) show greater amygdala activation and therefore, increased emotional respondingincludingfear and
anxiety responses.Those with other anxiety disorders,such as social anxiety disorder (SAD) and panic disorder (PD)
may also respond more strongly in their amygdala.
chronic stress can lead to an over-activefear and anxiety circuitin your brain,which also reduces the functioningof
other areas of the brain that help with inhibition of fear, such as the hippocampus and medial prefrontal cortex.
chronic stress can trigger more frequent amygdala hijacksand even subsequent problems with short-term memory.”
But Is possibleto say that this phenomena sincetoday is not measured or quantized in jurisdictional contest? To
differ pathological fromphysiological individuals?
In how many situation if availablemore time to think different actions could result?
To manage different and many informations in few seconds,or to control anger or other emotional reaction can be
difficultfor various subjects .
( activation of the rapid circuits :thalamus –amygdala or also the slowcircuits :involving also frontal cortex can
make the difference ).
Sensorial information arrivefrom thalamus to amygdala and from this startmotor signals.
Amygdala compare also pastexperiencewith the new intense stimulous .
Related this consideration is very importantto ask to justiceadministration to introducereally objectivemethods to
verify individualsreactivity in high stressingcondition.
A real measure of this condition make possibleto differ individual with normal management of minkset kinetics also
in high stressantcondition from whom present an abnormal reaction .
CHAPTER 3 MATERIAL AND METHODS
With an observational approach somerelevantliterature on PUBMED is analized to verify relationship between some
crime behavior and amigdala and limbic systemactivation in thevarious individuals involved in somecrime behavior.

6. After this review is submitted to researcher a global conclusion related to the topic of this work.
CHAPTER 4 RESULTS
From literature related to the topics of this work :
in articleAmygdala pharmacology and crimebehavior,dysfunctions to be considered as a disease.? Is reported that
: “we concludethat is needed to find an objective diagnostic systemto verify the basic level of activation status of
amygdala in stress conditions and also to find if a drugs
therapy systems can be considered if we have an organic pathology conditions.As others physiological apparatus:a
pathological activation and status can becontrolled by specific pharmacological therapy.”(1)
And related mindset kinetics article “ScientistlikeM. Planck,Einstein,Bohr, De Broglie,Schrödinger,Heisenberg et
others (involved in theory of quantum chemical physic field ),E. goldratt(Teory of constraints),Michaelis-Menten ( a
biochemistry kinetics theory), other biochemical and enzymatic reaction theory must be deeply investigated also in
other fields likeneuroscienceand applied in order to better clear some process .
The factor that can join the organic theories to the psychological approach can bean abnormal- pathological mindset
kinetics process or an overuse or saturation in somePsyco- neurological process.
And The singleresilienceability (or singlebuffer properties )in biochemical receptorial status mustbe also
objectivable
So a better objective way to verify the amount of stressingcondition, timeof exposure and quality mustbe
introduced.( in differente field like
Psycology,psychiatry ,forensic ) .
An useful instruments for healthcareprofessionalsand patients.(usingalso a toxicological approach:whattoxic
condition,amount and time of exposure and under a biochemical aspect( kinetics,max velocity of a system,
saturation) and not only the
receptorial status.
Observingbiochemistry kinetics lawcan we think that a Zero Order Kinetics in mindset kinetics can reducesome mind-
brain disorder? (Only a determinate quantum of stressingcondition in a definiteamount of time : really short,
medium or prolonged )” (6)
According Uri Maoz et al:
“A defendant is criminally responsiblefor his action only if he is shown to have engaged in a guilty act—actus reus (eg
for larceny,voluntarily takingsomeone else's property without permission)—whilepossessinga guilty mind—mens
rea (eg knowing that he had taken someone else's property without permission,intendingnot to return it)—and
lackingaffirmativedefenses ( in eg the insanity defense or self-defense). We firstreview neuroscientific studies that
bear on the nature of voluntary action,and so could,potentially,tell us something of importance about the actus reus
of crimes.Then we look at studies of intention, perception of risk, other mental states that matter to the mens rea of

7. crimes.we discuss studiesof self-control,which might be relevant to some formulations of the insanity defense. As
we show, to date, very littleis known about the brain thatis of significancefor understandingcriminal responsibility.
But there is no reason to think that neurosciencecannot provideevidence that will challengeour understandingof
criminal responsibility.”(7)
Sergio Canavero written :
“Although the definition of criminal behavior is fraughtwith controversy,with singleacts “criminalized”or
“decriminalized”accordingto time and place,and as such being observed in individualsof all sorts,there seems to be
an agreement across theboard that the truly dangerous subjects arepsycho-paths and the subjects affected by the
Anti-social Personality Disorder”(8)
And Rebecca Roache showed that :
“L Berlin reports that neuro-scientific data play an increasingrolein court.They have been used to argue that
criminalsarenotmorally responsiblefor their behaviour becausetheir brains are‘faulty’,and there is evidence that
such data lead judges to pass more lenient sentences.
I raise2 concerns about the view that neurosciencecan show criminalsnotto be morally responsible:
That the brains of (say) violentcriminalsdiffer frommost people’s brains does not straightforwardly showthatviolent
criminalsareless morally responsible.Behavioral states ariseinter aliafrombrain states,and sinceviolentcriminals’
behavioral states differ from those of most people, it is unsurprisingthatviolentcriminals’brainsshould differ from
most people’s brains.This no more shows violentcriminalsto have diminished moral responsibility than differences
between the brains of cheerful and uncheerful people show either group to have diminished moral responsibility.
Those who view brain abnormalities as evidenceof reduced moral responsibility rely on the assumptions thatpeople
with normal brains havefree will and that we know what sorts of brain activity underminefree will. both of these
assumptions arehighly controversial.As a result,neuroscience is not a reliablesourceof information aboutmoral
responsibility.
until we settle whether and under what circumstances brain activity i s incompatiblewith free will,neuroscience
cannot tell us anythinguseful about criminal accountability.”(8)
according Dean Mobbs et al :
“Archaeological discoveriesof traumatic injuries in primitivehominid skullsstrongly hintthatour species ha s a long
history of violence. Despite repeated attempts throughout history,includingefforts to eliminateviolencethrough the
imposition of criminal sanctions,we have yet to dispel our violentnature. Consequently, criminal violenceremains a
common feature of most societies.As policy-makers seek deeper understandings of criminally violentand anti-social
behavior,many contemporary neuro-scientists assumethatthe essential ingredients of the human condition,
includingfreewill,empathy, and morality,are the calculableconsequences of an immense assembly of neurons firing.
Intuitively,this view opposes Cartesian dualism(the brain and mind areseparate, but interacting,entities) and
assumes that violenceand antisocial behavioremanate from a mechanistically determined brain”(9)
Robert K. Naumann et al showed that :
A Primer on the reptile brain,in particular thelightitsheds on the structural and functional evolution of the
vertebrate neural circuits.

