Possible causes of damage to corpus callosum

The human brain has a complex anatomy due to its highly complex functions. This astonishing organ acts as a control center by receiving , interpreting and directing sensory information throughout the body. The brain also contains numerous structures that has a multitude of functions. The following essay focuses on the four structures mentioned in the title. The essay is divided into four sections, each section has information about anatomy, significance and causes of damage to every structure.

The corpus callosum (CC) is the largest interconnecting white matter tract in the brain, containing some 200 million axons [47] J. Tomasch, Size, distribution, and number of fibres in the human corpus callosum, Anat Rec 119 (1) (1954), pp. 119-135. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (78)traversing the subcortical white matter (Tomasch et al., 1954).CC is a very thick bundle of nerve fibres containing both myleinated and unmyleinated axons. Early in the 20th century it was assigned the mere role of preventing the collapsing of two hemispheres. Myers and Sperry in 1950s attributed the function of transferal of information between two hemispheres.

Each hemisphere contains neurons which project callosal axons not only to homologous (homotopic) areas in the contralateral hemisphere but also to heterologous (heterotopic) areas. The corpus callosum is the most important commissure to connect the two hemispheres, not only by virtue of its size, but also due to the wealth of its neural connections. It is through these projections that information is shared between the two halves of the brain. Very little is known about the neural signals that pass between the hemispheres, but recent studies have used modern tract tracing techniques to determine precisely the sites of origin and termination of neurons which project across the corpus callosum. Using a retrograde tracer (horseradish peroxidase), Lomber was able to link the functional divisions of the cerebral cortex to fiber trajectory through the corpus callosum. The motor cortex sends fibers through the rostrum and genu of the corpus callosum. The adjacent somatosensory cortex projects fibers through the anterior half of the corpus callosum whereas axons arising from auditory regions pass through the posterior two-thirds of the corpus callosum and the dorsal splenium. Axons from the limbic cortex also help to form these regions of the corpus callosum. Finally, axons from visual cortices which occupy the greatest single fraction of the cortical mantle pass through the largest portion of the corpus callosum; the fibers are present throughout the splenium and extend well into the body and the anterior portion.

Significance of corpus callosum can be seen in coordinating the activities of two hemispheres. It does not allow patients to match up concepts they see in one eye with concepts in the other half of the brain. For instance , If the corpus collosum structure gets damaged, a patient might have trouble with coordinating their hands, preventing them from matching sensations on one hand with movement on the other, because the information doesn’t get to where it’s needed. Corpus callosum also plays a significant role in visual orientation (Pollmann et al., 1997). The most common focal structural abnormality in individuals (adolescents) who were born 33 weeks prior to their gestation was thinning/atrophy of the corpus callosum, particularly posteriorly, which was noted in 43% of preterm individuals (Santhouse et al.,2002). The corpus callosum is known to be especially vulnerable to adverse consequences of premature birth such as ischaemia, haemorrhage and sepsis, because of its longer myelogenetic cycle (Valk and Njiokiktjien, 1991) and also because of its position adjacent to the periventricular region which is one of the most common sites of preterm hemorrhage in preterm infants (Fawer et al., 1984 ; Thorburn et al., 1981).

These abnormalities of the corpus callosum may have functional significance. For example, follow-up studies of preterm infants have indicated that callosal abnormalities underlie poor performance on the Kaufman Assessment Battery for Children (K-ABC) (Kaufman and Kaufman, 1983), and on the simultaneous processing scale and performance subscale of the WISC-R (Wechsler, 1974) at age eight (Roth et al., 1993). In adolescence, preterm individuals have more neurological, adjustment and reading impairments than controls born at term (Stewart et al., 1999) and have poorer educational outcome (Botting et al., 1998). The corpus callosum contributes

to the representation of the contralateral visual field near the vertical meridian of the temporal retina in both split-chiasm and normal cats. This is probably due to the scarcity of direct retinotectal projections from this part of the retina and to their supplementation by corticotectal neurons influenced by the callosal afferents (Antonini et al., 1979). Significance of corpus callosum can also be understood by understanding the significance of atrophy of corpus callosum in a mixed elderly population. In the research conducted by Ryberg , Rostrup and others in 2008 it was found that atrophy of the CC areas correlated significantly with impairments of global cognitive as well as motor functions. The strongest correlation was found for motor function, where reductions in the total area of the CC, as well as of all sub regions, correlated significantly with impaired walking speed. Furthermore, the area of CC rostrum, genu, rostral body, and splenium were significantly smaller in the subgroups of patients with subjective gait difficulty. The areas of CC rostrum, genu, and isthmus also correlated significantly with global cognitive function as assessed with the MMSE score. Though the researchers found no evidence for association between CC atrophy and mood disturbance. The impact of CC atrophy on global cognitive impairment and motor function was significant even after correction for relevant confounders (age, gender, handedness). The role of corpus callosum in attentional processing is also a subject of argument . In past researches it has been suggested that the corpus callosum should be considered a component in the network of neural structures that underlie attentional control (Banich 2002). Also , a relationship between multiple sclerosis and corpus callosum atrophy is established by  Dietemann and others in 1988. Damage to corpus callosum fibres can even cause refractory epilepsy (Clarke et al., 2007) thus corpus callosotomy has been suggested as a mode of treatment for the same. A number of clinical reports have cited memory disturbances in surgical cases involving section of the corpus callosum (Clark et al., 1989).

Damaged Corpus callosum is a rare neurological condition. Agenesis of CC is widely researched on and a dearth of literature has been found on other possible causes of damage to CC. Prenatal alcohol exposure can lead to damaged CC (Kellerman 2008). It is been pointed out by Kellerman children with FAS and ARND have smaller corpus callosum than normal and in some cases it is almost nonexistent. Teresa Kellerman derived this information from the MRI images. Another research has highlighted the relationship of high marijuana use and damage to CC. Heavy marijuana use has well established long term consequences for cognition and mental health, but the effect on brain structure is less well understood. Arnone , Barrick , Chengappa and others in 2008 used an MRI technique that is sensitive to the structural integrity of brain tissue combined with a white matter mapping tractography technique to investigate structural changes in the corpus callosum . Mean diffusivity (MD) and fractional anisotropy (FA) were analysed within the corpus callosum. MD was significantly increased in marijuana users relative to controls in the region of the CC where white matter passes between the prefrontal lobes. This observation suggests impaired structural integrity affecting the fiber tracts of the CC and is in keeping with previous reports of altered and diversified activation patterns in marijuana users. There was a trend towards a positive correlation between MD and length of use suggesting the possibility of a cumulative effect of marijuana over time and that a younger age at onset of use may predispose individuals to structural white matter damage. Structural abnormalities revealed in the CC may underlie cognitive and behavioural consequences of long term heavy marijuana use ( Barrick , Arnone et al., 2008). A very important but rare kind of neurological disorder is ACC which can be due to number of causes like chromosome errors, inherited genetic factors, prenatal infections or injuries, prenatal toxic exposures, structural blockage by cysts or other brain abnormalities, and metabolic disorders ( The University of Maine – College of Education and Human Development – What is ACC ). CC is highly likely to be attacked in multiple sclerosis (multiple Sclerosis.org). In a research conducted in University’s free hospital in Netherlands by Valk, Ramaekers and Njiokiktjien in 1988 they found out that Pre- or perinatally acquired damage to CC may have a mainly vascular, obstructive or hypoxic-ischemic etiology, whereas endotoxins and exotoxins might also play a role. Early postnatally acquired CC damage in children is mostly of vascular or traumatic origin. In some instances the CC is thinned after chronic pressure. Children with acquired CC anomalies have signs of supposed Interhemispheric Disconnection (ID), which is partly responsible for their clinical syndrome of mental and motor retardation.


The hippocampus has been of great interest for its role in processing spatial memory, where synaptic plasticity has been studied as a unitary cellular form of memory formation for the past three decades (Nishiyama et al., 2006). The earliest description of the ridge running along the floor of the temporal horn of the lateral ventricle comes from the Venetian anatomist, Julius Caesar Aranzi (1587) who initially likened it to a silkworm, and then a sea horse. Today, the structure is called the hippocampus (Duvernoy , 2005) De Garengeot’s “cornu Ammonis” survives in the names of the three main histological divisions of the hippocampus: CA1, CA2 and CA3.