8. “Deep insidethe skull of every one of us there is something likea brain of a crocodile.Surroundingthe R-complex is
the limbic systemor mammalian brain,which evolved tens of millions of years ago in ancestors who were mammal
but not yet primates. It is a major sourceof our moods and emotions, of our concern and carefor the young. And
finally,on the outside, livingin uneasy trucewith the more primitivebrains beneath,is the cerebral cortex; civilization
is a product of the cerebral cortex.”
— Carl Sagan,Cosmos p.276–277
“C. Sagan’s amusingwords of wisdom notwithstanding — is the H-bomb not also a productof the cerebral cortex? —
is the reptilian brain really justa mammalian brain missingmostof the parts? Some 320 million years ago,the
evolution of a protective membrane surrounding the embryo, the amnion,enabled vertebrates to develop outsideof
water and thus to invade new terrestrial niches.These amniotes were the ancestors of today’s mammals and
sauropsids(reptiles and birds).Present-day reptiles area diverse group of more than 10,000 species that comprise
sphenodons (‘Tuatara’), lizards,snakes,turtles and crocodilians.Although turtles were once thought to be the most
‘primitive’among reptiles,current genomic data point toward two major groupings:the Squamata (lizards and
snakes);and a group comprisingboth the turtles and the Archosauria (dinosaurs,modern birds and crocodilians) .
Dinosaurs inhabited the Earth from the Triassic (230 million years ago),ata time when the entire landmass formed a
singlePangaea.They flourished fromthe beginning of the Jurassicto the mass extinction atthe end of Cretaceous (65
million years ago),and birds aretheir only survivors.”(10)
According Hoerst M et al :
“Emotional dysfunction in a fronto-limbic network has been implicated in the pathophysiology of borderline
personality disorder (BPD).The amygdala is a key region of the limbic systemand plays an importantrolein
impulsivity,affectregulation,and emotional information processingand thus is likely related to BPD symptoms.
Alterations of the metabolismin the amygdala might be of interest for understandingthe pathophysiology of BPD.
the amygdala is a difficultregion from which to acquiremagnetic resonancespectra. We implemented a method for
proton magnetic resonance spectroscopy ((1)HMRS) at 3.0 T in which we acquiredata within only the small amygdala.
The purpose of this study was to determine alterations of the metabolismin the amygdala in BPD patients.
Twenty-one unmedicated BPD patients and 20 age-matched healthy control participantsunderwent (1)H MRS to
determine neurometabolite concentrations in the left amygdala.All participants underwent psycho-metric
assessments.
Significantly reduced total N-acetylaspartate(tNAA) and total creatine (tCr) concentrations in the left amygdala of
patients with BPD were founded. BPD patients with comorbid post-traumatic stress disorder (PTSD) showed lower
levels of tCr compared with BPD patients without PTSD and healthy control subjects.No significantcorrelations
between neurochemical concentrations and psychometric measures were founded.
Decreased tNAA and tCr might indicatedisturbed affectregulation and emotional information processingin the
amygdala of BPD patients.These findings are consistentwith many functional and structural neuro-imagingstudies
and may help to explain the greater emotional reactivity of BPD patients”(11)
Sakai Y et al written :
“The present work was performed to assess cerebral glucosemetabolismin patients with panic disorder using
positron emission tomography.F-fluoro-deoxyglucosepositron emission tomography with voxel-based analysiswas
used to compare regional brain glucoseutilization in 12 nonmedicated panic disorder patients,withouttheir
experiencingpanic attacks duringpositron emission tomography acquisition,with that in 22 healthy controls.Panic
disorder patients showed appreciably high stateanxiety before scanning,and exhibited significantly higher levels of