Anatomically hippocampus is an elaboration of the edge of cerebral cortex (Amaral and Lavenex, 2006). It can be distinguished as a one where the cortex narrows into a single layer of very densely packed neurons , which curls into a S shape. The structures that line the edge of the cortex make up the limbic system and includes the hippocampus. The hippocampus is the shape of a curved tube (Amaral and Lavenex, 2006) which has been analogized variously to a seahorse or a banana. It consists of ventral and dorsal portions both of which share similar composition but are parts of different neural circuits (Moser and Moser , 1998). In humans the portion of hippocampus near the base of the temporal lobe is much broader than the part at the top. The entorhinal cortex (EC), the greatest source of hippocampal input and target of hippocampal output, is strongly and reciprocally connected with many other parts of the cerebral cortex, and thereby serves as the main “interface” between the hippocampus and other parts of the brain. The superficial layers of the EC provide the most prominent input to the hippocampus, and the deep layers of the EC receive the most prominent output. Within the hippocampus, the flow of information is largely unidirectional, with signals propagating through a series of tightly packed cell layers, first to the dentate gyrus, then to the CA3 layer, then to the CA1 layer, then to the subiculum, then out of the hippocampus to the EC. Each of these layers also contains complex intrinsic circuitry and extensive longitudinal connections (Amaral and Lavenex, 2006).

The significance of hippocampus can be seen in memory. The research conducted in this field provides ample evidence for the same. Hippocampus plays a pivotal role in encoding and retrieving sequence of events that compose episodic memory (Fortin et al., 2002). The ability of humans, hippocampus underlies the ability to recall specific personal experiences (Vargha-Khadem et al., 1997). Hippocampal damage impairs memory for the order of a series of recently visited spatial locations (Kesner et al., 1992 and Chhiba et al., 1994). The role of hippocampus in declarative memory is also well established by now ( Tulving et al., 1996). It is generally accepted that the hippocampus is involved in the generation and recollection of episodic memories. However, not all experiences are remembered – it is mostly experiences that contribute to our understanding of the world that are remembered. The role of the hippocampus is to detect or extract the significant information for further memory consolidation from the less important, repetitive material that is already remembered. The hippocampus is involved in the ongoing comparison of cognitive expectations against reality for the purpose of maintaining accurate representation of reality that will aid future expectations (eg, Strange et al, 1999). In performing this process, the hippocampus constructs higher order or supramodal episodic representations that contain both stimulus and response information over time (Eichenbaum and Otto, 1993; Martin, Wiggs, Ungerleider & Haxby, 1996).

The hippocampus is a key structure in the detection of novelty or familiarity. Evidence indicates that activation along the anterior-posterior axis of the hippocampus reflects a distribution of stimulus novelty to familiarity. For instance, Strange et al (1999) report that anterior hippocampal regions respond to perceptual novelty, whereas posterior regions respond to stimuli that have response related familiarity. They propose that the anterior hippocampus registers mismatches of current stimulus information against an expected or predictive representation. When mismatches are identified and they have behavioural significance, greater attention and familiarity with the information engages posterior hippocampal regions. Furthermore, the activity along this hippocampal axis for the detection of novelty or familiarity may help to explain anterograde or retrograde amnesia. (Strange et al ., 1999) postulated that damage to the anterior hippocampus impairs novelty detection and episodic memory consolidation, which explains anterograde amnesia. Conversely, damage of the posterior hippocampus impairs recall of past experience, which explains retrograde amnesia (Strange et al, 1999).

There is a case to be made that hippocampal and parahippocampal regions are involved in detection of novelty, which subseqently or concurrently initiates more complex encoding strategies in frontal regions. The reports of Wagner et al (1998) and Brewer et al (1998) indicate that left prefrontal and parahippocampal regions are active during encoding and consolidation in an incidental memory task. Their task materials did not involve novelty and did not elicit activation in the hippocampus proper. It may be that the hippocampus is not directly involved in encoding or consolidation, but merely detects novelty and thereby initiates more complex evaluation, encoding, and consolidation processes. This interpretation is supported by a dissociation of frontal and hippocampal functions reported by Dolan and Fletcher (1997). They found that the left prefrontal cortex is engaged by changes in the content of linguistic category-exemplar encoding processes, implicating this brain area in the controlled transformation of auditory-verbal stimuli into meaningful information. On the other hand, left medial temporal lobe areas, including the hippocampus, were responsive to contextual novelty. The physical properties of the auditory-verbal stimuli were familiar; the novelty of the stimuli was related to the encoded associations of the verbal information – the medial temporal lobe structures responded to the associative or contextual novelty of the material, not simply the physical attributes of the stimuli (Dolan and Fletcher, 1997). The hippocampal detection of novelty may initiate frontal executive processes that alter encoding strategies. Hippocampus is also found to be one of the precipitating causes of diseases like epilepsy (Uesugi et al., 2002) and schizophrenia (Harrison e al.,2004).

A close association of hippocampus and amnesia and hippocampus and dementia is also seen. In fact a possible role of Hippocampal dysfunction in schizophrenic symptomatology is put forward by Daniel. J. Luchins in 2003. It is argued that such behaviors may have a neurobiology similar to schedule-induced behaviors or incentive-conditioned behaviors described in animal models, which involve the hippocampus, nucleus accumbens, and the neurotransmitter dopamine. Some scientists investigated the role of baseline hippocampal volume on later clinical emergence of dementia in a group of older, non-demented depressed individuals. Small left hippocampal volume was significantly associated with later dementia (hazard ratio=2.762). Also a close association between Hippocampal lesions and schizophrenia has also been reported. Parkinson’s disease also seem to be influenced by hippocampus. The research done by Bruck and others in 2003 has proven that Non-medicated, non-demented patients with early stage Parkinson’s disease show hippocampal and prefrontal atrophy. Impaired memory is related to hippocampal atrophy, whereas sustained attention is related to prefrontal atrophy. Hippocampal atrophy plays an important role in Alzheimer’s disease (Lakkso, 1996), however, the research concluded that volumetric Hippocampal atrophy is highly sensitive indicator in Alzheimer’s disease. A recent study has pointed out the significance of hippocampus in hyposmia in Parkinson’s disease with PET (positron Emission Tomography).

Furthermore, Eichenbaum (1997) proposes that the hippocampal inputs into associative memories can influence the latter retrieval cues for the memories. The quality or amount of episodic information and the manner of integration of that information into the associative memory networks will affect what type and how many cues can elicit memories and how much of the memories they elicit. For instance, an interleaved encoding of episodic with various multimodal or semantic representations can better facilitate retrieval of the whole episode and it’s specific representations (Eichenbaum, 1997). In general, the interactions of the cortex and parahippocampal structures serve to integrate and hold multimodal and semantic representations, while the hippocampus serves as a comparator and organiser of these representations (Dusek & Eichenbaum, 1997; Eichenbaum, Schoenbaum, Young & Bunsey, 1996; Goldman-Rakic, 1996). Implications of Hippocampal functions can be seen in PTSD (Post Traumatic Stress Disorder) as well. Damage to the anterior portion of the hippocampus in PTSD can affect the ability to accurately develop supramodal, episodic representations and accurately evaluate and incorporate new information into episodic memory. This lack of accuracy in episodic memory will continually generate mismatch activity in the hippocampus that will initially hyper arouse the BIS (Behavioural Inhibition system) and initiate excess stress reactions. These responses may attempt to habituate, but cannot do so due to impaired episodic memory evaluation and consolidation, which leads to cognitive, emotional, and endocrine exhaustion.

In this manner, PTSD patients are unable to incorporate new information after their trauma and the most recent episodic memories that were consolidated remain traumatic and continue to affect expectations of the world. This fundamentally alters their world view and psychic life.

Causes of damage to hippocampus has been attributed to various factors. It has been opined by Booze and Mactutus in 2005 that “developmental exposure to organic lead causes permanent Hippocampal damage.” The long-term consequences of neonatal exposure to triethyl lead, the putative neurotoxic metabolite of the anti-knock gasoline additive tetraethyl lead, were examined with respect to central nervous system (CNS) development in the experiment. A study on neurotrauma has revealed that repeated traumatic brain injury may result in cumulative damage to Hippocampal cells of the brain (Slemmer et al., 2002). Bacteremia and systemic complications are frequently associated with pneumococcal meningitis and, in approximately half of all fatal cases, are judged to be the primary causes of death (Samuelsson et al., 2005). Apoptosis in the dentate gyrus of hippocampus is an important histopathological finding in patients dying from bacterial meningitis (Bruck et al., 1998), and in experimental meningitis, hippocampal apoptosis has been associated with the development of learning deficits (Grandgirard et al., 2006). National institute of alcohol abuse and alcoholism has done a pioneering research to know more about the causes behind Hippocampal damage. Prenatal exposure to alcohol can result in fetal alcohol syndrome (FAS), characterized by growth retardation, facial dysmorphologies, and a host of neurobehavioral impairments ( Hannigan and Berman , 2000, p.94) . Neurobehavioral effects in FAS, and in alcohol-related neurodevelopmental disorder, include poor learning and memory, attentional deficits, and motor dysfunction (Hannigan and Berman , 2000, p.94). Neurobehavioral studies show that animals exposed prenatally to alcohol are impaired in many of the same spatial learning and memory tasks sensitive to hippocampal damage, including T-mazes, the Morris water maze, and the radial arm maze. Considered together, these observations demonstrate that prenatal exposure to alcohol can result in abnormal hippocampal development and function (Hannigan and Berman , 2000, p.94). Researchers have found that marijuana changes the way in which sensory information gets into and is acted on by the hippocampus. Investigations have shown that marijuana suppresses neurons in the information-processing system of the hippocampus. In addition, researchers have discovered that learned behaviors, which depend on the hippocampus, also deteriorate (National Institute of Drug Abuse). Studies investigating the effect of stress on hippocampus are done in a molecular level or at a hormonal level. Behavioral stress has detrimental effects on subsequent cognitive performance in many species, including humans ( Roy et al., 1996). The effects of stress on subsequent long term potentiation and enhancement of long term depression appear to be mediated through the activation of the NMDA subtype of glutamate receptors by the researchers. So it can be concluded that behavioral stress modifies hippocampal plasticity.