9. glucoseuptake in the bilateral amygdala,hippocampus, thalamus,in midbrain,caudal pons,medulla,and cerebellum
than controls.These results provided the firstfunctional neuroimagingsupportin human patients for the
neuroanatomical hypothesis of panic disorder focusingon the amygdala-based fear network.”(12)
And Sofi da Cunha-Bang et al :
“The ability to successfully suppressimpulses and angry affectis fundamental to control aggressivereactions
followingprovocations.Theaimof this work was to examine neural responses to provocations and aggression usinga
laboratory model of reactive aggression.Weused a novel functional magnetic resonanceimagingpoint-subtraction
aggression paradigmin 44 men, of whom 18 were incarcerated violentoffenders and 26 were control non-offenders.
We measured brain activation followingprovocations(monetary subtractions),whilethe subjects had the possibility
to behave aggressively or pursuemonetary rewards.The violentoffenders behaved more aggressively than controls
(aggression frequency 150 vs 84, P = 0.03) and showed significantly higher brain reactivity to provocations within the
amygdala and striatum,as well as reduced amygdala-prefrontal and striato-prefrontal connectivity.Amygdala
reactivity to provocations was positively correlated with task-related behavior in the violentoffenders. Across groups,
striatal and theprefrontal reactivity to provocations was positively associated with traitanger and traitaggression.
These results suggestthat violentindividualsdisplay abnormally high neural sensitivity to social provocations,a
sensitivity related to aggressivebehavior.These findings providenew insightinto the neural pathways that are
sensitiveto provocations,which is critical to more effectively shaped interventions that aimto reduce pathological
aggressivebehavior.“(13)
Larry J. Siever showed that :
“Acts of violenceaccountfor an estimated 1.43 million deaths world-wideannually.Whileviolence can occur in many
contexts, individual acts of aggression accountfor the majority of instances.In some individuals,repetitiveacts of
aggression aregrounded in an underlyingneuro-biological
susceptibility thatis justbeginningto be understood. The failureof “top-down” control systems in the prefrontal
cortex to modulate aggressiveacts that aretriggered by anger provokingstimuli appears to play an importantrole. An
imbalancebetween prefrontal regulatory influences and
hyper-responsivity of the amygdala and other limbic regions involved in affectiveevaluation are implicated.
Insufficientserotonergic facilitation of “top-down” control,excessivecatecholaminergic stimulation,and subcortical
imbalances of glutamatergic/ gabaminergic
systems as well as pathology in neuropeptide systems involved in the regulation of affiliative behavior may contribute
to abnormalities in this circuitry. pharmacological interventions such as mood stabilizers,which dampen limbic
irritability,or selectiveserotonin reuptake
inhibitors (SSRIs), which may enhance “top-down” control,as well as psychosocial interventions to develop alternative
copingskillsand reinforcereflectivedelays may be therapeutic.
Structural imaging—Whilelesion studies evaluateeffects of damage to specific brain regions,structural imaging
paradigms measurenaturalisticvariability in volumes and shapes of brain structures.Reductions in prefrontal gray
matter that arepresumably based in
aberrantdevelopment have been reported in individualswith antisocial personality disorder and areoften associated
with autonomic deficits . Significantvolumereductions havebeen demonstrated in the left orbital frontal- cortex and
rightanterior- cingulatecortex in
patients with borderlinepersonality disorder ,most marked in Brodmann’s area 24, which has also been implicated in
functional imagingstudies of these patients. The temporal cortex, particularly in themedial temporal cortex and
hippocampus,has also been

10. demonstrated to have structural alterations,includingaltered asymmetry in antisocial subjects.
Orbital frontal/cingulatecortical processingefficiency—Functional brain imaginingpermits an assessmentof brain
activation patterns in specific regions of interestin individualswith a history of recurrent episodic violentbehavior.
Initial studies focusingon
psychiatricpatients with a history of violencedemonstrated decreased glucosemetabolism usinga positron emission
tomography with [18]fluorodeoxyglucose(FDG-PET) paradigmin the temporal and frontal cortices . Similar results
were obtained in a study of murderers.
An inverserelationship hasalso been reported between the history of impulsive aggressivebehavior and glucose
metabolismin the orbital frontal cortex and right temporal cortex, with reductions of metabolism in prefrontal
Brodmann’s areas 46 and 6 in patients with borderlinepersonality disorder .In a PET study evaluatingresponses to
the probe metachlorophenylpiperazine,decrements in the lateral,medial,and orbital frontal cortices were found at
baselinein men with a history of physical aggression and in theorbital frontal cortex for both men and women with a
history of physical aggression .In an imaging study of an unrestrained aggressivescenario,healthy volunteers
demonstrated blood flow
reductions in the orbital frontal cortex,suggestinga releaseof “top-down” control of aggression .Whileparticipating
in a laboratory designed to provoke aggression,the Point Subtraction Aggression Paradigm,patients with intermittent
explosivedisorder,as
determined by integrated research criteria,and borderlinepersonality disorder mademore aggressiveresponses
relativeto comparison subjects .In the Point Subtraction Aggression Paradigm,patients with borderlinepersonality
disorder who were characterized
by anger dys-control showed diminished responses to provocation in the medial frontal cortex and the anterior frontal
cortex relativeto comparison subjects butgreater responses in the orbital frontal cortex,presumably to dampen
aggressiveresponses .In an fMRI
paradigm, when viewing negative pictures compared with rest, patients with borderline personality disorder showed
greater activity relativeto healthy comparison subjects in the amygdala,fusiformgyrus,para-hippocampul gyrus,
cerebellar declive,ventro-lateral
prefrontal cortex, occipital visual areas,and regions related to sensory,emotional, and facial processing,whilehealthy
comparison subjects showed greater activity in the insula, involved in visceral emotional processing,and the dorso-
medial/dorsolateral pre-frontal
cortex, involved in cognitiveprocessing. ”(14)
according Lara C.Foland-Ross ET AL :
“Recent evidence suggests that putting feelings into words activates the prefrontal cortex (PFC), and suppresses the
responseof the amygdala,potentially helpingto alleviateemotional distress.To further elucidatethe relationship
between brain structureand function in these regions,structural and functional magnetic resonanceimaging(MRI)
data were collected from a sampleof 20 healthy human subjects.Structural MRI data were processed usingcortical
pattern matchingalgorithms to produce spatially normalized maps of cortical thickness.Duringfunctional scanning,
subjects cognitively assessed an emotional target face by choosingone of two linguistic labels(label emotion
condition) or matched geometric forms (control condition).Manually prescribed regions of interestfor the left
amygdala were used to extract percent signal changein this region occurringduringthe contrastof “label emotion”
versus “match forms.” A correlation analysisbetween left amygdala activation and cortical thickness was then
performed alongeach pointof the cortical surface,resultingin a color coded r valueat each cortical point.Correlation
analyses revealed thatgray matter thickness in left ventro-medial PFC was inversely correlated with task-related