Thus it can be concluded that be due to developmental exposure to lead, neurotrauma, bacteremia and systematic complications, prenatal exposure to alcohol, drug abuse (marijuana in particular) and finally behavioral stress are the main causes of damage to hippocampus apart from a major head injury or accident.


The amygdala, an almond-sized and -shaped brain structure, has long been linked with a person’s mental and emotional state. Associated with a range of mental conditions from normalcy to depression to even autism, the amygdala has become the focal point of numerous research projects ( Black, 2001, p.15) .

According to Price , Russchen and Amaral (1987, p.279)The amygdala is a complex mass of gray matter buried in the anterior-medial portion of the temporal lobe, just rostral to the hippocampus. It comprises multiple, distinct subnuclei and is richly connected to nearby cortical areas on the medial aspect of the hemispheric surface. The amygdala contains three functional subdivisions, each of which has a unique set of connections with other parts of the brain. The medial group of subnuclei has extensive connections with the olfactory bulb and the olfactory cortex. The basolateral group, which is especially large in humans, has major connections with the cerebral cortex, especially the orbital and medial prefrontal cortex. The central and anterior group of nuclei is characterized by connections with the brainstem and hypothalamus and with visceral sensory structures, such as the nucleus of the solitary tract.

The amygdala thus links cortical regions that process sensory information with hypothalamic and brainstem effector systems. Cortical inputs provide information about highly processed visual, somatic sensory, visceral sensory, and auditory stimuli. These pathways from sensory cortical areas distinguish the amygdala from the hypothalamus, which receives relatively unprocessed visceral sensory inputs. The amygdala also receives sensory input directly from some thalamic nuclei, the olfactory bulb, and the nucleus of the solitary tract in the brainstem.

Significance of amygadala is established by physiological studies which has confirmed convergence of sensory information. It is widely accepted that the amygdala plays a role in emotion-related brain function (Le doux , 1994). However,its precise role in emotion-related processes is still under investigation.

Thus, many neurons in the amygdala respond to visual, auditory, somatic sensory, visceral sensory, gustatory, and olfactory stimuli. Moreover, highly complex stimuli (faces, for instance) are often required to evoke a response. In addition to sensory inputs, the prefrontal cortical connections of the amygdala give it access to more cognitive neocortical circuits, which integrate the emotional significance of sensory stimuli and guide complex behavior.Projections from the amygdala to the hypothalamus and brainstem allow it to play an important role in the expression of emotional behavior by influencing activity in both the somatic and visceral motor efferent systems (Price et al., 1987, p.279).