11. activation in the amygdala.These data add support to a general role of the ventro-medial PFC in regulatingactivity of
the amygdala.”(15)
Roee Admon et al :
“An intactamygdala is thought to be critical for advantaged processingof relevant stimuli in theenvironment via
efficient taggingof its emotional nature , whereas the hippocampus was found to be involved in forming episodic
representations of emotional events by taggingcontextual meaning to it . Therefore, itis possiblethatduringthe
second time point (i.e., After Stress), the limbic responseto a context in which the stressful experiencetook place(i.e.,
medical) is related to the fact that this context is a reminder of the stressful event, thus evoking emotions. This is
further supported by our findingthat the individual amygdalaand hippocampus activation levels After Stress were
positively correlated with the change in stress symptoms over time , implyingthat the more emotionally significant
the context is for the individual,the more intensely those regions respond to reminders of it. Similarly,thelevels of
amygdala activation and hippocampal volume were found to be correlated with symptom severity in PTSD . Our
current findings,however, show that even in the healthy brain the limbic responseto stress -related content within a
few months after the occurrence of a stressful lifeevent is related to an increasein stress symptoms. In that regard it
is importantto note, however, that our participantswere all adolescents,and itis widely recognized that during
adolescencethe brain shows remarkablechanges in both structure and function . Thus, stressors experienced during
adolescencemay have a different neural impactthan when experienced at adulthood,and future studies should
examine the age generality of our findings in older cohorts.”(16)
Altshuler L et al :
“This study sought to investigateneural activity in the amygdala duringepisodes of mania.
Nine manic subjects and nine healthy comparison subjects underwent functional magnetic resonance imaging(fMRI)
whileperforming a neuropsychological paradigmknown to activatethe amygdala.Subjects viewed faces displaying
affect (experimental task) and geometric forms (control task) and matched them to one of two simultaneously
presented similarimages.
Manic subjects had significantly increased activation in theleft amygdala and reduced bilateral activation in thelateral
orbitofrontal cortex relativeto the comparison subjects.
Increased activation in theamygdala and decreased activation in the orbitofrontal cortex may represent disruption of
a specific neuroanatomic circuitinvolved in mania. Thesebrain regions may be implicated in disorders involving
regulation of affect.” (17)
Sofi da Cunha-Ba et al :
“The ability to successfully suppressimpulses and angry affectis fundamental to control aggressivereactions following
provocations.The aimof this study was to examine neural responses to provocations and aggression usinga
laboratory model of reactive aggression.Weused a novel functional magnetic resonanceimagingpoint-subtraction
aggression paradigmin 44 men, of whom 18 were incarcerated violentoffenders and 26 were control non-offenders.
We measured brain activation followingprovocations(monetary subtractions),whilethe subjects had the possibility
to behave aggressively or pursuemonetary rewards.The violentoffenders behaved more aggressively than controls
(aggression frequency 150 vs 84, P = 0.03) and showed significantly higher brain reactivity to provocations within the
amygdala and striatum,as well as reduced amygdala-prefrontal and striato-prefrontal connectivity.Amygdala
reactivity to provocations was positively correlated with task-related behavior in the violentoffenders. Across groups,
striatal and prefrontal reactivity to provocations was positively associated with traitanger and traitaggression.These
results suggestthat violentindividualsdisplay abnormally high neural sensitivity to social provocations,a sensitivity
related to aggressivebehavior.These findings providenovel insightinto the neural pathways that are sensitiveto
provocations,which is critical to more effectively shaped interventions that aimto reduce pathological aggressive
behavior.Fig. 1 “(18)

12. M Brower et al :
“To establish thelink between frontal lobedysfunction and violentand criminal behaviour,based on a review of
relevant literature.
Articles relatingevidence of frontal lobedysfunction with violenceor crimewere collected through a MEDLINE search
usingthe keyword "frontal lobe" combined with the terms "aggression,""violence," "crime," "antisocial personality
disorder,""psychopathy," "impulsecontrol disorders",and "episodic dyscontrol."Reference lists werethen searched
for additional articles.
High rates of neuropsychiatric abnormalitiesreported in persons with violent and criminal behaviour suggestan
association between aggressivedyscontrol and brain injury,especially involvingthefrontal lobes.The studies
reviewed support an association between frontal lobedysfunction and increased aggressiveand antisocial behaviour.
Focal orbitofrontal injury is specifically associated with increased aggression.Deficitsin frontal executivefunction may
increasethe likelihood of future aggression,but no study has reliably demonstrated a characteristic pattern of frontal
network dysfunction predictiveof violent crime.
Clinically significantfocal frontal lobedysfunction isassociated with aggressivedyscontrol,butthe increased risk of
violenceseems less than is widely presumed. Evidence is strongestfor an association between focal prefrontal
damage and an impulsivesubtypeof aggressivebehaviour.” (19)
Hirono N et al :
“Aggressive behavior is common in patients with dementia disease.Temporo-limbic and prefrontal cortical lesions
can produce pathological aggression;involvement of these structures has not been established in aggressivepatients
with dementia.
To study the relation between the regional brain perfusion and aggressivebehavior in patients with dementia.
We compared the pattern of regional cerebral perfusion determined with technetium Tc 99m-labeled
hexamethylpropelene amineoxime singlephoton emission computed tomography in 2 groups of 10 patients with
dementia with and without aggression,thatwere comparablefor demographic factors,severity of cognitive
impairments,and other behavioral symptoms as measured by the Neuro-psychiatric Inventory.
Patients with aggression revealed significant(P<.001) hypo-perfusion in the left anterior temporal cortex; additional
bilateral dorso-frontal and rightparietal cortex were also found to be significantly hypo-perfused.
These results indicated an association between aggression and decreased perfusion in the left anterior temporal
cortex. “(20)
RaineAet al :
Major damage to gray and white matter in the pre-frontal cortex and autonomic deficits havebeen found to resultin
pseudo-psychopathic personality in patients with neurological disorders,butitis not known whether people with
antisocial personality disorder (APD) in the community who do not have discernablebrain trauma also havesubtle
prefrontal deficits.
Prefrontal gray and white matter volumes were assessed usingstructural magnetic resonanceimagingin 21
community volunteers with APD and in 2 control groups,comprising34 healthy subjects , 26 subjects with substance

13. dependence (substance-dependent group), and 21 psychiatric controls.Autonomic activity (skin conductanceand
heart rate) was also assessed duringa social stressor in which participants gavea video-taped speech on their faults.
The APD group showed an 11.0% reduction in prefrontal gray matter volume in the absence of ostensiblebrain lesions
and reduced autonomic activity duringthe stressor.These deficits predicted group membership independent of
psycho-social risk factors.
these findings providethe firstevidence for a structural brain deficitin APD. This prefrontal structural deficitmay
underliethe low arousal,poor fear conditioning,lack of conscience,and decision-makingdeficitsthathave been
found to characterizeanti-social,psycho-pathic behavior.”(21)
according VolkowND et al:
“Brain function was evaluated in four psychiatricpatients with a history of repetitive purposeless violentbehaviour ,
usingEEG, CT scan, positron emission tomography (PET). Three patients showed spikingactivity in lefttemporal
regions,and two showed CT scan abnormalities characterised by generalised cortical atrophy.The PET scans for the
four cases showed evidence of blood flow and metabolic abnormalities in theleft temporal lobe. 2 patients also had
derangement in the frontal cortex. The patients showing the largestdefects with the PET scans were those whose CT
scans were reported as normal.This work shows the utility of PET in investigatingpossiblebrain derangements that
could lead to violent behaviour.” (22)
Michael Wonget al showed that :
“To examine if different violentoffending behaviours areassociated with different clinical and neuro-imagingprofiles.
39 schizophrenic and schizo-affectiveoffenders from a maximum security mental hospital –20 repetitive violent
offenders (RVOs) and 19 non-repetitive violentoffenders (NRVOs) – were selected for clinical and neuroimaging
assessments.
Both groups had positivefamily history of mental illnessand violence.Age, diagnosis,duration of illness,victim
profiles and useof weapons at the time of the index offence were similar.RVOs had a higher prevalence of early
parental separation,juvenileconductproblem, previous convictions of crimes notinvolvingviolence,impulsivesuicide
attempts, delusion of their lives beingthreatened at the time of the index offence and electro-encephalographic (EEG)
abnormalities localized to temporal lobes. NRVOs had a higher prevalenceof sexual in-experienceand command
hallucinationsto kill atthe time of the index offence. Asymmetric gyral patterns at the temporo-parietal region were
particularly common in RVOs and absent in NRVOs. Non-specific whitematter changes in MRI and generalized cortical
hypo-metabolismin PET were present in both groups.

14. Different structural and metabolic changes in the brain were associated with different violentoffending behaviours.
The complex interaction between violent behaviour,clinical features and neuroimagingfindings in schizophrenia
requires further studies”.(23)
Armin H. Seidl et al :
“Timely delivery of information is essential for proper function of the nervous system. Precise regulation of nerve
conduction velocity is needed for correct exertion of motor skills,sensory integration and cognitivefunctions.In
vertebrates, the rapid transmission of signalsalong the nerve fibers is madepossibleby the myelination of axons and
the resultingsaltatory conduction in between nodes of Ranvier. Myelin is a specialization of glia cells and isprovided
by oligo-dendrocytes in the central nervous system. Myelination not only maximizes conduction velocity and provides
a means to systematically regulateconduction times in the NS
. Systematic regulation of conduction velocity alongaxons,and thus systematic regulation of conduction time in
between neural areas,is a common occurrence in the NS .
Little is understood about the mechanismthat underlies systematic conduction velocity regulation and conduction
time synchrony.Node assembly,internode distance(node spacing) and axon diameter - all parameters determining
the speed of signal propagation alongaxons –are controlled by myelinatingglia.an interaction between glial cells and
neurons has been
suggested.
This review work summarizes examples of neural systems in which conduction velocity is regulated by
anatomical variationsalongaxons.Whilefunctional implicationsin thesesystems arenot always clear,recentstudies
in the auditory system of birds and mammals present example. of conduction velocity regulation in systems with high
temporal precision and a defined biological function.
these findings suggestan activeprocess that shapes the interaction between axons and myelinatingglia to control
conduction velocity alongaxons.
conduction velocity is used for the speed of signal propagation,i.e.the speed at which an action potential travels.
Conduction time refers to the time ittakes for a specific signal to travel from its origin to its target, i.e. neuronal cell
body to axonal terminal.
An example of systematic regulation of conduction velocity in mammals is found in the fibers from the inferior olive
(IO) to cerebellar purkinjecellsin rats.Purkinje cellsin thecerebellar cortex display a high level of spiking
synchronicity,supported by
electrical couplingof IO cells through gap junctions.In rats,the olivocerebellar path length varies considerably
between the different parts of the cerebellar cortex (Sugihara et al., 1993),however their conduction times are fairly
equal (Sugihara et al.,1993; Lang and