Evidence from many different laboratories using a variety of experimental techniques and animal species indicates that the amygdala plays a crucial role in conditioned fear and anxiety, as well as attention ( Davis , 1997 , p. 382). Many amygdaloid projection areas are critically involved in specific signs used to measure fear and anxiety ( Davis , 1997 , p. 382). Electrical stimulation of the amygdala elicits a pattern of behaviors that mimic natural or conditioned fear ( Davis , 1997 , p. 382). Lesions of the amygdala block innate or conditioned fear, as well as various measures of attention, and local infusions of drugs into the amygdala have anxiolytic effects in several behavioral tests. N-methyl-D-aspartate (NMDA) receptors in the amygdala may be important in the acquisition of conditioned fear, whereas non-NMDA receptors are important for the expression of conditioned fear. The peptide corticotropin-releasing hormone appears to be especially important in fear or anxiety and may act within the amygdala to orchestrate part of the fear reaction ( Davis , 1997 , p. 382). As mentioned by Drevets A reciprocal relationship exists between persistent pain and negative affective states such as fear, anxiety, and depression. Accumulating evidence points to the amygdala as an important site of such interaction. Whereas a key role of the amygdala in the neuronal mechanisms of emotionality and affective disorders has been well established, the concept of the amygdala as an important contributor to pain and its emotional component is still emerging. Dependent on environmental conditions and affective states, the amygdala appears to play a dual facilitatory and inhibitory role in the modulation of pain behavior and nociceptive processing at different levels of the pain neuraxis (Davis , 1997 , p.382). It is also widely accepted that the amygdala enhances memory for emotional informationthrough its connections with the hippocampal formation (see review by McGaugh, 2000). Lesions of the basolateral nuclei of the amygdala,or its output pathways in the stria terminalis, canprevent emotion-enhanced memory (McGaugh,2000), and patients with amygdalar damage fail to show normal enhancement of memory by emotionally arousing stimuli (LaBar, Gatenby,Gore, LeDoux, & Phelps, 1998). In addition to enhancing memory consolidation,

the amygdala enhances sensory processing through its reciprocal connections with sensory cortical areas (Amaral, Behniea,&Kelly, 2003). The studies of Kluver and Bucy also significantly elucidated the role of the amygdala in social behavior. Amgdala-lesioned monkeys show

impaired facial expression and social withdrawal.Human patients with bilateral amygdalar damage show impaired identification of facial expressions; for example, such patients rated people with negative faces as more approachable and trustworthy than healthy controls did but had nonimpairment in judging verbal descriptions of people (Adolphs, Tranel,&Damasio, 1998). However, current views posit that the amgydala influences social behavior only so far as it signals the safetyof social stimuli (Amaral et al., 2003) and helps modulate emotional responses to ensure that they are appropriate to the social context (Bachevalier & Malkova, 2006). Functional magnetic resonance imaging (fMRI) studies of

subjective emotion have furthermore suggested a temporally limited role of the amygdala in subjective emotion (Garrett & Maddock, 2006). There is some debate about whether the amygdala directly mediates mood states. A

likely hypothesis is that the ongoing interaction of the amygdala with prefrontal modulatory regions and emotional response output regions

such as the striatumand insula, lead to subjective emotion and mood states. For example, the amygdala influences how events are perceived, the way memories are encoded, and how stimuli are associated with emotional responses. Amygdala also has a role in the etiology and progression of Bipolar disprder which is complex,and includes the interaction with multiple brain regions (Garett and King , 2008, p.1285). The amygdala appears to play a role in binge drinking, being damaged by repeated episodes of intoxication and withdrawal (Stephens and Duka , 2008 , p.3169).

Patients Alcoholism is associated with dampened activation in brain networks responsible for emotional processing, including the amygdala (Harris et al., 2009 , p.1880).

Patients who suffer from accidents or disesases also tend to damage their amygdala. The amygdala is no different from other regions of the brain in terms of its vulnerability to infection . Any bacterium or virus that penetrates the blood-brain barrier (certain forms of meningitis) can infect the amygdala, but its not likely.There is an interesting route for infection of the amygdala via the nose. With a chronic stress, neurons in the amygdala grow, they become larger,” says McEwen. “And there’s evidence that in depressive illness the amygdala may even become larger, and it certainly becomes more active.” So, after exposure to chronic stress, if the cells in in our amygdala are growing, “we may have all sorts of anxieties and anger and fear. So we may have generalized anxieties as a result of this.” It has been put forward that children with classic congential adrenal hyperplasia have decreases amygdalar volume ( Merker et al., 2003 , p.1760).

There is an interesting notion called “amygdala theory of autism” given by Cohen and Ring in 1996. They have proven their point by giving evidence of amygdalar abnormalty in autism through postmortem evidences, animal model of autism, similarities bettween autists and patirnts with amygdalotomy, effects of temporal lobe tubers , structural neuroimaging and functional neuroimaging. The degree of loss of dopamine-containing neurons in the substantia nigra pars compacta was related to the duration of the disease, and the cell loss followed a strict order

Substantia Nigra

The substantia nigra is a brain structure located in the mesencephalon (midbrain). Substantia nigra is Latin for “black substance”, as parts of the substantia nigra appear darker than neighboring areas due to high levels of melanin in dopaminergic neurons. The s

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