15. Rosenbluth, 2003). Variationsin axon diameter as well as differential myelination contribute to these isochronic
inputs (Sugihara et al.,1993; Lang and Rosenbluth, 2003). It should be noted that these findings arenot without
controversy; these results havenot been observed in the cat,suggesting that the iso-chronicity of the olivo-cerebellar
pathway is due to a restricted brain sizein smaller animals(Aggelopoulos et al., Baker and Edgley).
Another representation of intra-axonal variation of conduction velocity was illustrated in the Thalamo-cortical
pathway of mice by Salami and colleagues (Salami etal., ). Neurons in the ventro-basal nucleus of the thalamus
project to different areas in the cortex and their
projections differ widely in length. The axon partitions in the intra-cortical region,however, cover a similar distance,
due to the architecture of the cortical areas.Despitethe length difference of the projections,action potentials elicited
in the thalamus arrivearound the same time at their target. Within cortical areas,conduction velocity slows down
about 10- fold in thalamo-cortical axons,mostlikely the resultof decreased myelination.Thus, the longer, more
variableaxon segments propagateaction potentials quickly,whilethe shorter, uniform segments contribute most to
overall conduction time.
In the retina,variationsin conduction velocity minimizeconduction time differences among retinal ganglion cell axons
(Stanford ). This presumably ensures spatio-temporal representation of the retinal image so that differences between
conduction times to the
lateral geniculatenucleus areminimized.
This presumably ensures spatio-temporal representation of the retinal image so that differences between conduction
times to the
lateral geniculatenucleus areminimized.Another example is found in the projection from the lateral amygdala to
distributed perirhinal sites.Conduction times aresimilar, despitethe fact that the signalsmusttravel different
distances”(24)

16. Figure n. 8 Heightened amygdala and striatal reactivity to provocations in violentoffenders. (A) “Amygdala reactivity”
represents signal values extracted from left and right amygdala clusters significantly activated in responseto
provocations acrossall participants.Violentoffenders show significantly higher amygdala reactivity to provocations
(P¼0.02). (B) “Striatal Reactivity”represents signal values extracted from left and right striatal clusters significantly
activated in response to provocations acrossall participants.Violentoffenders show significantly higher amygdala
reactivity to provocations (P¼0.02).Squares represent group mean and error bars represent standard deviations.(
from reference n . 18)
• Front Psychol.2017 Jan 10;7:2029. doi: 10.3389/fpsyg.2016.02029.eCollection 2016. Amygdala Responseto
Emotional Stimuli without Awareness: Facts and Interpretations Matteo Diano1,2,Alessia Celeghin1,2*,Arianna
Bagnis2 and Marco Tamietto1,2,3
“One early study combiningMEG and MRI methods reported Early event-related synchronization in theAmgat 20–
30ms After stimulus onset,where as synchronization in the striate Cortex occurred later,atabout 40–50 ms after
stimulus onset(Luo etal., 2007). A more recen tMEG study revealed Dissociation between rapid Amg responses to
automatic fearful Face processingand later responses thatinteracted with voluntary
attention. One achtrial,participants had to discriminatethe orientation of peripheral bars whiletask-irrelevantneutral
or fearful faces were presented centrally.Rapid enhancement of neural activity in the gamma band triggered by
threatening faces(30–60ms)was independent of task load and occurred under attentional unawareness,wherease
motion processingand attention interacted at later latencies (280–340ms),subsequentto
fronto-parietal activity(Luo etal.,2010). Coherently,two other MEG studies applyingdynamic causal
modelling(DCM)tested The explanatory power of the automatic Amg responseallegedly
mediated via subcortical route,versus a model predictingonly cortical mediation associated with stimulus awareness
over Amg response.A model consideringalso automatic Amg responses mediated by a subcortical routeexplained
early brain activity”(25)
Luiz Pessoa et al :
“The evidence we have reviewed here suggests that the idea of a subcortical pathway thatis specialized for the
processingof emotional stimuli should berevised.Our reinterpretation has importantimplicationsfor the
conceptualization of the amygdala’s function in the processingof emotional visual information.Wesuggest two
revised roles for the amygdala.First,the amygdala has a mostly modulatory role in a wide array of networks. The
precisefunctional importanceof the amygdala in these networks remai ns to be investigated, but it is unlikely thatit
will map specifically onto emotion. Instead,we think that it corresponds to broader and more abstractdimensions of
information processing,includingprocessingof salience,significance,ambiguity,unpredictability21,97–99 and other
aspects of ‘biological value’.More broadly,we argue that the amygdala has a key role in solvingthe following
problem100: how can a limited-capacity information processingsystemthat receives a constant stream of diverse
inputs selectively process thoseinputs that are the most relevant to the goals of the animal101?
Thus, the amygdala serves to allocateprocessingresources to stimuli,atleastin partby modulating(through its
connectivity) the anatomical components that are required to prioritizeparticular features of information processing
in a given situation.Such a rolewould come into play not only for affectively significantstimuli butalso for other
stimuli.Notably,the amygdala may not be uniquein this respect as there are other, largely parallel,networks with
architectures that do not includethe amygdala but that also enablediversefunctions — notably the network
subserved by the connections between the cortex and the pulvinar.Wethink that our proposal is consistentwith the
majority of findings and can accommodateseveral views of amygdala function16,102,103,with the difference that it
provides a broader and more flexibleperspective.

17. The second aspectof our proposed revision is to stress the speed and temporal dispersion of cortical processing,
which render moot the assumed need for a fastsubcortical route.Many visual properties can beprocessed very
rapidly by the initial waveof cortical response,which suggests that there is ampletime for substantial feedback,even
within the cortex. Consequently, understandingthe flow of visual information within the cortex should help us to
understand how affective stimuli areprocessed.Ultimately,the fate of a biologically-relevantstimulusshould notbe
understood in terms of a ‘low road’ versus a ‘high road’,but in terms of the ‘multipleroads’that lead to the
expression of observed behaviours.
There is an enormous literatureimplicatingtheamygdala in affective dysfunction in nearly every psychiatrici llness,
most notably in mood disorders.The revised view in this Perspective suggests that rather than focusingon neurons
within the amygdala,we should focus on connections within the cortex and between the cortex and subcortical
structures such as the amygdala.This may not come as a bigsurpriseto some readers as,in the main,it simply reflects
the idea that the substrateof brain function is notso much to be found within neurons as within networks.” (26)
Sean McDougall et al :
“Myelination of prefrontal circuits duringadolescenceis thoughtto lead to enhanced cognitiveprocessingand
improved behavioral control.However, whilestandard neuroimagingtechniques commonly used in human and
animal studies can measurelargewhite matter bundles and residual conduction speed,they cannotdirectly measure
myelination of individual axons or howfastelectrical signals travel alongthese axons.Here we focused on a specific
population of prefrontal axons to directly measure conduction vel ocity and myelin microstructurein developingmale
rats.An in vitro electrophysiological approach enabled us to isolatemonosynaptic projectionsfromthe anterior
branches of the corpus callosum(corpus callosum-forceps minor,CCFM) to the anterior cingulatesubregion of the
medial prefrontal cortex (Cg1) and to measure the speed and direction of action potentials propagatingalongthese
axons.We found that a largenumber of axons projectingfrom the CCFM to neurons in Layer V of Cg1 areensheathed
with myelin between pre-adolescence[postnatal day (PD)15] and mid-adolescence(PD43). This robustincreasein
axonal myelination isaccompanied by a near doublingof transmission speed.As there was no age difference in the
diameter of these axons,myelin is likely thedrivingforcebehind faster transmission of electrical signalsin older
animals.Thesedevelopmental changes in axonal microstructureand physiology may extend to other axonal
populations as well,and could underliesomeof the improvements in cognitiveprocessingbetween childhood and
adolescence.”(27)
Ekaterina Likhtik et al :
“Accumulating evidence indicates thatphobic and posttraumatic anxiety disorders likely resultfroma failureto
extinguish fear memories. Extinction normally depends on a new learningthat competes with the original fear
memory and is driven by medial prefrontal cortex (mPFC) projections to the amygdala.Although mPFC stimulation
was reported to inhibitthe central medial (CEm) amygdala neurons that mediate fear responses via their brainstem
and hypothalamic projections,itis unclear howthis inhibition isgenerated. Because the mPFC has very sparse
projections to CEm output neurons, the mPFC-evoked inhibition of the CEm is likely indirect.Thus,this study tested
whether it resulted from a feedforward inhibition of basolateral amygdala(BLA) neurons that normally relay sensory
inputs to the CEm. However, our results indicatethat mPFC inputs excite rather than inhibitBLA neurons, implying
that the inhibition of CEm cells is mediated by an activegating mechanismdownstream of the BLA”(28)

18. JQuirk et al :
“Single neurons were recorded in freely behaving rats duringfear conditioningfromareas of auditory cortex that
project to the lateral nucleus of the amygdala (LA). The latency and rate of conditioningand extinction were analyzed,
and the results were compared to previous recordings fromLA itself.Auditory cortex neurons took more trials to
learn,and they responded more slowly than LA neurons within trials.Short-latency plasticity in LA, therefore, reflects
inputs from the auditory thalamus rather than the auditory cortex. Unlike LA cells,some auditory cortex cells showed
late conditioned responses that seemed to anticipatethe unconditioned stimulus,whileothers showed extinction-
resistantmemory storage. Thus, rapid conditioningof fear responses to potentially dangerous stimuli depends on
plasticity in the amygdala,whilecortical areas may be particularly involved in higher cognitive(mnemonic and
attentional) processingof fear experiences.” (29)
Yohan J. John et al :
“In a complex environment that contains both opportunities and threats, it is importantfor an organismto flexibly
directattention based on current events and prior plans.The amygdala,the hub of the brain's emotional system,is
involved in forming and signalingaffectiveassociationsbetween stimuli and their consequences. The inhibitory
thalamic reticularnucleus (TRN) is a hub of the attentional system that gates thalamo-cortical signaling.In the primate
brain,a recently discovered pathway from the amygdala sends robustproj ections to TRN. Here we used
computational modelingto demonstrate how the amygdala-TRN pathway, embedded in a wider neural circuit,can
mediate selectiveattention guided by emotions. Our Emotional Gatekeeper model demonstrates how this circuit
enables focused top-down, and flexiblebottom-up, allocation of attention. The model suggests that the amygdala-
TRN projection can serve as a unique mechanismfor emotion-guided selection of signalssentto cortex for further
processing.This inhibitory selection mechanismcan mediatea powerful affective ‘framing’ effect that may lead to
biased decision-makingin highly charged emotional situations.The model also supports the idea that the amygdala
can serve as a relevance detection system. Further, the model demonstrates how abnormal top-down drive and
dysregulated local inhibition in the amygdala and in the cortex can contribute to the attentional symptoms that
accompany several neuropsychiatric disorders. “(30)
CHAPTER 5 DISCUSSION
in vertebrates evolution ( also in humans ) some relevant neuronal circuitlike thalamus- amygdala arepresent but if
this circuits
in reptile was an evolutive advantages in humans today can be a wrong characterisctic in actual society .
Accurate legal psycologic or psychiatric opinion areasked by judges but there are really objectiveand instrumental
measured results?
Amygdala activation metabolismcan producedifferent reactions in different individualsalso under the same amount
of stilmulous.
Under an evolutive approach amygdala and limbic systemare “builded” to react in more rapid way versus cortex to
protect the organismfrom
Resque and sudden dangerous stimuli .
The rapid responsein this way is an evolutiveadvantages , but the same circuits can bedangerous if activated in
humans in actual days and society.

19. If in voluntary crimecortex play a relevant rolein the non voluntary amygdala and limbicsystemareinvolved in
priority ways.
( the rapid circuits activation ).
In an experimental is possibleto see in face money probability thatP = ½ = 0,5 to have heads
, but what happen in another situation involved humans in high stressingcondition in really shorttimelikeseconds?
Can we observe 0,5 of probalitity in shenario A( WITH OUT CRIME ) or scenario B( WITH CRIME ).
And what can be the responsein different amygdala ( anatomic- metabolic ) of different subjects?
How a littledifference in anatomy- metabolic status can influencethis kind of situation?
Figure n 9 matematic logaritmic function :this approach can be used to monitoring amygdala functionality related
time ( in determinate stressingcondition )
Is possibleto produce a global function- index related amygdala and limbic level of activation ( metabolism,imaging
or other ) related an increased stressantstimulus? Basal and after high stressantstimulus and related different time
of exposition ( short,medium , long). Fig. 2
Function likeother phisio-pathological charactheristic like(fig 3,4) :

20. Fig. 10 renal function - times years
Figure 11 heart failure and mathematical function
Figure n. 12 quantized atomic energy ( HIGH STRESSANT STIMULY CAN BE CONSIDERED QUANTIZED )
FIGURE 13 KINETCS ZERO ORDER (pharmaco- toxicology ) ----- example from other scienceto be investigated :
amount and level of high stressantstimulus and timeof exposition

21. Why also nowadays in jurisdictional contestrelated some non voluntary crime arenot used really objective amygdala
functionality profileto be added to the classic forensicpsychiatric- psycologial criminology legal report?
Why with forensic laboratory assay arecurrently detected nanoparticleor DNA molecule but not profi led amygdala
full functionality ?
CHAPTER 6 conclusion :
Related to the reference produced is relevant in jurisdictional settingto introducenew psycologic-psychiatric-
neurology diagnostic methods ( imaging,metabolic status , anatomic abnormality,lesions or other ) to verify level of
activation of limbic system – amigdala (metabolism,substratelevel , anatomy , kinetics , differential activation
between cortical –amigdala and other characteristics as level of activations,imaging,nuclear medicine ) to better
objectivate subjectattitude to react in high stressingcondition in very limited time ( emotional storm conditions) .
Is possiblethattoday we can classify in exampleheart diseasegivingan numeric valuein some property like heart
ejection fraction or in diabetes blood glucoselevel and after glucosecharge ,renal functionality ,body temperature,
blood PH, electromiography,urofluxometria and many other parameter and we not have possibility to objective
set the amygdala basal level of activation thedifferent humans in really high stressingcondition timerelated ? (
imaginglikef MRI, PET , SPECT , anatomy, lesions, biochemistry,substrate,neurotrasmitters , blood flux rate , time
of response, basal and after high stressingcondition in restricted time and other useful parameter ).
To measure related different level of stressantingcondition ( amount ( fig.5) and kinetics ,saturation of the system
fig. 6 ) in restricted time in different humans make possibleto verify phisio-patologial responceor abnormality in
reaction.
A global index of amygdala functionality –activation level can be :
AMYGDALA func- activ –level INDEX = log function of A ( anatomic- imaging – abnormality – local pathology ) x B
( physiology abnormality :metabolic substrate, metabolism ) x C ( neuronal circuitconductivity- velocity of neuronal
circuits –difference from average ).
In our opinion in jurisdictional settings in somenon voluntary crime to verify the really objectiveamygdala
functionality profileto be added to the classic forensicpsychiatric- psycologial criminology legal reportis relevantand
crucial to add also amygdala and limbicsystemfunctionality instrumental –imaging – biochemical assay.
Not a prove but an objective data to be considered in contestualizyngthe frame of the facts .
In example In a car crash a diabetic driver whitblood glucoselevel at 450 mg / dl how can control his car ? and in this
situation whatwill be the profileof responsibility ?
In 1700-1800 periods physician notused to test patients blood glucoselevel but this safelifeparameter is currently
tested in every emergency patients without any problems .
The same cardiac artimia isnormally classified related the singlecell membrane channel abnormality ( K, NA, CA) .
Why amygdala nowadays in nottested likeother organ and system? In example cardiac,renal,respiratory function?

22. Concepts from other sciencelikebiochemistry,toxicology,kinetics,imagingand many other contribute to better
clarify someorganic situation thatcan be co- responsibleof serious consequences .
In human evolution , due to various factors likesocial,religiousor other , emotional system has not adeguately
investigated as other organ but Is time to Introducemethods to clear some relevant aspectin the emotive
management and failure.
clarifications
this article is produced without any diagnostic or therapeutic intent , only to produce new research hipotesys under a
pharmaco- toxicological –phisio pathological approach .
Other implication (moral,ethical,) arenot considered in this paper.
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